cardiovascular Flashcards

1
Q

tell me about patent ductus arteriosus murmur

quality of sound? loudest when? causes? location best heard at?

A

continuous machine like murmur
loudest at S2
often from congenital rubella or prematurity
best heard at infraclavicular area

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2
Q
  1. autosomal recessive
  2. sensorineural deafness
  3. long QT

diagnosis?

A

Jervell and Lange-Nielsen syndrome

Romano Ward syndrome is autosomal dominant and no deafness

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3
Q

Brugada syndrome is esp Asian males. ECG pattern? prevention?

A

ECG pattern of pseudo right bundle branch block and ST elevations in v1-v3.

increased risk of ventricular tachyarrhythmias and SCD. prevent SCD with implantable defibrillator

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4
Q

true or false, LA pressure > LV pressure during diastole

A

true

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5
Q

where is u wave on ECG and when is it prominent?

A

after T wave. hypokalemia and bradycardia

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6
Q

speed of conduction pathway order from fastest to slowest

A

Purkinje fibers > atria > ventricles > AV node

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7
Q

mechanism that carotid massage decreases heartrate and fixes arrhythmia

A

increased afferent baroreceptor firing -> prolong AV node refractory period

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8
Q

Cushing reflex is reaction from increased intracranial pressure. whats the triad?

A

HTN, bradycardia, respiratory depression

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9
Q

what is Ebstein anomaly? Associations and cause?

A

tricuspid valves are placed too much in ventricle. “artificial atrializing the ventricle”
associated w/ tricuspid regurg and right heart failure. can be caused by lithium exposure in utero (teratogen)

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10
Q

outflow tract abnormalities (transposition, tetralogy, truncus arteriosus) is caused by failure of what?

A

failure of neural crest cells to migrate (possibly endocardial cells too)

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11
Q

aortic/pulmonary valves are derived from what

A

endocardial cushions of outflow tract

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12
Q

mitral/tricuspid valves are derived from ______

A

fused endocardial cushions of the AV canal

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13
Q

most posterior part of the heart is _____

A

left atrium.
if a Q asks about an enlarged heart causing dysphagia or hoarse voice, the part that’s pressing on the structures is left atrium.

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14
Q

which layers of pericardium is pericardial cavity in between?

A

in between parietal and visceral (fibrous is outermost layer)

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15
Q

cardiac abnormality of infant of diabetic mother

A

transposition of great vessels

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16
Q

cardiac abnormality of Downs kids

A

ASD, VSD, AV septal defect (bc of endocardial cushions)

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17
Q

cardiac abnormality from congenital rubella, besides PDA

A

pulmonary artery stenosis, septal defects

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18
Q

cardiac abnormality from alcohol exposure in utero

A

ASD, VSD, PDA, tetralogy of Fallot

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19
Q

between Temporal/giant cell arteritis and takayasu arteritis which are both large vessel vasculitis, which one has segmental lesions so that a negative biopsy does not exclude dz (specific but not sensitive)? and what does a positive biopsy of that look like?

A

Temporal/giant cell.

biopsy: giant cells and intimal fibrosis

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20
Q

vasculitis “transmural inflammation with fibrinoid necrosis” -> fibrosis healing -> string of pearls appearance on imaging

dx? treatment?

A

dx: Polyarteritis nodosa, which is a medium vessel vasculitis.
tx: corticosteroids, cyclophosphamide
(fatal if not treated)

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21
Q

which 3 organs does polyarteritis nodosa affect?

which one does it ALWAYS spare? (it can affect pretty much any other organ)

ASSOCIATED WITH SERUM WHAT????

A

commonly affects:

  1. renal artery -> HTN. also hella renal microaneurysms inside kidney seen on angiography
  2. mesenteric artery -> abdominal pain w/ melena
  3. neuro disturbances and skin lesions

SPARES THE LUNG

ASSOCIATED W/ SERUM HBsAG!!!

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22
Q

Kawasaki dz demographic? commonly affects which artery?

tx?

A

Asian children < 4 years old

coronary artery involvement -> thrombosis with MI, or aneurysm w/ rupture

tx: aspirin and IVIG. look out for that MI or aneurysm

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23
Q

young smoker male comes in with raynauds, gangrene, segmental necrotizing vasculitis of digits. what does he have and how do you treat?

A

Buerger Dz (NOT Berger Dz which is IgA nephropathy assocated w/ H S purpura)

stop smoking.

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24
Q

Microscopic polyangiitis is also a necrotizing vasculitis (small vessels) that affects lung and kidney like Wegeners. how does it differ from Wegener?

A
  1. no nasopharynx involvement
  2. no granulomas on biopsy
  3. p-ANCA instead of c-ANCA
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25
Q

“eosinophilic granulomatosis with polyangiitis”

is what?
clinical presentation?

A

Churg Strauss syndrome

lung and heart. asthma, pulmonary infiltrates, rhinosinusitis, peripheral eosinophilia,
mononeuritis multiplex = asymmetric multifocal neuropathy (like wrist drop)
skin - nodules, purpura

if renals involved, called pauci-immune glomerulonephritis

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26
Q

what part of neutrophils is the p-ANCA in Churg strauss syndrome staining?

A

myeloperoxidase

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27
Q

child presents with palpable purpura on butt and legs, colicky abdominal pain w/ GI bleed, and hematuria. had an URT infection a week ago
triad: purpuric rash, abdominal pain, polyarthralgia

dx? pathogenesis?

A

Henoch Schonlein Purpura

IgA (and C3) immune complex deposition
- makes sense since IgA increases during infection. and IgA nephropathy causes the hematuria)

28
Q

2 important causes of 2ndry HTN:

A

atherosclerosis in elderly males
fibromuscular dysplasia in young females (developmental defect, thickening of arrterial walls -> string of beads appearance)

29
Q

the 4 modifiable risk factors of atherosclerosis

A
  1. HTN
  2. dyslipidemia (high LDL, low HDL)
  3. smoking
  4. diabetes
30
Q

hyaline arteriosclerosis effect on renals is glomerular scarring (arteriolonephrosclerosis) that slowly progresses to chronic renal failure. what’s the effect on renals of hyperplastic arteriolosclerosis? (onion skinning)

A

acute renal failure with characteristic “flea bitten” appearance which are the pin point hemorrhages on the kidney surface

31
Q

pipestem appearance on x ray or mammography. dx? signficiance?

A

Monckeberg medial calcific sclerosis. of the media not intima (hence the name). not clniically significant, so don’t confuse it on mammography as something signficiant

32
Q

thoracic aortic aneurysm is classically due to _____

abdominal aortic aneurysm is due to ______

A

thoracic - tetiary syphilis -> tree bark appearance, complications are aortic regurg, compression of mediastinal structures (trachea or esophagus), and thrombosis/embolism

abdominal - from atherosclerosis, HTN
presentation triad of rupture: hypotension, pulsatile abdominal mass, flank pain

33
Q

do hemangiomas blanch with pressure?

2 most common organs involved?

A

yes, bc blood is in vessels, not trapped in interstitium, UNLIKE Kaposi sarcoma

skin and liver

34
Q

angiosarcomas is from what type of cell? 3 most common sites?

A

endothelial cells

skin, breast, liver

35
Q

liver angiosarcoma is associated w/ exposure to what 3 things?

A

polyvinyl chloride, arsenic, and Thorotrast

36
Q

what are the respective uses for measuring serum troponin I and CK-MB levels? time frame for rising and returning to normal? (both peak 24 hours after event)

A

elevated cardiac enzymes in MI.

troponin I is gold standard, most sensitive AND specific for MI. rise 2-4 hours post MI. normal in 7-10 days

CK-MB is useful for detecting reinfarction. returns to normal. levels rise 4-6 hours post MI. normal by 72 hours

37
Q

how does reperfusion from fibrinolysis or angioplasty cause contraction band necrosis?

A

if the cells reperfused are already irreversibly damaged cells, it results in calclium influx -> hypercontraction of myofibrils -> contraction band necrosis

note that this is different from the reperfusion injury simply from increased ROS and incoming of inflammatory cells

38
Q

post MI what do you see from 4-24 hours?

A

gross: dark discoloration
micro: coagulative necrosis ( nuclei missing)

39
Q

post MI what do you see from 1-3 days after?

A

gross: yellow pallor
micro: neutrophils

40
Q

post MI what do you see for days 4-7?

A

gross: yellow pallor
micro: macrophages

note: this is the pt where heart tissue is weakest bc macrophages are eating stuff, so this is when free wall rupture, papillary muscle and septum rupture all most occur

41
Q

post MI what do you see 1-3 weeks?

A

gross: red border
micro: granulation tissue at edges of infarct w/ fibroblasts, collagen, blood vessels

42
Q

tricuspid valve orifice fails to develop, _____ is hypoplastic, often associated w/ ______

what is required for viability?

A

RV is hypoplastic. associated w/ ASD -> R to L shunt -> early cyanosis

VSD and ASD both required for viability

43
Q

what is infantile form of coarctation of aorta associated w/?

adult form?

A

infantile - PDA and Turner

adult form: bicuspid aortic valve (FA says you can also get HF, berry aneurysms and aortic rupture as copmlications..)

44
Q

for some reason they named granulomatous inflammation specifically Aschoff bodies with Anitschkow cells for this one condition what is it?

A

the myocarditis seen in rheumatic fever. Anitschkow cells are “reactive histiocytes with slender wavy nuclei”

45
Q

acute rheumatic fever vs chronic on their effects on mitral (and sometimes aortic) valve

A

acute - vegetations -> regurg

chronic - scarring -> stenosis with fish mouth appearance

46
Q

if aortic stenosis is from rheumatic fever how can you tell? as opposed to some other cause (wear and tear)

A

fusion of commissures of aortic valve. also mitral stenosis is usually also present if due to rheumatic fever

47
Q

does mitral regurg murmur get louder or softer with expiration?

A

louder, because increased return to left atrium

48
Q

what microorganism is most common cause of endocarditis? (it’s low virulence)

A

strep viridans

49
Q

pt has endocarditis but blood cultures are negative. which organisms could be responsible?

A
HACEK:
Haemophilus
Actinobacillus
Cardiobacterium
Eikenella
Kingella
50
Q

Ouch Ouch Osler

A

Osler nodes are tender lesions on fingers and toes
Janeway lesions are erythematous nontender lesions on palms and soles

both are seen in infectious endocarditis

don’t forget you can also get anemia of chronic dz (increased ferritin, decreased TIBC and serum iron and % saturation)

51
Q

what imaging technique can you use to visualize lesions on heart valves? (like in infectious endocarditis)

A

Transesophageal echocardiogram

52
Q

Patient comes in with nonbacterial thrombotic endocarditis (sterile vegetations on heart) and you confirm it’s not lupus/Libman sacks. what’s your differential?

A

hypercoagulable state

UNDERLYING ADENOCARCINOMA or other malignancy

53
Q

what is the c-ANCA of Wegener’s specifically against?

A

anti-proteinase 3

54
Q

Osler Weber Rendu syndrome aka hereditary hemorrhagic telangiectasia

A

inherited disorder of blood vessels
blanching skin lesions (telangiectasias), recurrent epistaxis, skin discolorations, AV malformations, GI bleeding, hematuria

55
Q

“ventricular apical ballooning”

A

Takotsubo cardiomyopathy (broken heart syndrome)

56
Q

can chronic cocaine use and alcohol abuse result in dilated cardiomyopathy?

A

yes, yes it can

57
Q

you can get mitral and tricuspid regurg from dilated cardiomyopathy, duh. but did you know you can also get mitral valve regurg in hypertrophic cardiomyopathy?

A

well now you know.

58
Q

what is Loeffler syndrome and what is a complication of it?

A

endomyocaridal fibrosis w/ eosinophilic infiltrate and eosinophilia (btw remember that Churg strauss also has eosinophilia)

complication: restrictive cardiomyopathy

59
Q

“benign mesenchymal tumor w/ gelatinous appearance and abundant ground substance”

what kind of cardiac tumor? most common location? presentation?

A

myxoma

pedunculated mass in left atrium -> obstructs mitral valve -> episodic syncope

it’s the most common primary cardiac tumor in adults

60
Q

child has hamartoma of cardiac muscle. what is this the specific name for this and what is it associated with aka what does the child probably have? usual location?

A

Rhabdomyoma in ventricle

associated w/ tuberous sclerosis, in children

61
Q

most common places of cancer that metastasizes to heart (4). which specific part of heart does it usually metastasize to?

A

breast, lung, melanoma, lymphoma

goes to pericardium -> pericardial effusion

so if pt has cancer and also a pericardial effusion, suspect the cause is metastasis

62
Q

heart embryo: left horn of sinus venosus gives rise to_____

A

coronary sinus

63
Q

embryo: right common cardinal vein and right anterior cardinal vein give rise to ______

A

SVC

64
Q

embryo: right horn of sinus venosus gives rise to _____

A

smooth part of right atrium (sinus venarum)

65
Q

embryo: smooth part of left atrium comes from what embryo structure?

A

primitive pulmonary vein