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Clin Pathology > Cardiology > Flashcards

Cardiology Flashcards

1
Q

what layers does the pericardial sac consist of?

A

serous inner layer - visceral (inner) and parietal pericardium (fibrous outer)

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2
Q

how much clear liquid lies between the layers of the heart?

A

40-50mL

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3
Q

Which branches feed the LV?

A

PDA, Cx, LAD

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4
Q

Which branch is also known as a widowmaker?

A

Left Anterior Descending (LAD)

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5
Q

If a patient is having an inferior heart attack, which branch is this affecting?

A

PDA and leads 2&3

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6
Q

If a patient is having an ANTERIOR heart attack, which branch is this affecting?

A

LAD, v1 and v2

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7
Q

If a pt is having a LATERAL heart attack, which branch is this affecting?

A

Circumflex, L1

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8
Q

What percentage does the PDA supply blood of LV arising from RCA and Cx?

A

80%;20%

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9
Q

automaticity is another word for

A

pacemaker

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10
Q

what are the pacemakers and conductors of the heart? which have a faster velocity, why?

A

Pacemakers- SA/AV node
Conductors- His and Purkinje
conductors are faster bc the AV node has a delay in order to fill the heart

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11
Q

where is the electrical connection in the heart?

A

AV and His bundle

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12
Q

The ____ distal the pacemaker is, the ______ the heart rate

A

distal, slower

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13
Q

the p wave, QRS. and T wave measure…

A

P wave: atrial depolarization
Qrs: ventricular depolarization
T wave: atrial repolarization

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14
Q

What needs to be maintained in the heart?

A

Cardiac OUTPUT

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15
Q

What 3 parameters is the stroke volume dependent on?

A

preload, after load, contractility

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16
Q

what do catecholamines and inotropic drugs do to the heart?

A

increase calcium thus increasing contractility

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17
Q

are the nodal cells or the ventricular cells faster? Why?

A

phase 0 is faster so it spikes up in ventricular cells
-BUT depolarization is faster in phase 4 of the nodal (pacemaker) cells
…
“depolarization is faster but action potential is slower in nodal”

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18
Q

how do myosin and actin interact to give rise to ____?

A

CONTRACTION;

there’s calcium release that binds to troponin C

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19
Q

what two mechanisms consist of a Bradycardia

A

SA node and AV node block

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20
Q

In Sick Sinus Syndrome, what does the ekg read?

A

a Sinus pause, and Junctional rhythm where the AV node takes over to generate a beat.
a missing p wave

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21
Q

what are the 3 degrees of an AV block in Bradycardia?

A

1st- long AV conduction (lengthened PR interval > 0.22s) but still 1:1 AV conduction
2nd- not all atrial impulses are conducted to ventricles (missing QRS or random)
3rd- no association b/w atrial and ventricular activity

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22
Q

Which degree in bradycardia is pathological and in need of a pacemaker?

A

MOBITZ II- constant PR interval, but QRS is skipped (dropped randomly)

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23
Q

Which degree in bradycardia is in need of an organ donor?

A

3rd degree AV block

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24
Q

LONG PR INTERVAL

A

1st degree AV block

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25
Q

PR interval lengthens w/ each cycle until QRS is completely skipped

A

2nd - degree AV block : Wekebebach

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26
Q

PR remains constant but QRS is skipped

a. mobitz type 2
b. sick sinus syndrome
c. wekebach
d. 1st degree AV block

A

a.

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27
Q

reasons why AV blocks can occur?

A

increasing age, vagal input, side effect of drugs

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28
Q

Examples of congenital disorders

A

muscular dystrophy, lyme dz. Lupus, CAD, gout

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29
Q

what are 3 ways tachycardia can occur?

A

inc automaticity, re-entry, and late/delayed

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30
Q

a more rapid phase 4 depolarization can be due to:

a. inc automaticity
b. long QT syndrome
c. wolf-parkinson
d. reentry

A

a. increase automaticity = SA node firing faster, inc HR

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31
Q

a long QT syndrome:

a) inc automaticity
b) triggered tachycardia
c) supraventricular tachy
d) delay repolarization

A

b. AND d

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32
Q

what are some medications pts take and have polymorphic v tach (torsades de pointes) aka twisting of the points?

A

procainamide or quinidine and dig toxicity

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33
Q

what leads to a prolonged plateau in Long QT syndrome?

A

reduced fxn of K channels

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34
Q

what is the most common Reentry tachycardia and what is it indicated by on an ekg?

A

Wolf-Parkinson White- delta wave

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35
Q

if there is a short PR and slurred upstroke to QRS on an ekg, this would be indicative of?

A

Delta Wave

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36
Q

what occurs when an accessory pathway could block impulse due to refractory period

A

premature articular contraction (PAC) a form of reentry or Wolff-parkinson white

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37
Q

if the QRS is wide, the tachycardia arises from..?

A

from ventricular tissue or is an SVT w WPW

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38
Q

when p waves are occurring after QRS, this signifies

A

WPW reentry

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39
Q

LV failure etiology (5)

A

volume overload, pressure overload, restricted filling, myocyte loss, decreased myocyte contractility

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40
Q

pathophys of LV failure (3 changes)

A

hemodynamic changes, neuro-hormonal changes, cellular changes

41
Q

What are the two types of hemodynamic changes

A

HFrEF- decreased outside REDUCED

HFpEF- decreased filling PRESERVED

42
Q

what are the curve shifts in HFrEF and HFpEF?

A

HFrEF- contractility line decreases
HFpEF-compliance (bottom) line increases (left up)
both decrease SV

43
Q

what are 3 ways the heart tries to maintain CO during HFrEF? explain in shifting of curve as well

A
  1. Inc prelooad- shift of a’ to right
  2. Inc release of catecholamines- - contractility line up c’
  3. Hypertrophy and inc vent volume— compliance line to right
44
Q

a decreased relaxation, decreased elastic recoil, or increased stiffness of the ventricle is indicative of _____.
Examples include

A

HFpEF;

-HTN and Ischemia

45
Q

compensatory responses during neurohormonal changes in LV failure (4)

A

sympathetic system activation
RAAS
Vasopressin
Cytokine release

46
Q

what are the two major groups in cytokine release of LV failure that help myocyte hypertrophy?

A

Interleukins (ILs) and tumor necrosis factor

47
Q

elevated _____ levels cause increase cardiac contractility and an inc HR to help maintain CO

A

epinephrine

48
Q

what causes the production of Angiotensin II?

A

low BP stimulating release of renin

49
Q

what helps maintain GFR despite a reduced CO?

A

angiotensin II and sympathetic activation

50
Q

angio II stimulates aldosterone syntethsis which leads to ____ and potassium ____ by kidneys

A

sodium resorption and potassium excretion

51
Q

vasopressin helps ____ of water in renal tubules

A

reabsorption

52
Q

excessive endothelia release may be responsible for _____ in pulmonary arteries

A

hypertension

53
Q

what two sarcoplasmic reticulum proteins have reduced levels of mRNA from failing hearts

A

phospholamban and Ca2+ATPase

54
Q

there is a downstream of B-1 receptors, uncoupling of the signal transduction pathway and up regulation of inhibitory G proteins leading to….

A

desensitization of B adregenic receptors as a result of chronic sympathetic activation

55
Q

alpha1 receptors are slightly increased in heart failure for induction of….

A

myocardial HYPERTROPHY– to inc HR

56
Q

can cardiac proliferate during adult form?

A

no

57
Q

what is the function of myocytes that cannot proliferate, thus is a constant turnover producing large myocytes?

A

they do NOT contract normally and have decreased ATPase activity

58
Q

what causes holes in the myocardium?

A

myocyte loss via apoptosis (by TNF)

59
Q

what two things cause an inc in fibrous tissue in interstitial spaces of the heart?

A

collagen deposition

and endothelin release

60
Q

what sx occurs when there is a short blood supply to skeletal muscles?

A

fatigue

61
Q

what sx occurs when renal perfusion normalizes only at night?

A

nocturia

62
Q

what is a sx secondary to ischemia with CAD?

A

chest pain

63
Q

what are the 3 clinical presentations of a pt with RV failure?

A

SOB, pedal edema, abdominal pain

64
Q

What is the most common cause of RV failure?

A

LV failure bc of the inc afterload placed on RV

65
Q
  • in cardiomyopathy, a thicker and reduced chamber size indicates:
    a) cardiac dilation
    b) physiological hypertrophy
    c) Idiopathic DCM
    d) pathological hypertrophy
A

d) pathological hypertrophy

slide 92

66
Q

*What is the most common cause of cardiomyopathy? which one requires cardiac transplants?

A

dilated cardiomyopathy–> idiopathic DCM`

67
Q

alcohol is a cause in which cardiomyopathy?

A

dilated

68
Q

a biventricular characteristic is seen in which cardiomyopathy?

A

dilated

69
Q

*what is the number one cause of sudden death in young athletes?

A

HOCM

70
Q

what area of the heart is most affected in HOCM and what does it block?

A

septum –> thickens up closing off the outflow of blood through the aorta

71
Q

*cells appearing as whorls are indicative of?

A

HOCM

72
Q

signs and symptoms of HOCM

A

dyspnea and Angina

73
Q

what is the rarest form of cardiomyopathy?

A

restrictive cardiomyopathy

74
Q

which type of cardiomyopathy has a filling problem thus heart can’t relax?

A

restrictive cardiomyopathy

75
Q

which cardiomyopathy looks similar to normal heart?

A

restrictive cardiomyopathy

76
Q

define stenosis vs regurgitation

A

stenosis- narrow

regurgitation- leaky

77
Q

systole vs diastole murmurs

A

systole –> Mc Ao aortic stenosis or mitral regurgitation

diastole –> Mo Ac aortic regurgitation or mitral stenosis

78
Q

long latent period of slowly increasing obstruction before sx appear is seen in

a) aortic regurgitation
b) mitral stenosis
c) aortic stenosis
d) mitral regurgitation

A

c)

79
Q

what are the 3 cardinal symptoms of AS and the life expectancies of each one if left untreated?

A

chest pain–> 5 years, syncope–> 3 years, heart failure –> 2 years

80
Q

*comparison of carotid pulse and PMI in AS?

A

carotid pulse is decreased and delayed

pluses parvus & pulses tardus*

81
Q

You do an en echo on a pt’s (age30-70) heart and find tissue inflammation and adhesion/fusing of commissures, which type of AS is this?

a) congenital
b) rheumatic
c) degenerative
d) glue

A

b) rheumatic

slide 120*

  • congenital: partially fused, Abel flow–> fibrosis and calcification-> sx before 30y
    degenerative: inflexible leaflets, calcium deposits at bases, pt 70y
82
Q

if you see concentric hypertrophy and a prominent a wave, this indicative of

A

aortic stenosis

-causing LV hypertrophy; dependent on atrial kick

83
Q

in order to maintain the stroke volume in AS, what increases? think of the pressure/vol graph

A

LVED pressure increases, (preload to allow more blood out)

84
Q

The sound of AS is typically described as?

A

crescendo-decrescendo

quiet or silent S2 bc of hypertrophy

85
Q

what is the difference between HOCM and AS and how can this be tested?

A

decrease in preload in HOCM- valsalva maneuver–> HOCM murmur increase

similarities: hypertrophy, crescendo-decrescendo sound
* *slide 128

86
Q

What is the most common murmur sound in chronic AR?

A

Diastolic rumble –> Austin Flint murmur

87
Q

What signs are found in acute AR?

A

none bc it happens so fast

88
Q

Where does blood enter from in aortic regurgitation during diastole?

A

BOTH- the left atrium AND the aorta (leaking) thus increasing volume

89
Q

if you see eccentric hypertrophy, this is indicative of?

A

aortic regurgitation

90
Q

systemic diastolic BP inc or dec in Aortic regurgitation?

what about diastolic in the ventricle?

A

systemic diastolic pressure DECREASES because not squeezing enough blood out into the system***

  • diastolic in ventricle increases because there is more blood in the ventricle
  • slide 131*
91
Q

no relaxation/contraction exists in

a) aortic stenosis
b) aortic regurgitation
c) mitral stenosis
d) mitral regurgitation

A

b ***

92
Q

pathophysiology with a mitral valve of 1 cm^2

A

c) mitral stenosis

* aortic stenosis AVA = < 0.8 cm

93
Q

a main pathophysiologic abnormality is elevated pulm pressure and RIGHT sided pressure

a) aortic stenosis
b) aortic regurgitation
c) mitral stenosis
d) mitral regurgitation

A

c) mitral stenosis

94
Q

**hoarseness or Ortner Syndrome during Mitral Stenosis is due to

A

LA enlargement impinging on recurrent laryngeal nerve

95
Q

What is heard during mitral regurgitation?

A

holosystolic pitched regurgitant murmur

96
Q

most common cause of mitral stenosis?

A

rheumatic

97
Q

most common cause of mitral regurgitation?

A

mitral valve prolapse, followed by CAD

98
Q

atrial v waves are present in which valvular heart disease?

A

mitral regurgitation

-reuptake of the blood from ventricle through mitral valve

Clin Pathology (8 decks)

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