CV 1 Flashcards

1
Q

Mitral valve regurgitation

A

Holosystolic murmur

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

Myocarditis due to acute rheumatic fever

A
  • Develops after untreated strep
  • Aschoff bodies on microscopy (interstitial myocardial granulomas)
  • Aschoff bodies contain plump macros w/ abundant cytoplasm and central, slender ribbons of chromatin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Supine hypotension syndrom in preggers

A
=> Supine/right lateral decubitus position
=> Compression of IVC
=> reduced venous return
=> reduced preload
=> decreased CO
=> hypotension

Sx resolve when standing or sitting

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

Digoxin MOA

A
  • Directly inhibits Na-K-ATPase in myocardial cells
  • Causes v in Na efflux => ^ intracellular Na levels => reduces Na-Ca exchanger => ^ intracellular Ca => improved myocyte contractility and left ventricular systolic function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Go review blood vessel anatomy around the heart

A

NOW

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

V1-V2 ST elevation. Which coronary artery?

A

Left anterior descending

Anteroseptal infarct

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

V3-V4 ST elevation. Which coronary artery?

A

LAD distal

Anteroapical

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

V5-V6 ST elevation. Which coronary artery?

A

LAD or LCX

Anterolateral

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

I, aVL ST elevation. Which coronary artery?

A

LCX

Lateral

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

II, III, aVF

A

RCA

Inferior

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

Afib presentation

A
  • Palpitations
  • Tachycardia
  • Irregularly irregular rhythm

Precipitated by acute systemic illness, increased sympathetic tone, excessive alcohol consumption (holiday heart syndrome)

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

ECG of Afib

A
  • Absence of P waves

- Irregularly irregular rhythm with varying R-R intervals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Ergonovine

A

Ergot alkaloid

  • Stimulates alpha-adrenergic and serotonergic recetpors
  • In pts w/ pinzmetal’s angina, low doses can induce coronary spasm, chest pain, and ST elevation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

IV drug users and heart issues

A
  • Tricuspid (right sided) endocarditis
  • S. aureus (1) and P. aeruginosa (2)
  • Can develop multiple septic emboli in lungs
  • Pulm infarcts are almost always hemorrhagic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Turner syndrome cardiac anomalies

A
  • Aortic coarctation

- Bicuspid aortic valve

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

Aortic coarctation presentation

A

Infancy:

  • Cyanosis of LE
  • Severe form

Adolescent/youth

  • Decreased femoral pulses
  • Pain/cramping in legs during exercise
  • More common w/ Turner syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Which part of the heart makes up the anterior surface?

A

Right Ventricle

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

Penetrating injury to RV occurs where?

A

Left sternal border

Fourth intercostal space

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

Which layers would a penetrating injury to RV go through?

A

1) Skin/subcutis 2) Pectoralis major m.
3) External intercostal membrane
4) Internal intercostal m
5) Internal thoracic a. & v.
6) Transversus thoracis m
7) Parietal pleura
8) Pericardium
9) R. ventricular myocardium

Pleura of lungs is injured but not the actual lungs (no middle lobe on left side)

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

Dry beriberi

A
  • Peripheral neuropathy of distal L/UEs

- Sensory/motor impairments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Wet beriberi

A
  • Dry beriberi plus cardiac involvement

- Cardiomyopathy, high-output CHF, peripheral edema, tachy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Femoral triangle

A

Subfascial space in upper thigh:

  • Inguinal ligament (superior)
  • Adductor longus (medial)
  • Sartorius (lateral)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Path of LAD

A
  • arises off l. main a.

- courses along anterior aspect in the anterior interventricular groove toward apex of the heart

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

Pathogenesis of atherosclerotic plaques

A
  • Release of PDGF from locally adherent plts, endo cells, and macros
  • Promotes migration of SMCs into intima
25
Q

Which part of the body has the highest O2 extraction?

A

The heart!!!

Drains into coronary sinus

26
Q

Nitroglycerin affects which vessels?

A

Venous anything

Decreases preload => decreases ventricular wall stress => decreasing CO demand

Large veins are most susceptible

27
Q

What does the pulm cap wedge pressure measure?

A

L. atrial end diastolic pressure (LAEDP)

LAEDP = LVEDP in normal conditions

28
Q

Go review the LV pressure-volume relationship

A

NOW

29
Q

DiGeorge - lack of development of which embryologic structure

A
  • Third & Fourth branchial/pharyngeal pouch

Deletion of chr 22

Absent thymic shadow, hypocalcemia, cleft palate, mandibular deformity, low-set ears, aortic arch abnormalities

30
Q

VSD

A

presents in neonate period after pulm vascular resistance has declined (so not at birth)

HOLOsystolic murmur

31
Q

Prussian blue stains what?

A

Intracellular IRON

32
Q

Gold cytoplasmic granules in macros that turn blue with Prussian blue staining?

A

hemosiderin laden macrophases (siderophages)

33
Q

What is the significance of hemosiderin laden macros?

A
  • Indicates chronic elevation of pulm cap hydrostatic pressures
  • Most commonly due to left-sided HF
34
Q

Bicuspid aortic valve?

A

Common cause of aortic stenosis

Class auditory:

  • harsh, cres-descres systolic ejection murmur
  • heard best at R. 2nd intercostal space`
35
Q

adenosine and dipyridamole

A

Selective vasodilators of coronary vessels

36
Q

What is coronary steal?

A
  • Blood flow to ischemic areas (after an MI) is reduced
  • Because of arteriolar vasodilation in nonischemic areas
  • Can lead to hypoperfusion and worsening existing ischemia
37
Q

Right heart failure => ^ed CVP

What happens after that?

A
  • Increased cap hydrostatic pressure
  • Increased net plasma filtration
  • Increased interstitial fluid pressure => increased lymphatic drainage (prevents peripheral edema development)
38
Q

Cardiac AP (speed of conduction) slowest to fastest

A

AV node

39
Q

Blood flow radius and resistance

A

BF:
- Directly proportional to vessel radius^4

Resistance:
- BF is innersely proportional to radius^4

40
Q

Where do K sparing diuretics act on the kidney?

A

collecting duct

Blocks absorption of Na

Blocks excretion of K, H

41
Q

Where do loop diuretics act?

A

Thick ascending limb of loop of Henle

Blocks absorption of Na, Cl, K

42
Q

Where do thiazide diuretics act?

A

Distal convoluted tubule

Blocks absorption of Na, Cl

43
Q

Beta blocker MOA

A
  • Inhibits renin release from renal juxtaglomerular cells through antagonizing beta-1 receptors
  • Prevents activation of RAAS pathway => decreased vasoconstriction & renal Na &H20 retention
44
Q

Dobutamine

A
  • Beta- adrenergic agonist
  • Predominantly B1 receptors
  • Increases HR, contractility => increase myocardial O2 consumption
45
Q

Nitrates MOA

A

Vasodilation

  • ^ NO in VSMCs => ^ in cGMP and SM relaxation
  • Dilates veins&raquo_space;> arteries
  • Decrease preload
46
Q

Nitrates SEs

A
  • Reflex tachy
  • Hypotension
  • Flushing
  • HA
  • “Monday disease”
47
Q

Where is the MI with a ST elevation of II, III, aVF?

A

Inferior

RCA occlusion

Think RVMI

Presentation: hypotension, distended jugular veins, clear lungs

48
Q

Hemodynamic assessment of RVMI

A
  • Elevated RA and CVP
  • Reduced PCWP
  • Reduced CO
49
Q

Chlorthalidone MOA

A

Thiazide

  • Inhibits NaCl resorption in early DCT
  • Decreased Ca excretion
50
Q

Chlorthalidone SEs

A
  • Hypokalemic metabolic alkalosis
  • HYPOnateremia
  • HYPERglycemia/lipidemia/uricemia/calcemia

Sulfa allergy

51
Q

Coadmin of ACEIs and diuretics

A

Significant first-dose hypertension

ACEIs must be initiated at low doses to decrease the reaction

52
Q

Pros of using mineralcorticoid receptor antagonists (e.g. spironolactone, eplerenone) in pts with HF?

A
  • Improve survival
  • Regression of myocardial fibrosis & improvement of ventricular remodeling

Used in pts w/ decreased LVEF

53
Q

In transient ischemia, why do myocytes increase in size?

A

No O2 = No ATP

  • Can’t stimulate Na(going out)/K (going in) pump
  • Can’t maintain Na (going in)/Ca (going out) exchange
54
Q

MOA of statins

A

HMG-CoA reductase inhibitors

Lower total cholesterol and LDL

Most effective for prevention of CV events REGARDLESS of baseline lipid levels

55
Q

Anatomical findings in tetralogy of Fallot

A

PROV

1) Pulm infundibular stenosis
2) R. ventricular hypertrophy
3) Overriding aorta
4) VSD

56
Q

Cause of TOF

A

Anterosuperior displacement of infundibular septum

57
Q

Clinical Presentation of TOF

A

Early childhood cyanosis

Squatting: ^ SVR, v R-to-L shunt, improves cyanosis

Harsh systolic murmur (pulm stenosis)

58
Q

Hibernating myocardium

A
  • Presence of LV systolic dysfunction
  • Because of reduced coronary blood flow
  • Completely reversible by coronary revascularization