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USMLE Step 1 Systems > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Pulsus Paradoxus

  1. How is it manifested based on Korokoff sounds?
  2. What conditions assoc with it? Patho?
A
  1. Korokoff sounds: decrease in systolic BP > 10 mmHg with inspiration. First hear sounds during expiration, then at lower BP during all phases resp cycle.
  2. Constrictive pericarditis, tamponade, restrictive cardiomyopathy, obstructive pulmonary disease: during insp -> more blood flow -> RV can’t expand out so pushes IV septum -> less blood LV.
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2
Q

What are the aortic arch derivatives?

A

1st = maxillary artery

2nd = stapedial; hypid artery

3rd = common carotid, prox int. carotid

4th = L = aortic arch; R = prox R subclavian

6th = L = ductus arteriosus; R = pulmonary artery

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3
Q

Class I antiarrhythmics: strength of binding to Na channel?

A

Class IC > I A > IB

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4
Q

What endogenous substance dilates arteries and veins AND promotes diuresis?

A

Brain Natriuretic Peptide

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5
Q

Carcinoid Syndrome leads to what sx in the heart?

A

R-sided endocardial fibrosis esp near Tricuspid and Pulm valves -> Pulm Stenosis and Restrictive Endocarditis

(R sided bc on the L, serotonin inactivated by pulm vascular MAO)

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6
Q

What conditions does abnormal migration of neural crest cells result in?

A

TOF, Truncus Arteriosus, Transposition of the Great Arteries

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7
Q

Cardiac Pacemaker Cells (slow-response tissue; SA, AV node) - how does verapamil work?

A

Test ID: 36624218

CCB slows Diastolic Depolarization in phase 0 and latter part of phase 4 => decreased rate of SA firing and slows AV conduction

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8
Q

What endogenous factors increase coronary blood flow?

A
  1. NO
  2. Adenosine
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9
Q

Janeway Lesions vs. Osler Nodes

A

Janeway = painLESS, macular/flat lesions on palms and soles

  • due to septic microemboli. histo reveals microabscesses

Osler = painFUL, papular/raised on finger or toe pads

  • due to IC deposition
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10
Q

How is Ca lowered during myocyte relaxation?

A
  1. Ca-ATPase bring it back to SR
  2. Na/Ca exchanger on sarcolemma - 3 Na in, 1 Ca out
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11
Q

Where are the part of the heart located in relation to the chest? If stab wound to the apex (5th intercostal mid clav) what would get hurt?

A

Anterior = RV

Diaphragmatic = RV/LV

Posterior = LA

Apex = LV

If stabbed at apex = LUNGS would most likely be injured.

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12
Q

Endocarditis in an IVDU - which valve is most likely affected

A

Tricupsid! R-sided endocarditis.

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13
Q

What stimulates ANP and BNP to be secreted?

A

Hypertrophy, Stretch

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14
Q

1 year after a myocardial infarction - what type of collagen is deposited in the scar?

A

Collagen I = skin, bone, tendons

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15
Q

What vein/sinus has the LEAST oxygenated blood?

A

Coronary sinus - myocardium extracts 75-80% (resting) and 90% (increased demand) of oxygen from the blood. This is more than ANY OTHER TISSUE.

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16
Q

What are side effects of Verapamil?

A

AV Block (any degree), Bradycardia

Constipation

Gingival Hyperplasia

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17
Q

What is the best indicator of severity of MR?

A

S3.

MR causes LV overload bc of the increased rate of LV filling as a large volme of reguritant flow re-enters LV during diastole.

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18
Q

Formula for resistance.

A

R = nL/r^4 (n= viscosity)

Q = P/R (V=IR)

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19
Q

Congenital Long QT syndrome is associated with what?

A

Neurosensory Deafness.

Long QT can lead to syncopal episodes and sudden cardiac death due to Torsades.

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20
Q

What combination of lipid lowering agents causes the most myopathy?

A

Atorvastatin + Gemfibrozil (Fibrate)

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21
Q

Mechanism of action Niacin

A

Inhibit VLDL synthesis

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22
Q

What does consumption of appetite suppressants > 3 mo cause?

A

Pulmonary HTN -> cor pulmonale, RV hypertrophy -> can result in sudden death due to arrhythmia

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23
Q

Cardiac tissue conduction velocity

A

Fastest - Purkinje, Atrial, Ventricular, AV node - slowest

“Park At Ventura Ave”

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24
Q

Peripheral edema and flushing are adverse effects of what antihypertensive?

A

Amlodipine

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25
Q

CO in terms of measured oxygen values?

A

CO = O2 consumed/arteriovenous O2 difference

(CO = SV x HR)

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26
Q

Why is pO2 in the LA less than that in the pulmonary capillaries?

A

Oxygenated blood from the pulmonary veins + Deoxygenated blood from the bronchial arteries. (Q1542)

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27
Q

What class of antiarrhythmics inhibits phase 0 depol and prolongs the length of AP?

A

Class IA - Disopyramide, Quinidine, Procainamide

28
Q

Nonbacterial thrombotic endocarditis is associated with underlying disease? Similar to pathogenesis of what other disease.

A

Associated with underlying malignancy - procoagulant state. (ex: mucinous adenocarcinoma of the pancreas or lung).

Similar to Trousseau’s syndrome (migratory thrombophlebitis) due to tumor release of procoagulants.

29
Q

Myocardial Hibernation

A

Repetitive ischemia/hypoperfusion results in chronic but reverse loss of myocardial contractility. Reversed by reperfusion, ex: CABG.

30
Q

Myoxma presentation and histology.

A

Presentation: constitutional sx, positional dyspnea (better when lying down) and syncope, mid diastolic rumbling murmur at apex, large pedunculated mass

Histo: Scattered cells, with mucopolysaccharide stroma, angiogenesis (lots abnl blood vessels), and hemorrhage

31
Q

First step in pathogenesis of atherosclerosis?

A

Endothelial cell injury

  • > increased permeability -> macrophages come in
  • > subepithelial collagen -> plts
  • > macro and plts stimulate smooth muscle cells to prolif -> collagen, proteoglycans
  • > LDL gets in -> foam cells

Fibrofatty streak -> Fibrofatty atheroma (lipid debris surrounded by monocytes, lymphocytes, SMC, fibrous cap.

32
Q

Obstructive HCOM caused by what?

A

Hypertrophied interventricular septum + Anterior mitral valve leaflet

33
Q

What condition would lead to a dilation of the coronary sinus?

A

Coronary sinus drains into the RA. So, processes that dilate RA, such as pulmonary artery hypertension.

34
Q

Where is the great saphenous vein located?

A

Inferolateral to the pubic tubercle. Used for CABG.

Preferred vein is the left internal mammary artery (left internal thoracic) if only one is needed.

35
Q

ASD may lead to irreversible changes in what structure?

A

Pulmonary Artery!

May lead to Eisenmenger syndrome if uncorrected L-> R shunt -> pulmonary artery pressures > systemic pressure -> reversal of shunt. Will cause late cyanosis, clubbing, polycythemia.

36
Q

Histology of Temporal Arteritis?

A

Granlomatous Inflammation of the Media.

37
Q

How does NO change

  • end diastolic volume (preload)
  • blood pressure (afterload)
  • contractility
  • HR
  • LV end systolic volume
  • ejection time
  • MvO2
A
  • end-diastolic volume - decrease
  • blood pressure - decrease
  • contractility - increase reflexive
  • HR - increase reflexive
  • LV end systolic volume - decrease bc increase in cont
  • ejection time - decrease
  • MvO2 DECREASE
38
Q

Anticoagulation after Mechanical Valve Replacement?

A

WARFARIN, Bitch.

39
Q

At constant contractility, decreasing what would increase contraction velocity?

A

Decreasing afterload.

40
Q

How long before myocardium stops contracting is setting of complete ischemia? How long before damage is irreversible?

A

Stops contracting within 1 minute!

If < 30 minutes = reversible. Myocardial stunning - return of contractility gradually over the next several hours - days.

If > 30 minutes = irreversible!

41
Q

Major cause of AAA

A

ATHEROSCLEROSIS = intimal streak

(Atheromas weaken the underlying media of the arterial wall)

42
Q

What are the following buzzwords associated with?

intimal tear

intimal streak

medial degeneration

medial calcification

medial inflammation

vaso vasorum obliteration

onion like concentric thickening of arteriolar walls

A

intimal tear = Dissection

Intimal streak = Atherosclerosis

medial degeneration = AAA (but LESS common cause of AAA than atherosclerosis!)

medial calcification = form of atherosclerosis with calcification, usually > 50, can cause isolated systolic HTN due to arterial hardening

medial inflammation = arteritis

vaso vasorum obliteration = aortitis, thoracic AAA, syphillis, takayasu arteritis

onion like concentric thickening of arteriolar walls = HTN

43
Q

What are the 3 main groups of veins in embryologic development?

A
  1. Umbilical veins = degenerate
  2. Vitelline veins = become veins of portal venous system
  3. Cardinal veins = become veins of systemic circulation
44
Q

Vascular lesion with IgA and C3 deposition?

A

Henoch Schlonlein Purpura:

Mech: Vasculitis due to IgA and IgA Immune Complex Deposition!!!

Sx: commonly after a URI, children 3-11 yo

Classic Sx:

  1. Palpable Purpura
  2. Arthralgias
  3. Abd pain, Melena, Hematemesis
  4. Kidney: IgA nephropathy

Usually self-limited.

45
Q

What is histologic evidence of increased pulmonary capillary hydrostatic pressure and LV CHF?

A

Alveolar macrophages with golden cytoplasmic granules (either hemosiderin or lipofuschin) that stain with Prussian Blue (stains for hemosiderin).

When pressures are elevated, hemosiderin is extravasated into the alveoli where macrophages eat it.

46
Q

Morphologic changes in myocardium due to normal aging?

A
  1. LV decreases in size -> sigmoid shaped interventricular septum
  2. Increased interstitial connective tissue/collagen content in ventricular walls
  3. Brownish perinuclear cytoplasmic inclusion = Lipofuschin (result of indigestable byproduct of membrane lipid oxidation)
47
Q

Complete dissociation btwn P and QRS complex = ?

What paces the ventricle in this case? Is QRS wide or narrow?

A

Third degree AV block

AV node paces; QRS is narrow still bc ventricle depolarize normally.

48
Q

Pre-exercise: QRS 95, QTc 410

After-exercise: QRS 125, Qtc 400

What medication being used to treat his AFib?

A

Flecainide (Class IC Antiarrhythmic)

QRS = ventricular depolarization. Class IC strongly inhibits phase 0 depolarization with use (during exercise).

49
Q

How is digoxin cleared from the body?

A

Renally cleared! So older people should receive reduced doses to prevent toxicity.

50
Q

How does Carotid massage tx PSVT?

A

Increase refractory period of AV node (increase PNS)

51
Q

Endocarditis not due to infection mostly likely due to what?

A

SLE - Libman Sax endocarditis (sterile vegetations)

Also hypercoagulable states, malignancy.

52
Q

Most common cause of death in MI pt pre-hospital and in-hospital?

A

Pre-hospital: Ventricular Fibrillation (Arrhythmia) - esp if sudden cardiac death

In-hospital: Ventricular Failure - usually gradually if extensive MI over the next 2-10d

53
Q

Intimal Hyperplasia and Fibrosis is mediated by what?

A

Smooth muscle migration from media to intima.

54
Q

What major factor determines whether or not an occluded vessel will cause MI?

A

Growth rate. If slow, have time to develop collaterals.

Bad things: thin fibrous cap, lipid rich core, active inflam

55
Q

Pacemaker with what 3 leads? How to get there?

A

RA, RV - L subclavian -> SVC

LV - RA -> coronary sinus (atrioventricular groove) -> lateral venous tributaries

56
Q

What point on the LV curve is closest to opening snap?

A

Mitral valve opening, you idiot.

57
Q

What defect causes differential cyanosis - toes are cyanotic, but fingers are fine?

What defect causes whole body cyanosis?

A

Patient ductus arteriosus with reversal of flow now R -> L.

Septal defects with reversal of flow or TOF

Note: CoArc does NOT cause cyanosis - causes HF

58
Q

What kind of changes in arteries is associated with DM, long-standing non-malig HTN, and malig HTN?

A

DM, Long-standing nonmalig HTN = Hyaline Arteriolosclerosis

(homogenous deposition of eosinophilic hyaline material; probably due to production by SM in response to endothelial damage by HTN or DM)

Malignant HTN = Onion-like, concentric thickening

59
Q

Primary indiction and Adverse effects of :

Statin

Niacin

Fibric acid derivatives

Bile acid binding resins

A

Statin = high LDL = myopathy, hepatitis

Niacin = low HDL = vasodilation, hyperGLY, hyperUric acid, Hepatitis

Fibric acid derivatives = high TAG = gallstones, myopathy (worse with statins)

Bile acid binding resins = high LDL = GI upset, high TAG, malabsorption

60
Q

Pathogenesis of

Stable Angina

Unstable Angina/NSTEMI

MI

A

Stable Angina: Atherosclerotic plaque affecting >/= 75% of lumen (if < 75%, it’s asymptomatic still)

Unstable Angina/NSTEMI: Ulcerated plaque with partially obstructive thrombus

MI: Ruptured plaque with fully obstructive thrombus

61
Q

Most common site of atherosclerotic development

A

Abdominal Aorta

Then coronary , popliteal, int carotid, circle of willis.

62
Q

Systolic vs. Diastolic Dysfxn

A

Systolic

  • DILATED heart.
  • low EF, poor contractility
  • 2/2 ischemic heart diseae, dilated cardiomyopathy

Diastolic

  • HYPERTROPHIC heart
  • nl EF, nl contractility
  • impaired relaxation, compliance.
  • 2/2 HTN heart disease, HOCM
64
Q

Symmetric bilateral LE edema + prominent abd wall collateral venous circulation

A

Obstruction of IVC

  • such as from renal tumor
  • suspected when LE edema and collateral abd wall vessels, but with no signs of RHF, cirrhosis, nephrotic syndrome
65
Q

Why is paclitaxel used for drug eluting stents?

A

To prevent intimal hyperplasia

Prevents microtubule breakdown causing arrest of cell cycle in M phase.

USMLE Step 1 Systems (11 decks)

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