Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

STEP 1 > 03a: Cardio > Flashcards

03a: Cardio Flashcards

1
Q

Truncus arteriosus gives rise to:

A

Ascending aorta and pulmonary trunk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Bulbus cordis gives rise to:

A

Smooth parts (outflow tracts) of L and R ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Endocardial cushions give rise to:

A
  1. Atrial septum
  2. Membranous IV septum
  3. AV and semilunar valves
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Primitive atrium gives rise to:

A

Trabeculated parts of R and L atria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Primitive ventricle gives rise to:

A

Trabeculated parts of R and L ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Primitive pulmonary vein gives rise to:

A

Smooth part of L atrium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

L horn of sinus venosus gives rise to:

A

Coronary sinus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

R horn of sinus venosus gives rise to:

A

Smooth part of R atrium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Cardinal veins (R common and R anterior) give rise to:

A

SVC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Heart development: Foramen secundum is an opening in (X).

A

X = septum primium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

VSDs typically occur in (muscular/membranous) septum, which is the part (closer/further) from atria.

A

Membranous

Closer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

List the conotruncal abnormalities associated with failure of (X) process during heart development.

A

X = neural crest migration

  1. Persistent truncus arteriosus
  2. Transposition of great vessels
  3. Tetralogy of Fallot
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

PO2 of umbilical vein

A

30 mmHg (80% o2 sat)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

3 key shunts in fetus (in the order they’re encountered started at placenta)

A
  1. Ductus venosus
  2. Foramen ovale
  3. Ductus arteriosus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Ductus venosus: blood shunt from (X) to (Y)

A 
X = umbilical vein
Y = IVC

(bypasses hepatic circulation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

(X) keep PDA open

A

X = Prostaglandins E1, E2 (kEEp PDA open)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Allantois becomes urachus, which normally becomes (X) in adult. What does it connect?

A

X = mediaN (allaNtois) umbilical ligament

Bladder to umbilicus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Umbilical aa adult remnant

A

MediaL (umbiLical a) umbilical ligaments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Umbilical vein adult remnant

A

Ligamentum teres (round ligament)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Ligamentum teres, remnant of (X) and contained in (Y)

A 
X = umbilical vein
Y = falciform ligament
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

SA node blood supply off of (X) a. And AV node off of (Y) a.

A 
X = RCA
Y = PDA (off RCA in R dominant circ, off LCX in L dominant circ)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Coronary circulation: Most people are (R/L) dominant, which is defined by:

A

R (85%)

The a (RCA v LCA) from which which PDA arises

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

LCX artery supplies:

A
  1. Lat and Post walls of LV

2. Anterolateral papillary muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

LAD artery supplies:

A
  1. Anterior surface of LV and anterior 2/3 of IV septum

2. Anterolateral papillary muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

PDA of heart supplies:

A
  1. Post 1/3 of IV septum and Post 2/3 walls of ventricles

2. Posteromedial papillary muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Coronary blood flow peaks at what point in cardiac cycle?

A

Early diastole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Most of R cardiac silhouette on Xray is composed of which structure?

A

RA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Which structure in body has the most deoxygenated blood?

A

Coronary sinus (due to super high myocardial O2 extraction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Most common cause of coronary sinus dilation:

A

High RA P due to pulm HT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

List a valve abnormality that can lead to hoarseness or dysphagia. Why?

A

MR (dilated LA, which is most posterior chamber)

Enlargement can compress esophagus or L recurrent laryngeal n)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Transesophageal echo is used to visualize (X) heart structures. If rotated posteriorly, what else can be visualized?

A

X = LA, MV, atrial septum

Descending aorta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Pericarditis can cause referred pain to (X) due to innervation by (Y)

A 
X = shoulder
Y = phrenic n (C3-5)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Abnormal deviation of infundibular septum during development of heart leads to which abnormality?

A

Tetralogy of Fallot (anterior and cephalad deviation due to abnormal neural crest migration)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Loss of cardiomyocyte contractility occurs within (X) time after onset of total ischemia. After (Y) amount of time, injury is irreversible.

A 
X= 60s
Y = 30 min
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Which anti-anginal drugs work by (increasing/decreasing) coronary vasodilation?

A

Increasing

Nondihydropyridines and dihydropyridines; nitrates (mildly)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Nitrates work as anti-anginal drugs via which key mechanism?

A

Venodilation (decrease preload)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Which anti-anginal drugs work by decreasing HR?

A
  1. BB

2. Non-dihydropyridines (verapamil, dilitazem)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Which anti-anginal drugs work by decreasing afterload (arterial dilation)?

A

Dihydropyridines (amlodipine, nifedipine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Polyarteritis nodosa (PAN) spares which arteries?

A

Pulmonary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Nitroprusside is a (short/long)-acting (venous/arterial) (vasodilator/vasoconstrictor), functioning mainly to (increase/decrease) which cardiac values in hypertensive heart failure?

A

Short-acting, balanced venous and arterial vasodilator;

Decreases BOTH preload and afterload (thus, maintaining stroke volume)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Atrial muscle, ventricular muscle, Purkinje system, and AV node: list them in order of fastest to slowest conduction speed

A

“Park At Venture Ave”

  1. Purkinje (2.2 m/s)
  2. Atria (1.1 m/s)
  3. Ventricle (0.3 m/s)
  4. AV node (0.05 m/s)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Scar tissue in heart from an old MI has which type of collagen?

A

Type I

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Type (X) collagen seen about a week post-MI.

A

X = III (granulation tissue; eventually replaced by Type I with scar formation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Rare vascular tumor associated with arsenic or polyvinyl Cl exposure and positive for (X) cell marker.

A

X = CD31

Liver angiosarcoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Coagulation necrosis seen starting (X) days/weeks post-MI

A

X = 1-3 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Prominent neutrophilic infiltrate seen starting (X) days/weeks post-MI

A

X = 1-3 days (with coag necrosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Macrophage infiltration seen starting (X) days/weeks post-MI

A

X = 3-7 days

48
Q

Granulation tissue begins to form starting (X) days/weeks post-MI

A

X = 7 days

49
Q

Well-developed granulation tissue and neovascularization seen (X) days/weeks post-MI

A

X = 10-14 days

50
Q

Low extracellular Na will (increase/decrease) myocardial contractility. Why?

A

Increase;

Less Na/Ca exchange (remember: digoxin increases intracellular Na, which increases contractility because less Ca pumped out in exchange for Na)

51
Q

ACEi and ARB affect heart by (increasing/decreasing) (preload/afterload/contractility).

A

Decreasing

Preload and afterload

52
Q

The force of contraction of the myocardium is proportional to the (X) at the end of (systole/diastole).

A

X = length of cardiac muscle fibers

Diastole (aka preload)

53
Q

A profound impact on flow can be brought about by a minor change in:

A

Radius (decrease r by 50% will decrease flow by 16x! r^4)

54
Q

(X) vessels have the highest total cross sectional area

A

X = capillaries

55
Q

(X) vessels have the lowest flow velocity

A

X = capillaries

56
Q

(X) vessels account for most of TPR

A

X = arterioles

57
Q

Infusion of normal saline/fluid would alter (venous return/inotropy/TPR) in which manner?

A

Venous return increased

58
Q

Exercise overall (increases/decreases) SVR due to:

A

Decreases

Substantial arteriolar dilation in active muscles

59
Q

Absent jugular venous pulse a-wave

A

Atrial fibrillation (a-wave signifies atrial contraction)

60
Q

Jugular venous pulse waveform: absent y-wave

A

Cardiac tamponade (y-descent represents decline in P of RA during RV filling)

61
Q

Jugular venous pulse waveform: steep y-wave

A

Constrictive pericarditis

62
Q

Wide split between A2 and P2 is indicative of:

A

Condition that delays RV emptying (plumonic stenosis, RBBB)

63
Q

Fixed split between A2 and P2 is indicative of:

A

ASD (increased blood on R side of heart so high flow through pulmonic valve and delayed close, regardless of breath)

64
Q

Pt presents with split between A2 and P2 that is heard on expiration and disappears on inspiration. What’s this phenomenon and what are the underlying issues?

A

Paradoxical splitting (aortic valve sound A2 occurs after P2)

Delayed aortic valve closure (aortic stenosis, LBBB)

65
Q

Later onset of MVP click/murmur is brought about by which maneuvers?

A

Increasing afterload (thus increasing V in heart and maintaining tension along chordae tendinae)

Handgrip, rapid squat

66
Q

Early onset of MVP click/murmur is brought about by which maneuvers?

A

Decrease in preload (and thus decrease V in heart; more floppy, unsecure valve)

Valsalva, standing up

67
Q

In developed countries, (X) valve abnormality is the most common one to predispose pt to infective endocarditis

A

X = MVP

68
Q

(Increase/decrease) in interval between (S1/S2) and opening snap of (X) murmur indicates higher severity of valve disease.

A

Decrease (means P in LA is super high and opening valve more forcefully);
S2
X = MS

69
Q

Mitral regurg: best indicator of severity is (presence/absence) of which clinical finding?

A

Presence of S3 gallop - LV overload indicator

70
Q

Location of SA node

A

RA, near entrance of SVC

71
Q

Location of AV node

A

RA/Interatrial septum, near entrance of coronary sinus and septal cusp of tricuspid valve

72
Q

T wave inversion may indicate:

A

Ischemia or recent MI

73
Q

Child with sensorineural hearing loss since birth and FHx of sudden death. Most likely diagnosis?

A

Jervell and Lange-Nielsen syndrome - a long QT syndrome;

AR mutation in V-gated K channel (slow-acting, decreased K current)

74
Q

Romano-Ward syndrome:

A

AD mutation in ion channels, causing long QT syndrome

75
Q

Which electrolyte imbalances can lead to torsades?

A

Low K, low Mg

76
Q

Rx for Torsades includes:

A

Mg sulfate

77
Q

“Holiday heart syndrome” is:

A

Afib in pts after drinking EtOH excessively

78
Q

“Sawtooth” appearance on baseline of EKG (between QRS complexes). Diagnosis? Rx?

A

Atrial flutter;

Like A-fib (rhythm/rate control, anticoagulation)
Note: ablation for definitive treatment

79
Q

T/F: Atrial rate is greater than ventricular rate.

A

True - ventricular rate about 45-55 bpm

80
Q

Lyme disease can cause (first/second/third) degree heart block

A

Third

81
Q

ANP (atrial natriuretic peptide) works via (X) receptor/messenger system and has which key effects?

A

X = cGMP

  1. Vasodilation
  2. Increase GFR (constricts efferent arteriole, dilates afferent arteriole)
  3. Decreases Na absorption at collecting duct
82
Q

Carotid baroreceptors transmit to (X) and Aortic arch receptors transmit to (Y).

A

X = Y = solitary nucleus of medulla

carotid via CN IX, aortic via CN X

83
Q

Normal O2 sat of R heart chambers

A

70% (including SVC/IVC and pulm aa)

84
Q

Brain blood flow remains constant over wide range of perfusion pressures thanks to action of:

A

CO2 (pH) - local metabolite

85
Q

Skeletal muscle blood flow remains constant over wide range of perfusion pressures thanks to action of:

A

Local metabolites: LA, adenosine, K, H, CO2

86
Q

S. Bovis endocarditis is associated with which disease?

A

Colon cancer (part of normal flora of colon)

87
Q

Hydralazine MOA

A

Selective arteriolar vasodilator

88
Q

T/F: Hydralazine is an effective med for long-term BP control

A

False - since selective arteriolar vasodilation, increases sympathetic activity reflexively and increases RAAS (Na, water retention; limited longterm efficacy)

89
Q

Tricuspid atresia: which other defects required for viability?

A

BOTH ASD and VSD (since tricuspid valve absent)

90
Q

Boot-shaped heart on CXR

A

Tetralogy of fallot (RV hypertrophy)

91
Q

Kid with TOF runs around and then squats to relieve severe dyspnea. What’s the mechanism behind this?

A

Increases SVR (compared to PVR) and thus decreases R to L shunt/cyanosis

92
Q

Pulsatile vessels within intercostal spaces and notched appearance of ribs on CXR.

A

Coarctation of aorta (collateral circulation enlarges intercostal aa, which erode ribs)

93
Q

FAS associated with which congenital cardiac defects? Star the most common.

A

ASD*, VSD, PDA, ToF

94
Q

A complete AV canal defect (as well as either VSD/ASD) seen in which genetic/infectious disorder?

A

Down’s

95
Q

Marfan associated with which cardiac defects

A
  1. MVP
  2. Aortic regurg
  3. Thoracic aorta aneurysm and dissection
96
Q

DiGeorge associated with which congenital heart defects?

A

T-“q”bd (since 22q11 syndrome):

  1. ToF
  2. Truncus arteriosus
  3. Transposition of great vessels
97
Q

“String of beads” sign on renal a

A

Fibromuscular dysplasia

98
Q

Severe hypertension: (X) arteriolosclerosis. Diabetes and essential HT: (Y) arteriolosclerosis.

A 
X = hyperplastic ("onion skinning")
Y = hyaline (homogenous, glassy material that stains pink/eosinophilic with PAS)
99
Q

T/F: All arteriosclerosis causes eventual obstruction of blood flow

A

False - Mönckeberg sclerosis (medial calcific sclerosis) only causes vascular stiffening (“pipestem” appearance on xray) and doesn’t involve intima

100
Q

Arterial vasodilator and platelet aggregation inhibitor useful for symptomatic treatment of peripheral arterial disease

A

Cilostazol (PDE inhibitor)

101
Q

Rx for aortic dissection:

A 
Stanford A (ascending): surg
Stanford B (descending): BB then vasodilators
102
Q

Patient incapable of performing stress test can be infused with (X) and areas of ischemia will become evident by which phenomenon?

A

X = coronary vasodilator (ex: dipyridamole)

Coronary steal (normal coronary vessels dilate and shunt blood toward well-perfused areas/away from stenosed vessels)

103
Q

Key difference between STEMI and NSTEMI

A

STEMI: transmural infarct (full thickness involved)
NSTEMI: subendocardial infarct (inner 1/3 esp vulnerable to ischemia) with ST depression

104
Q

Gold standard MI diagnosis in first 6 hours

A

EKG

105
Q

(X) protein marker is the most specific for MI. It rises after (Y) hours, peaks at (Z) hours and remains high for:

A 
X = troponin I
Y = 4
Z = 24

7-10 days

106
Q

Pt 3 days post-MI is suspected to have a reinfarction. Which test can be useful in diagnosing this?

A

CK-MB (levels return to normal after 48 hours so useful to diagnose reinfarct)

107
Q

Post-infarct pericarditis usually occurs (X) hours/days post-MI and should be managed with:

A

X = 1-3 days

Aspirin
short-lived and localized reaction to necrosis

108
Q

Papillary muscle rupture occurs (X) days after MI. Most often, it’s the (anterolateral/posteromedial) papillary muscle ruptures because:

A

X = 2-7 days
Posteromedial

Single blood supply (PDA)

109
Q

Interventricular septal rupture occurs (X) days post-MI and pathogenesis involves:

A

X = 3-5 days

Macrophage-mediated degeneration

110
Q

T/F: Hx of previous MI puts patient at increased risk for cardiac tamponade in subsequent MI

A

False - previous MI (scar) and LV hypertrophy are protective against tamponade

111
Q

T/F: Under 10% of all MI deaths occur due to cardiac tamponade

A

True

112
Q

Fibrinous pericarditis that occurs several weeks after MI

A

Dressler syndrome (autoimmune)

113
Q

NSTEMI Rx:

A
  1. Anticoag (heparin)
  2. Antiplatelet (aspirin, clopidogrel)
  3. BB
  4. ACEi and statins
  5. Nitros and Morphine (Sx/pain management)
114
Q

STEMI v NSTEMI Rx involves which difference?

A

STEMI also includes reperfusion therapy (percutaneous coronary intervention); most important

115
Q

Which drugs must be avoided in hypertrophic cardiomyopathy?

A

Drugs that decrease preload or afterload (ex: vasodilators like nitros, diuretics, ACEi, etc)

116
Q

Drugs used to manage hypertrophic cardiomyopathy

A

BB and nondihydropyridine CCBs

117
Q

Isolated Asp aminotransferase (AST) increase in F with epigastric pain should prompt you to order which tests?

A

ECG and cardiac enzymes/markers (atypical presentation of ischemic heart disease common in females)

STEP 1 (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions