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usmle > amboss incorrects > Flashcards

amboss incorrects Flashcards

1
Q

how to differentiat between toxo retinitis and cmv retinitis

A

cmv=floaters/encephalitis,esophagitis/pneumonitis toxo however-causes eye pain/retrochoritdits, and fluffy lesions

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2
Q

noise induced hearing loss

A

destruction of cochelar hair cells

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3
Q

otoscleooris

A

chl mostly bilateral 3rd and 4th decade of life

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4
Q

acoustic neuroma

A

tinnitus gait instability

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5
Q

l4 herniation vs l5 herniation

A

decreased patella l5 decreased achilles

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6
Q

where is subependymal giant cell astrocytoma seen

A

TSC

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7
Q

oxygen induced retinopathy

A

inhibits vegf formation

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8
Q

common casses of meningioma

A

falx cerebri and spehnoid and foramen magnum

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9
Q

where does medulloblastma originate form

A

primitive neuroectoderm

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10
Q

what do arachnoid cells gve rise to

A

meningiomas

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11
Q

what do astroglial cells give rise to

A

astrocytomas

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12
Q

lymophocytic infiltrate of endoneurium seen in

A

gullian barre syndrome

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13
Q

MS is caused by which cells

A

th1 react to myelin basic protein=focal demyelination

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14
Q

what does mononeuritis simplex present as

A

painful sensory/motordefect it occurs in vasulitis

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15
Q

inhibition of 5ht /NE reuptake

A

amitryptiline

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16
Q

what alters perception of ascending pain impulse what is effect of opiod

A

vasodilation

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17
Q

what is there in alway s aneurologic stroke

A

PAINLESS FOCAL NEUROLOGIC DEFICIT

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18
Q

what is a complication of axillar node dissection

A

long thoracic nerve injury

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19
Q

what happens in excessive alcohol biochemically which enzyme fucked

A

pyruvate dehyrdogenase

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20
Q

clinical features of G6pd

A

Clinical findings include yellow-tinted skin, dark urine, and fatigue

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21
Q

advese effects of acetolazimide

A

sulfa allergy,hypokalemia and phyperamminome

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22
Q

why does acetolazimide cause hyperammoniema

A

cause inorder for ammonia to be excreted with need

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23
Q

all diuretics chave one adverse effect

A

hypokalemia

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24
Q

neurocyterosis vs toxoplasmosis how to differentiate

A

the latter one needs hiv

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25
Q

hyperammoniemia induced encephalopathy

A

astrocytes detoxify ammonia(glut dehydrogenase) and glutamine synthease water moves into cells=cerebral edema

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26
Q

worsening character for trochlear nevr lesion

A

downward gaze

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27
Q

a patient comes with confusion ataxia and mamillary body

A

wernicke

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28
Q

where do you see intraparenchymal cyst

A

neurocyticrosi

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29
Q

brainstem glioma

A

NF1, seixures cafe au lait

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30
Q

CJD classic symtooms

A

akinetic mutism/neuropsyhcatric symtoms

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31
Q

myoclonic jerks part of which isease

A

merrf mutation in mt k gene opsoclonus myoclus sundrome=myoclong jerks and atasia/ seen in neuroblastma as well

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32
Q

adenoma sebaceum seen in

A

tuberous sclerosis present with ataxia and nystagmus? hamartoma in cerebellum or subependymal astrocytoma causing hydrocephalus

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33
Q

beta amylkoid 1 42

A

alzehimers disease indicator

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34
Q

anti gangloside ab

A

gulian bare

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35
Q

what is the most common cause of anti yo antibodies

A

breast cancer

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36
Q

what produces anti nmda and anti hu

A

ovarian teratoma and small cell lung cancer

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37
Q

what causes hyperphosphrylation of tau

A

glycogen synthae 3

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38
Q

which nerve courses along parotid gland

A

facial nevr, does it innervate/ no

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39
Q

whiplash injury

A

central cord syndrome

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40
Q

a pregnant woman has toxoplasmosis infection what would you find on the baby

A

the baby would have spasticity of the lower leg with hydrocephalus

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41
Q

whend o msk nerve injury occurs

A

due to heavy liftint typically

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42
Q

a person has mengitis with gram + bacillis surrounded by rim what is it

A

listeria

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43
Q

what drugs cause glaucoma

A

atropine

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44
Q

how to dy/dx polymyositis with myasthenia gravis

A

polymyositis ocular muscles never affected

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45
Q

what causes spontaneus ruptures in the brian

A

amyloid angiopathy, causes microaneurysms which could rupture and result in stroke

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46
Q

what do flurionated anestheritc shave in common

A

they all increase in cerebral blood flow

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47
Q

what is alpha synuclein misfolding

A

parkinsons

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48
Q

typical locations of brain tumors

A
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49
Q

risk factors for ICH of newborn

A

<32 weeks

hypoxia

chorioamniotis

Infection of the amniotic fluid, fetal membranes, and placenta that is most commonly due to ascending cervicovaginal bacteria (e.g., Ureaplasma urealyticum or Mycoplasma hominis)

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50
Q

why do we have high arched palate in mytonic dystrophy

A

reducesd temporalis and ptyergoid muscle growth

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51
Q

how can subfalcine herniation cause hydrocephalus

A

it compresss foramen monro

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52
Q

brown sequard lesion

A
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53
Q

what is chromatolysis

A

A reaction of a neuronal cell body in response to an axonal injury; it is characterized by swelling of the neuronal body, dispersion of the Nissl bodies, and displacement of the nucleus to the periphery.

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54
Q
A
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55
Q

how does fish bone in pyiriform fossa fuck up laryngeal nerve

A

The superior laryngeal nerve divides into an internal and external branch beneath the internal carotid artery. The internal laryngeal nerve runs directly beneath the mucosa of the piriform recess, along with the recurrent laryngeal nerve, and is distributed to the mucous membrane of the larynx. The internal laryngeal nerve can be injured during surgery (e.g., thyroidectomy) or damaged by food items (e.g., a fishbone) being trapped in the piriform fossa. Damage to this nerve classically manifests with an impaired cough reflex, which increases the risk for recurrent aspiration pneumonia.

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56
Q

how does thambutol act

A

The mechanism of action of ethambutol is the inhibition of arabinosyltransferase, which subsequently inhibits the synthesis of arabinogalactan, an important mycobacterial cell wall polysaccharide

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57
Q

mercury posioning how he looks

A

buccal inflamation, blue white discolouration/ployneuropathy

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58
Q

diagnosis of narcolepsy which wave

periodic sharp waves seen in

old ppl

delirum

A

rapid onset of beta waves

cjd

delta waves decreased in old people

diffuse slow waves=delirum

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59
Q

can pregnant woman develop wernicke encephalopathy

A

yes metabolic demand of thiamine/ increaed hypermesis gravidarum

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60
Q

what are radial glial cells

A collection of nonspecific, reactive changes (e.g., proliferation, hypertrophy) to glial cells in response to CNS damage

A

line the ventricles

what is glial scleoriss

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61
Q

a pupillary dilator agonist increases nor e release what is it

A

ACH from preggl neuron, causes contractin of pylorus

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62
Q

inflammation of chorid plexus

A

Inflammation of the choroid plexus (choroid plexitis), which is most commonly caused by CNS infection (e.g., tuberculosis, cryptococcosis) can result in increased CSF production and thereby cause lateral ventricle enlargement, as seen here on the T2 weighted MRI. However, this patient does not have any clinical features of CNS infection (e.g., fever, headache, meningism) and there is no enlargement of the choroid plexus in the lateral ventricles on imaging to suggest choroid plexitis.

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63
Q

non communicationg hydrocephalus causes

A

Obstruction of the foramen of Monro, which is typically caused by a tumor (e.g., colloid cyst), would result in unilateral (asymmetrical) lateral ventricle enlargement, unlike this patient who has symmetrical enlargement of both the lateral ventricles on the T2 weighted MRI.

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64
Q

what is high pitched pericardial knock

A

early pericardial lesion which is high pitched occurs early diastole

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65
Q

temporal arteritis to development of thoracic aneurysm

A

lets say 10 years

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66
Q

why hand clenching increases vsd murmur

A

increased afterload therefore increase L-R shunt which causes systolic sound (holosystolic)

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67
Q

why ASD has systolic ejection murmur

why ASD has soft midiastolic murmur

A

Relative pulmonary stenosis due to an increase in stroke volume

Soft mid-diastolic murmur over the lower left sternal border

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68
Q

what is differential cyanosis / reverse dy/dx cyanosis

A

The reversal of the shunt results in a mixture of deoxygenated and oxygenated blood reaching the lower extremities.

reverse is the opposute

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69
Q

a continuous murumur that become loud on the second heart sound is

A

PDA

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70
Q

what is brugada syndrome

A

present as syncope with tacchyarthmia

incolmplete RBBB, and elevation in v123

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71
Q

a person is alcoholic takes diuretics and has diarrhea he develops torsades des pointes why?

A

hypomagensemia

which diruetics

loop

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72
Q

where is the aortic isthmus what are the symotoms

A

is located just distal to the origin of the left subclavian artery and is tethered by the ligamentum arteriosum

(hematoma seen on the chest typically hand sized)

however if injury to IVC it can result in (retropertioneal bleed)

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73
Q

if you have injury to aortic isthmus if coronary artery injured how would it manifest as

A

increased st segment

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74
Q

how can presence of vasopsatic angina be confirmed

A

coronary angiography with ACh released

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75
Q

HCMo is highly variable why?

in restrictive cardiomyoapthy MOA of death

remember one thing aortic stenosis never results in sudden cardiac death why

A

some patients develop symmetric however other patients are asyymetric

not sudden

because it manifes as SAD

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76
Q

what other disease can cause lebiman sack endocarditis

are libeman sack endocarditis dangerous

a person has fever and new murmur what it ocould eb

A

advanced cancer /rheumatoid arthiritis

it is dangerous since it can be dislodged and embolizied

infective endocarditis

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77
Q

what is exactly coarctation of aorta medial and intimal hypertrophy causes narrowin preductal and postfuctal types of cyanosis and when does rib notching occur

what are the symotoms of coarctation of aorta

A

rib notching doesnt occur before 5 years

dyx cyanosis can occur delayed towards the leg, if subclavian artery involved will lead to high right arm pa anddifferential cyanosis of the the right arm

LVhypertrophy and symptoms dont produce in utero because of Patent ductus arteriosus

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78
Q

where and why do you hear murmur of coarctation of aorta

A

Systolic ejection murmur over left posterior hemithorax

becausestenosis of aorta there

continous murmur b/w scapular space due to collateral flow

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79
Q

what are the consequeunces of brachial hypertension

A

headache eppxistasix and tinnitus

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80
Q

what happens if in coartcation PDA suddenly closes

A

it can cause hypotension and shock

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81
Q

wjhy we have pericarditis after neutrophilic inflammation

A

e.g., TNF-α, IL-2, IL-6) from neutrophils causes exudation of fibrin and leukocytes into the pericardial space, resulting in fibrinous pericarditis.

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82
Q

EARLY MI

late mi

A

release of cytokines from cells, early recruitment of neutophils can lead to motlling

hypercontraction of myofibrils

and after 12 24 hours dark mottling

if contraction band it is repurfusion injury

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83
Q

what is the MOA of prostacyclin analogs

A

ncreased activation of protein kinase A is the mechanism of action of prostacyclin analogs, a class of drugs used to treat pulmonary hypertension. Prostacyclin analogs bind to prostacyclin receptors and activate G protein, which in turn stimulates adenylyl cyclase, resulting in increased intracellular cAMP. Intracellular cAMP activates protein kinase A, which causes vasodilation by inhibiting myosin light chain kinase, the structure responsible for smooth muscle contraction. Ho

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84
Q

why we dont have JVD on normal inspiration

A

During inspiration, there is increased systemic venous return and increased volume in the right heart, which is compensated for by expansion into the pericardial space

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85
Q

which conditions leads to high A wave

when is v wave seen

A

A prominent a wave may be seen in patients with right ventricular hypertrophy or pulmonic stenosis

seen in tricuspid regurgitation and right heart failure. This patient’s v wave should not be significantly changed.

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86
Q

what is holiday heart syndrome

A

particular, acute alcohol consumption often triggers paroxysmal A-fib (also known as “holiday heart syndrome”), which subsides within 7 days without intervention

presens with syncope and dizziness

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87
Q

why do you have JVP in constirctive vs tamponade u dont

A

noncompliant ventricle doesn expand

tamponade-imapired rv filling due to cardiac compression

when does jvp occur only in poulsus paradoxus

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88
Q

Pulmonary artery hptn

pcwp lfh

A

>25

>18

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89
Q

What does RHF lead to in kidney

what is coronary sinus dilation

A

Right heart failure is a condition that can cause systemic hypoperfusion. For this reason dilatation (not constriction) of the renal afferent arteriole would rather be expected in this patient.

Reduced right-sided cardiac output leads to venous congestion in the vessels that drain into the right heart, including the coronary sinus, which can become dilated as a result

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90
Q

how do nitrates work

when are they contraindicated

A

Nitrates work by forming free radical nitric oxide,

rhf, HCOM

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91
Q

side effects of exitimidbe

A

hepatotoxicity

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92
Q

Developed countries

A

radiastion therapy dangerous

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93
Q

mutation in fibrillin

A

predispose to mucoid extracellular matrix accumulation, medial fibrosis, and loss of smooth muscle cell nucle

94
Q

Pressure gradient location in aortic stenosis vs HCOM

A

HCOM is below aortic valve wheras aortic stenosis across aortic valce

95
Q

is thrombosis of bowel common or emboli

if emboli where does it occur

A

emboli mor comomon,sma/ima

96
Q

IN ami how are the coronary arteries

how nitroglucerin improves venticular compliance

A

they are in acute state of dilation due to impaired o2 delivery Nitroglycerin actually improves ventricular compliance by reduction of myocardial preload and its effects.

97
Q

what features confirm diagnosis of TOF

A

Echocardiography showing a pulmonary artery arising from the left ventricle and aorta arising from the right ventricle confirms the diagnosis of transposition of the great arteries,

98
Q

why high cardiac output causes volume overload

A

However, despite increased cardiac output, low systemic vascular resistance results in arterial underfilling, decreased renal perfusion, and retention of salt and water, which leads to volume overload and heart failure.

99
Q

when is d dimer test used in DVT

A

to rule out DVT in low pretet probability

100
Q

stasis dermatitis

A

n inflammatory skin condition characterized by a scaly, pruritic rash on the lower extremities. Most commonly occurs as a consequence of chronic venous insufficiency and edema.

101
Q

cholestrol embolization syndrome

A

This patient presents with the classic symptoms of blue toe syndrome, livedo reticularis, and acute kidney failure. Eosinophilia and eosinophiluria in the setting of cholesterol embolism are very suggestive findings.

102
Q

action of fibrates

A

Fibrates are associated with an increased risk of cholesterol gallstones because they inhibit the cytochrome p450 enzyme cholesterol 7-α hydroxylase (↑ cholesterol and ↓ bile acid concentration in bile

103
Q

why do we have tet spells

which CHD cause pulmonary congestion

A

due to contractions of infinduibular septum, how to manage it beta blockers, volume expansion and iv morphinet

runcus arteriosus, total anomalous pulmonary venous return)

104
Q

TAPVR

how could it cause pulmonary edema

A

All four pulmonary veins drain into the systemic venous circulationminsted of there could be a right to atrial shunt

obstruction of pulmonary vein =pulmonary congetion

Pulmonary venous obstruction: obstruction of pulmonary venous return → ↑ pulmonary venous pressure → ↑ pulmonary edema → ↑ PVR → RVH, ventricular dilation, and heart failure

105
Q

perioral parethesia is side effect of antiarrythmic drug

and sedation

A

Perioral paresthesia is a side effect of lidocaine, a class IB antiarrhythmic agent used to treat ventricular tachycardia.

Sedation is a known side effect of beta blockers (e.g., metoprolol, labetalol) and class IB antiarrhythmics (e.g., lidocaine, mexiletine). These agents are lipophilic and can penetrate the blood-brain barrier, resulting in CNS side effe

106
Q

Great saphenous vein coryse

A

The great saphenous vein (GSV) originates at the base of the hallux, continues proximally by passing anterior to the medial malleolus and then courses along the posterior aspect of the medial femoral condyle before running deep into the thigh to join the femoral vein.

107
Q

inhaled NO

A

nhaled nitric oxide (NO) is the mainstay treatment for PPHN because of its ability to potently vasodilate the pulmonary vasculature (reducing V/Q mismatch) without decreasing systemic vascular resistance.

108
Q

PDA=

pvr in relationt o hypovolemic shock

A

a continuous machinery murmur best heard in the left infraclavicular area.

include an increased respiratory rate (as a compensatory response to lactic acidosis) and increased alveolar-capillary permeability.

109
Q

The antitoxin can only neutralize unbound toxin and should therefore be administered early in the course of the dise

A
110
Q

whats the difference in lovation b/w mVP and mitral regurgtation

A

one radiates to acxilla, the other is associates to 5th intercostal space

111
Q

how do statins cause myalgia MOA

A

Statins can decrease the synthesis of coenzyme Q10 and impair energy production within muscle, which can result in myalgia, muscle weakness, and increased serum creatine kinase (CK)

112
Q

causes of increased tags

A

serum triglyceride concentrations include beta blockers, glucocorticoids, cyclosporine, and some HIV antiretroviral drugs.

113
Q

what will hemopericardium due to MI cause

Px of free wall rupture

PX of interventricualr septum

A

Ventricular wall rupture can occur within 2 weeks of myocardial infarction and typically results in hemopericardium and cardiac tamponade, which can manifest with profound right heart failure, shock, and often death.

so its symptoms are of obstructive shock

new-onset chest pain and cardiogenic shock due to cardiac tamponade.

signs of RHF

114
Q

explain pathophys cardiorenal syndrome

A

Systolic dysfunction → reduced cardiac output → renal hypoperfusion → prerenal kidney failure

Diastolic dysfunction → systemic venous congestion → renal venous congestion → decreased transglomerular pressure gradient → ↓ GFR → worsening kidney function

RAAS activation → salt and fluid retention → hypertension → hypertensive nephropathy

115
Q

where would thrombus of abdominal aneurysm normally occur

A

Occlusion at the opening of the IMA by a thrombus within an aortic aneurysm (suggested by the filling defect) would cause acute mesenteric ischemia and, potentially, necrosis of the bowel segments supplied by this artery

116
Q

how does ACE inhibitor cause reoaxtaion moa

A

Angiotensin-converting enzyme (ACE) inactivates bradykinin, an inflammatory mediator that increases intracellular calcium in endothelial cells. Intracellular calcium stimulates nitric oxide synthase to convert arginine to nitric oxide, which mediates the relaxation of vascular smooth muscle cells to cause vasodilation.

117
Q

why isnt heparin used for long term treatment

A

it is only adminstred subcutaneously requires monitoring

118
Q

timiolol is passively absorbed into the eyse

A
119
Q

why thiazides good for salt secretion

A

causes hyponatremia due to decresed salt but increased water absorption however loop diuretics destroy the gradient so technically hypernatremia

120
Q

thyroid artery

what lies posterior to esophagus

which CCB blocker cause Peripheral edema, which causes gingival hyperplasia

A

sup-eca

inf-thyrocervical trunk

include the thoracic duct and azygos vein.

PE=amlodipine

GH-non dihydropyridine

121
Q

Granulomatous nodules on mitral valve is

Formation of giant cells in the tunica media is characteristic of giant cell arteritis (GCA) and Takayasu arteritis, both of which are large vessel vasculitides and can result in an AAA. H

A

Granulomatous nodules on the mitral valve are associated with rheumatic heart disease (RHD

122
Q

what causes intrapulmonary shunting

\where it occurs

A

Some common conditions that can cause intrapulmonary shunt include pulmonary AVM, hepatopulmonary syndrome, severe cases of pulmonary edema, and lobar atelectasis.

perfusion no ventalation

123
Q

what causes arthesosclerotic plaque to rupture

marfan syndrome how does it look on ct/arthropathy

A

increase metalloproteinase

which causes thrombus to form over

with Marfan syndrome have hypermobile joints, which predisposes them to chronic arthralgia as a result of recurrent sprains, bursitis, and/or early-onset osteoarthritis. Cystic medial degeneration,

124
Q

prolonged qt interval

A

Prolongation of the QTc interval is a possible ECG change seen on cardiac stress testing in patients taking class IA and class III antiarrhythmic drugs, which block potassium channels, resulting in a prolonged repolarization phase of the cardiac action potential. Flecainide has minimal effects on the ventricular repolarization but can result in shortening (rather than prolongation) of the QTc interval on stress testing.

125
Q

what heart sound would be expected in aortic stenosis

A

Moreover, in aortic stenosis, a paradoxical split of S2 would be expected on cardiac auscultation rather than a wide splitting of S2.

126
Q

why pulmonary edema has bats wing appearence

compare ards with PE

A

In pulmonary edema, the opacification can often assume a perihilar distribution (a so-called “batwing” or “butterfly-shaped” pattern), which is seen here, because the periphery of the lung has better lymphatic drainage than the central regions

127
Q

pathogensis of thromboarteries

A

infolatmition of intima, neutrophil migration microabscess formation

interal elastic lamina remains intact

128
Q

limiing factor of coronary blood flow

A

excercise

129
Q

isruption of an atherosclerotic plaque with a non-occlusive coronary artery thrombus can could be wht

A

unstable angina pectoris

130
Q

what exaccebrates symtooms of aortic stnosis

how do fatty streaks appear

whaich murmur is seen in mitral regurgtation and mitral regurg exaccebration

A

a fib and why

Fatty streaks appear macroscopically as flat yellow discolorations with irregular borders on the luminal surfaces of blood vessels, including the aorta. Sta

MR exaccebration axilla murmur not seen

131
Q

continutity equation

A

his concept is expressed mathematically via the continuity equation: A1V1 = A2V2

132
Q

HIT 1 vs HIT 2

A

Direct interaction between heparin and platelets (e.g., heparin directly induces platelet aggregation)

No antibodies involved (nonimmunologic)

Heparin and platelet factor 4 (PF4) form a complex → production of IgG antibodies against the heparin-PF4 complex → IgG antibody-heparin-PF4 immunocomplex binds on platelet surface → platelet activation and aggregation → consumption of platelets (thrombocytopenia) and arterial/venous thrombosis

133
Q

cml vs pcv

A

tear drop cells

134
Q

pathophys of splenomegaly in hairy cell, vs cml

A
135
Q

pica is associated with

altered sense of smell

A

Pica is also associated with zinc deficiency, pregnancy, and psychiatric conditions, though its etiology is not entirely understoo

zinc deficiency

136
Q

how does tyrosine kinae inhibtor work

A

It binds to the active site for ATP on the abnormal BCR-ABL tyrosine kinase (caused by the Philadelphia chromosome) and prevents the phosphorylation of tyrosine residues on the enzyme’s substrates. In turn, this inhibits proliferation

137
Q

what happens to people with sickle cell disease

which bleeding location is epitaxis correlated to

talk about oxygen changes in anemia

A

they develop functional asplenia

vwf disease

Dyspnea, tachycardia, and evidence of hyperdynamic circulation (e.g., loud S1/S2, systolic ejection murmur due to increased blood flow) are features of severe anemia. In patients with anemia, the arterial partial pressure of oxygen (PaO2), which reflects dissolved oxygen content, and the arterial hemoglobin oxygen saturation (SaO2) remain normal. However, the total arterial oxygen content (CaO2), which is given by the formula [1.34 x SaO2 x hemoglobin concentration] + [0.003 x PaO2])

138
Q

how to diagnosie antiphosophlipid antibody

A

Lupus anticoagulant (LA): leads to a prolonged aPTT

Mixing study: The patient’s plasma is mixed with normal plasma. If the prolonged aPTT is caused by a lack of clotting factors, the factors contained in the normal plasma will normalize the aPTT. In the presence of lupus anticoagulants, the aPTT will remain unchanged.

Dilute Russell viper venom test: Lupus anticoagulant interacts with Russell viper venom, which usually induces the formation of blood clots. As LA binds the venom, this effect is suppressed, resulting in a prolonged aPTT.

139
Q

MOA of all trans retinoic acid

A

Retinoic acid binds its nuclear receptors to stimulate histone acetylation, which promotes gene expression that regulates the maturation and proliferation of granulocytes.

140
Q

effect of bence jones protien on tubules what other causes of renal dysfucntion in MM

A

causes tubular atrophy(Bj) proteinincluding AL amyloidosis (usually presenting with nephrotic syndrome due to glomerular dysfunction) or hypercalcemia (causing nephrocalcinosis).

141
Q

febrile non hemolytic reaction=

A

Serum antibodies directed against donor HLA antigens have been associated with febrile non-hemolytic transfusion reactions (FNHTRs), as the antibodies may bind to HLA antigens on residual donor leukocytes in blood products and possibly stimulate the release of inflammatory cytokines.

142
Q

if a patient has hemoglobinuria and flank pain what would the patient have

A

intravasuclar hemolysis

143
Q

name.2 different types of hemolytic reaction

cold agglutins associated with which disease

A

major and minor( a person with scd will develop alloimmunization which could result in transfusion reaction)

CLL,HEPC,mYoco penumo

144
Q

allogenic vs autologus stem cell transplantation

A
145
Q

anti b2 glycoprotein MOA

A

These antibodies inactivate anticoagulant proteins (e.g., protein C and protein S, antithrombin III) and activate platelets and vascular endothelium, thereby resulting in a hypercoagulable state with an increased risk of arterial and venous thrombi.

146
Q

AML risk factors

A

downs, cml,and radiation

147
Q

explain role of ribavirin in HCV treatment and MOA of adverse effect

A

. Ribavirin-induced hemolytic anemia results from the accumulation of phosphorylated forms of ribavirin within red blood cells; since RBCs lack dephosphorylating enzymes, ribavirin accumulates within cells, leading to hemolysis. Because of the advent of newer HCV medications, ribavirin is typically used as an adjunct in patients with refractory hepatitis C infection.

Binds to rna polymerase/prevents gmp synthesis

148
Q

hypocellular bone marrow seen in

A

HAIRY cell leukemia and myelofibrosis

149
Q

what is the cause of fractures in Multiple myeloma how to diagnose from ideny

how can they develop analgesic nephropathy

A

proliferation of cells in the bone marrow inhibtis synthesis of cells, causing pancytopenia and skelatal destruction

since cells grow it causes hypercalcemia, non funtincal antibodies forme

A test in which sulfosalicylic acid is added to urine to measure urine proteins.

150
Q

how to differentiate between myxedema and lymphedema

A

fluid is protein rich/gag rich

the other is lipid rich protein rich

if neutrophilic rich, it would be due to inflammation

151
Q

how to differentiate between alpha thalesemia and beta thealesmeia

A

HB a2 would be seen in beta thalesemia

152
Q

what sort of infarction does sickle cell disease have

Transient synovitis is a common cause of self-limited hip pain and limping in children and is often preceded by upper respiratory tract infection. However, most patients with transient synovitis are slightly younger (< 10 years), and this patient’s underlying sickle cell disease makes a different diagnosis more likel

A

trabeculae bone infarction

153
Q

hemophius influenza non tybale B

and staph aureus

A

patients who have cystic fibrosis, alcohol use disorder, a history of IV drug use, or an immunocompromised status

heam has milder infections compared to the rest

154
Q

what is porphria cutane

A
155
Q

beta thaleesamia mutation

A

intron and promotor

if intron splice site mutation if promoto =point mutation

156
Q

breastfeeding jaundice vs breat failure jaundice

a person with herditary spherocytosis will have folic acid deficiency or b12 deficiency

A

Pathophysiology: insufficient breast milk intake → lack of calories and inadequate quantities of bowel movements to remove bilirubin from the body → ↑ enterohepatic circulation → increased reabsorption of bilirubin from the intestines → unconjugated hyperbilirubinemia

Clinical features: onset within 1 week

Treatment: increase breastfeeding sessions, rehydration

Breast milk jaundice [2]

Pathophysiology: increased concentration of β-glucuronidase in breast milk → ↑ deconjugation and reabsorption of bilirubin → persistence of physiologic jaundice with unconjugated hyperbilirubinemia

Clinical features: onset within 2 weeks after birth; lasts for 4–13 weeks

157
Q

what. is the indication of celcoxib and why is it used in genetic disorder of glantzmann thrombasthenia

A

glanzmann thromboasthenia needs coz 1 for formationo f thromboxane a 2 which stimulates aggregation so if cox 1 inhibited coul be a problem

158
Q

lack of nucleus in RBC

mitochondria syntehsizes what

A

globin is not synthesized

heme is not hindered

ferrocheleatase/aminoleuviniv acid

159
Q

person with epidural mass on vertebra of beta thalesmeia

A
160
Q

clotting factors mutation leads to venous thromboembolism

antiphospholipid syndrome leads to both venous and arterial thromboembolism

A
161
Q

a person with g6pd deficinecy how are ribose 5 phosphate produced

A

R5P is produced by the enzymes transketolase and transaldolase using byproducts of glycolysis, namely, fructose-6-phosphate (F6P) and glyceraldehyde-3-phosphate (G3P). F6P is formed by isomerization of G6P and G3P is produced by transaldolase. Therefore, transaldolase is one of the essential enzymes for the production of R5P, and thus nucleotide synthesis, in patients with G6PD deficiency.

162
Q

what does lipid a activate

how can ecoli cause tubovarian abscess

A

The lipid A component of endotoxin activates tissue factor, the complement system, and macrophages,probably due to bacteremia

163
Q

why is leuprolide combined with flutamide intially ot treat prostate cancer

A
164
Q

tolterodine B3 receptor relaxation

cockroft gault equation

A
165
Q

why cant creatinine clearence be used to assess kidney function>60

A

Because a significant GFR drop is required before serum creatinine increases, serum creatinine cannot be used to assess kidney function at a GFR of > 60 mL/min/1.73m2. This is termed the “creatinine-blind” range.

166
Q

which is a better indicatiro serum creatine vs creatine clearnece

1.23 for males and 1.04 for females

A

obviously kideny creatinine why?

because serum creatinie Serum creatinine levels do not start rising until the GFR is reduced by approx. 50%.

167
Q

anti phospholipase a2 antibodies

A

Anti-phospholipase A2 receptor antibodies (anti-PLA2R antibodies) bind to PLA2R (an autoantigen in glomerular podocytes) and thereby form immune complexes that activate the complement system, leading to podocyte injury. [15]

168
Q

diabetic nephropathy pathophys

A

Chronic hyperglycemia and hyperinsulinemia stimulate collagen and glycoprotein synthesis within the GBM and mesangial matrix (protein glycosylation). I

169
Q

why ace inhibitors increase renal plasma flow

A

Simultaneously, renal plasma flow (RPF) is increased and filtration fraction (FF) is decreased. The underlying mechanism is inhibition of angiotensin II synthesis, causing dilation of the efferent arteriole. This increases RPF and reduces GFR due to a decrease in glomerular filtration pressure. Also, the FF is decreased because GFR is decreased and RPF is increased (FF = GFR / RPF).

170
Q

why cant we give ace inhibotors in heart failure

albuminuria coorelates with future risk of what

A

In patients with a preexisting reduction in RPF (e.g. heart failure), initiation of ACE inhibitors may lead to acute kidney injury.

cardiovasuclar events

171
Q

treat good pasture

where does the lower third of ureter lie

A

cyclophosphamide

below the cardinal ligament

The ureters lie below the ovarian arteries within the infundibulopelvic ligament and are also susceptible to injury during ovarian surgeries (e.g., oophorectomy).

172
Q

horse shoe kideny is always

A

incidentl

173
Q

why do we have hypovoluemia in rhabdomyolisis

A

third fluid spacing in damaged muscle could preciptate kidney injury release phosokinase andserum myoglobin could lead to pigment nephropahty

174
Q

How rapid progressive GN impairs renal function

A

so the cresecent =finbrin plus proliferating cells, compresses the glomerulus therefore could cause anuria

extracpaillary cell rpoliferation displaces glomerulus

175
Q

why you have vitamin d and thyroxine defciciency in nephrotic compare mcd vs other disorders

very high prtoein diet why not allowed in nephrotic

why they can develop heparin resistance

metabolic disturnbances in nephrtoic and their consequences

A
176
Q

Git manifestations of APCKD

A
177
Q

how do you differentiate between selective and nonselective proteinuria\

gitelman syndrome symotoms

wjhat causes mesangial expansion in diabetic kidney

A

selective proteinuria will be loss of negative charge

nonselective proteinuria will be loss of glomeular archeticture

selective proteinuria predominantly albumin

non selective will be mid prtoeins

chondrocalcinosis

178
Q

which drugs preciptate in kideny

A

Drugs such as acyclovir, indinavir, methotrexate, and ciprofloxacin are poorly soluble in urine and can cause renal tubule obstruction due to drug precipitation, building up as crystals that cause AKI within days to a week. This patient has not been exposed to any drugs that commonly cause crystal-induced AKI and has been sympto

179
Q

xanthaloma glomeularnephritis

A

A rare form of chronic pyelonephritis characterized by chronic destructive granuloma formation

Associated with Proteus mirabilis and Escherichia coli infections

Large, irregular, yellow-orange masses on gross examination of the kidney (may be mistaken for a true renal neoplasm)

Histology: granulomatous tissue with lipid-laden foamy macrophages and multinucleated giant cells

180
Q

Moa of pyelopnephritis

A

bacteria attaches to tubule cells, release cytokine s thereofre makes it more permeable therefore polynuclear cells enter the urine

181
Q

why we give low sodium diet in renal stones

A

High sodium levels ultimately cause an increase in urine output, which results in both dehydration and increased amounts of calcium excreted in the urine. This increases the risk of calcium phosphate stones or calcium oxalate stones formation. This patient would benefit from a low-sodium, not a high-sodium, d

182
Q

injury to pelvic splanchic nerves can

A

decrese sensation of bladdder fullness therefore can lead to overflow incontinecne

183
Q

role of citrate in stone formation

A

Citrate inhibits stone formation by forming a soluble complex with calcium in the renal tubule, which reduces the amount of free calcium in the urine to bind with oxalate or phosphate. Citrate excretion in the kidney is strongly influenced by pH (systemic, tubular, and intracellular). Alkalosis increases renal citrate excretion, whereas acidosis decreases it.

184
Q

hyperuricoria in stone formation

A

Associated with decreased solubility of calcium oxalate.

185
Q

mechanism of gynecomastia in spirnolactone

A

Spironolactone inhibits the binding of androgens to their receptors as well as the activity of enzymes involved in androgen synthesis (e.g., 17,20-desmolase, 17α-hydroxylase). It also increases the peripheral conversion of testosterone to estradiol and displaces estradiol from SHBG.

186
Q

changes in gfr/ ff in prfuse diarrhea

A

Profuse diarrhea can quickly lead to severe dehydration and hypovolemia, which would present with hypotension, tachycardia, and possibly, loss of consciousness. Hypovolemia leads to decreased renal plasma flow (RPF), and subsequently, a reduction in glomerular filtration rate. However, hypovolemia also stimulates the renin-angiotensin-aldosterone system, which attempts to mitigate the decrease in GFR by constricting the efferent arteriole. Therefore, in hypovolemic patients, the percentage reduction in GFR is less than the percentage reduction in RPF. The net effect is an increase in the filtration fraction.

PHYSIOLOGY OF THE KIDNEY

187
Q

where is creatinine synthesized

A

Creatine is synthesized from arginine and glycine in two steps in the kidneys and liver and is then transported to the muscle cells and phosphorylated intracellularly to creatine phosphate

188
Q

ARPCKD

A

Mutation in PKHD1 gene on chromosome 6, the gene that encodes for fibrocystin, a protein involved in the maintenance of primary cilia of the renal collecting duct and biliary epithelial cells

189
Q

causes of hyoreninism hypoadlostrenism

A

In acute glomerulonephritis, hyporeninism occurs as a result of volume expansion Due to damage to the juxtaglomerular apparatus(diabeties) heparin ace increase renin supppress aldoestrone

190
Q

how aldoestrone inhibits formation of ammonia

A

intracellular alkalosis

191
Q

pseudohypoaldoestrinism aldoestrone resitance what are the causes what is liddle syndrome,

A

type 1 /type2 could be caused by obstructive uropathy and analgesic nephropathy liddle syndrome is basically gain of functionm utation ( decreased ubiquintin degradation by proteasomes), causes pseudohyperaldoestrinsim

192
Q

glucogonoma what causes erythema

A

Nutritional deficiencies (e.g., decreased amino acid levels) are thought to be the underlying pathomechanism for the development of the erythema.

193
Q

acanthosis nigricans see where and pathophys

A

acromegaly, Elevated levels of insulin stimulate keratinocyte and dermal fibroblast proliferation via interaction with insulin-like growth factor 1, resulting in epidermal hyperplasia and plaque-like lesions, as seen in this patient. In addition,

194
Q

pcos what is the main hypothesis of SHBG decrease and how it affects

A

An inverse relationship between insulin levels and SHBG production has been suggested.

195
Q

features of de querivian thyroididtis

A

Painful, diffuse, firm goiter, jaw pain(swalling cough

196
Q

what are symtoms of thyroid malignancy

A

Also, this patient does not have symptoms suggestive of a thyroid malignancy (e.g., thyroid swelling, cervical lymphadenopathy, vocal cord palsy).

197
Q

spindle cells in kidney

A

Sheets of spindle cells in the kidney can be seen in patients with angiomyolipoma

198
Q

HPL b cell hyperplasia

A

Human placental lactogen causes pancreatic beta-cell hyperplasia and leads to an increase in insulin (and C-peptide) secretion as well as maternal insulin resistance. This ensures adequate glucose availability for the fetus. If maternal pancreatic function does not overcome insulin resistance, patients can develop gestational diabetes. In response to increased serum glucose concentrations, fetal production of insulin increases, which leads to increased fetal growth (macrosomia) as seen in this case.

199
Q

which sort of diabetic patients are at increased risk of fetal abnormalities

A

Infants born to mothers with pregestational diabetes, not gestational diabetes, are at risk for intrauterine growth restriction. Infants born to mothers with gestational diabetes are at increased risk for macrosomia due to the anabolic effects of high insulin levels.

200
Q

effects of graves diseas and fiabeties on fetus

A

Untreated diabetes during pregnancy can have teratogenic effects, putting infants at increased risk for congenital malformations including hypertrophic cardiomyopathy and small left colon syndrome. They are not, however, at increased risk for omphalocele. Pregestational diabetes (but not gestational diabetes) puts infants at increased risk of caudal regression syndrome.

201
Q

cns causes of galactorhhea

A

anything destroying the dopamine pathway in pitutary stalk or prolactinoma

202
Q

hypocalcemia causes what ecg findings

A

QT prolongation is seen in hypocalcemia due to slower calcium influx during phase 2 of the myocardial action potential and lengthening of the ST segment, whereas the T wave remains unaffected. Hypoparathyroidism, caused by trauma during thyroidectomy or parathyroidectomy, is the most common cause of hypocalcemia. Other, less common causes include vitamin D deficiency, PTH resistance, increased phosphate binding (rhabdomyolysis or tumor lysis syndrome), and hypomagnesemia.

HYPOCALCEMIA

203
Q

what would increase with use of levothyroxine

A

Levothyroxine is a synthetic form of T4, which is converted to reverse T3 (biologically inactive) and T3 (biologically active) by a deiodinase in the blood. Since an increase of reactants leads to an increase in products, rT3 would be expected to increase after several weeks of levothyroxine therapy. T3 and T4 negatively regulate the secretion of TRH from the hypothalamus and of TSH from the anterior pituitary.

204
Q

which molevular mechanism is involved in follicular adenoma

A

PAX8-PPAR gamma gene rearrangement is involved in the pathogenesis of follicular thyroid adenoma and follicular thyroid cancer, the second most common type of thyroid cancer. Unlike benign thyroid adenomas, follicular thyroid cancer is more likely to cause early invasion of the thyroid capsule and vasculature, making it the most likely diagnosis here.

205
Q

where do parafollicular cells of thyroid gland come from

A

ultimobrachial body sepcifically thyroid aalange

206
Q

what is adiponectin

A

A hormone produced by adipose tissue. Modulates insulin sensitivity, enhances fatty acid breakdown and has anti-inflammatory effects. Inversely related to adiposity.

207
Q

which diabetics drugs have delayed onset

A

tzds enhances transcription

208
Q

differentiate between classic and nonclassic 21 hydroxylase deficiency which is more common what are the sumtoms

A
209
Q

what happens to TOTAL calcium ions when you infuse phosphate in it

A

calcium exists in three forms there will be a decrease in free ion calcium but an increase in total calcium

210
Q

what antidiabetics used in gestational diabeties

A

Metformin and glyburide can

211
Q

mechanism of hyperuriciemia in vongireke disease

A
212
Q

calcitonin effects

A

its main goal is to decrease serum calcium so it inhibtis osteoclasts number 1 calcitonin keeps it in the bone

213
Q

why we use high glucorticoids in acute adrenal insufficiency but we need both glucorticoids and aldoestrone in chronic adrenal insfufficiency

A
214
Q

how to differentiate partial diabeties insipdus from central diapdies insipidus

A

The degree of responsiveness to desmopressin allows partial DI to be differentiated from complete central DI: In partial central DI, urine osmolality increases by approximately 10%, while in complete central DI, urine osmolality increases by over 50%. This patient’s urine osmolality increased from 310 to 355 mOsm/kg H2O, an approximate 15% increase, which is sufficient to diagnose partial central DI.

215
Q

siabeties insipuds cental

A

production problem or secretion problem ADH is produced in the hypothalamus and secreted from the posterior pituitary gland. Defects in the synthesis or secretion of ADH, e.g., those caused by brain tumors (craniopharyngioma), neurosurgery, traumatic brain injury, pituitary ischemia (Sheehan syndrome), or infection (meningitis), can cause central DI.

216
Q

CF of siadh

A

SIADH patients are usually euvolemic, normotensive, and have no edema

217
Q

symtoms of pitutary apoplexy

A

Pituitary apoplexy is often caused by hemorrhage into the pituitary gland. Intracerebral bleeding increases intracranial pressure, causing sudden, severe headache. The hematoma compresses the oculomotor nerves, which lie adjacent to the pituitary, causing acute onset of double vision. The disruption of pituitary secretion and release of ACTH can cause severe hypotension, as seen in this patient. Hemorrhage into the pituitary gland usually occurs into a previously existing pituitary adenoma (e.g., prolactinoma), which explains this patient’s history of amenorrhea, recurrent headaches, and bitemporal hemianopsia.

218
Q

a pt comes with charcort bouchard aneursym autospy findings hsow glomeulasa hyperplasia what is the mechanism of death

A
219
Q

which drugs are associated with aki(diabetic)

A

Because SGLT2 inhibitors are associated with acute kidney injury, patients taking these agents should undergo regular renal function testing, and their use is contraindicated in patients with severe renal impairment. Other adverse effects of SGLT2 inhibitors include weight loss and (orthostatic) hypotension.

ANTIDIABETIC DRUGS

220
Q

which diabetic drug causes agranulocytosis

A

Agranulocytosis is a rare complication of first-generation sulfonylurea use (chlorpropamide, tolbutamide) via an unknown mechanism.

221
Q

what are brown tumors and why is it brown bone changes in hypperpth

A

Consist of osteoclasts and hemosiderin (hemosiderin accumulates in bone cysts as a result of hemorrhage)

Subperiosteal thinning

Most commonly seen in primary hyperparathyroidism but can also occur in secondary hyperparathyroidism (↑ PTH → activation of osteoclasts)

222
Q

how to differentiate between brachial cyst and thyroglossal cyst

A

braachial cyst does not arise after URTI, however thyroid cyst can enlarge after urti

223
Q

what degrades thyroglobulin after endocytosis

A

Instead, they degrade the prohormone thyroglobulin into T4 and T3 after its endocytosis into thyr

224
Q

what is not destryoed in sheehan syndrome

A

In contrast, the posterior pituitary gland is thought to receive its blood supply from a higher-pressure arterial system. Accordingly, the posterior pituitary gland hormones, including antidiuretic hormone and oxytocin, are not typically affected in patients with Sheehan syndrome.

225
Q

types of MODY and complication

A

n contrast to other subtypes of MODY, patients with MODY type II are not at risk for micro- or macrovascular complications, despite mild fasting hyperglycemia and chronically elevated HbA1c.

DIABETES MELLITUS

226
Q

talk about islet amyloidosis

A

The pancreatic proteolytic enzymes that convert proinsulin and proamylin into insulin and amylin are not able to keep up with the high levels of production, which leads to the accumulation of proamyli

227
Q

humoral calcium of malignancy

A

These laboratory values are seen in humoral hypercalcemia of malignancy, which is caused by PTHrP secretion from solid tumors (most commonly renal cancer, bladder cancer, ovarian cancer, or squamous cell cancers of the head, neck, or lung). PTHrP can activate PTH receptors and increase bone resorption, renal calcium absorption and phosphate excretion, leading to severe hypercalcemia and hypophosphatemia. Hypercalcemia further suppresses the secretion of PTH, causing decreased serum PTH levels. Unlike PTH, PTHrP does not stimulate the hydroxylation of 25-dihydroxyvitamin D to 1,25-dihydroxyvitamin D.

228
Q

hyperechogenic on ultrasound is seen in what cancer,what will papillary cancer always have

A

thyroid cancer typically papillary why psammoma bodies,papillary cancer will always have lymphatic spread

229
Q

thyroid nodule when to do monitoring, when do you do thyroid scintigraphy

A

If TSH levels are normal or elevated, this patient should undergo regular monitoring in case the tumor grows to ≥ 1 cm, , we do a thyroid scintigraphy to evaluate the functional status of a nodule

230
Q

what is pathogensis of antiphospholipid antibody and give clinical features of livedoreticularis

A

Antibodies form complexes with anticoagulant proteins, thereby inactivating them (e.g., protein C, protein S, antithrombin III)

Antibodies activate platelets and vascular endothelium

blood clots in capillaries leads to swelling net like appearnece of skin

usmle (38 decks)

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