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NPLEX I 2024 > Cardio Pathology > Flashcards

Cardio Pathology Flashcards

1
Q

what is defined as systemic HTN?

A

persistent systolic 130+ and/or diastolic 80+

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2
Q

what is the most common secondary cause of systemic HTN?

A

kidney pathology

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3
Q

what are types of complications of systemic HTN?

A

heart
kidneys (CKD due to hypertensive nepropathy)
vessels
eyes

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4
Q

explain the pathogenesis of systemic HTN

A

multifactoral:
- genetics
- activation of SNS
- activation of renin-angiotension-aldosterone system

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5
Q

what can cause increased BP?

A

BP = CO x TPR

inc CO: inc HR (exercise, anxiety), inc contractility, inc preload (filling), dec afterload

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6
Q

what is defined at pulmonary HTN?

A

elevation of 20-25+ in pulmonary artery pressure at rest

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7
Q

what are some RF for pulmonary HTN?

A

heart - harder to pumpo blood to pulm vasculature; CHF, MI, anemia
lung - COPD, thromboembolism, pulmonary arterial HTN
fibrosis - scleroderma, CT dz

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8
Q

what are some complications of pulmonary HTN?

A

arteriosclerosis
medial hypertrophy
intimal fibrosis of PAs

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9
Q

describe the pathogenesis of pulmonary HTN

A

inc pulmonary vasculature resistance > inc RV pressure > RV hypertrophy > RHF

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10
Q

what are the main causes of RHF?

A

LHF**
pulmonary HTN/pulmonary etiology

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11
Q

what are the signs/sx of pulmonary HTN?

A

microscopic plexiform lesions (“spider veins” in lungs from remodeled PAs)

medial hypertrophy of muscular and elastic arteries

fatigue
dyspnea
syncope
edema
chest pain w exertion
palpitations

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12
Q

what are the causes of pulmonary HTN? which is most common?

A

group 1 - pulmonary arterial HTN; PAH (drugs/toxins, CT, idiopathic)
2 - due to LHD (most common)
3 - due to lung dz/hypoxemia
4 - due to chronic emboli
5 - unclear mechanism

Genetic component- smooth muscle proliferation bc of decreased apoptosis from BMPR2 morphogenic protein mutation (vasculature is stuck in place from all the smooth muscle, can’t vasodilate)

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13
Q

what is CHF?

A

cardiac pump dysfunction > heart congestion > dec CO > low perfusion

left and right sided

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14
Q

what are the two types of LCHF? how are they differentiated?

A

systolic dysfunction:
- reduced EF (HFrEF)
- inc EDV
- dec contractility

diastolic dysfunction:
- preserved EF (HFpEF)
- normal EDV
- dec compliance/inc end diastolic pressure

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15
Q

describe the etiology of LCHF

A

ischemic causes:

IHD
HTN
Atrial and mitral valve dz
myocardial dz

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16
Q

what are some signs/sx of LCHF? explain the pathogensis for those you know.

A
  • S3
  • rales
  • JVD
  • pitting edema
  • dyspnea
  • orthopnea (SOB supine due to inc venous return worsening pulm congestion)
  • fatigue
  • paroxysmal noctural dyspnea (wakening SOB due to inc venous return and edema resorption)
  • pulm edema (inc pulm venous pressure > distention)
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17
Q

what is a sign that could be seen microscopically due to pulmonary edema present with LCHF?

A

HF cells in the lung (hemosideran laden macrophages)

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18
Q

what are some complications of LCHF?

A

a fib
RCHF
thrombosis/stroke
hypoxic encephalopathy

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19
Q

what is cor pulmonale?

A

RCHF due to a pulmonary etiology

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20
Q

what is the most common cause of RCHF?

A

LCHF

21
Q

what are some signs of RCHF and their pathogenesis?

A
  • congestive hepatomegaly: inc central venous pressure > inc resistance to portal flow > NUTMEG LIVER (mottled liver on cadaver)
  • JVD (inc venous pressure)
  • peripheral edema (inc venous pressure > fluid transudation)
22
Q

what are examples of ischemic heart disease (IHD)?

A

angina, chronic IHD, MI

23
Q

what are the types of angina? which is most common?

A

stable (most common) - secondary to atherosclerosis
vasospastic - at rest due to CA spasm
unstable - thrombosis with incomplete CA occlusion

24
Q

what nerve innervates the carotid sinus?

A

glossopharyngeal

25
Q

how does the renin-angiotensin-aldosterone system increase BP?

A

direct systemic vasoconstriction via increasing sympathetic output

26
Q

regarding the three types of angina, for each of them describe the characteristic of pain and when/if it occurs

A

stable - on exertion
vasospastic - at rest
unstable - mild exertion or at rest

27
Q

regarding the three types of angina, for each of them describe the changes to troponin levels

A

NO elevation for any type of angina

28
Q

regarding the three types of angina, for each of them describe the type/degree of infarction

A

NONE for any type of angina

29
Q

regarding the three types of angina, for each of them describe the ECG changes

A

stable - none
vasospastic - transient ST elevation
unstable - possible ST depression, possible T wave inversion

30
Q

regarding the three types of angina, for each of them describe the triggers

A

stable - atherosclerosis, activity, HR/BP
vasospastic - cocaine, alcohol, triptans
unstable - atherosclerosis, activity, HR/BP

31
Q

regarding the three types of angina, for each of them describe the RF

A

stable - HTN, HLD, tobacco, other MI RF
vasospastic - tobacco
unstable - HTN, HLD, tobacco, other MI RF

32
Q

what is described as chronic IHD?

A

progressive HF with onset from chronic ischemic myocardial damage (myocardial ischemia)

33
Q

RF for chronic IHD

A

CAD RF (HLD, HTN, tobacco, etoh, age, SAD diet, sedentary lifestyle)

34
Q

complications of chronic IHD

A

leading cause of death worldwide
progressive CHF > heart transplant

35
Q

pathogenesis chronic IHD

A

long and slow - late manifestations of coronary atherosclerosis

often appears post-infarction due to functional decompensation of hypertrophied non-infarcted myocardium

36
Q

etiology chronic IHD

A

dec blood flow due to obstructive atherosclerotic lesions in CAs

typically preceded by MI

37
Q

sx chronic IHD

A
  • enlarged, heavy heart with LV hypertrophy + dilation
  • obstructive coronary atherosclerosis
  • scars from healed infarcts
38
Q

complications of MI by time frame

A

0-24 hours: cardiogenic shock, CHF (d/t dec EF), ventricular arrythmia (conduction system damaged)

1-3 days: fibrinous pericarditis

4-7 days: cardiac tamponade (rupture of ventricular free wall), mitral regurgitation (rupture of papillary muscle, more common w RCA occlusion), shunt (rupture of IV septum)

months: dressler syndrome (inf pericardium > ab to pericardium), aneurysm, mural thrombus

39
Q

pathogenesis of an MI

A

change in atherosclerotic plaque (hemorrhage, rupture, erosion, etc) > necrotic plaque contents exposed to subendothelial collagen > platelets adhere and release granule contents, aggregating to form microthrombi (they think the vessel is damaged) > vasospasm stimulated by platelet released mediators

> TF activates coagulation pathway, adding to bulk of thrombus

40
Q

biochemistry of an MI

A

cessation of aerobic metabolism within seconds

> dec ATP production
accumulation of lactic acid

41
Q

name the microscopic changes of an MI by time period

A

4-24 hours: coagulative necrosis

1-3 days (inflammation: neutrophils

4-7 days (inflammation): macrophages

1-3 weeks: granulation tissue with plump fibroblasts, type I collagen, and BV (scar formation process)

Months: fibrosis (scar); scar is not as strong as myocardium, can be stasis along scar

42
Q

name the gross changes of an MI by time period

A

4-24 hours: dark discoloration

1-7 days: yellow pallor (due to dec WBC in myocardium)

1-3 weeks: red border (BVs) emerges as granulation tissue enters from edge of infarct

Months: white scar

43
Q

compare the following for an NSTEMI and STEMI: pain

A

pain at rest with both

44
Q

compare the following for an NSTEMI and STEMI: troponin

A

troponin elevated for both

45
Q

compare the following for an NSTEMI and STEMI: infarction type

A

NSTEMI: subendocardial (inner 1/3)
STEMI: transmural (full thickness myocardial wall)

46
Q

compare the following for an NSTEMI and STEMI: ECG changes

A

NSTEMI: ST depression
STEMI: ST elevation, pathologic Q waves

47
Q

list the most common arteries affected in an MI

A

LAD > RCA > circumflex

48
Q
A

NPLEX I 2024 (23 decks)

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