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NIMS(Nepal Index Of Medical Specialities) has been design to provide information on drugs that are marketed in Nepal by Pharma company from around the world .

NIMS DRUGS DIRECTORY

NIMS(Nepal Index Of Medical Specialities) has been design to provide information on drugs that are marketed in Nepal by Pharma company from around the world .

NIMS DRUGS DIRECTORY

NIMS(Nepal Index Of Medical Specialities) has been design to provide information on drugs that are marketed in Nepal by Pharma company from around the world .

NIMS DRUGS DIRECTORY

NIMS(Nepal Index Of Medical Specialities) has been design to provide information on drugs that are marketed in Nepal by Pharma company from around the world .

NIMS DRUGS DIRECTORY

NIMS(Nepal Index Of Medical Specialities) has been design to provide information on drugs that are marketed in Nepal by Pharma company from around the world .

Saturday, January 31, 2015

Fetal alcohol syndrome

The infant pictured as follows was small for gestational age.

He also was found to have a ventricular septal defect on cardiac evaluation. This infant appeared to have features consistent with

a. Perinatal phenytoin exposure
b. Trisomy 21
c. Alport syndrome
d. Fetal alcohol syndrome
e. Infant of diabetic mother


Ans is D:
Fetal alcohol syndrome is a preventable cause of birth defects. Prenatal exposure to ethanol is the cause. Findings include microcephaly, small palpebral fissures, short nose, smooth philtrum, thin upper lip, ptosis, microphthalmia, cleft lip and palate, and central nervous system abnormalities including mental retardation (average IQ = 67).
Common findings with trisomy 21 include protruding tongue, Brushfield’s
spots, redundant neck skin, mental retardation, brachycephaly,
upslanting palpebral fissures, epicanthal folds, flat face, small ears, cardiac
abnormalities (especially ventricular septal defect or endocardial cushing
defect), palmar creases, and clinodactyly of the fifth digit.
Dilantin exposure causes midface hypoplasia, low nasal bridge, ocular
hypertelorism, and accentuated cupid’s bow of the upper lip. Other features
include cleft lip and palate, growth retardation, mental deficiency, distal
phalangeal hyperplasia, cardiovascular anomalies, and skeletal defects.
Alport syndrome is the most common of the hereditary nephritis conditions,
frequently leading to end-stage renal disease. In 85% of patients
with Alport syndrome, an X-linked dominant form of inheritance is found;
about 15% are autosomal recessive. All cause hematuria and progressive
nephritis. Other findings include deafness and ocular defects.
Infants of diabetic mothers have an increased chance of congenital
heart disease, caudal regression syndrome, and a small left colon; are large
for gestation age; and have a number of biochemical abnormalities such as
hypoglycemia or hypocalcemia.

Friday, January 30, 2015

The most sensitive and specific test to confirm the diagnosis of acute cholecystitis is:

The most sensitive and specific test to confirm the diagnosis of acute cholecystitis is:


biliary system

a. Oral cholecystogram.
b. HIDA radioisotope scan.
c. Ultrasound.
d. Plain film of the abdomen.
e. The triad of fever, elevated bilirubin, and elevated alkaline phosphatase.




The answer is b. Ultrasonography has an unadjusted 94% sensitivity and 78% specificity for the diagnosis of acute cholecystitis. The 50% sensitivity of CT scanning is insufficient for it to be used in place of ultrasonography.

Technetium-iminoacetic acid analogue-based radioisotope scintigraphy (HIDA) has 97% sensitivity and 90% specificity. Within 1 hour of injection, a normal patient will have a clearly outlined gallbladder and cystic duct. Failure to demonstrate the gallbladder within this time frame is consistent with cystic duct obstruction.

Thursday, January 29, 2015

e. Any of the above.

Operative intervention for neurotrauma is indicated in a patient suffering from:


a. Significant mass effect from contusion or hemorrhage, resulting in a 5-mm shift of intracranial structures.
b. Penetrating head injury with necrotic foreign body tracks.
c. Significantly depressed skull fractures.
d. Foreign body removal if compromising neurologic function.
e. Any of the above.


The answer is e. Indications for operative treatment in patients with neurotrauma are indicated for all of the above situations and, additionally, in the instance of extra-axial collections.

Wednesday, January 28, 2015

management for a child with Kawasaki disease is

The most appropriate choice of management for a child with Kawasaki disease is:


a. Admission for IV gamma-globulin and high-dose aspirin therapy.
b. Admission for antibiotics and steroids.
c. Discharge on high-dose aspirin therapy and follow up in 2–3 days.
d. Discharge on high-dose aspirin therapy and a second-generation cephalosporin.
e. Discharge on high-dose steroids.



kawasaki baby


The answer is a. Kawasaki disease, the most frequent cause of acquired pediatric cardiac disease, is an acute multisystem vasculitis of small and medium sized arteries. It occurs primarily in infants and children, with a peak incidence between 1 and 2 years of age. Diagnosis is based on the presence of fever for 5 or more days in association with four of the following five conditions: bilateral conjunctivitis, cervical lymphadenopathy, polymorphous rash, mucous membrane changes, and extremity findings. Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are often markedly elevated. The clinical course is divided into three phases. The acute phase (days 1–11) is
characterized by fever and myocarditis. The subacute phase (days 11–20) is characterized by resolution of the fever, rash, and adenopathy as well as the development of thrombocytosis and periungal desquamation. 

Risk for developing coronary artery thrombosis and sudden death is the greatest at this time. The convalescent phase (days 21–60) begins when the clinical findings have resolved and continues until the ESR is normal. All patients should be admitted for IV gamma-globulin and high-dose aspirin therapy. Neither steroids nor antibiotics are indicated. Steroids may actually be detrimental.

Tuesday, January 27, 2015

c. Active immunization and antibiotics.

A 6-year-old girl who recently emigrated from Sri Lanka with her parents complains of severe sore throat, headache, difficulty swallowing, and generalized weakness and malaise. Her previous medical history is not known. Her oral temperature is 103.2◦F. You note prominent cervical lymph nodes and an adherent gray pseudomembrane in her posterior oropharynx. Treatment must include antitoxin therapy plus:



a. Active immunization.
b. Passive immunization.
c. Active immunization and antibiotics.
d. Passive immunization and high-dose acyclovir.
e. Active immunization and steroids.


The answer is c. This patient has a classic case of diphtheria, a respiratory infection caused by Corynebacterium diptheriae. Management should focus on airway protection, limiting additional C. diptheriae growth and toxin production, and minimizing the effects of toxin that has already been produced. Equine serum diphtheria antitoxin should be administered promptly after the clinical diagnosis of respiratory diphtheria. Antitoxin can be obtained by contacting the CDC. The size and location of the membrane, the duration of illness, and the patient’s overall degree of toxicity determine the dosage of antitoxin. The Committee on Infectious Diseases of the American
Academy of Pediatrics (AAP) recommends 20,000–40,000 units for pharyngeal or laryngeal involvement of 48 hours’ duration, 40,000–60,000 units for nasopharyngeal lesions, and 80,000–100,000 units for extensive disease of 3 or more days’ duration or for diffuse swelling of the neck. In addition to antitoxin therapy, antibiotics should be administered for 14 days. Erythromycin, 40–50 mg/kg/d (up to 2 g) IV or orally in divided doses; intramuscular (IM) aqueous crystalline penicillin, 100,000–150,000 U/kg/d in four divided doses; or procaine penicillin,25,000–50,000 U/kg/d in two divided doses for 14 days given IM every 12 hours is acceptable. Patients should be admitted to respiratory isolation.

Monday, January 26, 2015

DKA vs HONK , Diabetic ketoacidosis , hyperosmolar nonketotic hyperglycemia


A helpful clue to differentiate diabetic ketoacidosis (DKA) from hyperosmolar nonketotic hyperglycemia (HONK) is:

a. Serum glucose of 500 mg/dL is most consistent with the diagnosis of HONK.
b. Fluid deficits are typically greater in DKA.
c. Most patients who develop HONK have a prior history of complications of their IDDM.
d. HONK most commonly presents as an acute event with illness developing over several hours, and coma             is required to make the diagnosis.
e. Focal neurologic symptoms occur more frequently in HONK.


The answer is e. HONK and DKA have similar features: hyperglycemia (patients with HONK usually have a serum glucose >800 mg/dL), hyperosmolality, and dehydration; however, no ketoacidosis. HONK most
commonly occurs in patients with non–insulin-dependent diabetes, usually the elderly. Precipitating illnesses
include myocardial infarction, stroke, upper GI bleeding, sepsis, and renal failure. Some drugs that can cause
HONK include thiazide diuretics, calcium channel blockers, phenytoin, and propranolol. There are no specific signs on physical examination, although neurologic pathology is most prominent and may present as hemisensory or hemiparesis, altered mental status, and focal motor seizures. Treatment for HONK includes correction of hypovolemia—the average fluid deficit is between 8 and 12 L—and hyperglycemia.

Lyme disease


The most common manifestation of Lyme disease is:

Erythema migrans

a. Erythema migrans.
b. Meningitis.
c. Cognitive impairment.
d. Recurrent arthritis.
e. Heart block


The answer is a. Lyme disease is caused by the spirochete Borrelia burgdorferi. After B. burgdorferi is introduced into the skin, it spreads locally. The local spread leads to erythema migrans (EM), a rash that is found in approximately two-thirds of patients. Keep in mind that a rash may not be present in up to 20% of cases and even if present may be mild, nonspecific, and easily missed by the patient, family, caregivers, and/or the initial treating physicians.

Sunday, January 25, 2015

Lactulose removes ammonia ions from the gut by:


Lactulose removes ammonia ions from the gut by:


a. Being converted to lactic acid by colonic bacteria; this acidifies the feces, resulting in the trapping of ammonia as ammonium in the stool.
b. Causing ammonia to be transmitted to the intracellular region through the sodium–potassium membrane
pump, where it is safely used in the tricarboxylic acid cycle.
c. Forcing renal excretion of chloride, leading to compensatory hyperpnea and respiratory alkalosis, which keeps
ammonia nontoxic.
d. Providing a protective coating on the gut’s brush border, which blocks ammonia absorption.
e. Mycelizing preammonia prior to its harmonic conversion.


The answer is a. Lactulose is a poorly absorbed sugar metabolized by colonic bacteria yielding lactic acid. The salutary effects of this agent are related both to the acidification of the fecal stream, resulting in the trapping of ammonia as ammonium in the stool, and to its cathartic action. The usual dosage of lactulose is 15–30 mL orally 3 or 4 times daily or in a quantity sufficient to result in several loose bowel movements daily. The principal adverse effect is excessive diarrhea, with resultant fluid and electrolyte imbalance.

Friday, January 23, 2015

The answer is a. The FEV1 (forced expiratory volume in 1 second) as a fraction of the FV


In managing the patient with COPD, the measurement or finding which best corresponds with day-to-day
function and long-term prognosis is the:
a. Forced expiratory volume in 1 second as a fraction of the forced vital capacity (FEV1%).
b. Arterial blood gas.
c. Dead-space volume.
d. Chest radiograph.
e. Forced vital capacity.


The answer is a. The FEV1 (forced expiratory volume in 1 second) as a fraction of the FVC (forced vital capacity) correlates well with physiologic function. An increase in dead space is common in COPD but is poorly correlated with function or prognosis. CXR is often misleading in predicting performance, although it can rule out superimposed complications. A single blood gas is not predictive of long-term prognosis. A combination of physiologic and laboratory tests is necessary to accurately stage the severity of disease.

Sunday, January 11, 2015

The answer is C. Marfan’s syndrome

More than 90% of patients with Marfan’s syndrome have mutations in which gene?


A. BMPR2
B. COL1A1
C. Fibrillin
D. TGFb
E. Type IV collagen

The answer is C. Marfan’s syndrome is an autosomal dominant syndrome characterized
by skeletal changes including long, thin extremities; loose joints; lens dislocation
with reduced vision; and aortic aneurysms. The incidence is high, affecting 1 in 3000–5000
live births in most racial and ethnic groups. More than 90% of Marfan’s syndrome patients
have mutations in the fibrillin-1 gene. Although Marfan’s syndrome is rarely associated
with mutations in TGFb, recent work has highlighted the close interaction between fibrillin
mutation and alterations in TGFβ signaling, offering new therapeutic potential. BMPR2
mutation is associated with heritable pulmonary arterial hypertension. COL1A1 mutation
is found in Ehlers-Danlos syndrome and osteogenesis imperfecta. Type IV collagen mutations
have been described in Alport’s syndrome.

Saturday, January 10, 2015

Waardenburg Syndrome Type 1.

WAARDENBURG SYNDROME. WS, 


described by the Dutch physician Petrus Waardenburg in 1951,104 is the prototypic congenital disorder of pigmentation. Although it was originally described as a syndrome combining pigmentary defects of the hair (poliosis or white forelock) and iris, congenital deafness, and developmental craniofacial abnormalities, it was subsequently realized that additional phenotypic manifestations could be part of the same syndrome. Four types of WS, WS1 through WS4. The discovery of molecular mutations accounting for the different types of WS has helped to explain its wide variety of manifestations as well as to illuminate the importance of specific genes for the development of different tissues and organs . While practically all cases of WS1 and WS3 show mutated PAX3,105,105,109,110 WS4 individuals either have homozygous mutations in EDN3 (the endothelin- 3 gene)111–113 or EDNRB (the endothelin-B receptor gene)114 or heterozygous mutations in SOX10.115 On the other hand, WS2 appears to arise more heterogeneously, as a mutation in MITF has been shown in only a small fraction of WS2 patients

Waardenburg Syndrome Type 1. 

Note poliosis (white forelock) and dystopia canthorum (lateral displacement of the medial canthi of the eyes).

Individuals

with WS1  are usually heterozygous for mutations in PAX3; hence, WS1 is autosomal dominant in inheritance. Although many different mutations in PAX3 have been associated with WS1, these mutations are thought either to be functionally null alleles or to abrogate the interactions of PAX3 with DNA.

Individuals with WS1 have pigmentation abnormalities associated with craniofacial abnormalities
(see Fig). Dystopia canthorum, which is lateral displacement of the medial canthi of the eyes, is the hallmark craniofacial defect found in virtually all cases of WS1. A broadening of the nasal root, the presence of hypoplastic alae nasi, and synophrys are other craniofacial abnormalities associated with WS1. Poliosis, such as the presence of a white forelock, is the most common pigmentation abnormality associated with WS1. Depigmented white spots on the skin occur less commonly, but are often located at the ventral midline reflecting the compromised migration of dysfunctional
melanocyte precursors from their origin in the dorsal neural crest. Pigmentary abnormalities of the iris, including complete heterochromia irides (differently colored irises), partial heterochromia irides (variations of color within an iris), or hypoplastic blue irides, can also be associated with WS1. Premature graying may also be observed in WS1. Congenital deafness is present in 57% of cases.117
The importance of PAX3 for the expression of MITF,118,119 with consequent effects upon melanocyte survival during development, is likely to account for the pigmentary defects of WS1. A role for PAX3 in governing the development of neural crest derivatives that contribute to bony and cartilaginous structures of the face,120 particularly those contributing to the formation of the frontal bone, explain the craniofacial anomalies observed in WS1. Sensorineural deafness, observed with
incomplete penetrance in WS1, results from the variable failure of melanoblasts to migrate to or to survive in the stria vascularis in the lateral wall of the cochlea.

Friday, January 9, 2015

d. Small arteries and arterioles.

Under normal circumstances, the largest drop in blood pressure in the systemic circulatory system occurs in the:


a. Vena cava.
b. Small and large veins and venules.
c. Aorta.
d. Small arteries and arterioles.
e. Capillaries and venules.


The answer is d. The small arteries and arterioles have the highest resistance and therefore cause the largest drop in pressure along this segment of the vascular system.

Wednesday, January 7, 2015

The answer is e.

Which of the following fractures is most likely to cause hypovolemic shock and life-threatening blood loss?

a. Femur
b. Spine
c. Tibia
d. Radius
e. Pelvis

The answer is e.  The greatest amount of blood loss generally occurs in fractures of the pelvis (retroperitoneal hemorrhage), followed by those of the femur and spine. Patients with pelvic
fractures should be evaluated for hypovolemic shock. Common manifestations include tachycardia, hypotension, oliguria, a clouded sensorium, and cool extremities.

A 9-day-old baby presents to the emergency department with purulent conjunctivitis.

A 9-day-old baby presents to the emergency department with purulent conjunctivitis. Topical erythromycin  prophylaxis was given in the nursery. The most likely cause of this neonate’s conjunctivitis is:



a. Syphilis.
b. Neisseria gonorrhoeae.
c. Group B Streptococcus.
d. Herpes simplex virus.
e. Chlamydia trachomatis.



The answer is e. Neonatal conjunctivitis (ophthalmia neonatorum) occurs within the first month of life. Previously, the most common cause was chemical irritation from application of silver nitrate eyedrops as antimicrobial prophylaxis at birth, which is usually seen 1–2 days after birth. Presently, most hospitals use erythromycin ointment as the standard prophylaxis and as a result, the incidence of chemical conjunctivitis has gone down. However, erythromycin ointment does not prevent all gonococcal and other bacterial ocular infections and is not effective against C. trachomatis. Although N. gonorrhoeae is no longer a major cause of neonatal conjunctivitis in the United States, it should be presumed in infants who have purulent conjunctivitis until proven otherwise. Corneal perforation is a known complication. You should do a Gram stain of the eye discharge looking  for Gram–negative diplococci, as well as gonococcal and chlamydial cultures or nucleic acid amplication (PCR)
tests. Gonococcal conjunctivitis is commonly seen between 3 and 5 days after birth. By the end of first week of life and throughout the first month of life, C. trachomatis becomes the most frequent cause of conjunctivitis. Other important but less common bacterial causes are Haemophilus influenzae and Streptococcus pneumoniae.

Tuesday, January 6, 2015

PYODERMA GANGRENOSUM

PYODERMA GANGRENOSUM


multiple early lesions at the site of previous surgery.


DEFINITION
This clinically diagnosed entity presents as pustules and is frequently associated with various conditions, especially inflammatory bowel disease, arthritis and plasma cell dyscrasias, at
times occurring at sites of prior surgery

.
PHYSICAL FINDINGS AND CLINICAL PRESENTATION

● Typically, the ulcers have undermined edges and red-purple borders . They may be solitary or multiple, and occur most often on the lower limbs.

● The ulcers are painful and tender, and may persist for months or years.

● There is a risk of disfi guring scarring.


TREATMENT
● Treatment of associated disorders
 ● Topical corticosteroids, clofazimine, dapsone, intralesional steroids, minocycline, cyclosporine, systemic corticosteroids

Monday, January 5, 2015

A 47-year-old woman with known HIV/AIDS (CD4+ lymphocyte, 106/μL and viral load,

A 47-year-old woman with known HIV/AIDS (CD4+ lymphocyte, 106/μL and viral load, 35,000/mL) presents with painful growths on the side of her tongue as shown in Figure.


What is the most likely diagnosis?

A. Aphthous ulcers
B. Hairy leukoplakia
C. Herpes stomatitis
D. Oral candidiasis
E. Oral Kaposi’s sarcoma

The answer is B.  Oral hairy leukoplakia is caused by a severe overgrowth of
Epstein-Barr virus infection in T-cell–deficient patients. It is not premalignant and is often
unrecognized by the patient but is sometimes a cosmetic, symptomatic, and therapeutic
nuisance. The white, thickened folds on the side of the tongue can be pruritic or painful
and sometimes resolve with acyclovir derivatives or topical podophyllin resin. Ultimate
resolution occurs after immune reconstitution with antiretroviral therapy. Oral candidiasis
or thrush is a very common, relatively easy-to-treat condition in HIV patients and
takes on an appearance of white plaques on the tongue, palate, and buccal mucosa that
bleed with blunt removal. Herpes simplex virus (HSV) recurrences or aphthous ulcers
present as painful ulcerating lesions. The latter should be considered when oral ulcers persist,
do not respond to acyclovir, and do not culture HSV. Kaposi’s sarcoma is uncommon
in the oropharynx and takes on a violet hue, suggesting its highly vascularized content.

Saturday, January 3, 2015

A 68-year-old woman seeks evaluation for an ulcerative lesion on her right hand.

A 68-year-old woman seeks evaluation for an ulcerative lesion on her right hand. She reports that the area on the back of her right hand was initially red and not painful.


There appeared to be a puncture wound in the center of the area, and she thought she had a simple scratch acquired while gardening.

Over the next several days, the lesion became verrucous and ulcerated. Now the patient has noticed several nodular areas along the arm, one of which ulcerated and began draining a serous fluid today. She is also noted to have an enlarged and tender epitrochlear lymph node on the right arm.

A biopsy of the edge of the lesion shows ovoid and cigar-shaped yeasts.

Sporotrichosis is diagnosed.




What is the most appropriate therapy for this patient?


A. Amphotericin B intravenously
B. Caspofungin intravenously
C. Clotrimazole topically

D. Itraconazole orally

E. Selenium sulfide topically

The answer is D. Sporothrix schenckii is a thermally dimorphic fungus found
in soil, plants, and moss and occurs most commonly in gardeners, farmers, florists, and
forestry workers. Sporotrichosis develops after inoculation of the organism into the skin
with a contaminated puncture or scratch.

 The disease typically presents as a fixed cutaneous lesion or with lymphocutaneous spread. The initial lesion typically ulcerates and become verrucous in appearance. The draining lymphatic channels become affected in up to 80% of cases. This presents as painless nodules along the lymphatic channel, which ulcerate. A definitive diagnosis is made by culturing the organism. A biopsy of the lesion may show ovoid or cigar-shaped yeast forms. Treatment for sporotrichosis is systemic therapy. Options include oral itraconazole, saturated solution of potassium iodide, and terbinafine.

 However, terbinafine has not been approved for this indication in the United States. Topical antifungals are not effective. In cases of serious system disease such as pulmonary sporotrichosis,
amphotericin B is the treatment of choice. Caspofungin is not effective against S. schenckii.

Friday, January 2, 2015

What is the mechanism of target cell formation?

What is the mechanism of target cell formation?



a. Precipitation of hemoglobin in the red blood cell (RBC) membrane
b. Excess cell membrane bunching up on the surface
c. Loss of membrane from protein loss
d. Cellular dehydration
e. Ankyrin and spectrin deficiency

Answer b. Excess cell membrane bunching up on the surface

Target cells are formed exclusively from excess RBC membrane. The amount of hemoglobin is too small for the size of the covering. The excess membrane “bunches up” on the cell surface.