Page 1 of 45: aiims standard refrence series part-2 november 2007

aayush138 · Credits: 25241 My Scrapbook

due to members repeated request this thread has been promoted to a sticky one with an faq tag and will stay on top of AIIMS list of threads with a tag faq which will make it even more visible . any comment on this work are highly welcome

ok guys starting my work again.and let me tell you again that work will not be as fast as other thread.but will surely try to complete as i did in AIIMS may thread.

and once again thank you for over wheming response to the previous thread.

hope this thread also lives up to expectation.as i am receiveing many scraps for this thread.

aayush138 · Credits: 25241 My Scrapbook

lets start with a bouncer from AIIMS

child with H/O respiratory problem. best investigation to rule out cystic fibrosis after sweat chloride test 25 and 35
1)f508 mutation
2) Foecal fat estimation
3) CT chest
4) potential difference at nasal epithelium

refrence nelson 17th edition page 1442

More than 60?mEq/L of chloride in sweat is diagnostic of CF when one or more other criteria are present. Threshold levels of 40?mEq/L for infants have been suggested. Values between 40 and 60?mEq/L suggest CF at all ages and have been reported in cases with typical involvement. In healthy adults, the sweat chloride values increase slightly, but a value of 60?mEq/L still adequately differentiates CF from other conditions. Chloride concentrations in sweat are somewhat lower in individuals who retain exocrine pancreatic function but remain within the diagnostic range. False-negative test results may be encountered in children with hypoproteinemic edema.

so here you can say that sweat chloride is normal

now read following lines

The finding of increased potential differences across nasal epithelium, the loss of this difference with topical amiloride application, and the absence of a voltage response to a ß-adrenergic agonist have been used to confirm the diagnosis in patients with equivocal or frankly normal sweat chloride values.

other refrence harrison 16th 1545 1546

Because of the large number of CF mutations, DNA analysis is not
used for primary diagnosis. The diagnosis of CF rests on a combination
of clinical criteria and analyses of sweat Cl values. The values for
the Na and Cl concentration in sweat vary with age, but typically
in adults a Cl concentration of 70 meq/L discriminates between
patients with CF and patients with other lung diseases.DNA analyses are being performed increasingly in patients with
CF. Comprehensive genotype-phenotype relationships have not yet
been established sufficiently for prognosis. A relationship between
F508 homozygosity and pancreatic insufficiency has been established,
but no predictive relationship holds for F508 homozygosity and lung
disease.[/b][b]Between 1 and 2% of patients with the clinical syndrome of CF
have normal sweat Cl values. In most of these patients, the nasal
transepithelial potential difference is raised into the diagnostic range
for CF, and sweat acini do not secrete in response to injected -
adrenergic agonists.

so you can see that there no predictive value between 508 mutation and lung disease value and second thing they have clearly given potential differnce is the diagnostic test for normal sweat chloride test.

and 25 and 35 is normal range as you can see that it should be greater than 60.

so answer is 4 potential difference at nasal epithelium.

aayush138 · Credits: 25241 My Scrapbook

reye’s syndrome, histopathological finding
1) Mitochondrial blebs and enlarged mitochondria
2) Endoplasmic reticulum/lysosome
3) Glycogen depletion
4) Perinuclear staining

answer 1 mitochondrial blebs and enlarged mitochondria

harrison 16th edition page 1871

There is mitochondrial dysfunction with decreased activity of hepatic
mitochondrial enzymes

schiff diseases of liver 10th edition page 1319 1320

This disorder shares many features with mitochondrial hepatopathy, and indeed, abnormal mitochondria are an important
ultrastructural feature.

electrom microscopy reveals marked microvesicular steatosis (Fig. 47.9) and characteristic
mitochondrial changes with swelling of matrix, dissolution of cristae and intramatrical granules, and ameboid shapes

sfors · Credits: 275 My Scrapbook

hi ayush gr8 work. howz ur paper?kep gng buddy!

catar · Credits: 1005 My Scrapbook

good work aayush

aayush138 · Credits: 25241 My Scrapbook

3. fracture penis with intact Buck’s facia. Blood extravasates in
1) butterfly shaped
2) scrotum and penis only
3) Scrotum, penis, anterior abdominal wall
4) penile shaft only

answer 4 penile shaft only

refrence campbell urology 9th edition

The diagnosis of penile fracture is often straightforward and can be made reliably by history and physical examination alone. Patients usually describe a cracking or popping sound as the tunica tears, followed by pain, rapid detumescence, and discoloration and swelling of the penile shaft. If Buck's fascia remains intact, the penile hematoma remains contained between the skin and tunica, resulting in a typical eggplant deformity ( Fig. 83-1 ). If Buck's fascia is disrupted, hematoma can extend to the scrotum, perineum, and suprapubic regions.

euphoria · Credits: 688 My Scrapbook

Que. A child presents with non blanching rash over the extensor aspect of arm with swelling over knee urine analysis show proteinurea 1 + and RBC 3+ on kidney biopsy which finding will be seen
a) fusion of podocytes
b) ATN
c) depositions of Ig A
d)thickening of membrane

ANS- c) depositions of Ig A.
This is a case of IgA NEPHROPATHY (BERGER DISEASE)/HENOCH-SCHONLEIN PURPURA,
This syndrome consists of purpuric skin lesions characteristically involving the extensor surfaces of arms and legs as well as buttocks; abdominal manifestations including pain, vomiting, and intestinal bleeding; nonmigratory arthralgia; and renal abnormalities. The renal manifestations occur in one-third of patients and include gross or microscopic hematuria, proteinuria, and nephrotic syndrome.This form of glomerulonephritis is characterized by the presence of prominent IgA deposits in the mesangial regions, detected by immunofluorescence microscopy. A small number of patients, mostly adults, develop a rapidly progressive form of glomerulonephritis with many crescents. Not all components of the syndrome need to be present, and individual patients may have purpura, abdominal pain, or urinary abnormalities as the dominant feature. The disease is most common in children 3 to 8 years old, but it also occurs in adults, in whom the renal manifestations are usually more severe. There is a strong background of atopy in about one-third of patients, and onset often follows an upper respiratory infection. IgA is deposited in the glomerular mesangium in a distribution similar to that of IgA nephropathy. This has led to the concept that IgA nephropathy and Henoch-Schönlein purpura are spectra of the same disease.

ROBBIN'S Pathology 7th ed pg-990

euphoria · Credits: 688 My Scrapbook

Que. Collapsing glomarulopathy following is seen
A) proliferation of parietal cells
B) tuft necrosis
C)visceral epithelial cell destruction
d)

ANS-C)visceral epithelial cell destruction.

A morphologic variant of focal segmental glomerulosclerosis, called collapsing glomerulopathy, is characterized by collapse and sclerosis of the entire glomerular tuft in addition to the usual focal segmental glomerulosclerosis lesions.A characteristic feature is proliferation and hypertrophy of glomerular visceral epithelial cells. This lesion may be seen in situations in which it is idiopathic, but it is the most characteristic lesion of HIV-associated nephropathy.
PATHOGENESIS-
The characteristic degeneration and focal disruption of visceral epithelial cells are thought to represent an accentuation of the diffuse epithelial cell change typical of minimal change disease. It is this epithelial damage that is the hallmark of focal segmental glomerulosclerosis. The hyalinosis and sclerosis represent entrapment of plasma proteins in extremely hyperpermeable foci with increased ECM deposition.

ROBBIN'S Pathology 7th Ed Pg- 9 8 3

euphoria · Credits: 688 My Scrapbook

Phenytoin, all are true except-

a) Induces enzymes
b) Zero order kinetics at low dose
c) Half life increases with increasing dose
d) Highly protein bound

ANS-b) Zero order kinetics at low dose.

The elimination of phenytoin is dose-dependent. At very low blood levels, phenytoin metabolism follows first-order kinetics.Further increases in dosage, even though relatively small, may produce very large changes in phenytoin concentrations. In such cases, the half-life of the drug increases markedly
-Phenytoin is highly bound to plasma proteins(90% bound to plasma proteins).
-Phenytoin has been shown to induce microsomal enzymes responsible for the metabolism of a number of drugs.

Ref- Katzung Basic & Clinical Pharmacology , 10th Ed

euphoria · Credits: 688 My Scrapbook

bisphosphonates are used in all except
a) hypercalcemia
b) cancer
c) osteoporosis
d) hypervitaminosis D

Ans- d) hypervitaminosis D

chronic hypercalcemia of sarcoidosis, vitamin D intoxication, and certain cancers may respond within several days to glucocorticoid therapy.The treatment of hypervitaminosis D with glucocorticoids probably does not alter vitamin D metabolism significantly but is thought to reduce vitamin D-mediated intestinal calcium transport
-bisphosphonates are useful for the treatment of hypercalcemia associated with malignancy, for Paget's disease, and for osteoporosis.

Ref- Katzung Basic & Clinical Pharmacology , 10th Ed

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