Continuing health education

Melasma

Mon, 27 Nov 2023 05:29:46 GMT

Unlocking the Secrets to Radiant Skin: A Comprehensive Guide to Treating Melasma Naturally and Effectively

Melasma is a common skin problem caused by brown to gray-brown patches on the face. Most people get it on their cheeks, chin, nose bridge, forehead, and above the upper lip. It is more common in women than men. Pregnancy is a common cause of melasma. It also affects woman taking oral contraceptives and hormones.

Etiologic factors include genetic influences, ultraviolet (UV) radiation, pregnancy, hormonal therapies, cosmetics, phototoxic drugs, and antiseizure medications.

Melasma stimulates melanocytes by the female sex hormones estrogen and progesterone, producing more melanin pigments when the skin is exposed to the sun

Sunlight Exposure

UV radiation can cause lipids peroxidation in cellular membranes, resulting in free radicals which could stimulate melanocytes to produce excess melanin.

Sunscreens that block UV-B radiation (290-320 nm) do not block the longer wavelengths of UV-A and visible radiation (320-700 nm) which also stimulate melanocytes to produce melanin .

Hormonal Influences

Hormones may play a role in developing melasma in some individuals.

The mask of pregnancy is known to occur in obstetric patients. The exact mechanism is unknown. Estrogen, progesterone, and melanocyte-stimulating hormone levels are normally increased during the third trimester of pregnancy and may be a factor.
Patients with melasma who are nulliparous have no increased levels of estrogen or MSH but show elevated levels of estrogen receptors within the lesions. In addition, melasma with estrogen- and progesterone-containing oral contraceptive pills and diethylstilbestrol treatment for prostate cancer have been observed.
A woman who is postmenopausal and given progesterone may develop melasma, while those who are given estrogen alone do not; this implicates progesterone as playing a primary role in the development of melasma.

Treatment

Sunscreen
Topical depigmenting agents :

-Hydroquinone:

Contraindications

History of sensitivity or allergic reaction to hydroquinone or any ingredient in the formulation.

Warnings/Precautions

Warnings

Cosmetic Effects

May produce undesired cosmetic effects (e.g., excessive skin bleaching) if not used as directed. Clinician should be familiar with the use, adverse effects, precautions, and contraindications before prescribing or dispensing the drug.

Exposure to Sunlight or Ultraviolet Light

Exposure to sunlight or ultraviolet light may cause repigmentation of bleached areas. [ref] Avoid unnecessary exposure to sunlight during and after therapy.

Sunscreen agents and/or protective clothing recommended if preparations which do not contain sunscreen are applied during the daytime. [ref] Preparations containing sunscreen may provide sufficient protection from sunlight.

After reduction of hyperpigmentation and during maintenance therapy, continue the use of sunscreen agents and/or protective clothing.

Sensitivity Reactions

Sulfite Sensitivity

Some formulations contain sulfites, which may cause allergic-type reactions (including anaphylaxis and life-threatening or less severe asthmatic episodes) in certain susceptible individuals.

Other Sensitivity Reactions

Contact dermatitis reported. If contact dermatitis occurs, discontinue immediately and contact a clinician.

Major Toxicities

Rarely, ochronosis (gradual blue-black darkening of the skin) and colloid milium reported with chronic use (up to 8 years) of 5% hydroquinone cream. If affected skin changes to a blue-black color, discontinue immediately and contact a clinician.

General Precautions

Topical Use

For external use only. Not for topical application in the eyes, ears, or mouth; to cut, abraded, or sunburned skin; after shaving or using a depilatory agent; or over miliaria rubra (prickly heat).

Dermatologic Effects

Possible local skin irritation (e.g., burning, stinging, mild erythema). Dryness and fissuring of paranasal and infraorbital areas reported.

Use of Fixed Combinations

When hydroquinone is used in fixed combination with topical sunscreens (e.g., dioxybenzone, oxybenzone, and padimate), fluocinolone, or retinoids (e.g., tretinoin), consider the cautions, precautions, and contraindications associated with these agents.

Specific Populations

Pregnancy

Category C.

Lactation

Not known if topical hydroquinone is distributed into milk. [ref] Caution advised if topical hydroquinone is used.

Pediatric Use

Safety and efficacy of hydroquinone preparations not established in children <12 years of age.

Safety and efficacy of the fixed-combination hydroquinone, fluocinolone, and tretinoin cream not established in pediatric patients of any age.

-Rucinol:

https://pubmed.ncbi.nlm.nih.gov/17388924/

Cat-scratch disease

Mon, 27 Nov 2023 04:49:09 GMT

Explore the Depths of Cat-Scratch Disease

Definition: a benign, self-limiting infectious disease that is transmitted mainly by cats (via scratching, biting, or licking)
Epidemiology: predominantly affects children and adolescents
Pathogen: Bartonella henselae (gram negative, aerobic bacillus)
Clinical features
General: malaise, loss of appetite, fever
Localized
One or more 5–10 mm large, erythematous, nontender cutaneous papules or vesicles develop approx. 3–10 days after exposure at the site of inoculation.
Swollen, tender lymph nodes 7–60 days following exposure
Develops as primary lesions disappear
Usually unilateral, occasionally suppurative
Most commonly involves lymph nodes of axillae, neck, or groin (nearest the site of inoculation)
Resolves after 2–4 months
In immunocompromised individuals (e.g., patients with HIV) Bacillary angiomatosis (red-purple papules that bleed easily)
Hepatic peliosis: a benign vascular condition characterized by multiple blood-filled cysts and vascular sinuses in the liver
Can be asymptomatic or cause abdominal pain, jaundice, and/or liver failure
In rare cases, cysts may rupture, causing intraperitoneal hemorrhage
Bacteremia and endocarditis
Diagnostics
Bacterial culture from blood, swabs, or lymph node aspirate
Antibody testing
Histological study
Warthin-Starry staining of the involved lymph node may show clusters of rod-shaped bacteria.
H&E staining of cutaneous lesions may show necrotizing granuloma formation and neutrophilic infiltrate.
Differential diagnosis: Kaposi sarcoma (has lymphocytic infiltrate as opposed to bacillary angiomatosis)
Treatment
Mild or moderate cases: azithromycin (5-day course) to decrease lymphadenopathy and the duration of illness
In the case of persistent and/or disseminated disease (e.g., bacillary angiomatosis): erythromycin OR doxycycline
In the case of CNS involvement or endocarditis: rifampicin PLUS either erythromycin OR doxycycline

References

GREER WER, KEEFER CS. Cat-scratch fever; a disease entity. N Engl J Med. 1951 Apr 12;244(15):545–548. [ PubMed ] [ Google Scholar ]
SPAULDING WB, HENNESSY JN. Cat scratch disease. A study of eighty-three cases. Am J Med. 1960 Apr;28:504–509. [ PubMed ] [ Google Scholar ]
FOWLER RS, BAILEY JD. Cat scratch disease in childhood. Can Med Assoc J. 1961 Jun 17;84:1365–1368. [ PMC free article ] [ PubMed ] [ Google Scholar ]
SMALL WT, SNIFFEN RC. Nonbacterial regional lymphadenitis (cat-stratch fever); evaluation of surgical treatment. N Engl J Med. 1956 Nov 29;255(22):1029–1033. [ PubMed ] [ Google Scholar ]
McGOVERN JJ, KUNZ LJ, BLODGETT FM. Nonbacterial regional lymphadenitis (cat-scratch fever); an evaluation of the diagnostic intradermal test. N Engl J Med. 1955 Feb 3;252(5):166–172. [ PubMed ] [ Google Scholar ]
DANIELS WB, MacMURRAY FG. Cat-scratch disease; nonbacterial regional lymphadenitis. AMA Arch Intern Med. 1951 Dec;88(6):736–751. [ PubMed ] [ Google Scholar ]
CASSADY JV, CULBERTSON CS. Cat-scratch disease and Parinaud's oculoglandular syndrome. AMA Arch Ophthalmol. 1953 Jul;50(1):68–74. [ PubMed ] [ Google Scholar ]
MARGILETH AM. Cat scratch disease as a cause of the oculoglandular syndrome of Parinaud. Pediatrics. 1957 Dec;20(6):1000–1005. [ PubMed ] [ Google Scholar ]
LEVITT JM. The oculoglandular form of cat-scratch disease. J Am Med Assoc. 1957 Dec 14;165(15):1955–1956. [ PubMed ] [ Google Scholar ]
DANIELS WB, MACMURRAY FG. Cat scratch disease; report of one hundred sixty cases. J Am Med Assoc. 1954 Apr 10;154(15):1247–1251. [ PubMed ] [ Google Scholar ]
DANIELS WB, MACMURRAY FG. Cat scratch disease; nonbacterial regional lymphadenitis: a report of 60 cases. Ann Intern Med. 1952 Oct;37(4):697–713. [ PubMed ] [ Google Scholar ]
PHILPOTT OS, WOODBURNE AR, PHILPOTT JA., Jr Cat-scratch fever. Rocky Mt Med J. 1955 Sep;52(9):789–790. [ PubMed ] [ Google Scholar ]
KALTER SS, PRIER JE, PRIOR JT. Recent studies on the diagnosis of cat scratch fever. Ann Intern Med. 1955 Mar;42(3):562–573. [ PubMed ] [ Google Scholar ]
BELBER JP, DAVIS AE, EPSTEIN EH. Thrombocytopenic purpura associated with cat-scratch disease; response of cat-scratch disease to steroid hormones. AMA Arch Intern Med. 1954 Aug;94(2):321–325. [ PubMed ] [ Google Scholar ]
JIM RT. Thrombocytopenic purpura in cat-scratch disease. JAMA. 1961 Jun 24;176:1036–1037. [ PubMed ] [ Google Scholar ]
DEVITO JJ. Cat scratch disease. J Fla Med Assoc. 1954 Mar;40(9):638–640. [ PubMed ] [ Google Scholar ]
PELNER L. Cat-scratch disease or benign lymphoreticulosis; a disease to be ruled out in the differential diagnosis of Hodgkin's disease. Am Pract Dig Treat. 1955 Aug;6(8):1164–1166. [ PubMed ] [ Google Scholar ]
GUTTMAN PH. Pathology of cat-scratch disease. Calif Med. 1955 Jan;82(1):25–31. [ PMC free article ] [ PubMed ] [ Google Scholar ]
TURNER W, BIGLEY NJ, DODD MC, ANDERSON G. Hemagglutinating virus isolated from cat scratch disease. J Bacteriol. 1960 Oct;80:430–435. [ PMC free article ] [ PubMed ] [ Google Scholar

Serotonin syndrome

Sat, 25 Nov 2023 20:43:12 GMT

Serotonin Syndrome Alert: Recognizing Early Signs and Ensuring Timely Intervention

Serotonin syndrome is a potentially life-threatening condition caused by serotonergic overactivity due to the use of serotonergic drugs. It can be caused by a therapeutic dose or overdose of a serotonergic drug, concomitant use of multiple serotonergic drugs, or interactions with CYP450 inhibitors. Onset is typically rapid, occurring within 24 hours of drug administration. Classic features include autonomic dysfunction, neuromuscular excitability (e.g., rigidity, hyperreflexia), and altered mental status. Increased neuromuscular activity can also lead to hyperthermia. Serotonin syndrome is a clinical diagnosis but laboratory studies may be used to assess for complications such as rhabdomyolysis. Management involves discontinuation of serotonergic drugs and treatment of features of serotonin syndrome (e.g., agitation, hyperthermia). In most cases, symptoms resolve within 24 hours of cessation of serotonergic drugs. In moderate to severe cases, pharmacological treatment with cyproheptadine may be indicated. Patients with features of severe disease, e.g., life-threatening hyperthermia, may also require sedation and intubation .

Serotonergic drugs

Antidepressants (e.g., MAOIs, SSRIs, SNRIs, tricyclic antidepressants, vortioxetine, vilazodone, trazodone)
Anxiolytics (e.g., buspirone)
Anticonvulsants (e.g., valproate)
Opioids (e.g., tramadol, meperidine)
NMDA receptor antagonists (e.g., dextromethorphan)
5-HT3 receptor antagonists (e.g., ondansetron)
Serotonin receptor agonists (e.g., triptans, ritonavir)
Antibiotics (e.g., linezolid)
Herbal supplements (e.g., St. John's wort, ginseng, tryptophan)
Recreational stimulants (e.g., MDMA, cocaine)

Risk factors

Concurrent use of:
Two or more serotonergic drugs (e.g., an MAOI with an SSRI)
One or more serotonergic drug with certain CYP450 inhibitors (e.g., ciprofloxacin)
Switching from one serotonergic drug to another without tapering
Accidental or intentional overdose
Patient-specific pharmacokinetic and/or pharmacodynamic factors

Clinical features

Symptom progression :

Onset : acute, typically within 24 hours of administration of the causative drug
Resolution : rapid, typically within 24 hours of treatment initiation

Presentation :

Classic triad:

Autonomic dysfunction
Diaphoresis
Tachycardia
Hypertension
Mydriasis
Neuromuscular excitability: can lead to hyperthermia
Hyperreflexia
Myoclonus
Clonus
Horizontal ocular clonus
Hypertonicity
Rigidity (especially in the lower extremities)
Altered mental status
Delirium
Psychomotor agitation
Coma

Other features:

Nausea, diarrhea, vomiting
Anxiety
Hypotension (due to MAOI poisoning)
Seizure

HAHA! Serotonin syndrome is no joke: H yperthermia, A utonomic dysfunction, H yperreflexia, A ltered mental status

To differentiate between serotonin syndrome and other drug-induced hyperthermia conditions, remember that only SErotonin Shakes your Extremities (myoclonus and hyperreflexia, mostly of the lower limbs ).

Diagnostics

General principles

Serotonin syndrome is a clinical diagnosis.
Diagnosis is made based on diagnostic criteria, e.g., Hunter serotonin toxicity criteria.
Laboratory studies may be used to assess for complications related to muscle rigidity and hyperthermia.

Diagnostic criteria

Presence of any of the following in patients with exposure to ≥ 1 serotonergic drug :

Spontaneous clonus
Inducible clonus or ocular clonus plus ≥ 1 of the following:
Agitation
Diaphoresis
Hypertonia and temperature > 38°C (100.4°F)
Tremor and hyperreflexia

Laboratory studies

BMP
↑ Creatinine in acute kidney injury
↓ Bicarbonate in metabolic acidosis
CBC: ↓ platelets, ↓ Hb, ↑ D-dimer, ↑ aPTT, and ↑ PT in DIC
↑ CPK in rhabdomyolysis
Liver chemistries: ↑ transaminases

Management

All patients

The goal of management is the stabilization of vital signs.

Discontinue all serotonergic drugs immediately.
Provide supportive care: e.g., oxygen therapy, IV fluid therapy
Give symptom-specific treatments.
Determine severity: For moderate to severe and/or refractory cases, consider treatment with an antidote.
Mild: tachycardia, hyperreflexia, shivering, diaphoresis, mydriasis, tremor
Moderate: agitation, hyperthermia < 40°C (104°F), clonus, diarrhea
Severe: hemodynamic instability, agitated delirium, muscle rigidity, hyperthermia ≥ 40°C (104°F), multiorgan failure

Symptom-specific management

Agitation and excessive muscle activity : Treat with benzodiazepines.
Mild symptoms: e.g., low-dose diazepam DOSAGE (off-label)
Moderate to severe symptoms: higher starting dose, e.g., diazepam DOSAGE (off-label) and repeat doses as needed
Hyperthermia : Initiate cooling measures, e.g., by reducing ambient temperature, applying cooling blankets or ice packs, administering cold IV fluids.
Autonomic instability : Use short-acting or titratable medications, as rapid changes in blood pressure and heart rate are common.
Give antihypertensive treatment.
Short-acting agents, e.g., esmolol, nitroprusside

Treat MAOI-induced hypotension or shock.
Titratable vasopressors, e.g., norepinephrine

Avoid physical restraints, as they can lead to worsening hyperthermia and lactic acidosis.

Moderate to severe and/or refractory cases

Consider treatment with 5-HT2A receptor antagonists: cyproheptadine DOSAGE (off-label)
Temperature > 41.1°C: Sedate, paralyze, and intubate patients.
Use nondepolarizing NMJ blocker as paralytic agent for intubation, e.g., rocuronium.
See “Endotracheal intubation” for preparation and procedure.

Rule out anticholinergic syndrome prior to administration of cyproheptadine, as cyproheptadine can worsen anticholinergic syndrome.

Avoid bromocriptine and dantrolene, as bromocriptine may worsen symptoms of serotonin syndrome and dantrolene has not been shown to be effective.

Agents other than cyproheptadine, e.g., chlorpromazine, are not currently recommended for the treatment of serotonin syndrome .

Staphylococcal diseases

Sat, 11 Nov 2023 19:12:34 GMT

Staphylococcal diseases

The Staphylococci are gram-positive, spherical-shaped bacteria that form clusters and are commonly found on the skin and mucous membranes. Clinically, the most important species include Staphylococcus aureus and Staphylococcus epidermidis , which are categorized according to their coagulase activity.

S. aureus is coagulase positive and expresses several virulence factors which support evasion of the host immune response.

S. epidermidis is coagulase negative and is usually less virulent, although it can evade the host immune system by forming and subsequently hiding in a biofilm.

S. aureus is commonly responsible for many localized infections (e.g., folliculitis, cervical lymphadenopathy) and also severe organ infections in the setting of bacteremia (e.g., endocarditis, osteomyelitis). As a toxin producer, S. aureus can cause food poisoning (see Staphylococcal food poisoning) and, in severe cases, life-threatening diseases such as staphylococcal scalded skin syndrome (SSSS) or toxic shock syndrome (TSS). Methicillin-resistant S. aureu s (MRSA), in particular, poses a major threat to both immunocompromised and multimorbid patients and is a considerable challenge to hospital hygiene.

S. epidermidis is mostly responsible for foreign body infections caused by, for example, contaminated peripheral lines or prosthetic joints. The treatment of choice is anti-staphylococcal penicillins (e.g., oxacillin, flucloxacillin) or first and second-generation cephalosporins..

Treatment :

Staphylococcus aureus

Anti-staphylococcal penicillins: oxacillin , flucloxacillin
First and second generation cephalosporins
In case of penicillin allergy: clindamycin
MRSA: drugs of last resort such as vancomycin and linezolid

Coagulase-negative staphylococcus (particularly S. epidermidis )

Methicillin-sensitive: oxacillin, nafcillin, or cefazolin
Methicillin-resistant: vancomycin or daptomycin
Second-line treatment (if susceptible): levofloxacin and rifampici n

References

Tong SYC, Davis JS, Eichenberger E, Holland TL, Fowler VG. Staphylococcus aureus Infections: Epidemiology, Pathophysiology, Clinical Manifestations, and Management. Clin Microbiol Rev. 2015; 28(3): p.603-661. doi: 10.1128/cmr.00134-14 . | Open in Read by QxMD

Xu SX, McCormick JK. Staphylococcal superantigens in colonization and disease. Frontiers in Cellular and Infection Microbiology. 2012; 2. doi: 10.3389/fcimb.2012.00052 . | Open in Read by QxMD

Ghasemian A, Najar Peerayeh S, Bakhshi B, Mirzaee M. The Microbial Surface Components Recognizing Adhesive Matrix Molecules (MSCRAMMs) Genes among Clinical Isolates of Staphylococcus aureus from Hospitalized Children.. Iranian journal of pathology. 2015; 10(4): p.258-64. pmid: 26351495. | Open in Read by QxMD

Source: " ID#: 11155 ", CDC/ Matthew J. Arduino, DRPH, Centers for Disease Control and Prevention (CDC) licensed under Public Domain

Source: " ID#: 18168 ", CDC/ National Institute of Allergy and Infectious Diseases (NIAID), Centers for Disease Control and Prevention (CDC) licensed under Public Domain

Visual assessment of melanoma

site-X7cQHw — Tue, 28 Mar 2023 09:27:40 GMT

Visual assessment of melanoma

Melanoma is a type of skin cancer that develops in the cells that produce melanin, which is the pigment that gives color to the skin, hair, and eyes. Melanoma can occur anywhere on the body but most commonly develops on areas that are exposed to the sun, such as the face, neck, arms, and legs.

Melanoma is usually curable if it is detected and treated early. However, if it is not diagnosed and treated in its early stages, melanoma can spread to other parts of the body and become life-threatening. Risk factors for melanoma include a history of sunburns, a family history of melanoma, having fair skin, and having a large number of moles or atypical moles.

The ABCDE criteria for melanoma :

Are a set of visual signs that can help identify suspicious moles or lesions that may be cancerous. The criteria are as follows:

A - Asymmetry: One half of the mole or lesion does not match the other half.

B - Border irregularity: The edges of the mole or lesion are not smooth, but rather uneven or notched.

C - Color variation: The mole or lesion has different colors or shades within it, such as brown, black, white, red, or blue.

D - Diameter: The mole or lesion is larger than 6 mm (about the size of a pencil eraser).

E - Evolving: The mole or lesion is changing in size, shape, or color.

The additional features that can help diagnose melanoma and are known as the 'CRETERA' criteria:

C - Color variegation: different colors or shades of the same color within the mole or lesion

R - Regular shape: the lesion should have a round or oval shape

E - Elevated: the lesion should be raised or elevated above the skin

T - Texture: the lesion should have an irregular texture or feel uneven to the touch

E - Enlarging: the mole or lesion is getting larger in size over time

R - Regression: part of the lesion is disappearing or fading away

A - Age: new lesions in people over 50 years of age are more suspicious for melanoma.

It's important to note that not all melanomas exhibit all of these signs, and some melanomas may not exhibit any of them.

The additional visual criteria for assessing the risk of melanoma include:

The "ugly duckling sign": a lesion that is substantially different from the others in a patient with multiple pigmented lesions may represent melanoma. This sign has a sensitivity of up to 90% for melanoma.

Palpable nodularity: this often corresponds with vertical growth of a melanoma and increases metastatic risk.

Breslow depth: this is the distance from the epidermal granular cell layer to the deepest visible melanoma cells and is the most important prognostic indicator in malignant melanoma.

Biopsy consideration: benign pigmented lesions are usually asymptomatic, and biopsy should be considered for moles that itch, bleed, or are associated with local sensory symptoms (e.g., tingling).

Lichen Sclerosus(affects the genital and anal regions)

Tue, 28 Mar 2023 09:23:24 GMT

Lichen Sclerosus

Lichen sclerosus (LS) is a chronic autoimmune disease first described by Hallopeau in 1881. It has had various names over the years, including leukoplakia, kraurosis vulvae, balanitis xerotica obliterans, and lichen sclerosis et atrophicus, but in 1976, the International Society for the Study of Vulvovaginal Disease adopted the term lichen sclerosus. LS primarily affects the genital skin, with hypopigmentation and skin atrophy as its hallmarks. Women are more commonly affected than men, and LS can lead to phimosis or scarring of the vaginal introitus. Diagnosis is based on clinical features, but biopsy confirmation is often necessary. If left untreated, LS can result in the destruction of anatomic structures, functional impairment, and an increased risk of malignant evolution. Treatment and long-term follow-up are therefore essential.

LS primarily affects the genital skin and less commonly the extragenital areas.
Typical lesions begin as erythema and progress to thin, hypopigmented, ivory-white, porcelain-like, and sclerotic plaques.
Itching is the main symptom and can be worse at night.
Other symptoms may include telangiectasias, purpura, fissures, ulcerations, and edema.
Common complaints include significant pruritus, local burning sensation, pain, and painful defecation.
LS typically spares the vagina and cervix but can affect the periclitoral hood in girls and the foreskin, glans penis, and coronal sulcus penis in boys and men.
Extragenital lesions can occur on any part of the skin but are usually asymptomatic.
Oral mucosa involvement presents as bluish-white papules on the buccal mucosa or under the tongue.
LS lesions can be asymptomatic, and sexual abuse can aggravate lesions in cases where they coexist.

Treatment / Management

The goals of treatment for LS are to relieve symptoms, prevent scarring and anatomical distortion, and prevent malignant transformation.
General care includes avoiding irritating products and using emollients.
Topical treatments are the first line of therapy for genital LS and include high potency topical steroids such as clobetasol propionate. Second-line therapies include topical calcineurin inhibitors and imiquimod.
Early circumcision may be recommended for men with LS.
Surgery is only indicated for complications associated with LS.
Treatment options for extragenital LS are limited and include phototherapy, ultrapotent topical steroids, tacrolimus ointment, and systemic steroids or methotrexate.
Follow-up examinations should be conducted indefinitely.

Lichen Planus( flat-topped, purplish, itchy bumps or patches on the skin)

Tue, 28 Mar 2023 07:50:21 GMT

Lichen Planus

Lichen Planus is a common inflammatory skin condition that affects around 1-2% of the general population. It can occur at any age, but it is most common in middle-aged adults. The exact cause of lichen planus is unknown, but it is believed to be an autoimmune disorder, in which the body's immune system attacks the skin and mucous membranes.

Lichen planus typically appears as flat-topped, purplish, itchy bumps or patches on the skin, often with a network of white lines called Wickham's striae. It can also affect the mouth, genital area, nails, and scalp. In the mouth, it can cause white, lacy patches or sores that can be painful and make eating difficult.

Lichen planus can occur on the skin, mucous membranes, nails, and scalp. The most commonly affected regions include:

Skin: Lichen planus can appear on any part of the skin, but it is most commonly found on the inner wrist, ankle, lower back, neck, and genitals.
Mouth: Lichen planus can affect the lining of the mouth, including the gums, tongue, and inner cheeks. It can cause white, lacy patches or sores that can be painful and make eating difficult.
Genital area: Lichen planus can affect the skin around the genitals and anus, causing itching, burning, and soreness.
Nails: Lichen planus can affect the nails, causing them to become thin, ridged, and discolored.
Scalp: Lichen planus can cause hair loss and scarring on the scalp, which can be permanent if left untreated.

Overall, the most common regions affected by lichen planus are the skin, mouth, and genital area. However, it can also affect other areas of the body, such as the nails and scalp

Drug-induced lichen planus, or lichenoid drug eruption, is a type of lichen planus that is caused by a reaction to certain medications.

Blood pressure medications: lisinopril, captopril, enalapril
Nonsteroidal anti-inflammatory drugs (NSAIDs): ibuprofen, naproxen, diclofenac
Antibiotics: penicillin, tetracycline, sulfonamides
Antimalarials: hydroxychloroquine, chloroquine
Anticonvulsants: carbamazepine, phenytoin, valproic acid

Treatment/management of lichen planus:

Cutaneous Lichen Planus:

Treatment is aimed at reducing pruritus and time to resolution, as cutaneous LP typically clears spontaneously within 1 to 2 years.
For limited LP, first-line treatment is superpotent topical steroids (clobetasol 0.05%) twice daily for 2 to 4 weeks.
Inadequate response to topical steroids may be augmented with intralesional steroid injections (triamcinolone 5 to 10 mg/mL).
For diffuse LP, first-line treatment is daily oral corticosteroids (prednisone 30 to 60 mg) tapered over 2 to 6 weeks.
If no change is seen, second-line therapy may include metronidazole, sulfasalazine, isotretinoin, acitretin, PUVA, UVB, topical calcineurin inhibitors, or methotrexate.
Third-line treatment may include trimethoprim-sulfamethoxazole, griseofulvin, terbinafine, antimalarials, tetracyclines, ciclosporin, mycophenolate mofetil, azathioprine, etanercept, adalimumab, or low-molecular-weight heparin.

Oral Lichen Planus:

Asymptomatic oral LP should not be treated as the side-effect burden of treatment is high, but symptomatic oral LP should be treated to reduce pain and allow normal food intake.
Patients should be instructed to avoid spicy or acidic foods as well as alcohol and tobacco as these exacerbate symptoms.
First-line treatment is very high potency topical steroids three times daily until remission.
No improvement after 6 weeks should prompt escalation of therapy to second-line treatment, which may include oral corticosteroids or application of topical calcineurin inhibitors.
Third-line treatment may include cyclosporine, azathioprine, mycophenolate mofetil, or methotrexate.

Shingles

Tue, 28 Mar 2023 01:52:16 GMT

Shingles

Shingles:

Is caused by varicella zoster virus (VZV), the same virus that causes chickenpox. After a person recovers from chickenpox, the virus stays dormant (inactive) in the body. This virus can reactivate years later, causing shingles.

Clinical Features of Herpes Zoster:

Localized zoster: most common presentation with rash in one or two adjacent dermatomes; commonly seen on the trunk along a thoracic dermatome.
Disseminated zoster: less common presentation affecting three or more dermatomes; usually seen in people with compromised or suppressed immune systems.
Painful, itchy, or tingly rash: usually preceded by several days of prodromal symptoms like headache, photophobia, and malaise.
Vesicular rash: clusters of vesicles develop and new vesicles continue to form over three to five days, eventually drying and crusting over.
Healing time: usually takes two to four weeks for the rash to heal, but permanent pigmentation changes and scarring may occur.

Complications of Herpes Zoster:

Postherpetic neuralgia (PHN): the most common complication , with persistent pain in the area where the rash was for more than 90 days after rash onset.
Ophthalmic involvement: herpes zoster ophthalmicus with acute or chronic ocular sequelae, including vision loss.
Bacterial superinfection: of the lesions, usually due to Staphylococcus aureus and, less commonly, due to group A beta-hemolytic streptococcus.
Cranial and peripheral nerve palsies: nerve damage that can cause weakness, paralysis, or other complications.
Visceral involvement: such as meningoencephalitis, pneumonitis, hepatitis, and acute retinal necrosis.
Complications in immunocompromised individuals : more severe, long-lasting rash and higher risk of developing disseminated herpes zoster.

Vaccination for Herpes Zoster:

Recombinant zoster vaccine (RZV, Shingrix): recommended vaccine to prevent shingles and its complications.
Recommended age group: adults 50 years and older.
Immunocompetent adults: should get two doses of Shingrix, 2 to 6 months apart, whether or not they have already had herpes zoster or previously received Zostavax®.
Protection against herpes zoster and PHN: two doses of Shingrix are more than 90% effective at preventing herpes zoster and PHN.
Long-lasting protection: protection stays above 85% for at least the first four years after vaccination.

Overall, the recombinant zoster vaccine (RZV, Shingrix) is highly effective at preventing herpes zoster and its complications, including PHN. Vaccination is recommended for adults 50 years and older, whether or not they have previously had herpes zoster or received Zostavax.

Zostavax is no longer available for use in the United States, as of November 18, 2020.

Disease Rates, Recurrence, Complications, and Deaths for Herpes Zoster:

Annual incidence: approximately 4 cases per 1,000 U.S. population, with an estimated one million cases occurring annually in the United States.
Incidence among people 60 years and older: about 1 case per 100 U.S. population annually.
Repeat episodes: multiple episodes of herpes zoster can occur, but the precise incidence of recurrence is not known. Most people have only one episode of herpes zoster in their lifetime.
Complications: approximately 1 to 4% of people with herpes zoster get hospitalized for complications. About 30% of all people hospitalized with herpes zoster have compromised or suppressed immune systems. About 1 in 10 adults with herpes zoster develop PHN.
Deaths: one study estimated that 96 deaths occur each year in which herpes zoster was the actual underlying cause (0.28 to 0.69 per 1 million population). Almost all deaths occur in older adults and those with compromised or suppressed immune systems.

Overall, herpes zoster is a relatively common disease with the majority of cases occurring in older adults. While most people have only one episode of herpes zoster in their lifetime, complications such as hospitalization and PHN can occur in a significant percentage of cases. Vaccination with the recommended vaccine, Shingrix, can help prevent herpes zoster and its complications.

References

CDC. Prevention of herpes zoster: recommendations of the Advisory Committee on Immunization Practices (ACIP) Recommendations for use of Herpes Zoster Vaccines . MMWR Recomm Rep. 2018;67(03):103-108.
Thomas SL, Hall AJ. What does epidemiology tell us about risk factors for herpes zoster? Lancet Infect Dis. 2004;4(1):26-33.
Tseng HF, Smith N, Harpaz R, Bialek SR, Sy LS, Jacobsen SJ. Herpes zoster vaccine in older adults and the risk of subsequent herpes zoster disease . JAMA. 2011 Jan 12;305(2):160-6.
Mahamud A, Marin M, Nickell SP, Shoemaker T, Zhang JX, Bialek SR. Herpes zoster-related deaths in the United States: validity of death certificates and mortality rates, 1979-2007 . Clin Infect Dis.2012 Oct;55(7):960-6.
Leung J, Harpaz R, Molinari NA, Jumaan A, Zhou F. Herpes zoster incidence among insured persons in the United States, 1993-2006: evaluation of impact of varicella vaccination . Clinical Infectious Diseases. 2011;52(3):332-340.
Yih W, Brooks D, Lett S, Jumaan A, Zhang Z, Clements K, Seward J. The Incidence of varicella and herpes zoster in Massachusetts as measured by the Behavioral Risk Factor Surveillance System (BRFSS) during a period of increasing varicella vaccine coverage . BMC Public Health. 2005;5(68).
Jumaan AO, Yu O, Jackson LA, Bohlke K, Galil K, Seward JF. Incidence of herpes zoster, before and after varicella vaccination-associated decreases in the incidence of varicella . Journal of Infectious Diseases. 2005;191:2002-7.
Hales CM, Harpaz R, Joesoef MR, Bialek SR (2013). Examination of links between herpes zoster incidence and childhood varicella vaccination . Annals of Internal Medicine. 159(11):739-45
Russell ML, Dover DC, Simmonds KA, Svenson LW. Shingles in Alberta: before and after publicly funded varicella vaccination . Vaccine. DOI 10.1016/j.vaccine.2013.09.018.
Weinmann S, Chun C, Schmid DS, Roberts M, Vandermeer M, Riedlinger K, et al. Incidence and clinical characteristics of herpes zoster among children in the varicella vaccine era, 2005–2009 . Journal of Infection Diseases. 2013;208(11):1859-68.
Hardy I, Gershon AA, Steinberg SP, LaRussa P. The incidence of zoster after immunization with live attenuated varicella vaccine. A study in children with leukemia. Varicella Vaccine Collaborative Study Group . N Engl J Med. 1991;325(22):1545-50.

Montreal Cognitive Assessment score

Thu, 09 Mar 2023 21:06:34 GMT

The Montreal Cognitive Assessment (MoCA)

The Montreal Cognitive Assessment (MoCA) is a cognitive screening tool that assesses various cognitive domains, including attention, memory, language, visuospatial abilities, and executive functions. The maximum score on the MoCA is 30, with higher scores indicating better cognitive functioning.

A MoCA score of 26 or higher is generally considered normal or healthy cognitive functioning for most individuals. However, it's important to note that the interpretation of MoCA scores should be done in the context of an individual's age, education level, and other relevant factors. Additionally, a MoCA score is only one aspect of a comprehensive cognitive evaluation, and further assessment may be needed to fully evaluate an individual's cognitive functioning.

The Montreal Cognitive Assessment (MoCA) is a brief cognitive screening tool that assesses various cognitive domains, including:

Visuospatial/executive functions: This domain assesses an individual's ability to perceive and manipulate visual information, as well as their ability to plan and execute complex tasks.
Naming: This domain assesses an individual's ability to name objects and animals.
Memory: This domain assesses an individual's ability to learn and recall information, including immediate and delayed recall.
Attention: This domain assesses an individual's ability to sustain attention and concentrate on tasks.
Language: This domain assesses an individual's ability to understand and use language, including verbal fluency and comprehension.
Abstraction: This domain assesses an individual's ability to think abstractly and make inferences.
Delayed recall: This domain assesses an individual's ability to recall information after a delay.

The MoCA test consists of 30 items, and each item is worth one point, resulting in a maximum score of 30. The test takes approximately 10-15 minutes to administer and is designed to be used by a trained healthcare professional.

It's important to note that the MoCA is a screening tool and is not a diagnostic instrument. If an individual scores below the established cut-off, further assessment and evaluation are needed to confirm a diagnosis of cognitive impairment. Additionally, MoCA scores should be interpreted in the context of an individual's age, education level, cultural and linguistic background, and medical history

Advantages vs. Disadvantages

Advantages of the Montreal Cognitive Assessment (MoCA) include :

Quick and easy to administer: The MoCA is a brief and easy-to-administer test that takes only 10-15 minutes to complete, making it an efficient way to screen for cognitive impairment.
Assess a range of cognitive domains: The MoCA assesses various cognitive domains, including attention, memory, language, visuospatial abilities, and executive functions, providing a comprehensive assessment of an individual's cognitive functioning.
Validated in diverse populations: The MoCA has been validated in various populations and cultural contexts, making it a useful tool for assessing cognitive functioning across diverse groups.
Can identify mild cognitive impairment: The MoCA can identify mild cognitive impairment, which is an early stage of cognitive decline and can indicate the risk of developing dementia.

However, there are also some potential disadvantages of the MoCA, including:

Limited diagnostic value: The MoCA is a screening tool and is not a diagnostic instrument. Further evaluation and testing are necessary to confirm a diagnosis of cognitive impairment.
Affected by various factors: MoCA scores can be influenced by various factors, including age, education level, cultural and linguistic background, and medical conditions or medications, making it essential to interpret scores in the context of an individual's unique circumstances.
Limited sensitivity for some cognitive domains: The MoCA may have limited sensitivity for some cognitive domains, such as executive functions, and may miss some cases of cognitive impairment in these areas.

In summary, the MoCA is a useful cognitive screening tool that has several advantages, including being quick and easy to administer, assessing a range of cognitive domains, and being validated in diverse populations. However, it also has some potential limitations, such as limited diagnostic value and sensitivity for some cognitive domain

References that you may find helpful for further information on the Montreal Cognitive Assessment (MoCA):

Nasreddine, Z. S., Phillips, N. A., Bédirian, V., Charbonneau, S., Whitehead, V., Collin, I., ... & Chertkow, H. (2005). The Montreal Cognitive Assessment, MoCA: a brief screening tool for mild cognitive impairment. Journal of the American Geriatrics Society, 53(4), 695-699.
Carson, N., Leach, L., & Murphy, K. J. (2018). A re-examination of Montreal Cognitive Assessment (MoCA) cutoff scores. International Journal of Geriatric Psychiatry, 33(2), 379-388.
Ciesielska, N., Sokołowski, R., Mazur, E., Podhorecka, M., & Polak-Szabela, A. (2016). Validation of the Polish version of the Montreal Cognitive Assessment (MoCA-P) in Parkinson's disease patients. Journal of the Neurological Sciences, 368, 127-131.
Malek-Ahmadi, M., & Davis, K. (2015). The Montreal Cognitive Assessment (MoCA) for Alzheimer's Disease Screening in Primary Care: A Systematic Review. Journal of Alzheimer's Disease & Parkinsonism, 5(3), 194.
Pendlebury, S. T., Cuthbertson, F. C., Welch, S. J., Mehta, Z., & Rothwell, P. M. (2010). Underestimation of cognitive impairment by Mini-Mental State Examination versus the Montreal Cognitive Assessment in patients with transient ischemic attack and stroke: a population-based study. Stroke, 41(6), 1290-1293.

links to resources related to the Montreal Cognitive Assessment (MoCA) that you may find helpful:

MoCA website: https://www.mocatest.org/
This website provides information about the MoCA test, including how to administer and score the test, training and certification for healthcare professionals, and resources for patients and caregivers.
MoCA Test App: https://www.mocatest.org/moca-test-app/
This app is available for download on iOS and Android devices and provides a digital version of the MoCA test that can be administered by a trained healthcare professional.
Alzheimer's Association: https://www.alz.org/alzheimers-dementia/what-is-dementia/brain_tests
The Alzheimer's Association provides information about different types of cognitive tests, including the MoCA, and how they are used to assess cognitive functioning.
National Institute on Aging: https://www.nia.nih.gov/health/cognitive-health-and-older-adults

loss of libido? memory impairment? lack of motivation? salt craving? reduced body hair?

Wed, 08 Feb 2023 04:35:35 GMT

Addison's disease

Is a chronic endocrine disorder that results in the destruction of the adrenal glands, which are small hormone-producing glands located on top of each kidney. It affects the body's ability to produce sufficient amounts of cortisol and aldosterone, two hormones that play critical roles in regulating metabolism, blood pressure, and other physiological processes.

Common signs and symptoms include:

Fatigue and weakness
Weight loss and decreased appetite
Low blood pressure, dizziness, and fainting
Darkening of the skin, especially on areas exposed to the sun
Muscle and joint pains
Irritability and depression
Salt craving

In severe cases, individuals with Addison's disease may experience an acute adrenal crisis, characterized by sudden and severe symptoms such as severe abdominal pain, vomiting, dehydration, low blood pressure, and even loss of consciousness. This is a life-threatening condition that requires immediate medical attention.

It is important to note that the symptoms of Addison's disease may be subtle and may be easily confused with other conditions. A definitive diagnosis requires a comprehensive evaluation by a healthcare provider, who may consider the patient's medical history, symptoms, physical examination, and test results

Primary adrenal insufficiency (Primary AI) and Secondary adrenal insufficiency (Secondary AI) are two different forms of adrenal insufficiency, which is characterized by a deficiency of cortisol production by the adrenal glands.

The main difference between the two forms is the cause of the adrenal insufficiency.

Primary adrenal insufficiency , also known as Addison's disease, occurs when the adrenal glands themselves are damaged or destroyed, leading to a deficiency of cortisol and aldosterone production. This may be due to autoimmune destruction, infection, or other forms of adrenal gland damage.

Secondary adrenal insufficiency , on the other hand, occurs when the adrenal glands are functioning normally, but the production of cortisol is not stimulated adequately. This is typically due to a problem with the pituitary gland , which is responsible for producing adrenocorticotropic hormone (ACTH), the hormone that stimulates cortisol production by the adrenal glands. In secondary adrenal insufficiency, cortisol production is not stimulated adequately, leading to a deficiency of cortisol production by the adrenal glands.

Cosyntropin stimulation testing is a diagnostic test used to evaluate adrenal gland function. It involves the administration of a synthetic form of adrenocorticotropic hormone (ACTH), known as cosyntropin, to stimulate the adrenal glands to produce cortisol. The test is used to differentiate between primary adrenal insufficiency (Addison's disease) and secondary adrenal insufficiency.

In primary adrenal insufficiency, the adrenal glands are damaged or destroyed, leading to a deficiency of cortisol production. In secondary adrenal insufficiency, cortisol production is normal, but the production is not stimulated adequately. The cosyntropin stimulation test is used to determine whether the problem lies with the adrenal glands or the pituitary gland.

The test is performed by administering cosyntropin and measuring cortisol levels in the blood before and after the injection. In individuals with normal adrenal gland function, cortisol levels should increase in response to cosyntropin stimulation. In individuals with primary adrenal insufficiency, cortisol levels will remain low or may not increase adequately in response to cosyntropin stimulation. In secondary adrenal insufficiency, cortisol levels may increase, but not as much as in individuals with normal adrenal gland function.

It is important to note that the results of the cosyntropin stimulation test should be interpreted in the context of the individual's medical history, symptoms, physical examination, and other test results. A definitive diagnosis of adrenal insufficiency requires a comprehensive evaluation by a healthcare provider.

There are several conditions that can mimic the symptoms of Addison's disease and should be considered in the differential diagnosis, including:

Adrenal insufficiency secondary to pituitary disease (secondary adrenal insufficiency)
Chronic fatigue syndrome
Depression and other psychiatric disorders
Anemia
Hypothyroidism
Malnutrition and eating disorders
Hypoglycemia (low blood sugar)
Sepsis and other systemic infections
Dehydration and electrolyte imbalances
Chronic obstructive pulmonary disease (COPD) and other chronic respiratory disorders

Diagnostic tests that may be used to confirm the diagnosis of Addison's disease include:

Adrenocorticotropic hormone (ACTH) stimulation test
Cortisol levels measurement in the blood and/or urine
Aldosterone levels measurement
Antibody testing to detect autoimmune destruction of the adrenal glands

The gold standard for diagnosing Addison's disease is the adrenocorticotropic hormone (ACTH) stimulation test. This test measures the body's response to a synthetic form of ACTH, which stimulates the adrenal glands to produce cortisol. In a healthy individual, cortisol levels should increase after ACTH administration. However, in individuals with Addison's disease, cortisol levels will not increase adequately, indicating a deficiency of cortisol production by the adrenal glands.

In addition to the ACTH stimulation test, the diagnosis of Addison's disease may also be supported by laboratory tests that measure cortisol and aldosterone levels, as well as by imaging studies to visualize the adrenal glands.

It is important to note that a definitive diagnosis of Addison's disease requires a comprehensive evaluation by a healthcare provider, who may consider the patient's medical history, symptoms, physical examination, and test results.

Treatment of Addison's disease:

Involves replacing the hormones that the adrenal glands are not producing. This is usually done through daily doses of cortisol and aldosterone, either in the form of oral medications or injections. In addition, treatment may also involve management of the underlying cause, such as immunosuppressive therapy for autoimmune destruction .

The medications used to treat Addison's disease are hormone replacement therapy drugs that aim to replace the hormones that the adrenal glands are not producing. Some common drugs used for this purpose include:

Hydrocortisone (Cortef)
Fludrocortisone (Florinef)
Desoxycorticosterone pivalate (DOCP, Percorten-V)
Cortisone acetate (Cortone Acetate)

It is important to note that the specific treatment plan and medication regimen may vary from person to person, based on individual needs and the underlying cause of the disease. Your doctor will determine the best course of treatment based on your specific situation.

References :

Bouloux PM, Hindmarsh PC. Addison's disease. In: Jameson JL, De Groot LJ, de Kretser DM, et al., eds. Endocrinology: Adult and Pediatric. 7th ed. Philadelphia, PA: Elsevier Saunders; 2016:chap 83.
New M, Maclaren N. Adrenal insufficiency. In: Kumar P, Clark M, eds. Clinical Medicine. 6th ed. London: Elsevier; 2009:chap 19.
Addison's Disease - NIDDK. National Institute of Diabetes and Digestive and Kidney Diseases. https://www.niddk.nih.gov/health-information/endocrine-diseases/addisons-disease . Published June 2018.
Addison's Disease. American College of Endocrinology. https://www.aace.com/publications/brochures/addisons-disease . Published 2019.
Addison's Disease. American Academy of Pediatrics. https://pedclerk.bsd.uchicago.edu/page/addisons-disease . Published 2022.

Addison's Disease - MedlinePlus: https://medlineplus.gov/addisonsdisease.html
Addison's Disease - Mayo Clinic: https://www.mayoclinic.org/diseases-conditions/addisons-disease/symptoms-causes/syc-20351310
Adrenal Insufficiency (Addison's Disease) - EndocrineWeb: https://www.endocrineweb.com/conditions/adrenal-insufficiency-addisons-disease
Addison's Disease - NHS: https://www.nhs.uk/conditions/addisons-disease/
Addison's Disease - American Academy of Pediatrics: https://pedclerk.bsd.uchicago.edu/page/addisons-disease
Primary Adrenal Insufficiency (Addison's Disease) - UpToDate: https://www.uptodate.com/contents/primary-adrenal-insufficiency-addisons-disease

Vitamin deficiencies

Sun, 05 Feb 2023 18:37:16 GMT

Vitamin deficiencies

- Are a common problem worldwide, and can have serious health consequences. A balanced diet that includes a variety of fruits, vegetables, whole grains, and lean proteins is the best way to get enough essential vitamins and minerals. However, some populations are at higher risk of certain deficiencies due to factors such as poverty, poor dietary choices, and health conditions that interfere with nutrient absorption.

Here is a summary of some of the most common vitamin deficiencies and their health consequences:

Vitamin A deficiency: This deficiency affects approximately 19% of the world's population, particularly children and pregnant women. Vitamin A deficiency can cause vision problems, including night blindness and increased risk of blindness, as well as increased susceptibility to infections.
Vitamin D deficiency: This deficiency affects approximately 1 billion people worldwide, or 15% of the world's population. Vitamin D is important for bone health and deficiency can cause rickets in children and osteomalacia in adults, leading to weak bones and increased risk of fractures.
Vitamin B12 deficiency: This deficiency affects approximately 15-20% of older adults and up to 30% of people who follow a vegetarian or vegan diet. Vitamin B12 is important for nerve function and red blood cell production. Deficiency can cause anemia, nerve damage, and cognitive decline.
Iron deficiency: This deficiency affects approximately 25% of the world's population, with women and young children being most at risk. Iron is important for carrying oxygen in the blood, and deficiency can cause anemia, fatigue, and weakened immune system.
Folate deficiency: This deficiency affects approximately 11% of the world's population, with women of reproductive age being particularly vulnerable. Folate is important for cell division and DNA synthesis, and deficiency can cause neural tube defects in newborns and anemia.
Vitamin C deficiency: This deficiency affects approximately 10% of the world's population, particularly in developing countries. Vitamin C is important for skin and wound healing, as well as immune system function. Deficiency can cause scurvy, which is characterized by gum disease and skin bruising.
Thiamin (Vitamin B1) deficiency: This deficiency affects approximately 10% of the world's population, particularly in developing countries. Thiamin is important for energy production and nerve function, and deficiency can cause beriberi, which is characterized by muscle weakness and heart problems.
Niacin (Vitamin B3) deficiency: This deficiency affects approximately 10% of the world's population, particularly in developing countries. Niacin is important for energy production and skin health, and deficiency can cause pellagra, which is characterized by skin rashes, diarrhea, and dementia.
Riboflavin (Vitamin B2) deficiency: This deficiency is relatively rare, but can occur in populations with poor diets or high alcohol consumption. Riboflavin is important for energy production and skin health, and deficiency can cause ariboflavinosis, which is characterized by skin rashes and mouth sores.
Calcium deficiency: This deficiency affects approximately 10% of the world's population, particularly in developing countries and postmenopausal women. Calcium is important for bone and teeth health, and deficiency can cause osteoporosis, which is characterized by weak bones and increased risk of fractures.

References:

World Health Organization (WHO). (2019). Vitamin and mineral deficiencies. Retrieved from https://www.who.int/nutrition/topics/vad/en/
World Health Organization (WHO). (2020). Vitamin A deficiency. Retrieved from https://www.who.int/news-room/fact-sheets/detail/vitamin-a-deficiency
World Health Organization (WHO). (2020). Vitamin D. Retrieved from https://www.who.int/news-room/fact-sheets/detail/vitamin-d
National Institutes of Health (NIH). (2021). Vitamin B12. Retrieved from https://ods.od.nih.gov/factsheets/VitaminB12-Consumer/
National Institutes of Health (NIH). (2021). Iron. Retrieved from https://ods.od.nih.gov/factsheets/Iron-Consumer/
National Institutes of Health (NIH). (2021). Folate. Retrieved from https://ods.od.nih.gov/factsheets/Folate-Consumer/

World Health Organization (WHO). (2019). Vitamin and mineral deficiencies. Retrieved from https://www.who.int/nutrition/topics/vad/en/
World Health Organization (WHO). (2020). Vitamin C. Retrieved from https://www.who.int/news-room/fact-sheets/detail/vitamin-c
World Health Organization (WHO). (2020). Thiamin (Vitamin B1). Retrieved from https://www.who.int/news-room/fact-sheets/detail/thiamin-(vitamin-b1)
World Health Organization (WHO). (2020). Niacin (Vitamin B3). Retrieved from https://www.who.int/news-room/fact-sheets/detail/niacin-(vitamin-b3)
World Health Organization (WHO). (2020). Riboflavin (Vitamin B2). Retrieved from https://www.who.int/news-room/fact-sheets/detail/riboflavin-(vitamin-b2)
National Institutes of Health (NIH). (2021). Calcium. Retrieved from https://ods.od.nih.gov/factsheets/Calcium-Consumer/

World Health Organization (WHO). (2019). Global report on osteoporosis. Retrieved from https://www.who.int/publications/i/item/global-report-on-osteoporosis

Vitamin E

Sat, 28 Jan 2023 20:18:40 GMT

What is vitamin E and what does it do

Vitamin E is a powerful antioxidant that helps to protect the body's cells from damage caused by harmful free radicals. Found in a variety of foods including nuts, seeds, and leafy green vegetables, it also helps to boost the immune system, promote healthy blood flow, and maintain the health of the skin and eyes. It plays a critical role in cell signaling, gene expression and enzyme activity regulation. With the ability to scavenge free radicals, Vitamin E helps to keep the body functioning at optimal levels, making it an essential nutrient for overall health and well-being. With its wide range of benefits, it's no wonder that many choose to supplement their diet with Vitamin E.

Functions of Vitamin E

Vitamin E in Disease Prevention

Vitamin E has been found to be very effective in the prevention and reversal of various disease complications due to its function as an antioxidant, its role in anti-inflammatory processes, its inhibition of platelet aggregation and its immune-enhancing activity.

While developing a differential diagnosis, clinicians must consider other possible vitamin deficiencies as well as the following:

Friedreich ataxia
Ataxia with vitamin E deficiency (AVED)
Stroke
Cerebral palsy
Paraneoplastic syndrome
Biliary disease
Short-Bowl syndrome
Mutations in the tocopherol transfer protein causing impaired fat metabolism
Cystic fibrosis
Chronic cholestatic hepatobiliary disease
Crohn disease
Exocrine pancreatic insufficiency
Liver disease
Abetalipoproteinemia
Isolated vitamin E deficiency

References

Kim HK, Han SN. Vitamin E: Regulatory role on gene and protein expression and metabolomics profiles. IUBMB Life. 2019 Apr;71(4):442-455. [ PubMed ]

Suzuki H, Kume A, Herbas MS. Potential of Vitamin E Deficiency, Induced by Inhibition of α-Tocopherol Efflux, in Murine Malaria Infection. Int J Mol Sci. 2018 Dec 24;20(1) [ PMC free article ] [ PubMed ]

Jilani T, Iqbal MP. Vitamin E deficiency in South Asian population and the therapeutic use of alpha-tocopherol (Vitamin E) for correction of anemia. Pak J Med Sci. 2018 Nov-Dec;34(6):1571-1575. [ PMC free article ] [ PubMed ]

Khadangi F, Azzi A. Vitamin E - The Next 100 Years. IUBMB Life. 2019 Apr;71(4):411-415. [ PubMed ]

Sapiejka E, Krzyżanowska-Jankowska P, Wenska-Chyży E, Szczepanik M, Walkowiak D, Cofta S, Pogorzelski A, Skorupa W, Walkowiak J. Vitamin E status and its determinants in patients with cystic fibrosis. Adv Med Sci. 2018 Sep;63(2):341-346. [ PubMed ]

Boltshauser E, Weber KP. Laboratory investigations. Handb Clin Neurol. 2018;154:287-298. [ PubMed ]

Tokgöz Y, Terlemez S, Karul A. Fat soluble vitamin levels in children with newly diagnosed celiac disease, a case control study. BMC Pediatr. 2018 Apr 09;18(1):130. [ PMC free article ] [ PubMed ]

Teriaky A, Mosli M, Chandok N, Al-Judaibi B, Marotta P, Qumosani K. Prevalence of fat-soluble vitamin (A, D, and E) and zinc deficiency in patients with cirrhosis being assessed for liver transplantation. Acta Gastroenterol Belg. 2017 Apr-Jun;80(2):237-241. [ PubMed ]

Gomez-Pomar E, Hatfield E, Garlitz K, Westgate PM, Bada HS. Vitamin E in the Preterm Infant: A Forgotten Cause of Hemolytic Anemia. Am J Perinatol. 2018 Feb;35(3):305-310. [ PubMed ]

The Benefits of Eating Vitamin-Rich Foods

site-X7cQHw — Wed, 18 Jan 2023 04:48:45 GMT

Boost Your Health with Vitamin-Rich Foods: The Top 10 Benefits

E ating foods that are rich in vitamins can provide a range of health benefits. Some of the key benefits include:

Improved Immune Function: Vitamins, particularly Vitamin C and Vitamin E, can help boost the immune system and protect against infections and illnesses.
Better Skin Health: Vitamins A, C, and E can help improve skin health by promoting collagen production, fighting free radicals and protecting against UV damage.
Better Eye Health: Vitamins A, C and E can help protect against age-related eye conditions such as macular degeneration and cataracts.
Improved Heart Health: Vitamins B6, B12, and folate can help lower homocysteine levels in the blood, which is a risk factor for heart disease.
Better Brain Health: Vitamins B6, B12, and folate can also help improve brain health and reduce the risk of cognitive decline as we age.
Increased Energy: B-vitamins are essential for energy production, and a deficiency can lead to fatigue and weakness.
Weight Management: Eating a diet rich in vitamins can help control appetite and cravings, making it easier to maintain a healthy weight.
Improved Digestion: Vitamins such as Vitamin A and Vitamin D can help support the health of the digestive tract and promote regular bowel movements.
Stronger Bones: Vitamins D and K are essential for maintaining strong bones, and a deficiency in these vitamins can lead to osteoporosis.
Reduced Inflammation: Vitamins C and E, along with other antioxidants, can help reduce inflammation in the body, which is linked to a range of chronic diseases.
Mood Boost: Vitamin B12 and folate are important for the production of neurotransmitters, which help regulate mood and emotional well-being.
Blood Pressure Control: Vitamin D and potassium can help regulate blood pressure, and a deficiency in these vitamins can lead to hypertension.
Blood Sugar Control: Vitamin B1 and chromium can help regulate blood sugar levels, and a deficiency in these vitamins can lead to diabetes.

It is also important to note that certain groups of people may be at greater risk of vitamin deficiencies, such as vegetarians, pregnant women, and the elderly. Consultation with a doctor or dietitian is recommended to understand which vitamins may be lacking in a particular diet and to find the best way to supplement and balance the diet.

LIST OF BLOOD DISORDERS

Sun, 08 Jan 2023 22:14:37 GMT

LIST OF BLOOD DISORDERS

Anemia: a condition in which the body doesn't have enough red blood cells or the red blood cells don't function properly.
Bleeding disorders: conditions that affect the body's ability to form blood clots, including hemophilia and von Willebrand disease.
Blood cancers: cancers that affect the blood cells, such as leukemia and lymphoma.
Blood clotting disorders: conditions that cause abnormal blood clotting, such as thrombophilia. .

Anemia

is a condition in which the body doesn't have enough red blood cells or the red blood cells don't function properly. Red blood cells are responsible for carrying oxygen from the lungs to the rest of the body. When there aren't enough healthy red blood cells, the body's tissues and organs don't get enough oxygen, leading to fatigue and other symptoms.

There are several types of anemia, including iron deficiency anemia (the most common type), anemia caused by vitamin deficiencies (such as folic acid and vitamin B-12 deficiency), and anemia caused by chronic diseases (such as kidney disease or cancer).

Symptoms of anemia include:

Fatigue
Weakness
Pale skin
Shortness of breath
Rapid heartbeat
Chest pain
Dizziness
Cold hands and feet
Headache

Anemia can be treated with medications, blood transfusions, and lifestyle changes such as eating a healthy diet that includes iron-rich foods. The specific treatment will depend on the underlying cause of the anemia.

Bleeding disorders

Are conditions that affect the body's ability to stop bleeding or clotting after an injury. Some bleeding disorders are inherited, while others can be acquired. Examples of inherited bleeding disorders include hemophilia, von Willebrand disease, and inherited platelet disorders. Acquired bleeding disorders can be caused by certain medications, liver disease, or other medical conditions. Symptoms of a bleeding disorder may include prolonged bleeding after an injury or surgery, easy bruising, and the presence of blood in the urine or stool. Treatment for a bleeding disorder may include medications to help the blood clot, dietary changes, and avoiding activities that could cause injury. It's important to seek medical attention if you or someone you know is experiencing symptoms of a bleeding disorder.

Blood cancers

Also called hematologic cancers, are cancers that affect the cells of the blood, bone marrow, or lymphatic system. There are several types of blood cancers, including leukemia, lymphoma, and myeloma.

Leukemia is a cancer of the white blood cells, which are important for fighting infection. There are several subtypes of leukemia, including acute leukemia and chronic leukemia, which differ based on the rate at which the cancer progresses.

Lymphoma is a cancer of the lymphatic system, which is part of the immune system. There are two main types of lymphoma: Hodgkin lymphoma and non-Hodgkin lymphoma.

Myeloma is a cancer of the plasma cells, which are a type of white blood cell that produces antibodies.

Symptoms of blood cancer can include fatigue, fever, weight loss, and swollen lymph nodes. Treatment options may include chemotherapy, radiation therapy, and bone marrow or stem cell transplant. It's important to speak with a healthcare provider if you have any concerns about blood cancer.

Blood clotting disorders

Also called coagulation disorders, are conditions that affect the body's ability to stop bleeding or form clots. Blood clotting is a complex process that involves several factors, including platelets and proteins called clotting factors. When a blood vessel is damaged, platelets and clotting factors work together to form a blood clot, which helps to stop the bleeding. However, if there is a problem with any of these factors, it can lead to a blood clotting disorder.

There are several types of blood clotting disorders, including inherited disorders, such as hemophilia and von Willebrand disease, and acquired disorders, which can be caused by medications, medical conditions, or other factors. Symptoms of a blood clotting disorder can include prolonged bleeding after an injury or surgery, easy bruising, and the presence of blood in the urine or stool. Treatment for a blood clotting disorder may include medications to help the blood clot, dietary changes, and avoiding activities that could cause injury. It's important to seek medical attention if you or someone you know is experiencing symptoms of a blood clotting disorder.

Clinical features of type 2 heparin-induced thrombocytopenia

Mon, 19 Dec 2022 16:14:04 GMT

Heparin-induced thrombocytopenia

Heparin-induced thrombocytopenia (HIT) is a life—threatening complication of heparin therapy. Heparin induces a conformational change in a platelet surface protein (platelet factor 4), which exposes a neoantigen. In patients with HIT, HIT antibodies form in response to the neoantigen and bind to the surface of platelets, causing platelet aggregation, thrombocytopenia

Clinical signs

Suspected with heparin exposure >5 days and any of the following:

Platelet count reduction >50% from baseline
Arterial or venous thrombosis
Necrotic skin lesions at heparin injection sites
Acute systemic (anaphylactoid) reactions after heparin

Diagnostic

Serotonin release assay: Gold standard confirmatory test evaluation a Start treatment in suspected cases prior to confirmatory tests

Treatment

Stop ALL heparin products a Start a direct thrombin inhibitor (eg, argatroban) orfondaparinux (synthetic pentasaccharide)

Plasma cell neoplasms

Wed, 14 Dec 2022 14:12:41 GMT

Plasma cell neoplasms

General Information About Plasma Cell Neoplasms

KEY POINTS

Plasma cell neoplasms are diseases in which the body makes too many plasma cells.
Plasma cell neoplasms can be benign (not cancer) or malignant (cancer).
There are several types of plasma cell neoplasms.
Monoclonal gammopathy of undetermined significance (MGUS)
Plasmacytoma
Multiple myeloma
Multiple myeloma and other plasma cell neoplasms may cause a condition called amyloidosis.
Age can affect the risk of plasma cell neoplasms.
Tests that examine the blood, bone marrow, and urine are used to diagnose multiple myeloma and other plasma cell neoplasms.
Certain factors affect prognosis (chance of recovery) and treatment options.

Plasma cell neoplasms are diseases in which abnormal plasma cells or cells form tumors in the bones or soft tissues of the body. The plasma cells also make an antibody protein, called M protein, that is not needed by the body and does not help fight infection. These antibody proteins build up in the bone marrow and can cause the blood to thicken or can damage the kidneys.

Plasma cell neoplasms can be benign (not cancer) or malignant (cancer).

Monoclonal gammopathy of undetermined significance (MGUS) is not cancer but can become cancer. The following types of plasma cell neoplasms are cancer:

Lymphoplasmacytic lymphoma (also called Waldenström macroglobulinemia) .
Plasmacytoma.
Multiple myeloma.

There are several types of plasma cell neoplasms.

Plasma cell neoplasms include the following:

Monoclonal gammopathy of undetermined significance (MGUS)

In this type of plasma cell neoplasm, less than 10% of the bone marrow is made up of abnormal plasma cells and there is no cancer. The abnormal plasma cells make M protein, which is sometimes found during a routine blood or urine test. In most patients, the amount of M protein stays the same and there are no signs, symptoms, or health problems.

In some patients, MGUS may later become a more serious condition, such as amyloidosis, or cause problems with the kidneys, heart, or nerves. MGUS can also become cancer, such as multiple myeloma, lymphoplasmacytic lymphoma, or chronic lymphocytic leukemia.

Plasmacytoma

In this type of plasma cell neoplasm, the abnormal plasma cells (myeloma cells) are in one place and form one tumor, called a plasmacytoma. Sometimes plasmacytoma can be cured. There are two types of plasmacytoma.

In isolated plasmacytoma of bone, one plasma cell tumor is found in the bone, less than 10% of the bone marrow is made up of plasma cells, and there are no other signs of cancer. Plasmacytoma of the bone often becomes multiple myeloma.
In extramedullary plasmacytoma, one plasma cell tumor is found in soft tissue but not in the bone or the bone marrow. Extramedullary plasmacytomas commonly form in tissues of the throat, tonsil, and paranasal sinuses.

Signs and symptoms depend on where the tumor is.

In bone, the plasmacytoma may cause pain or broken bones.
In soft tissue, the tumor may press on nearby areas and cause pain or other problems. For example, a plasmacytoma in the throat can make it hard to swallow.

Multiple myeloma

In multiple myeloma, abnormal plasma cells (myeloma cells) build up in the bone marrow and form tumors in many bones of the body. These tumors may keep the bone marrow from making enough healthy blood cells. Normally, the bone marrow makes stem cells (immature cells) that become three types of mature blood cells:

Red blood cells that carry oxygen and other substances to all tissues of the body.
White blood cells that fight infection and disease.
Platelets that form blood clots to help prevent bleeding.

As the number of myeloma cells increases, fewer red blood cells, white blood cells, and platelets are made. The myeloma cells also damage and weaken the bone.

Sometimes multiple myeloma does not cause any signs or symptoms. This is called smoldering multiple myeloma. It may be found when a blood or urine test is done for another condition. Signs and symptoms may be caused by multiple myeloma or other conditions. Check with your doctor if you have any of the following:

Bone pain, especially in the back or ribs.
Bones that break easily.
Fever for no known reason or frequent infections.
Easy bruising or bleeding.
Trouble breathing.
Weakness of the arms or legs.
Feeling very tired.

A tumor can damage the bone and cause hypercalcemia (too much calcium in the blood). This can affect many organs in the body, including the kidneys, nerves, heart, muscles, and digestive tract, and cause serious health problems.

Hypercalcemia may cause the following signs and symptoms:

Loss of appetite.
Nausea or vomiting.
Feeling thirsty.
Frequent urination.
Constipation.
Feeling very tired.
Muscle weakness.
Restlessness.
Confusion or trouble thinking.

Multiple myeloma and other plasma cell neoplasms may cause a condition called amyloidosis.

In rare cases, multiple myeloma can cause peripheral nerves (nerves that are not in the brain or spinal cord) and organs to fail. This may be caused by a condition called amyloidosis. Antibody proteins build up and stick together in peripheral nerves and organs, such as the kidney and heart. This can cause the nerves and organs to become stiff and unable to work the way they should.

Amyloidosis may cause the following signs and symptoms:

Feeling very tired.
Purple spots on the skin.
Enlarged tongue.
Diarrhea.
Swelling caused by fluid in your body's tissues.
Tingling or numbness in your legs and feet.

Age can affect the risk of plasma cell neoplasms.

Anything that increases your risk of getting a disease is called a risk factor. Having a risk factor does not mean that you will get cancer; not having risk factors doesn't mean that you will not get cancer. Talk with your doctor if you think you may be at risk.

Plasma cell neoplasms are most common in people who are middle aged or older. For multiple myeloma and plasmacytoma, other risk factors include the following:

Being Black.
Being male.
Having a personal history of MGUS or plasmacytoma.
Being exposed to radiation or certain chemicals.

Studies about how racial, social, and financial factors affect access to treatment and rates of plasma cell neoplasms are ongoing .

Tests that examine the blood, bone marrow, and urine are used to diagnose multiple myeloma and other plasma cell neoplasms.

The following tests and procedures may be used:

Physical exam and health history: An exam of the body to check general signs of health, including checking for signs of disease, such as lumps or anything else that seems unusual. A history of the patient’s health habits and past illnesses and treatments will also be taken.
Blood and urine immunoglobulin studies: A procedure in which a blood or urine sample is checked to measure the amounts of certain antibodies (immunoglobulins). For multiple myeloma, beta-2-microglobulin, M protein, free light chains, and other proteins made by the myeloma cells are measured. A higher-than-normal amount of these substances can be a sign of disease.
Bone marrow aspiration and biopsy: The removal of bone marrow, blood, and a small piece of bone by inserting a hollow needle into the hipbone or breastbone. A pathologist views the bone marrow, blood, and bone under a microscope to look for abnormal cells.

KEY POINTS:

Waldenstrom macroglobulinemia (WM) is a lymphoplasmocytic malignancy characterized by the excessive production of monoclonal lgM antibody. Clinical manifestations of WM stem from elevated serum lgM (hyper viscosity syndrome, neuropathy, cryoglobulinemia) and neoplastic infiltration of tissue (hepatosplenomegaly, lymphadenopathy, cytopenia). Peripheral blood smear may show rouleaux formation (or erythrocyte agglutination) due to elevated serum protein. Serum protein electrophoresis (SPEP) is an important screening study; patients with WM have a monoclonal spike (M-spike) of IgM. Diagnosis is then confirmed by bone marrow biopsy showing >10% clonal B cells with specific cytogenetic features . The patient presents with manifestations of hyper viscosity syndrome (diplopia, tinnitus, headache, dilated/segmented funduscopic findings), neuropathy (electric sensation), and evidence of infillralive disease (hepatosplenomegaly, anemia, thrombocytopenia), suggesting WM.
A minority of patients with chronic lymphocytic leukemia (CLL) have high levels of monoclonal lgM, However, patients with CLL tend to have a dramatic lymphocytic predominant leukocytosis (often >100,000/mm3) on complete blood count.
Patients with monoclonal gammopathy of undetermined significance (MGUS) also have M spikes, but they are most commonly due to lgA, lgG, or lgD (lgM is seen in 15% of cases). MGUS is marked by smaller M spikes (<3 g/dL), bone marrow biopsy with <10% monoclonal plasma cells

ARDS require mechanical ventilation with the following goals:

Thu, 17 Nov 2022 21:35:30 GMT

Clinical points in ARDS

The management of acute respiratory distress syndrome (ARDS) involves avoiding complications of mechanical ventilation by using lung protective strategies such as low tidal volume ventilation (LTVV). LTVV results in lower pulmonary pressures, decreasing the likelihood of over distending alveoli. In addition, it improves mortality in patients with ARDS.

Avoiding complications of mechanical ventilation by using lung-protective strategies such as low tidal volume ventilation (LTVV):

LTVV (6 ml/kg of ideal body weight) decreases the likelihood of over distending alveoli and provoking barotrauma due to high plateau pressures (pressure applied to small airways and alveoli).
LTVV improves mortality in patients with ARDS. In contrast, higher tidal volumes in ARDS may result in elevated pulmonary pressures due to the work of forcing larger volumes into stiff lungs (decreased compliance), leading to increased alveolar distension.

Providing adequate oxygenation:

Increasing the fraction of inspired oxygen (Fi02) administered by the ventilator improves oxygenation; however, prolonged FiO2 levels >6 are associated with oxygen toxicity.
Increasing positive end—expiratory pressure (PEEP) also improves oxygenation by preventing alveolar collapse at the end of expiration, thereby decreasing shunting and the work of breathing.
Given the severe hypoxemia seen in ARDS, PEEP levels up to 15—20 cm H2O may be necessary to maintain oxygenation.
The goal is arterial partial pressure of oxygen (PaO2) at 55-80 mm Hg or peripheral saturation (Sp02) at 88%-95% (ie, preventing Spo2<88%, not <92%)

Optic neuritis

site-X7cQHw — Sun, 30 Oct 2022 03:47:56 GMT

Optic neuritis

Optic neuritis , an inflammatory demyelination of the optic nerve.

Optic neuritis is thought to be immune-mediated and is most commonly seen in women age 20-40 Symptoms develop acutely and usually include monocular vision loss, pain with eye movement, and “washed—out" color vision.

Examination typically reveals an afferent pupillary defect (paradoxical pupillary dilation of the affected eye with the swinging—flashlight test) and central scotoma.

Funduscopy is usually normal as inflammation occurs behind the optic nerve head

Optic neuritis is strongly associated with multiple sclerosis and is frequently the heralding symptom of this condition.

As such, patients are typically evaluated with MRI of the orbits and the brain to look for other areas of inflammation .

Criteria for thrombolytics in stroke

site-X7cQHw — Sat, 29 Oct 2022 03:51:01 GMT

Criteria for thrombolytics in stroke

Inclusion criteria:

Ischemic stroke with measurable neuro deficits Symptom onset <3—4V5 hours before treatment initiation

Strict exclusion criteria:

Hemorrhage or multilobe infarct involving >33% of cerebral hemisphere on CT scan Stroke
head trauma in the past 3 months
History of intracranial hemorrhage, neoplasm, or vascular malformation
Recent intracranial/spinal surgery
Active bleeding or arterial puncture in the past 7 days at noncompressible site
Blood pressure >180 mm Hg Platelets less than 100.000‘mm3 or glucose <50 mg/dL
Anticoagulant use with INR >1.7 PT >15 sec, or high active PTT

Relative exclusion criteria :

Minor or rapidly improving neuro deficits
Major surgery/trauma in past 14 days
Myocardial infarction in the past 3 months GU or GI bleeding in the past 21 days
Seizure at stroke onset
Pregnancy

What is syringomyelia?

Sat, 29 Oct 2022 03:24:10 GMT

Syringomyelia

Syringomyelia is a disorder in which a fluid-filled cyst (called a syrinx) forms within the spinal cord. Over time, the syrinx can get bigger and can damage the spinal cord and compress and injure the nerve fibers that carry information to the brain and from the brain to the rest of the body

The syrinx may represent dilation of the central canal or a separate cavity within the spinal parenchyma and is usually located within the cervical or thoracic spine Syringomyelia is most associated with Chiari type 1 malformation but may also occur with spinal cord inflammation, infection, neoplasms, or trauma.

Patients frequently have loss of pain/temperature sensation in the dermatomes corresponding to the site of spinal involvement (eg, " cape" distribution ). This is due to disturbance of the crossing spinothalamic tracts (STTs) in the anterior white commissure.

In contrast, vibratory/proprioceptive sensation is typically intact due to preservation of the dorsal columns (ie, dissociated sensory loss).

Continued syrinx enlargement can encroach on the central aspect of the lateral corticospinal tracts (LCTs) (in which the upper extremity fibers are somatotopically arranged more centrally) and/or the anterior horn gray matter. This produces weakness that disproportionately affects the upper extremities compared with the lower extremities

https://www.webmd.com/brain/what-is-syringomyelia

https://www.neurosurgery.columbia.edu/patient-care/conditions/syringomyelia

lateral medullary infarction (Wallenberg syndrome)

Thu, 27 Oct 2022 03:17:39 GMT

Wallenberg described the first case in 1895

Wallenberg syndrome is also known as lateral medullary syndrome and posterior inferior cerebellar artery syndrome. This neurological disorder is associated with a variety of symptoms that occur as a result of damage to the lateral segment of the medulla posterior to the inferior olivary nucleus. It is the most common posterior circulation ischemic stroke syndrome

Etiology

Wallenberg syndrome is caused most commonly by atherothrombotic occlusion of the vertebral artery, followed most frequently by the posterior inferior cerebellar artery, and least often, the medullary arteries. Hypertension is the most prevalent risk factor, followed by smoking and diabetes . Cerebral embolism is a less frequent cause of the infarction. The other important cause to remember is vertebral artery dissection , which may have risk factors including neck manipulation or injury, Marfan syndrome, Ehlers Danlos syndrome, and fibromuscular dysplasia. Vertebral artery dissection is the commonest cause of Wallenberg syndrome in younger patients

Epidemiology

It can be estimated that there are more than 60,000 new cases of Wallenberg syndrome each year in the United States.

Presentation suggests right—sided lateral medullary infarction (Wallenberg syndrome)

Vestibulocerebellar symptoms

Nystagmus (both horizontal and rotational),
Vertigo with falling to the side of the lesion, and difficulty sitting upright without support.

Sensory symptoms

loss of pain and temperature in the ipsilateral face (spinal trigeminal nucleus and tract) and contralateral trunk/limbs (spinothalamic tract).
Despite the loss of sensation, pain in the face is sometimes prominent, also likely due to spinal trigeminal nucleus and tract lesions.

Ipsilateral bulbar muscle weakness

(eg, dysphagia, dysarthria, hoarseness) due to involvement of the nucleus ambiguus

Autonomic dysfunction

(eg, ipsilateral Horner syndrome). The corneal reflex may be diminished due to disruption of the spinal trigeminal nucleus (located within the lateral medulla), which interrupts the reflex pathway.

Treatment / Management

1-Ogawa K, Suzuki Y, Oishi M, Kamei S. Clinical study of 46 patients with lateral medullary infarction. J Stroke Cerebrovasc Dis. 2015 May;24(5):1065-74. [ PubMed ]

Lui F, Tadi P, Anilkumar AC. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Jul 4, 2022. Wallenberg Syndrome. [ PubMed ]

Amarenco P, Hauw JJ. [Anatomy of the cerebellar arteries]. Rev Neurol (Paris). 1989;145(4):267-76. [ PubMed ]

Inamasu J, Nakae S, Kato Y, Hirose Y. Clinical Characteristics of Cerebellar Infarction Due to Arterial Dissection. Asian J Neurosurg. 2018 Oct-Dec;13(4):995-1000. [ PMC free article ] [ PubMed ]

Park MG, Choi JH, Yang TI, Oh SJ, Baik SK, Park KP. Spontaneous isolated posterior inferior cerebellar artery dissection: rare but underdiagnosed cause of ischemic stroke. J Stroke Cerebrovasc Dis. 2014 Aug;23(7):1865-70. [ PubMed ]

Saleem F, M Das J. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Aug 11, 2021. Lateral Medullary Syndrome. [ PubMed ]

Hong YH, Zhou LX, Yao M, Zhu YC, Cui LY, Ni J, Peng B. Lesion Topography and Its Correlation With Etiology in Medullary Infarction: Analysis From a Multi-Center Stroke Study in China. Front Neurol. 2018;9:813. [ PMC free article ] [ PubMed ]

Kim JS, Caplan LR. Clinical Stroke Syndromes. Front Neurol Neurosci. 2016;40:72-92. [ PubMed ]

Caplan LR. Lacunar infarction and small vessel disease: pathology and pathophysiology. J Stroke. 2015 Jan;17(1):2-6. [ PMC free article ] [ PubMed ]

10.

Ferbert A, Brückmann H, Drummen R. Clinical features of proven basilar artery occlusion. Stroke. 1990 Aug;21(8):1135-42. [ PubMed ]

11.

Kim YK, Schulman S. Cervical artery dissection: pathology, epidemiology and management. Thromb Res. 2009 Apr;123(6):810-21. [ PubMed ]

12.

Saber Tehrani AS, DeSanto JR, Kattah JC. Neuroimaging "HINTS" of the Lateral Medullary Syndrome. J Neuroophthalmol. 2017 Dec;37(4):403-404. [ PubMed ]

13.

Chen K, Schneider AL, Llinas RH, Marsh EB. Keep it simple: vascular risk factors and focal exam findings correctly identify posterior circulation ischemia in "dizzy" patients. BMC Emerg Med. 2016 Sep 13;16(1):37. [ PMC free article ] [ PubMed ]

14.

De Cocker LJ, Lövblad KO, Hendrikse J. MRI of Cerebellar Infarction. Eur Neurol. 2017;77(3-4):137-146. [ PubMed ]

15.

Makin SD, Doubal FN, Dennis MS, Wardlaw JM. Clinically Confirmed Stroke With Negative Diffusion-Weighted Imaging Magnetic Resonance Imaging: Longitudinal Study of Clinical Outcomes, Stroke Recurrence, and Systematic Review. Stroke. 2015 Nov;46(11):3142-8. [ PMC free article ] [ PubMed ]

16.

Kumral E, Kisabay A, Ataç C, Calli C, Yunten N. Spectrum of the posterior inferior cerebellar artery territory infarcts. Clinical-diffusion-weighted imaging correlates. Cerebrovasc Dis. 2005;20(5):370-80. [ PubMed ]

17.

Salerno A, Cotter BV, Winters ME. The Use of Tissue Plasminogen Activator in the Treatment of Wallenberg Syndrome Caused by Vertebral Artery Dissection. J Emerg Med. 2017 May;52(5):738-740. [ PubMed ]

18.

Malik MT, Kenton Iii EJ, Vanino D, Dalal SS, Zand R. Lateral Medullary Ischemic Infarct Caused by Posterior Inferior Cerebellar Artery Aneurysm. Case Rep Neurol. 2017 Sep-Dec;9(3):316-319. [ PMC free article ] [ PubMed ]

19.

Nesbitt J, Moxham S, Ramadurai G, Williams L. Improving pain assessment and managment in stroke patients. BMJ Qual Improv Rep. 2015;4(1) [ PMC free article ] [ PubMed ]

20.

Meschia JF, Bushnell C, Boden-Albala B, Braun LT, Bravata DM, Chaturvedi S, Creager MA, Eckel RH, Elkind MS, Fornage M, Goldstein LB, Greenberg SM, Horvath SE, Iadecola C, Jauch EC, Moore WS, Wilson JA., American Heart Association Stroke Council. Council on Cardiovascular and Stroke Nursing. Council on Clinical Cardiology. Council on Functional Genomics and Translational Biology. Council on Hypertension. Guidelines for the primary prevention of stroke: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2014 Dec;45(12):3754-832. [ PMC free article ] [ PubMed ]

21.

Yuan MZ, Li F, Tian X, Wang W, Jia M, Wang XF, Liu GW. Risk factors for lung infection in stroke patients: a meta-analysis of observational studies. Expert Rev Anti Infect Ther. 2015;13(10):1289-98. [ PubMed ]

22.

Guler A, Karbek Akarca F, Eraslan C, Tarhan C, Bilgen C, Kirazli T, Celebisoy N. Clinical and video head impulse test in the diagnosis of posterior circulation stroke presenting as acute vestibular syndrome in the emergency department. J Vestib Res. 2017;27(4):233-242. [ PubMed ]

23.

Roley SS, DeLany JV, Barrows CJ, Brownrigg S, Honaker D, Sava DI, Talley V, Voelkerding K, Amini DA, Smith E, Toto P, King S, Lieberman D, Baum MC, Cohen ES, Cleveland PA, Youngstrom MJ., American Occupational Therapy Association Commission on Practice. Occupational therapy practice framework: domain & practice, 2nd edition. Am J Occup Ther. 2008 Nov-Dec;62(6):625-83. [ PubMed ]

24.

Gupta H, Banerjee A. Recovery of Dysphagia in lateral medullary stroke. Case Rep Neurol Med. 2014;2014:404871. [ PMC free article ] [ PubMed ]

25.

Ekechukwu END, Olowoyo P, Nwankwo KO, Olaleye OA, Ogbodo VE, Hamzat TK, Owolabi MO. Pragmatic Solutions for Stroke Recovery and Improved Quality of Life in Low- and Middle-Income Countries-A Systematic Review. Front Neurol. 2020;11:337. [ PMC free article ] [ PubMed ]

Absence Seizures

site-X7cQHw — Thu, 27 Oct 2022 01:52:34 GMT

Absence seizures

According to the Epilepsy Foundation , an advocacy group, absence seizures generally last less than 10 to 20 seconds. Typical symptoms include:

staring off into space
smacking the lips together
fluttering eyelids
stopping speech in the middle of a sentence
making sudden hand movements
leaning forward or backward
appearing suddenly motionless

Adults may mistake absence seizures in children as misbehaving or being inattentive. A child’s teacher is often the first to notice absence seizure symptoms. The child will appear temporarily absent from their body.

You can often tell if a person is experiencing an absence seizure because they become unaware of their surroundings, touch, and sound. Absence seizures typically occur suddenly and with no warning. This makes taking precautions to protect the person having a seizure important.

Risk factors for absence seizures

Risk factors for developing absence seizures include:

Age. Absence seizures most often occur in children ages 4 to 12Trusted Source
. Based on a 2019 studyTrusted Source
, they peak around ages 6 to 7.
Triggers. Hyperventilation or flashing lights may trigger an absence seizure in some people, according to a 2021 review .
Gender. In a 2019 studyTrusted Source
, absence seizures occurred more often in girls than in boys.
Family history. A family history of epilepsy has been reported in 41.8 percentTrusted Source
of children with juvenile absence epilepsy. Juvenile absence epilepsy is an epileptic syndrome characterized by absence seizures and generalized tonic-clonic seizures.

How to tell the difference between absence seizures and focal impaired awareness seizures

Focal onset seizures , or partial seizures, start on one side of your brain. The Epilepsy Foundation says that they’re the most common type of seizure in adults. These seizures are referred to as focal impaired awareness seizures when they cause changes in your level of awareness. Some focal impaired awareness seizures are misdiagnosed as absence seizures.

Some of the key features that are more typical of focal impaired awareness seizures than absence seizures include:

less than daily frequency
lasting longer than 30 to 45 seconds
confusion and sleepiness after seizures
aura or strange feeling before the seizure

Educational objective:

Episodes of impaired concentration (eg, pause, blank stare) that occur in multiple settings with a sudden onset and resolution.

These episodes are suggestive of absence seizures, which are generalized seizures that typically last <20 seconds and occur in children age 4-10. During these episodes, which are often mistaken for inattention, patients maintain postural tone but are unresponsive to vocal or tactile stimulation.
Motor automatisms during the seizure are common and can include oral (eg, lip smacking, chewing) or eyelid (eg, blinking, fluttering) movements.
Many patients have a personal history of febrile seizures and/or a family history of seizures.
Hyperventilation can trigger an episode, but baseline neurologic examination is normal.
Diagnosis of absence seizures is confirmed by demonstration of a classic 3-Hz spike and wave pattern on electroencephalogram.
Ethosuximide is the first—line therapy. Most patients can discontinue medication before puberty with no long—term sequelae

Pediatric traumatic brain injury (PECARN rule)

Wed, 26 Oct 2022 21:04:42 GMT

PECARN rule

High-risk features age <2 :

Altered mental status (fussy behavior)
Loss of consciousness
Severe mechanism of injury (fall >09 in [3 ft], high impact, MVC)
Nonfrontal scalp hematoma
Palpable skull fractur e

High-risk features age more 2 to 18:

Altered mental status (eg, somnolence, agitation)
Loss of consciousness
Severe mechanism of injury (fall >1.5 m [5 ft], high impact, MVC)
Vomiting, severe headache
Basilar skull fracture signs (eg, CSF rhinorrhea)

Management - Head CT scan without contrast

https://www.uptodate.com/contents/severe-traumatic-brain-injury-tbi-in-children-initial-evaluation-and-management

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7254418/

https://canchild.ca/en/resources/249-concussion-mild-traumatic-brain-injury-guideline-brochures

https://canchild.ca/system/tenon/assets/attachments/000/002/643/original/RTARTS_Suggestion_by_stage.pdf

Brain hemorrhage

Sun, 23 Oct 2022 02:39:46 GMT

Site of hemorrhage, Neurologic findings

Basal ganglia Neurologic findings:

Contralateral herniparesis & hemisensory loss
Homonymous hemianopsia
Gaze palsy

Cerebellum Neurologic findings:

Usually NO hemiparesis
Facial weakness
Ataxia & nystagmus
Occipital headache & neck stuffiness

Thalamus Neurologic findings :

Contralateral hemiparesis & hemisensory loss
Nonreactive miotic pupils
Upgaze palsy
Eyes deviate Toward hemiparesis

Cerebral lobe Neurologic findings:

Contralateral hemiparesis (frontal lobe)
Contralateral hemisensory loss (parietal lobe)
Cerebral lobe Homonymous hemianopsia (occipital lobe)
Eyes deviate away from hemiparesis
High incidence of seizures

PONS Neurologic findings:

Deep coma & total paralysis within minutes
Pinpoint reactive pupils

4 Causes itchy skin in pregnancy

Tue, 20 Sep 2022 22:00:13 GMT

Intrahepatic cholestasis of pregnancy

Although most cases of pruritus can be attributed to itchy dry skin, there are conditions unique to pregnancy that involve pruritus as a leading symptom. These include :

A-Pemphigoid gestations

Pemphigoid gestationis, formerly known as herpes gestationis, is a rare autoimmune sub-epidermal bullous dermatosis of that shares some clinical and pathogenic features with bullous pemphigoid. Pemphigoid gestationis typically presents during the third trimester, though it can present in any trimester or even after delivery. It manifests with inflammatory skin lesions and severe pruritus. It tends to recur in subsequent pregnancies earlier and with a more severe course. This activity describes the pathophysiology, etiology, evaluation, and management of pemphigoid gestationis and highlights the role of the interprofessional team in the care of affected patients.

B- Pruritic urticarial papules and plaques of pregnancy

Pruritic urticarial papules and plaques of pregnancy (PUPPP) rash is an itchy rash that appears in stretch marks of the stomach during late pregnancy.

While the exact cause of PUPPP rash isn’t known, the stretching of the skin seems to be a trigger for the rash to occur. PUPPP rash occurs in about 1 in every 150 pregnancies.

C- Intrahepatic cholestasis of pregnancy

Intrahepatic cholestasis of pregnancy (ICP) is a cholestatic disorder characterized by (i) pruritus with onset in the second or third trimester of pregnancy, (ii) elevated serum aminotransferases and bile acid levels, and (iii) spontaneous relief of signs and symptoms within two to three weeks after delivery . ICP is observed in 0.4–1% of pregnancies in most areas of Central and Western Europe and North America, while in Chile and Bolivia as well as Scandinavia and the Baltic states roughly 5–15% and 1–2%, respectively, of pregnancies are associated with ICP. Genetic and hormonal factors, but also environmental factors may contribute to the pathogenesis of ICP.

Intrahepatic cholestasis of pregnancy increases the risk of preterm delivery (19–60%), meconium staining of amniotic fluid (27%), fetal bradycardia (14%), fetal distress (22–41%), and fetal loss (0.4–4.1%), particularly when associated with fasting serum bile acid levels > 40 μmol/L. The hydrophilic bile acid ursodeoxycholic acid (10–20 mg/kg/d) is today regarded as the first line treatment for intrahepatic cholestasis of pregnancy.

Delivery has been recommended in the 38th week when lung maturity has been established

D- Atopic eruption of pregnancy

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1891276/

The use of acetylsalicylic acid (ASA or Aspirin®) has been strongly linked to Reye Syndrome.

site-X7cQHw — Sat, 17 Sep 2022 21:50:03 GMT

What is Reye Syndrome?

Reye Syndrome

is a rare disease that mainly affects children and teenagers when they have, or recently had, a viral infection such as chickenpox or influenza. Reye Syndrome causes swelling of the liver and brain, and it can also cause death.

How can I prevent Reye Syndrome?

The use of acetylsalicylic acid (ASA or Aspirin®) has been strongly linked to Reye Syndrome. Do not give ASA or Aspirin® to anyone under 18 years of age to manage symptoms such as fever, headache and muscle aches.

Instead, use acetaminophen for anyone under 18 years of age. Examples of medications with acetaminophen are Tylenol®, Tempra® and Atasol®.

You can also use ibuprofen for relief of symptoms in children under 18 years of age. Examples of ibuprofen include Advil® and Motrin®. Do not use products containing ibuprofen in children under 6 months of age without first talking to your health care provider.

Always use the dosage indicated in the product instructions or as recommended by your health care provider.

What are the symptoms of Reye Syndrome?

Symptoms of Reye Syndrome include:

Unusual sleepiness or lack of energy
Diarrhea and rapid breathing in infants and toddlers
Persistent vomiting in children and teenagers
Changes in personality or behaviour such as confusion, irritability or aggression. Reye Syndrome may also cause strange behavior such as staring and slurred speech
Seizures and comas
Loss of consciousness

Reye Syndrome occurs 3 to 7 days after the beginning of an infection or illness caused by a virus, or during recovery from the infection or illness. Reye Syndrome can be misdiagnosed as swelling of the brain, also known as encephalitis or swelling of the lining of the brain (meningitis), diabetes, drug overdose, poisoning, sudden infant death syndrome (SIDS) or a psychiatric illness.

What is the treatment?

Early diagnosis and treatment in a hospital can save your child’s life. Treatment includes reducing brain swelling, preventing damage to the liver and other organs and monitoring the heart.

Most people recover completely, but Reye Syndrome can cause permanent brain damage or death.

https://www.healthlinkbc.ca/healthlinkbc-files/reye-syndrome

Blunt abdominal trauma

Wed, 14 Sep 2022 05:56:57 GMT

ABDOMINAL TRAUMA

Abdominal trauma caused by blunt force is a common presentation in the emergency room seen in adults and children. The chief cause of blunt abdominal trauma in the United States is motor vehicle accidents. This activity describes the clinical presentation, evaluation, and management of blunt abdominal trauma and the importance of the interprofessional team in educating patients on prevention of abdominal injuries .

Etiology

The chief cause of blunt abdominal trauma in the United States is motor vehicle accidents. Other rare causes include falls from heights, bicycle injuries, injuries sustained during sporting activities, and industrial accidents. In children, the most common causes are due to motor vehicle injuries and bicycle accidents

History and Physical

Because the presentation is often not straightforward, the diagnosis can be difficult and often time-consuming. Besides pain, the patient may present with bleeding per rectum, unstable vital signs, and the presence of peritonitis. The physical exam may reveal marks from a lap belt, ecchymosis, abdominal distention, absent bowel sounds and tenderness to palpation. If peritonitis is present, abdominal rigidity, guarding and rebound tenderness may be present. The mechanism of injury, motor vehicle speed, associated deaths at the scene, uses of alcohol or other substance of abuse must be taken into account so as not to miss an injury.

Evaluation

The evaluation of any trauma patient begins with evaluating the airway, accessing the breathing, and managing the circulation. The diagnosis of intra-abdominal injury following blunt trauma depends primarily on the hemodynamic status of the patient. If the patient is hemodynamically stable , CT scan is the ideal test to look for solid organ injury in the abdomen and pelvis. For unstable patients , one may perform an ultrasound (Extended Focused Assessment with Sonography for Trauma (EFAST)) or diagnostic peritoneal lavage, both of which are associated with a high rate of false negatives and false positives

The Extended Focused Assessment with Sonography for Trauma (EFAST) exam

1. RUQ (right upper quadrant)

2. Perisplenic space LUQ (left upper quadrant)

3. Pelvis (bladder)

4. Cardiac view

5. Normal Lung

Pearls and Other Issues

A-When a hollow viscus (eg, duodenum, ascending or descending colon) perforates within the retroperitoneum, gastrointestinal spillage may be initially sequestered away from the intraperitoneal space (which is separated from the retroperitoneum by the posterior peritoneal lining). This may delay the development of classic symptoms and signs of perforation (eg, fever, diffuse abdominal pain), . In addition, back or flank pain (eg, right flank pain) may be present due to retropentoneal inflammation.

-Aspects of duodenal anatomy that increase the duodenum's susceptibility to perforation include:

. Its location anterior to the vertebral column: compression against the vertebral column during BAT can rapidly increase intraluminal pressure, causing rupture.

. Its multiple attachments (eg, hepatoduodenal ligament, ligament of Treitz): abrupt force against the duodenum can cause duodenal tearing at fixed points of attachment rather than stretching.

C-The stomach and transverse colon are also susceptible to rupture from rapid change in intraluminal pressure during BAT. However, both are intraperitoneal (vs retroperitoneal) structures. Therefore, intraperitoneal free air (eg, free air under the diaphragm on chest x—ray) would be expected on imaging .

BAT can injure the pancreas or kidney, causing spillage of pancreatic enzymes or urine into the retroperitoneal space. Although both renal pelvis laceration and traumatic pancreatitis could result in a delayed presentation of abdominal and right flank pain, they would typically cause free fluid rather than free air on

Treatment / Management

Treatment of patients with blunt abdominal injury requires the routine ABCs (Airway, Breathing, and Circulation). Once the airway is protected, it is mandatory to protect the cervical spine. After the primary survey is complete, patients who are hypotensive require aggressive fluid resuscitation. If hemodynamic instability persists, blood should be typed and crossed, but in the meantime, immediate transfusion with O negative blood can be done (O+ for males and women past childbearing years). All patients with blunt abdominal trauma who have signs of peritonitis, frank bleeding, or worsening of clinical signs require an immediate laparotomy. Non-surgical treatment in patients with blunt abdominal injury depends on the clinical features, hemodynamic stability and results of the CT scan. Advances in angiography can now help control hemorrhage with the use of embolization therapy, which is more cost effective than laparotomy. In general, the prognosis of patients with blunt abdominal trauma is good

References

Authors

Maria C. O'Rourke1; Ryan Landis2; Bracken Burns3

Garside G, Khan O, Mukhtar Z, Sinha C. Paediatric duodenal injury complicated by common bile duct rupture due to blunt trauma: a multispecialist approach. BMJ Case Rep. 2018 Aug 29;2018 [ PMC free article ] [ PubMed ]

Zhou H, Ma X, Sheng M, Lai C, Fu J. Evolution of intramural duodenal hematomas on magnetic resonance imaging. Pediatr Radiol. 2018 Oct;48(11):1593-1599. [ PubMed ]

Molinelli V, Iosca S, Duka E, De Marchi G, Lucchina N, Bracchi E, Carcano G, Novario R, Fugazzola C. Ability of specific and nonspecific signs of multidetector computed tomography (MDCT) in the diagnosis of blunt surgically important bowel and mesenteric injuries. Radiol Med. 2018 Dec;123(12):891-903. [ PubMed ]

Taghavi S, Askari R. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Jul 22, 2021. Liver Trauma. [ PubMed ]

Renson A, Musser B, Schubert FD, Bjurlin MA. Seatbelt use is associated with lower risk of high-grade hepatic injury in motor vehicle crashes in a national sample. J Epidemiol Community Health. 2018 Aug;72(8):746-751. [ PubMed ]

Pelletti G, Cecchetto G, Viero A, De Matteis M, Viel G, Montisci M. Traumatic fatal aortic rupture in motorcycle drivers. Forensic Sci Int. 2017 Dec;281:121-126. [ PubMed ]

Tarchouli M, Elabsi M, Njoumi N, Essarghini M, Echarrab M, Chkoff MR. Liver trauma: What current management? Hepatobiliary Pancreat Dis Int. 2018 Feb;17(1):39-44. [ PubMed ]

So HF, Nabi H. Handlebar hernia - A rare complication from blunt trauma. Int J Surg Case Rep. 2018;49:118-120. [ PMC free article ] [ PubMed ]

Wortman JR, Uyeda JW, Fulwadhva UP, Sodickson AD. Dual-Energy CT for Abdominal and Pelvic Trauma. Radiographics. 2018 Mar-Apr;38(2):586-602. [ PubMed ]

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Tsai R, Raptis D, Raptis C, Mellnick VM. Traumatic abdominal aortic injury: clinical considerations for the diagnostic radiologist. Abdom Radiol (NY). 2018 May;43(5):1084-1093. [ PubMed ]

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Tomic I, Dragas M, Vasin D, Loncar Z, Fatic N, Davidovic L. Seat-Belt Abdominal Aortic Injury-Treatment Modalities. Ann Vasc Surg. 2018 Nov;53:270.e13-270.e16. [ PubMed ]

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Inukai K, Uehara S, Furuta Y, Miura M. Nonoperative management of blunt liver injury in hemodynamically stable versus unstable patients: a retrospective study. Emerg Radiol. 2018 Dec;25(6):647-652. [ PubMed ]

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Sarychev LP, Sarychev YV, Pustovoyt HL, Sukhomlin SA, Suprunenko SM. Management of the patients with blunt renal trauma: 20 years of clinical experience. Wiad Lek. 2018;71(3 pt 2):719-722. [ PubMed ]

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Cunningham AJ, Lofberg KM, Krishnaswami S, Butler MW, Azarow KS, Hamilton NA, Fialkowski EA, Bilyeu P, Ohm E, Burns EC, Hendrickson M, Krishnan P, Gingalewski C, Jafri MA. Minimizing variance in Care of Pediatric Blunt Solid Organ Injury through Utilization of a hemodynamic-driven protocol: a multi-institution study. J Pediatr Surg. 2017 Dec;52(12):2026-2030. [ PubMed ]

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Aeberhard P, Weber M. [Sigmoid colon injuries caused by blunt abdominal trauma]. Helv Chir Acta. 1979 Feb;45(6):719-22. [ PubMed ]

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Waheed KB, Baig AA, Raza A, Ul Hassan MZ, Khattab MA, Raza U. Diagnostic accuracy of Focused Assessment with Sonography for Trauma for blunt abdominal trauma in the Eastern Region of Saudi Arabia. Saudi Med J. 2018 Jun;39(6):598-602. [ PMC free article ] [ PubMed ]

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Margari S, Garozzo Velloni F, Tonolini M, Colombo E, Artioli D, Allievi NE, Sammartano F, Chiara O, Vanzulli A. Emergency CT for assessment and management of blunt traumatic splenic injuries at a Level 1 Trauma Center: 13-year study. Emerg Radiol. 2018 Oct;25(5):489-497. [ PubMed ]

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Guillen B, Cassaro S. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Jul 15, 2021. Traumatic Open Abd omen. [ PubMed ]

Serum alpha—fetoprotein level

Tue, 13 Sep 2022 03:22:26 GMT

Alpha Fetoprotein

https://www.ncbi.nlm.nih.gov/books/NBK430750/

Introduction

Alpha-fetoprotein (AFP) is a plasma protein produced by the embryonic yolk sac and the fetal liver. AFP levels in serum, amniotic fluid, and urine functions as a screening test for congenital disabilities, chromosomal abnormalities, as well as some other adult occurring tumors and pathologies. This tumor marker is a glycoprotein encoded by the AFP gene on chromosome 4q25. Prenatal levels in developing human embryo rise from the end of the first trimester and begin to fall after 32 weeks of gestation. Maternal serum AFP forms part of the triple or quadruple screening tests for fetal anomaly. [1][2][3]

Potential Diagnosis

Pregnant maternal serum AFP levels elevated:

Neural tube defects (e.g., spina bifida, anencephaly)
Omphalocele
Gastroschisis

Pregnant maternal serum AFP low levels:

Down syndrome

Non-pregnant female or male adult AFP elevated:

Hepatocellular cancer
Metastatic liver cancer
Liver cirrhosis
Hepatitis
Germ cell tumors
Yolk sac tumor
Ataxia telangiectasia

References

Sharony R, Dayan D, Kidron D, Manor M, Berkovitz A, Biron-Shental T, Maymon R. Is the ratio of maternal serum to amniotic fluid AFP superior to serum levels as a predictor of pregnancy complications? Arch Gynecol Obstet. 2016 Apr;293(4):767-70. [ PubMed ]

Öztürk H, Erkaya S, Altınbaş S, Karadağ B, Vanlı Tonyalı N, Özkan D. The role of unexplained high serum alpha-fetoprotein (AFP) and human chorionic gonadotropin (hCG) levels in the second trimester to determine poor obstetric outcomes. Turk J Obstet Gynecol. 2014 Sep;11(3):142-147. [ PMC free article ] [ PubMed ]

Rood K, Stiller R. Hereditary persistence of alpha-fetoprotein: a rare cause for unexplained alpha-fetoprotein elevations in pregnancy. Conn Med. 2013 Jan;77(1):43-5. [ PubMed ]

Gkogkos P, Androutsopoulos G, Vassilakos P, Panayiotakis G, Kourounis G, Decavalas G. Mid-trimester maternal serum AFP levels in predicting adverse pregnancy outcome. Clin Exp Obstet Gynecol. 2008;35(3):208-10. [ PubMed ]

Chen CP, Chern SR, Cheng SJ, Chang TY, Yeh LF, Lee CC, Pan CW, Wang W, Tzen CY. Second-trimester diagnosis of complete trisomy 9 associated with abnormal maternal serum screen results, open sacral spina bifida and congenital diaphragmatic hernia, and review of the literature. Prenat Diagn. 2004 Jun;24(6):455-62. [ PubMed ]

Shipp TD, Wilkins-Haug L. The association of early-onset fetal growth restriction, elevated maternal serum alpha-fetoprotein, and the development of severe pre-eclampsia. Prenat Diagn. 1997 Apr;17(4):305-9. [ PubMed ]

Benn PA, Horne D, Briganti S, Rodis JF, Clive JM. Elevated second-trimester maternal serum hCG alone or in combination with elevated alpha-fetoprotein. Obstet Gynecol. 1996 Feb;87(2):217-22. [ PubMed ]

Wenstrom KD, Owen J, Davis RO, Brumfield CG. Prognostic significance of unexplained elevated amniotic fluid alpha-fetoprotein. Obstet Gynecol. 1996 Feb;87(2):213-6. [ PubMed ]

Ursodeoxycholic acid therapy

Tue, 13 Sep 2022 03:05:01 GMT

Ursodeoxycholic acid therapy

https://www.ncbi.nlm.nih.gov/books/NBK545303/

Ursodeoxycholic acid is a medication used in the management and treatment of cholestatic liver disease. This activity reviews the indications, mechanism of action, and contraindications for UDCA as a valuable agent in managing liver disease. This activity will highlight the mechanism of action, adverse event profile, and other key factors (e.g., off-label uses, dosing, pharmacodynamics, pharmacokinetics, monitoring, relevant interactions) pertinent for members of the interprofessional team performing patient management of cholestatic liver disease and related conditions.

Objectives:

Identify the mechanism of action of ursodeoxycholic acid.
Describe the potential adverse effects of ursodeoxycholic acid.
Review appropriate monitoring needed for patients receiving therapy with ursodeoxycholic acid.
Explain interprofessional team strategies for improving care coordination and communication to advance the use of ursodeoxycholic acid and improve outcomes.

Access free multiple choice questions on this topic.

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Indications

The use of ursodeoxycholic acid (UDCA), also known as ursodiol, in treating liver disease dates back more than a hundred years when it was first employed in traditional Chinese medicine by herbalists and physicians alike. Before discovering its effectiveness in dissolving gallstones, its primary use was as a liver tonic. [1][2] Today, there is extensive evidence suggesting that UDCA is beneficial in various types of liver pathology. However, the greatest amount of data still points to its therapeutic effect in treating gallstone disease.

Gallstone disease is a common and exceedingly costly digestive disorder if considering the number of hospital admissions and cholecystectomies performed in the United States annually. It is a complex disorder where both genetic and environmental factors contribute to the susceptibility of the disease. The primary non-invasive treatment for cholesterol gallstones is oral litholysis with bile acids. UDCA has been shown to decrease the biliary cholesterol saturation markedly and has found use as an alternative to cholecystectomy in patients with gallstone disease. [3] Currently, gallstone disease is not an FDA-approved indication for UDCA use.

Biliary sludge is considered to be another therapeutic target of UDCA therapy. It’s an occurrence commonly precipitated by rapid weight loss, pregnancy, and total parenteral nutrition. A clinical study in which patients with idiopathic acute pancreatitis attributed to microscopic gallstones or biliary sludge showed complete resolution of gallbladder microlithiasis after UDCA treatment, demonstrating its therapeutic effect. [4][1]

UDCA is commonly used to treat patients with primary biliary cholangitis (formerly known as primary biliary cirrhosis), an immune-mediated cholestatic liver disease characterized by the destruction of intrahepatic bile ducts. UDCA is the only drug approved by the U.S Food and Drug Administration to treat primary biliary cholangitis. Studies suggest that UDCA can significantly delay the progression of liver cirrhosis in patients with early stages of PBC. [5][6] In one study, the probability of remaining free of extensive fibrosis or cirrhosis after UDCA treatment was 76% and 61% after being treated for 4 and 8 years, respectively. [7] Similar results have been observed in other case-control studies as well.

UDCA has been shown to have a role in treating patients with primary sclerosing cholangitis. However, its use in PSC has not come without controversy. Primary biliary cirrhosis is a rare, progressive, immuno-mediated hepatobiliary disease. Currently, there is no proven medical therapy for patients with PSC, but UDCA has been established as first-line therapy for those suffering from the condition. The most significant two clinical trials of UDCA in PSC had somewhat disappointing results. One trial only showed a minimal trend toward statistically significant benefit with moderate doses of UDCA, and researchers terminated the other trial where high dose UDCA was used due to excessive adverse effects. Despite the lack of data regarding long-term efficacy, many experts still recommend moderate doses of UDCA in PSC. Lack of sufficient data regarding long-term efficacy might explain why PSC is not an FDA-approved indication for UDCA treatment. [8]

Current data also supports UDCA treatment in intrahepatic cholestasis of pregnancy, a unique pregnancy-related disorder that can manifest during the late third trimester of pregnancy. In a recent meta-analysis that looked at 12 RCTs involving 662 patients with ICP, UDCA was associated with resolution of pruritus, reduced serum levels of bile acids, and decreased serum levels of alanine aminotransferase. The same meta-analysis also demonstrated reduced adverse maternal and fetal outcomes among pregnant women with ICP. [9] Despite the current data, the FDA does not list ICP as an indication for UDCA treatment.

UDCA has also found use in the treatment of cystic fibrosis, graft vs. host disease involving the liver, liver allograft rejection, bile duct-paucity syndromes such as biliary atresia, and non-alcoholic steatohepatitis. However, more studies are needed to determine the therapeutic potential of UDCA in these disorders, and the FDA has not approved the drug for treating these liver conditions.

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Mechanism of Action

Ursodeoxycholic acid acts on the liver through various complex and complementary mechanisms, including alterations in the bile acid pool, serving as a cytoprotectant, immunomodulating substance, and choleretic. Furthermore, UDCA markedly decreases biliary cholesterol saturation by inhibiting the absorption of cholesterol in the intestine and its secretion into bile, demonstrated by reduced cholesterol fraction of biliary lipids. [1][3]

The cytoprotective effect of UDCA is attributable to its ability to protect hepatocytes and cholangiocytes from bile acid-induced damage. Bile acids stimulate the formation of reactive oxygen species, which induce inflammatory processes and cholecystitis. [10] Evidence suggests that bile acids damage cells by causing mitochondrial dysfunction. UDCA offers cytoprotection in hepatic epithelia by preserving cell structures, including plasma membranes and mitochondria, while stimulating anti-apoptotic pathways. Additionally, UDCA can prevent Kupffer cells, the resident macrophages in the liver, from generating reactive oxygen species, thus decreasing the level of oxidate stress in hepatocytes. [3][11]

Therapeutic concentrations of ursodeoxycholic acid can shift the concentration of bile acids from hydrophobicity to hydrophilicity. [12] Hydrophobic bile acids, including deoxycholic acid and chenodeoxycholic acid, have been shown to have a toxic effect on hepatocytes by increasing cell membrane permeability and inducing apoptosis. There are suggestions that UDCA competitively displaces the endogenous bile acids at the level of ileal absorption or the hepatocyte level, thus decreasing the concentration of toxic hydrophobic bile acids while simultaneously increasing the absorption of hydrophilic bile acids. [4] Depending on the dosage, UDCA and its conjugates account for approximately 19 to 64% of total biliary bile acids. [3]

The choleretic effect of UDCA is attributable to its ability to induce the secretion of bile acids. This effect is comparable to endogenous bile acids; however, without the potential toxicity, which makes it useful in treating cholestatic disorders. In fact, prior studies have shown that in patients with primary biliary cirrhosis and primary sclerosing cholangitis, UDCA therapy improved the excretion rates and transit time of bile acid analogs. [4][13] UDCA induces vesicular exocytosis in cholestatic hepatocytes by indirectly increasing intracellular calcium levels. In animal models, high levels of intracellular calcium were shown to stimulate transport proteins and vesicular exocytosis. [4][14] Other proposed mechanisms behind UDCA-induced choleresis include modulation of membrane transport proteins such as the chloride-bicarb anion exchanger (AE2), which research found to be diminished in biliary epithelia of PBC patients. UDCA administration was found to upregulate the expression of AE2 transporter when compared to the placebo group. [4][15]

UDCA has also been shown to have an immunomodulating effect on hepatocytes. In rats with extrahepatic obstruction caused by bile duct ligation, researchers observed an increased hepatic expression of major histocompatibility complex (MHC) class I antigens. Similarly, patients with cholestasis resulting from primary biliary cirrhosis have the same aberrant expression of MHC class I antigens on hepatocytes and bile duct cells. Expression of these antigens could lead to immune-mediated destruction by activated lymphocytes, causing hepatic injury. UDCA has been shown to reduce the expression of class I antigens in several cholestatic liver disorders. [16]

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Administration

Ursodeoxycholic acid is a film-coated tablet available for oral administration. The absorption of the drug is enhanced by other bile acids; therefore, it is recommended to take the drug during meals with food to facilitate biliary secretion by the gallbladder. [17]

The dosing of UDCA is as follows:

For gallstone dissolution: 8 to 10 mg/kg/day orally divided into three or four doses.

For gallstone prophylaxis: 300 mg orally twice daily.

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Adverse Effects

Ursodeoxycholic acid is a mostly well-tolerated drug. In most clinical trials, diarrhea was the most frequent adverse event observed during UDCA treatment in patients with gallstone disease, with a reported incidence of 2 to 9%. The mechanism behind this side effect is unclear. However, researchers have proposed that bacterial conversion of UDCA to chenodeoxycholic acid, which serves as a potent secretory substance, could significantly contribute to this side effect. In patients with primary biliary cirrhosis, right upper quadrant abdominal pain was the most common reported side effect. Reports also exist of skin reactions in those with primary biliary cirrhosis. The most common dermatological manifestation was an exacerbation of pruritus, even though UDCA has demonstrated effectiveness in relieving pruritus in patients with PBC in other trials. [18]

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Contraindications

The use of ursodeoxycholic acid is contraindicated in patients with obstructive cholestasis due to a potential risk of biliary integrity disruption. Also, UDCA has not received approval for use in early pregnancy because of insufficient data regarding the risk of UDCA on the fetus during the first trimester of pregnancy. [19]

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Monitoring

There is limited data on the therapeutic index of ursodeoxycholic acid. However, most data suggest that UDCA in doses of 5 to 25 mg/kg appears safe and well-tolerated. In patients with PBC, a dose of 13 to 15 mg/kg is preferred. The dose of 10 to 15 mg/kg used in most large trials was mostly for gallstone dissolution. [20]

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Toxicity

UDCA has been shown to have potentially toxic molecular properties. UDCA breaks down into toxic lithocholic acid. After being absorbed in the small intestine, UDCA undergoes hepatic conjugation. Beyond conjugation, UDCA does not experience further breakdown by the liver or intestinal mucosa. It becomes oxidized or reduced, yielding either 7-keto-lithocholic acid or lithocholic acid. Litcholic acid can be toxic to liver cells and even cause liver failure in those with compromised sulfation. It also leads to segmental bile duct injury, hepatocyte failure, and death. [21]

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Enhancing Healthcare Team Outcomes

The large number of studies and data published on UDCA demonstrates the therapeutic effect of this drug on various forms of cholestatic liver disease. The efficacy of UDCA in primary biliary cholangitis is evident. Prolonged administration of ursodeoxycholic acid for patients with primary biliary cholangitis (PBC) is associated with a survival benefit and delaying of liver transplantation. There is evidence that it might even prevent the progression of the histologic stage of PBC. A comprehensive review of three randomized trials from the United States, Canada, and France included more than 500 patients with PBC treated with UDCA, with a median length of follow-up of 4 years. Patients treated with UDCA had significantly longer transplant-free survival, with a 32% reduced risk of death or transplantation. However, it is essential to note that up to 40% percent of patients with PBC exhibit an inadequate response to UDCA and may continue to experience disease progression. In these cases, second-line agents merit consideration. [22]

Recent data also suggest UDCA might have a role in managing PSC, cystic fibrosis, graft-versus-host-disease, and other hepatobiliary disorders; however, concrete data regarding therapeutic potential and long-term effects are currently lacking. Due to its multi-functionality, it is difficult to envision a viable substitute agent for UDCA that combines as many hepatoprotective effects with similar efficacy. The significant progress made in understanding the anti-cholestatic mechanisms of UDCA has allowed for successful testing of new therapeutic applications, even beyond liver and gallbladder disease. Several alternative drugs are under investigation in pre-clinical trials; however, unless there's an agent proven to be more effective than the current therapy, UDCA will most likely remain the go-to agent for treating cholestatic liver disease.

The use of UDCA requires the involvement of the entire interprofessional healthcare team. Management of the drug includes monitoring by the pharmacist in tandem with the prescribing clinician (MD, DO, NP, PA). While the drug is safe, it can exacerbate pruritis and cause abdominal discomfort. The pharmacist should notify the clinician if the side effects become intolerable. Nursing can assess for therapeutic effectiveness and adverse events at follow-up visits, which is particularly important if the drug is used off-label, and report these to the rest of the team. As more data regarding indications and use of UDCA becomes available from ongoing research, all interprofessional healthcare team members need to keep current to drive patient outcomes optimally to effectively use ursodeoxycholic acid, where it can provide therapeutic benefit. [Level 5]

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Review Questions

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References

Guarino MP, Cocca S, Altomare A, Emerenziani S, Cicala M. Ursodeoxycholic acid therapy in gallbladder disease, a story not yet completed. World J Gastroenterol. 2013 Aug 21;19(31):5029-34. [ PMC free article ] [ PubMed ]

Makino I, Tanaka H. From a choleretic to an immunomodulator: historical review of ursodeoxycholic acid as a medicament. J Gastroenterol Hepatol. 1998 Jun;13(6):659-64. [ PubMed ]

Roma MG, Toledo FD, Boaglio AC, Basiglio CL, Crocenzi FA, Sánchez Pozzi EJ. Ursodeoxycholic acid in cholestasis: linking action mechanisms to therapeutic applications. Clin Sci (Lond). 2011 Dec;121(12):523-44. [ PubMed ]

Lazaridis KN, Gores GJ, Lindor KD. Ursodeoxycholic acid 'mechanisms of action and clinical use in hepatobiliary disorders'. J Hepatol. 2001 Jul;35(1):134-46. [ PubMed ]

Copaci I, Micu L, Iliescu L, Voiculescu M. New therapeutical indications of ursodeoxycholic acid. Rom J Gastroenterol. 2005 Sep;14(3):259-66. [ PubMed ]

Chascsa D, Carey EJ, Lindor KD. Old and new treatments for primary biliary cholangitis. Liver Int. 2017 Apr;37(4):490-499. [ PubMed ]

Patel A, Seetharam A. Primary Biliary Cholangitis: Disease Pathogenesis and Implications for Established and Novel Therapeutics. J Clin Exp Hepatol. 2016 Dec;6(4):311-318. [ PMC free article ] [ PubMed ]

Tabibian JH, Ali AH, Lindor KD. Primary Sclerosing Cholangitis, Part 1: Epidemiology, Etiopathogenesis, Clinical Features, and Treatment. Gastroenterol Hepatol (N Y). 2018 May;14(5):293-304. [ PMC free article ] [ PubMed ]

Kong X, Kong Y, Zhang F, Wang T, Yan J. Evaluating the effectiveness and safety of ursodeoxycholic acid in treatment of intrahepatic cholestasis of pregnancy: A meta-analysis (a prisma-compliant study). Medicine (Baltimore). 2016 Oct;95(40):e4949. [ PMC free article ] [ PubMed ]

10.

Ward JBJ, Lajczak NK, Kelly OB, O'Dwyer AM, Giddam AK, Ní Gabhann J, Franco P, Tambuwala MM, Jefferies CA, Keely S, Roda A, Keely SJ. Ursodeoxycholic acid and lithocholic acid exert anti-inflammatory actions in the colon. Am J Physiol Gastrointest Liver Physiol. 2017 Jun 01;312(6):G550-G558. [ PubMed ]

11.

Ljubuncic P, Fuhrman B, Oiknine J, Aviram M, Bomzon A. Effect of deoxycholic acid and ursodeoxycholic acid on lipid peroxidation in cultured macrophages. Gut. 1996 Sep;39(3):475-8. [ PMC free article ] [ PubMed ]

12.

Combes B, Carithers RL, Maddrey WC, Munoz S, Garcia-Tsao G, Bonner GF, Boyer JL, Luketic VA, Shiffman ML, Peters MG, White H, Zetterman RK, Risser R, Rossi SS, Hofmann AF. Biliary bile acids in primary biliary cirrhosis: effect of ursodeoxycholic acid. Hepatology. 1999 Jun;29(6):1649-54. [ PMC free article ] [ PubMed ]

13.

Jazrawi RP, de Caestecker JS, Goggin PM, Britten AJ, Joseph AE, Maxwell JD, Northfield TC. Kinetics of hepatic bile acid handling in cholestatic liver disease: effect of ursodeoxycholic acid. Gastroenterology. 1994 Jan;106(1):134-42. [ PubMed ]

14.

Heuman DM. Hepatoprotective properties of ursodeoxycholic acid. Gastroenterology. 1993 Jun;104(6):1865-70. [ PubMed ]

15.

Medina JF, Martínez-Ansó, Vazquez JJ, Prieto J. Decreased anion exchanger 2 immunoreactivity in the liver of patients with primary biliary cirrhosis. Hepatology. 1997 Jan;25(1):12-7. [ PubMed ]

16.

Hillaire S, Boucher E, Calmus Y, Gane P, Ballet F, Franco D, Moukthar M, Poupon R. Effects of bile acids and cholestasis on major histocompatibility complex class I in human and rat hepatocytes. Gastroenterology. 1994 Sep;107(3):781-8. [ PubMed ]

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Saksena S, Tandon RK. Ursodeoxycholic acid in the treatment of liver diseases. Postgrad Med J. 1997 Feb;73(856):75-80. [ PMC free article ] [ PubMed ]

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Hempfling W, Dilger K, Beuers U. Systematic review: ursodeoxycholic acid--adverse effects and drug interactions. Aliment Pharmacol Ther. 2003 Nov 15;18(10):963-72. [ PubMed ]

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Bessone F, Roma MG. Is ursodeoxycholic acid detrimental in obstructive cholestasis? A propos of a case of malignant biliary obstruction. Ann Hepatol. 2016 May-Jun;15(3):442-7. [ PubMed ]

20.

Verma A, Jazrawi RP, Ahmed HA, Davis T, Bland JM, Benson M, Orchard RT, Theodossi A, Maxwell JD, Northfield TC. Optimum dose of ursodeoxycholic acid in primary biliary cirrhosis. Eur J Gastroenterol Hepatol. 1999 Oct;11(10):1069-76. [ PubMed ]

21.

Kotb MA. Molecular mechanisms of ursodeoxycholic acid toxicity & side effects: ursodeoxycholic acid freezes regeneration & induces hibernation mode. Int J Mol Sci. 2012;13(7):8882-914. [ PMC free article ] [ PubMed ]

22.

Bahar R, Wong KA, Liu CH, Bowlus CL. Update on New Drugs and Those in Development for the Treatment of Primary Biliary Cholangitis. Gastroenterol Hepatol (N Y). 2018 Mar;14(3):154-163. [ PMC free article ] [ PubMed ]

Small intestinal bacterial overgrowth (SIBO).

Wed, 07 Sep 2022 04:28:58 GMT

Small intestinal bacterial overgrowth (SIBO)

SIBO results when bacteria originating from the colon grow in excess in the small bowel. It can develop in patients with altered small bowel motility (eg, uncontrolled diabetes mellitus, chronic opiate use, scleroderma) or in those who have had surgery involving the ileocecal valve. Other predisposing conditions include small intestinal diverticula, chronic pancreatitis, and gastric hypochlorhydria (eg, chronic proton pump inhibitor use).

Patients typically have mild abdominal pain, bloating, flatulence, and watery diarrhea. Vitamin B12 deficiency is common due to bacterial consumption; however, folate levels may be elevated due to bacterial production of the nutrient.

The gold standard for diagnosis is a jejunal aspiration demonstrating a high bacterial concentration (eg, >103 colony—forming units/mL); however, this test is invasive and not easily performed. SIBO is more commonly diagnosed by a carbohydrate breath test using either glucose or lactulose. Patients with SIBO have an early peak in breath hydrogen/methane (due to carbohydrate metabolism by bacteria in the small intestine) compared to those without SIBO (in whom carbohydrate metabolism primarily occurs in the colon).

Treatment is with oral antibiotics (eg, rifaximin , neomycin) to reduce bacterial load.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1954873/

Trousseau syndrome

Wed, 07 Sep 2022 04:06:42 GMT

Trousseau syndrome

Migratory superficial thrombophlebitis, classically known as Trousseau syndrome.

Trousseau syndrome is a hypercoagulable disorder that usually presents with unexplained superficial venous s thrombosis at unusual sites (eg, arm, chest area). The syndrome is usually diagnosed prior to (sometimes months to years before) or at the same time as an occult visceral malignancy.

Trousseau syndrome is usually associated with cancer involving the pancreas (most common), lung, prostate, stomach, and colon, and acute leukemias.

The tumor likely releases mucins that react with platelets to form platelet—rich microthrombi.

Trousseau syndrome is a hypercoagulability disorder presenting with recurrent and migratory superficial thrombophlebitis at unusual sites (eg, arm, chest area). It is usually associated with an occult visceral malignancy such as pancreatic (most common), stomach, lung, or prostate carcinoma

non-alcoholic fatty liver disease (NAFLD).

Tue, 06 Sep 2022 22:25:39 GMT

Non-alcoholic fatty liver disease (NAFLD)

Most patients are asymptomatic; some may have hepatomegaly on examination or minimal right upper quadrant pain.

Risk factors for NAFLD include type 2 diabetes mellitus, obesity, dyslipidemia, and metabolic syndrome. Insulin resistance causes unregulated hepatic triglyceride synthesis, peripheral Lipolysis, and free fatty acid uptake into the liver—all of which promote hepatic fat deposition (ie, hepatic steatosis),

Laboratory findings include elevated aminotransferases (usually 2-5 times the upper limit of normal) with an AST/ALT ratio <1. An ultrasound is performed to help confirm the diagnosis and usually demonstrates a hyperechoic— appearing liver, which reflects hepatic fatty infiltration

As NAFLD progresses, steatohepatitis can occur, putting patients at risk for liver fibrosis and cirrhosis. The mainstay of therapy is weight loss, which can reverse NAFLD-related liver damage

https://www.mayoclinic.org/diseases-conditions/nonalcoholic-fatty-liver-disease/symptoms-causes/syc-20354567

10 Common causes of ascites

Mon, 05 Sep 2022 20:14:04 GMT

Common causes of ascites :

1-Extraperitoneal

-Acute liver failure

-Alcoholic hepatitis

-Heart failure

-Hypoalbuminemia

- Malnutrition

-Budd-Chiari syndrome

-Nephrotic syndrome

-Cirrhosis

2- Peritoneal causes :.

-Malignancy (ovarian, pancreatic)

-Infection (tuberculosis, fungal)

Ascites fluid characteristics (Cell count and differential)

A-Color:

Bloody : trauma, malignancy, TB (rarely)

Milky : chylous

Turbid : possible infection

Straw color : likely more benign causes

B- Neutrophils:

2250/mm: peritonitis (secondary or spontaneous bacterial)

C-Total protein

-more than 22.5 g/dL (high-protein ascites)

CHF, constrictive pericarditis, peritoneal carcinomatosis, TB, Budd-Chiari syndrome, fungal

-lees than 2.5 g/dL (low—protein ascites)

Cirrhosis, nephrotic syndrome

D-SAAG (serum—ascites albumin gradient)

-more than 1.1 g/dL (indicates portal hypertension)

Cardiac ascites, cirrhosis, Budd—Chiari syndrome

-lees than 1.1 g/dL (absence of portal hypertension)

TB, peritoneal carcinomatosis, pancreatic ascites, nephrotic syndrome

https://my.clevelandclinic.org/health/diseases/14792-ascites

https://www.webmd.com/digestive-disorders/ascites-medref

https://www.liver.ca/patients-caregivers/liver-diseases/cirrhosis/?gclid=CjwKCAjwvNaYBhA3EiwACgndgs77iCwoynyUU5OeYTt9X-J9so6wubYlO2uhYKjbghqnWzBhbt2ckxoCGCcQAvD_BwE

How to know irritable bowel syndrome

Sun, 04 Sep 2022 04:59:02 GMT

Irritable bowel syndrome

a functional disorder of the gastrointestinal tract (with no identifiable organic cause). It is the most common gastrointestinal diagnosis in North America, with a prevalence of 10%-15%. IBS presents most commonly in young women as chronic, crampy abdominal pain with alternating episodes of constipation and diarrhea. Passage of stool often relieves the pain.

It can also present with nonspecific symptoms such as gastroesophageal reflux, dysphagia, early satiety, and chest pain.

IBS is further subclassified as diarrhea—predominant, constipation—predominant , or mixed .

IBS was previously considered a diagnosis of exclusion. However, patients with IBS :: symptoms based on the ROME I criteria, no alarm features, and no family history of inflammatory bowel disease or colorectal cancer do not require extensive workup. Colonoscopy performed on IBS patients typically shows normal colonic mucosa.

https://www.niddk.nih.gov/health-information/digestive-diseases/irritable-bowel-syndrome

Sickle hemoglobin mutations

Sun, 04 Sep 2022 04:44:36 GMT

Sickle hemoglobin

Sickle hemoglobin mutations are often linked to Sub-Saharan Africa but are also common in other regions that have a high burden of malaria, including Central/South America, the Caribbean, the Middle East, the Mediterranean, and India. Most patients with sickle cell trait (eg, one altered beta—hemoglobin chain) are asymptomatic and considered benign carriers; however, certain stressors, such as flying at high attitude or dehydration due to alcohol consumption, can sometimes lead to intravascular hemolysis, tissue ischemia (eg, splenic infarction), and/or vasoocclusive pain. Hemoglobin electrophoresis is diagnostic

Splenic infarction usually occurs in the setting of splenic artery (or subbranch) occlusion due to hypercoagulable states, embolic disease, or hemoglobinopathy (eg, sickle cell disease or trait). Although patients with sickle cell trait are generally asymptomatic, they occasionally develop splenic infarction and intravascular hemolysis in the setting of certain stressors such as air travel or dehydration. Diagnosis of most hemoglobinopathies is made by hemoglobin electrophoresis.

https://www.cdc.gov/ncbddd/sicklecell/facts.html

https://www.nih.gov/news-events/nih-research-matters/fixing-sickle-cell-disease-gene#:~:text=Sickle%20cell%20disease%20(SCD)%20is,sickle%2Dshaped%20red%20blood%20cells.

3 degree of dehydration child's

Sat, 03 Sep 2022 21:10:57 GMT

Dehydration

which can be divided into the following categories:

1. Mild dehydration (3-5% volume loss) presents with a history of decreased intake or increased fluid loss with minimal or no clinical symptoms.

2. Moderate dehydration (6—9% volume loss) presents with decreased skin turgor, dry mucus membranes, tachycardia, irritability, a delayed capillary refill (2—3 seconds), and decreased urine output.

3. Severe dehydration (10—15% volume loss) presents with cool, clammy skin, a delayed capillary refill (>3 seconds), cracked lips, dry mucous membranes, sunken eyes, sunken fontanelle (if still present), tachycardia, lethargy, and minimal or no urine output. Patients can present with hypotension and signs of shock when severely dehydrated

12 Signs alcoholic cirrhosis of the liver.

Sat, 03 Sep 2022 20:50:04 GMT

12 Signs alcoholic cirrhosis of the liver.

In patients with cirrhosis, spider angioma and palmar erythema both arise from hyperestrinism due to impaired hepatic metabolism of circulating estrogens, a process that begins in the cytochrome P450 system. Circulating estrogens affect vascular wall dilation. Spider angioma consists of a central, dilated arteriole surrounded by smaller radiating vessels. Palmar erythema is a result of increased normal speckling of the palm due to increased vasodilation, especially at the thenar and hypothenar eminences. Other manifestations of hyperestrinism in patients with cirrhosis include gynecomastia, testicular atrophy, and decreased body hair in males.

Dupuytren contracture occurs when the palmar fascia thickens and shortens, deforming the hand. It is usually most notable initially in the fourth and fifth digits and occurs due to fibroblast proliferation and collagen deposition, which are likely worsened by oxidative stress from increased free radical productionaragraph

Caput medusae arise from the dilation of superficial veins on the abdominal wall due to portal hypertension (PH). PH results from increased resistance to portal flow at the sinusoids and leads to increased pressure at the portosystemic collateral veins in the anterior abdomen, rectum, and distal esophagus. This then predisposes to esophageal varices, rectal varices, and caput medusae. Similal1y, PH causes enlargement of the spleen (which drains into the portal vein via the splenic vein) due to vascular congestion

The liver is the primary site of protein synthesis, and the cirrhotic liver typically produces insufiicient amounts of proteins, including albumin. Hypoalbuminemia leads to both a decrease in the intravascular oncotic pressure and fluid shifts to the extravascular space, predisposing to edema of the lower extremities.

Delayed passage of meconium

Sat, 03 Sep 2022 02:43:25 GMT

Passage of meconium

Meconium ileus and Hirschsprung disease (congenital aganglionic megacolon) should be considered in any neonate with delayed passage of meconium as 99% of healthy, infants pass stool within 48 hours of birth. These 2 conditions have overlapping clinical features but can usually be differentiated by the level of intestinal obstruction and meconium consistency.

Meconium ileus is virtually diagnostic for CF. Although only 20% of patients with CF develop meconium ileus, almost all newborns with meconium ileus have CF. A mutation in the CF transmembrane conductance regulator gene results in abnormal chloride and sodium transport and thick, viscous secretions in multiple organs. Thick, inspissated meconium is difficult to propel, resulting in obstruction at the level of the ileum and a narrow, underdeveloped colon (microcolon).

Nearly all patients with CF develop sinopulmonary disease. Opacification of all sinuses can be seen as early as age 8 months, and often require surgical debridement of sinuses

Hirschsprung disease is associated with Down syndrome, which in turn is associated with an increased risk of Alzheimer disease and hypothyroidism. It typically presents with increased rectal tone, "squirt sign" (forceful expulsion of stool after rectal examination), and obstruction at the rectosigmoid region with a transition zone between the aganglionic rectum and proximal dilated colon. Patients with CF are no more likely to develop Alzheimer disease or hypothyroidism than individuals in the general population.

Although men with CF are typically infertile due to congenital absence of the vas deferens, only 20% of women with CF have fertility problems. Infertility is due to the combination of secondary amenorrhea from malnutrition and thick cervical mucus obstructing sperm entry

Approximately 20% of patients with CF develop sensorineural hearing loss due to frequent treatment with aminoglycosides for gram-negative infections (eg, Pseudomonas aeruginosa)

Biliary colic in pregnancy

Fri, 02 Sep 2022 21:11:46 GMT

Symptomatic cholelithiasis.

Pregnant women (particularly those with concomitant obesity) are at increased risk for symptomatic cholelithiasis because they have elevated estrogen levels, which increases cholesterol excretion into bile, and elevated progesterone levels, which decreases gallbladder motility and emptying. As gallstones form and become too large to pass through the cystic duct, they intermittently obstruct the cystic duct when the gallbladder contracts (eg, with fatty meals). This obstruction causes increased intraluminal pressure, leading to the characteristic intermittent RUQ pain that can radiate to the back. Diagnosis is confirmed with RUQ ultrasound, which may show gallstones or biliary sludge (appearing as echogenic foci within the gallbladder). Management during pregnancy is conservative because most cases resolve with supportive care (eg, pain control). Cholecystectomy is usually delayed until the postpartum period.

Zenker (pharyngoesophageal) diverticulum (ZD)

Fri, 02 Sep 2022 20:56:34 GMT

Zenker (ZD)

The diverticular pouch can trap food and medication Patients often regurgitate the undigested food or medications several hours after eating. This can be more pronounced when the individual lies supine, as in this patient. Abnormal spasm or diminished relaxation of the cricopharyngeal muscles during swallowing (cricopharyngeal motor dysfunction) is thought to be the underlying mechanism of ZD formation. Increased intraluminal pressure above the cricopharyngeus muscle eventually results in herniation of the mucosa through an area of weakness Therefore, ZD is classified as a pulsion (resulting from increased intraluminal forces), rather than a traction (resulting from external tugging forces), pseudodiverticulum. Treatment of symptomatic patients involves surgical division of the cricopharyngeus muscle (cricopharyngeal myotomy). The diverticular pouch can be removed or combined with the esophageal lumen.

Mitral stenosis in adults

site-X7cQHw — Wed, 31 Aug 2022 20:25:47 GMT

Mitral stenosis

-Etiology

1-Rheumatic heart disease (vast majority of cases)

2-Age-related calcification, radiation-Induced

-Clinical

1-Exertional dyspnea, orthopnea, PND, hemoptysis

2-Pulmonary edema t right-sided heart failure

3-Atrial fibrillation, T risk for systemic embolization

-Diagnosis

1-Opening snap with mid diastolic rumble at the apex

2-Echocardiography increase trans mitral flow velocity

-Treatment

- Percutaneous valvotomy or surgical repair/replacement

What is healthy weight loss?

Mon, 01 Jul 2019 11:38:31 GMT

Losing Weight

It’s natural for anyone trying to lose weight to want to lose it very quickly. But people who lose weight gradually and steadily (about 1 to 2 pounds per week) are more successful at keeping weight off. Healthy weight loss isn’t just about a “diet” or “program”. It’s about an ongoing lifestyle that includes healthy eating patterns and regular physical activity.

Once you’ve achieved a healthy weight, rely on healthy eating and physical activity to help you keep the weight off over the long term.

Losing weight is not easy, and it takes commitment. But if you’re ready to get started, we’ve got a step-by-step guide to help get you on the road to weight loss and better health.

latex allergy

sites@tailorbrands.com — Mon, 15 Apr 2019 12:41:17 GMT

Latex is a plant-derived material that became widely used in the medical community (eg, surgical gloves) in the late 20th century

A high rate of allergic reaction among patients and health care workers was soon recognized, and recent efforts have been made to minimize the use of latex. However, latex gloves continue to be used in some surgical/procedural settings, and many short-term Foley catheters still contain latex

Latex can lead to a spectmm of lgE—mediated type 1 hypersensitivity reactions, including isolated urticarial skin rashes, erythema, wheals), rhino conjunctivitis, and anaphylaxis. Anaphylaxis is the result of a widespread response to antigen, leading to massive release of histamine and other substances from mast cells and basophils. Multiple organ systems are afiected;

High-output heart failure

sites@tailorbrands.com — Sun, 01 Jul 2018 11:37:25 GMT

High-output heart failure usually involves increased cardiac output (CO) in response to a disturbance causing reduced systemic vascular resistance

Such disturbances include:

- Peripheral vasodilation due to unmet metabolic demand (eg, hyperthyroidism, severe anemia)

- Increased quantity of peripheral vessels (eg, Paget disease, morbid obesity)

- Bypass of systemic arteriolar resistance due to an enlarged arteriovenous fistula (as in this patient's case)

Secondary hypertension

sites@tailorbrands.com — Wed, 19 Apr 2017 12:40:28 GMT

Secondary causes of hypertension

1-Renal parenchymal disease:

Clinical clues features - Abnormal urinalysis (proteinuria, red blood cell casts)- Elevated serum creatinine

2-Renovascular disease:

Clinical clues features - Severe hypertension with onset afler age 55-Recurrent flash pulmonary edema- Rise in serum creatinine-- Abdominal bruit

3-Primary aldosteronism:

Clinical clues features Spontaneous or easily provoked hypokalemia

4-Pheochrornocytoma:

Clinical clues features - Paroxysmal hypertension with tachycardia- Pounding headaches, palpitations,

5-Cushing syndrome:

Clinical clues features Cushingoid body habitus +Proximal muscle weakness+Hyperglycemia

6-Hypothyroidism

Clinical clues features Fatigue, dry skin, cold intolerance+Constipation, weight gain, bradycardia

7-Primary hyperparalhyroidism

8-Coarctation of the aorta

Continuing health education

Melasma

Unlocking the Secrets to Radiant Skin: A Comprehensive Guide to Treating Melasma Naturally and Effectively

Contraindications

Warnings/Precautions

Warnings

Cosmetic Effects

Exposure to Sunlight or Ultraviolet Light

Sensitivity Reactions

Sulfite Sensitivity

Other Sensitivity Reactions

Major Toxicities

General Precautions

Topical Use

Dermatologic Effects

Use of Fixed Combinations

Specific Populations

Pregnancy

Lactation

Pediatric Use

Cat-scratch disease

Explore the Depths of Cat-Scratch Disease

Serotonin syndrome

Serotonin Syndrome Alert: Recognizing Early Signs and Ensuring Timely Intervention

Serotonergic drugs

Risk factors

Clinical features

Staphylococcal diseases

Staphylococcal diseases

Treatment :

Staphylococcus aureus

Coagulase-negative staphylococcus (particularly S. epidermidis )

Visual assessment of melanoma

Visual assessment of melanoma

The ABCDE criteria for melanoma :

Lichen Sclerosus(affects the genital and anal regions)

Lichen Sclerosus

Treatment / Management

Lichen Planus( flat-topped, purplish, itchy bumps or patches on the skin)

Lichen Planus

Lichen planus can occur on the skin, mucous membranes, nails, and scalp. The most commonly affected regions include:

Drug-induced lichen planus, or lichenoid drug eruption, is a type of lichen planus that is caused by a reaction to certain medications.

Treatment/management of lichen planus:

Cutaneous Lichen Planus:

Oral Lichen Planus:

Shingles

Shingles

Shingles:

Is caused by varicella zoster virus (VZV), the same virus that causes chickenpox. After a person recovers from chickenpox, the virus stays dormant (inactive) in the body. This virus can reactivate years later, causing shingles.

Clinical Features of Herpes Zoster:

Complications of Herpes Zoster:

Vaccination for Herpes Zoster:

Disease Rates, Recurrence, Complications, and Deaths for Herpes Zoster:

References

Montreal Cognitive Assessment score

The Montreal Cognitive Assessment (MoCA)

loss of libido? memory impairment? lack of motivation? salt craving? reduced body hair?

Addison's disease

Addison's disease

Common signs and symptoms include:

Diagnostic tests that may be used to confirm the diagnosis of Addison's disease include:

Treatment of Addison's disease:

References :

Vitamin deficiencies

Vitamin deficiencies

Vitamin deficiencies

Here is a summary of some of the most common vitamin deficiencies and their health consequences:

Vitamin E

What is vitamin E and what does it do

﻿

Functions of Vitamin E

Vitamin E in Disease Prevention

While developing a differential diagnosis, clinicians must consider other possible vitamin deficiencies as well as the following:

References

The Benefits of Eating Vitamin-Rich Foods

Boost Your Health with Vitamin-Rich Foods: The Top 10 Benefits

LIST OF BLOOD DISORDERS

LIST OF BLOOD DISORDERS

Anemia

Bleeding disorders