uworld incorrect 4

Question 1

what kind of mutation caused in lysch nyhan

Answer 1

activating mutations involving phosphoribosyl

Question 2

how does colichine act on neutrophils

Answer 2

decreases tyrosine phosphrylation decreasing neutrophil activation and also prevents microtubbule polymerization

Question 3

what sort of chest is seen in cystic fibrosis

Answer 3

barrel shaped chest

Question 4

what is diffference between dna polymerase 1 and 3

Answer 4

1 removes rna primer replaces it withdna. 3

Question 5

what is sympathia opthalmia

Answer 5

when eye injured self antigens released=autoimmune reaction

Question 6

which body parts have immune privilge

Answer 6

testis and eyes

Question 7

immune privilge

Answer 7

ack of lymphatics, low expression of MHC class Ia); t

Question 8

explain pathogenis of sympathy opthamia

Answer 8

Self-antigens located in immune-privileged sites can be recognized by T cells that escape negative selection in the thymus. Therefore, if these self-antigens are released into the lymphatic system as a result of trauma, T cells may recognize these self-antigens as foreign and mount a response in both the injured eye and the contralateral eye

Question 9

function of dnase

Answer 9

degrades dna in pus helping spread of orgasm

Question 10

possible diagnosis if staph aureus in urine

Answer 10

If S. aureus is cultured from the urine you should suspect a metastatic infection from another location in the body (an abscess or infective endocarditis etc.)

Question 11

jc virus clinical px

Answer 11

Hemiparesis, visual field defects+cognitive impairemtn

Question 12

how is cmv transmitted how to prevent it and what other cases u see cmv

Answer 12

CMV can be acquired during the transfusion of leukocyte-laden blood products, as the virus infects leukocytes of granulocyte-macrophage lineage

HSv 6, HIV and toxo

Question 13

why lipohilic drugs require loading dose

Answer 13

they distribute into fat

Question 14

dosing how it varies with weight

Answer 14

dosing based on body weight=for narrow therapeutic index
it affects Vd/clearence
lean mass increases vd high
obesity causes disporptional increase in adipose therefore variable effect
aminoglycosides have minimal plasma protein binding and can distribute extensively into the interstitial compartment.

Question 15

causes of serum sickness? symotoms? time?

Answer 15

Monoclonal Ab, nonhuman Ig, penicillin, cefaclor, TMP/SMX

Fever, pruritic skin rash, arthralgias 7- 14 days after exposure (takes time to make

Question 16

how does serum sickness cause neutropenia

Answer 16

c5a acts as a chemotaxin

Question 17

anticholinergics, sympathomimetics, dopaminergic antagonists, diuretics how they mess up with heat regulation

Answer 17

Anticholinergics (eg, amitriptyline, scopolamine) inhibit diaphoresis, limiting the body’s primary mechanism of heat dissipation.

Sympathomimetics (eg, amphetamines, cocaine) impair peripheral vasodilation, limiting heat transfer to the skin (Choice E).

Dopaminergic antagonists (eg, chlorpromazine, haloperidol) disrupt hypothalamic thermoregulation, likely by blocking dopamine transmission in the hypothalamus (Choice C).

Diuretics (eg, furosemide) and beta blockers (eg, metoprolol) limit the cardiac response to heat stress by reducing blood volume or heart rate, thereby decreasing blood

Question 18

chagas disease explain acute vs chronic

Answer 18

acute chagas
-circulating trypomastig pts assymotmatic, nonspecific symotoms, inflmmation of eyes

chronic phase-elimination=resolution
assmotmatic chronic infection serology+ but no paraseitemia
complication of chagas-BIventricular HF+aneurysm

Question 19

does urea have a tmax

Answer 19

urea has no tmax since its passively reabsorbed

Question 20

which joint is involved in hemochromatosis

Answer 20

econd and third metacarpophalangeal (MCP) joint

Question 21

osteoarthritis involves which joint

Answer 21

proximal and distal interphalangeal joints and the first carpometacarpal joint

Question 22

moa of e6 and e7 in hpv virus cancwer formation

Answer 22

Ubiquitination of the E6-p53 complex induces degradation of p53, leading to unregulated cellular growth.

Question 23

Define dermatoform herpes histo

Answer 23

microabscesses containing fibrin and neutrophils at the dermal papillae tips

Question 24

explain pathogenesis of herpes demetoformis

Answer 24

iadin is deaminated by tissue transglutaminase in a process involving formation of covalent crosslinks between the twoubsequent immune response against gliadin also targets tissue transglutaminase, leading to the production of IgA and IgG tissue transglutaminase autoantibodies.

Question 25

2 skin lesions associated with diabeties | skin manifestation of poryphria cutanea tarda

Answer 25

Necrobiosis lipoidica diabeticorum+acathosis nigricans | This condition is characterized by skin fragility and blistering lesions in sun-exposed areas

Question 26

histopath of leukocytoplastic vascukutus

Answer 26

perivascular neutrophil depris

Question 27

histopath of giant cell arteritis

Answer 27

Transmural granulomatous inflammation with fragmentation of elastic fibers is a typical finding of giant cell arteritis, seen in adults age

Question 28

explain causes and pathogeneis of Mitral VP

Answer 28

Seen in Marfans and Ehlers danlos and OI • Proliferation of spongiosa in leaflets, fragmentation of elastin fibers with increase mucopolysaccharides and type 3 collagen deposition

Question 29

how is c1 activated which AB more effective

Answer 29

C1 must bind the Fc portions of two different antibodies at specific C1 binding sites.

Question 30

why prostate cancer goes to bone

Answer 30

pericytes and bone marrow stromal cells | osteoblast differentiation factors

Question 31

explain patho of osteomyeltis | which bone children gets affected and why

Answer 31

metaphysis of long bones due to the slower blood flow and cap fenestrae in this region

Question 32

chronic osteomyeltis

Answer 32

Persistent inflammation within the confined bony space leads to increased intramedullary pressure, which compromises blood flow and forces infectious exudate into the cortex and periosteum. Without treatment, the infection can progress to chronic suppurative osteomyelitis, in which necrotic bone (ie, sequestrum) serves as an infectious reservoir and sinus tracts develop to drain away the purulent material.

Question 33

hematogenous spread of bacteria in vertebra

Answer 33

Hematogenous osteomyelitis in adults occurs more commonly in the vertebral bodies due to increasing vertebral vascularity with age as well as epiphyseal closure during puberty

Question 34

allergy to shellfish

Answer 34

urticaria, angioedema, and/or anaphylaxis immediately after food consumptio

Question 35

arsenic posion

Answer 35

binds to sulfadryyl groups inhibits cell respir/gluconeogensis pyruvate DEhydrogenase acute-garlic breath, vomiting high qt chronic -hypo.hyper pigment, hyperkeratosis and glove and stocking

Question 36

whats a dhole body

Answer 36

Leukocytosis with high LAP | • Dohle bodies: light blue (ribosome) basophilic peripheral granules in neutrophils

Question 37

neutrophil left shift vs hypersegmented neutrphils

Answer 37

Increased neutrophil precursors (eg, bands, metamyelocytes, myelocytes) are also typically present (referred to as "left shift") due to early release from the marrow in response to the increased demand of the inflammatory co

Question 38

clinic features of chest xray in decompensate hf

Answer 38

caridomegaly, highly atteunated vessels, pulmonary edema/pleural efffusion

Question 39

monoamioxidase receptors why delayed clinical effects in Monoamine receptor

Answer 39

Monoamine receptor are GCPR | • Can be downregulated if overstimulated > explains delayed clinical effects

Question 40

how do ssris/tca work

Answer 40

block reuptake