uWorld 37 Flashcards

1
Q

korsakoff syndrome is associated with damage to what

A

ANTERIOR and DORSOMEDIAL THALAMIC NUCLEI

results in memory loss (permanent) and confabulation (if they dont know a fact they will fill in the gaps with made up shit they think is true)

inability to form new memories (anterograde amnesia)

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2
Q

QT interval represents what

A

ventricular depolarization and repolarization

can be though of as a rough estimate of the action potential duration (APD)

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3
Q

what antiarrythmics prolong QT

A

class IA and III

amiodorone has very little risk of torsades tho

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4
Q

how does adenosine work ni treating PSVT

A

A1 rectors on cardiac cells to activate POTASSIUM channels, increasing potassium conductance

transient conduction delay through AV node is used for acute termination of PSVT

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5
Q

CD14 is a surface marker of what

A

monocyte-MACROPHAGE cell lineage

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6
Q

if mom with a son with sickle cell wants to have a kid with another man whats best way to see if her next child will have sickle cell

A

since her son has it we know she has sickle cell TRAIT (sickle cell disease is AR)

do PATERNAL HEMOGlOBIN ELECTROPHORESIS to see if the new partner also has sickle cell trait

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7
Q

inappropriate activation of what causes acute pancreatitis

A

TRYPSINOGEN

either ductal obstruction or direct parenchymal injury leads to ACINAR cell INJURY which results in INTRA-ACINAR CONVERSION of TRYPSINOGEN to TRYPSIN (done by lysosomal enzymes)

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8
Q

what do amylases do

A

hydrolyze starch to produce maltose (glucose-glucose disaccharide), trisaccharide maltotriose, and limit dextrins

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9
Q

impairment of what system can contribute to the development of neurodegenerative disorders such as parkinson’s and alzheimers

A

Ubiquitin-Proteasome system

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10
Q

mutations of the NOD2 gene have shown a particularly strong association with what

A

Crohn disease

it encodes an intracellular microbial receptor that recognizes bacterial lipopolysaccharides and subsequently activates NF-kappaB pathway

NK-kappaB is PROINFLAMMATORY TRANSCRIPTION FACTOR that increases CYTOKINE PRODUCTION

mutations in Crohns = impaired innate immune response

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11
Q

pertussis toxin incases cAMP production (via ribosylation of Gi) which leads to what

A

↑ INSULIN production
lymphocyte and neutrophil dysfunction
↑ SENSTIVITY to HISTAMINE

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12
Q

exogenous androgen (steroid) abuse INCREASES HEMATOCRIT in a dose-dependent mannor, why

A

testosterone stimulates red blood cell production (this is why normal hematocrit is higher in males than females)

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13
Q

lack of t-tubules in some myofibrils leads to what

A

uncoordinated contraction of individual fibers

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14
Q

impaired relaxation of the muscle after a SINGLE contraction occurs in what condition

A

myotonic dystrophy

AD disease due to abnormality of myotonia protein kinase resulting form a CTG trinucleotide repeat expansion

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15
Q

what forms the right lateral cardiac border on frontal chest xray

A

RIGHT ATRIUM

SVC

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16
Q

what form the anterior (sternal) surface and most of inferior border of the heart

A

right atrium

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17
Q

what is seen directly posterior to the esophagus on tranesophageal electrocardiography (TEE)

A

DESCENDING AORTA

good b/c you can see if it is dissected or aneurysm or something

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18
Q

the pulmonary artery ascends anteriorly and to the left of the ascending aorta and is directed toward the left shoulder, what is the course after it bifurcates

A

right pulmonary artery travels horizontally under the aortic arch posterior to the SVC

left pulmonary artery courses superiorly over the left main bronchus

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19
Q

what is the spread of neisseria causing meningitis

A

pharynx → blood → choroid plexus → meninges

transmitted via respiratory droplets (usuali asymptomatic carriers with nasopharyngeal colonization)

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20
Q

pharynx → lymphatics → meninges is how what organism causes meningitis

A

H. flu

infants and young children

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21
Q

middle ear → contiguous tissues → meninges how what organism causes meningitis

A

S. pneumonia (unusual way but its possible after an acute infection of the middle ear)

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22
Q

traumatic wound → leaking CSF → meninges how what organism causes meningitis

A

MCC of S AUREUS MENINGITIS or CNS ABSCESS

following penetrating skull injury or neurosurgery

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23
Q

primary lung focus → blood → meninges how what organism causes meningitis

A

TB or S. pneumonia

TB meningitis is chronic and characterized by monocytes and lymphocytes in the CSG primarily affecting the basal meningines

24
Q

hemosiderin-containing macrophages in alveoli are suggestive of what

A

PRIOR episodes of pulmonary congestion and edema that arose due to chronic left heart failure

25
Q

EPISODIC HYPERTENSION, TREMORS, HEADACHE, TACHYCARDIA, and DIAPHORESIS are highly suggestive of what

A

PHEOCHROMOCYTOMA (PC)

episodic due to fluctuation in catecholamine synthesis by the tumor

26
Q

what are the hemodynamics of acute mitral valve regurgitation

A
↑↑ Preload (EDV)
↓ Afterload
↑↑ Ejection fraction
↓ foraward stroke volume
↓ ESV
↓ CO
no change in contractile function
27
Q

what are the hemodynamics of compensated mitral valve regurgitation

A

↑ Preload
↑ Ejection fraction
No change in after load, contractile function, or forward stroke volume

28
Q

what are the hemodynamics of decompensated mitral valve regurgitation

A
↑ Preload (EDV)
↑ After load
↓ Contractile function
↓ ejection fraction
↓ forward stroke volume
29
Q

what causes the hemodynamic changes seen in acute mitral valve regurgitation

A

high LA pressures and PULMONARY EDEMA so the LV need to accommodate regurgitated blood plus what normally comes from venous return, ↑ LV EDV (PRELOAD)

↑ preload and ↓ after load together = ↑ ejection fraction

however much of total stroke volume is lost to regurgitation into the LA, resulting in decreased forward stroke volume and reduced cardiac output (manifesting as HYPOTENSION and cardiogenic shock)

30
Q

what causes the hemodynamic changes seen in chronic mitral valve regurgitation

A

compensatory LA enlargements allows the LA to receive the regurgicatnat column at lower filling pressure preventing pulmonary edema

chronic volume overload causes LV to undergo substantial enlargement due to eccentric hypertrophy

early on this will maintain forward stroke volume even in the setting of substantial regurgitant flow

after a while remodeling cause LV to becomes maladaptive and decompensated state occurs. IMPAIRED CONTRACTILITY reduces forward SV and increases left-sided filling pressures, causing decreased cardiac output and pulmonary edema

31
Q

baby with CF on a HOT SUMMER DAY is vomiting and sleepy what is the electrolyte problem

A

HYPONATREMIA (they sweat out lots of SODIUM and CHLORIDE, hence the salt test)

they hypochloremia is typically asymptomatic so doesn’t cause the vomiting or sleepiness

32
Q

what are risk factors for babies with CF getting hyponatremia, how is this managed

A

exclusive breast or formula feeding prior to the introduction of sodium rich, solid foods
high temperature environments
exercise (more sweating)

SALT SUPPLEMENTATION is recommended for patients with CF

33
Q

CONSTIPATION, syncope and 2nd degree heart block in the setting of A FIB is likely due to what medication

A

calcium channel blocker (VERAPAMIL or DILTIAZEM)

frequently used for hypertension, angina pectoris, and supra ventricular arrhythmias

CONSTIPATION is a major side effect of non-DHP calcium channel blockers (verapil more than diltiazem)

34
Q

what is indapamide

A

thiazide diuretic

35
Q

what are the side effects of ethambutol

A

optic neuropathy:

decreased visual acuity, central scotoma, red/green color blindness

36
Q

the ixodes tick is the vector for what

A

lyme
babesiosis (asplenic patients)
Anaplasma spp

37
Q

what does babesiosis present as in a splenetomized patient

A

dyspnea
coarse crackles
bilateral infiltrates on CXR

38
Q

procainamide, hydralazine, and isoniazid are all metabolized how

A

phase II ACETYLATION in the liver

SLOW ACETYLATORS are more susceptible to drug induced lupus

39
Q

liver hydroxylation and hydrolysis are what type of metabolism

A

phase I

addition of of hydroxyl group reduces lipid solubility and facilitates excretion

40
Q

liver sulfate conjugation is what type of metabolism

A

phase II

biotransforms drugs into MORE POLAR compounds that are more water soluble and easily excreted

41
Q

succinylcholine, tetracaine, and remifentanil (all used for anesthesia) are metabolized how

A

plasma hydrolysis (esterase)

42
Q

what type of nose bleed are most common

A

ANTERIOR
occur within the vascular watershed area of the NASAL SPETUM (anteroinferior part of the nasal septal mucosa) known as KIESSELBACH PLEXUS

several anastomosis in Kiesselbach plexus:
septal branch of the ANTERIOR ETHMOIDAL ARTERY
lateral nasal branch of the SPHENOPALATINE ARTERY
septal branch of the SUPERIOR LABIAL ARTERY (brach of the facial artery)

can be TREATED with CAUTERY (silver nitrate)

43
Q

compression of the nasal alae while leaning forward stops a nose bleed from where

A

Kiesselbach plexus

44
Q

what do the turbines (conchae) do

A

warm, humidify, and filter inspired air

expand and contract in response to environmental changes (temp, allergens, humidity)

they have a corresponding meatus which is a drainage pathway

45
Q

the middle meatus drains what

A

frontal, maxillary, and anterior ethmoidal sinuses

MC site of NASAL POLYP

46
Q

what is the most common site of a nasal polyp

A

middle meatus

47
Q

the superior meatus proves drainage for what

A

sphenoidal and posterior ethmoid sinuses

48
Q

posterior nose bleed are more severe and usually not treatable with cautery, what arteries are involved

A

branches of the sphenopalatine artery (also supply the posterior conchae)

49
Q

co-adminsitration of phenytoin with what decreases the concentration of phenytoin in the plasma

A

CYP450 inducers (carbamazepine, barbs, griseofulvin, chronic alcohol consumption, rifampin)

50
Q

most cases of SPORADIC colorectal cancer arise how

A

classic ADENOMA-CARCINOMA SEQUENCE (APC/beta-catenin pathway)

FIRST MUTATION is usually APC TUMOR SUPPRESSOR (regulates cell growth/adhesion)

seen in the LEFT side of the GI tract

51
Q

micro satellite instability pathway of colorectal cancer is seen when

A

DNA mismatch repair gene mutations

implicated in Lynch Syndrome (HNPCC)

52
Q

what are lab values in kleinfelters

A

↓ testosterone
↑ FSH, LH
↑ estradiol

53
Q

new onset neurologic symptoms, anemia with schistocytes, thrombocytopenia, and acute kidney injury suggest what

A

THROMBOTIC THROMBOYTOPENIC PURPURA (TTP)

impaired function of ADAMTS13 which is a von-willebrand cleaving protease

excess von willebrant multipliers aid in hemostasis resulting in diffuse MICROVASCULAR THROMBOSIS

54
Q

when the endometrium is no longer exposed to estrogen what happens

A

prostaglandin production increases, leading to VASOCONSTRICTION of SPIRAL ARTERIES

secretion of metallopreases by endometrial stromal cells (degradation of the extracellular matrix) and APOPTOSIS of the endometrium epithelium

55
Q

under hypoxic conditions what drives conversion of pyruvate to lactate via lactate dehydrogenase

A

build up of NADH (due to hypoxia) inhibits PYRUVATE DEHYDROGENASE

56
Q

patient who recently came back from mexico with maculopapular rash, purpuric lesions, hepatomegaly, thombocytopenia, leukopenia, and elevate liver aminotransferases

they had been to mexico 5 years before and got similar sickness that went away on its own

what they got, why is it worse this time?

A

DENGUE FEVER

worse because its a DIFFERENT SEROTYPE (SECONDARY infection can cause MORE SEVERE illness)

he has life long immunity to the first serotype he was infected with

57
Q

what are the symptoms of dengue fever

A

classic:

  • flu like febrile illness with marked myalgia and joint pains (“bone break fever”)
  • RETRO ORBITAL PAIN
  • rash (white islands in a sea of red)
Hemorrhagic fever:
-increased vascular permeability
thrombocytopenia
spontaneous bleeding → SHOCK
PROSITIE TOURNIQUET TEST (petechiae after sphygmomanometer cuff inflation for 5 infuse)

TX: supportive care