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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
CO in terms of measured oxygen values?
CO = O2 consumed/arteriovenous O2 difference (CO = SV x HR)
26
Why is pO2 in the LA less than that in the pulmonary capillaries?
Oxygenated blood from the pulmonary veins + Deoxygenated blood from the bronchial arteries. (Q1542)
27
What class of antiarrhythmics inhibits phase 0 depol and prolongs the length of AP?
Class IA - Disopyramide, Quinidine, Procainamide
28
Nonbacterial thrombotic endocarditis is associated with underlying disease? Similar to pathogenesis of what other disease.
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
Myocardial Hibernation
Repetitive ischemia/hypoperfusion results in chronic but reverse loss of myocardial contractility. Reversed by reperfusion, ex: CABG.
30
Myoxma presentation and histology.
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
First step in pathogenesis of atherosclerosis?
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
Obstructive HCOM caused by what?
Hypertrophied interventricular septum + Anterior mitral valve leaflet
33
What condition would lead to a dilation of the coronary sinus?
Coronary sinus drains into the RA. So, processes that dilate RA, such as pulmonary artery hypertension.
34
Where is the great saphenous vein located?
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
ASD may lead to irreversible changes in what structure?
Pulmonary Artery! ## Footnote 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
Histology of Temporal Arteritis?
Granlomatous Inflammation of the Media.
37
How does NO change * end diastolic volume (preload) * blood pressure (afterload) * contractility * HR * LV end systolic volume * ejection time * MvO2
* 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
Anticoagulation after Mechanical Valve Replacement?
WARFARIN, Bitch.
39
At constant contractility, decreasing what would increase contraction velocity?
Decreasing afterload.
40
How long before myocardium stops contracting is setting of complete ischemia? How long before damage is irreversible?
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
Major cause of AAA
ATHEROSCLEROSIS = intimal streak ## Footnote (Atheromas weaken the underlying media of the arterial wall)
42
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
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
What are the 3 main groups of veins in embryologic development?
1. Umbilical veins = degenerate 2. Vitelline veins = become veins of portal venous system 3. Cardinal veins = become veins of systemic circulation
44
Vascular lesion with IgA and C3 deposition?
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
What is histologic evidence of increased pulmonary capillary hydrostatic pressure and LV CHF?
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
Morphologic changes in myocardium due to normal aging?
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
Complete dissociation btwn P and QRS complex = ? What paces the ventricle in this case? Is QRS wide or narrow?
Third degree AV block AV node paces; QRS is narrow still bc ventricle depolarize normally.
48
Pre-exercise: QRS 95, QTc 410 After-exercise: QRS 125, Qtc 400 What medication being used to treat his AFib?
Flecainide (Class IC Antiarrhythmic) QRS = ventricular depolarization. Class IC strongly inhibits phase 0 depolarization with use (during exercise).
49
How is digoxin cleared from the body?
Renally cleared! So older people should receive reduced doses to prevent toxicity.
50
How does Carotid massage tx PSVT?
Increase refractory period of AV node (increase PNS)
51
Endocarditis not due to infection mostly likely due to what?
SLE - Libman Sax endocarditis (sterile vegetations) Also hypercoagulable states, malignancy.
52
Most common cause of death in MI pt pre-hospital and in-hospital?
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
Intimal Hyperplasia and Fibrosis is mediated by what?
Smooth muscle migration from media to intima.
54
What major factor determines whether or not an occluded vessel will cause MI?
Growth rate. If slow, have time to develop collaterals. Bad things: thin fibrous cap, lipid rich core, active inflam
55
Pacemaker with what 3 leads? How to get there?
RA, RV - L subclavian -\> SVC LV - RA -\> coronary sinus (atrioventricular groove) -\> lateral venous tributaries
56
What point on the LV curve is closest to opening snap?
Mitral valve opening, you idiot.
57
What defect causes differential cyanosis - toes are cyanotic, but fingers are fine? What defect causes whole body cyanosis?
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
What kind of changes in arteries is associated with DM, long-standing non-malig HTN, and malig HTN?
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
Primary indiction and Adverse effects of : Statin Niacin Fibric acid derivatives Bile acid binding resins
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
Pathogenesis of Stable Angina Unstable Angina/NSTEMI MI
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
Most common site of atherosclerotic development
Abdominal Aorta Then coronary , popliteal, int carotid, circle of willis.
62
Systolic vs. Diastolic Dysfxn
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
63
64
Symmetric bilateral LE edema + prominent abd wall collateral venous circulation
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
Why is paclitaxel used for drug eluting stents?
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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