Cardio Pathology Flashcards by tia meechan

what is defined as systemic HTN?

persistent systolic 130+ and/or diastolic 80+

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what is the most common secondary cause of systemic HTN?

kidney pathology

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what are types of complications of systemic HTN?

heart
kidneys (CKD due to hypertensive nepropathy)
vessels
eyes

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explain the pathogenesis of systemic HTN

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

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what can cause increased BP?

BP = CO x TPR

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

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what is defined at pulmonary HTN?

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

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what are some RF for pulmonary HTN?

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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what are some complications of pulmonary HTN?

arteriosclerosis
medial hypertrophy
intimal fibrosis of PAs

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describe the pathogenesis of pulmonary HTN

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

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what are the main causes of RHF?

LHF**
pulmonary HTN/pulmonary etiology

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what are the signs/sx of pulmonary HTN?

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

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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what is CHF?

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

left and right sided

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

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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describe the etiology of LCHF

ischemic causes:

IHD
HTN
Atrial and mitral valve dz
myocardial dz

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

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

HF cells in the lung (hemosideran laden macrophages)

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what are some complications of LCHF?

a fib
RCHF
thrombosis/stroke
hypoxic encephalopathy

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what is cor pulmonale?

RCHF due to a pulmonary etiology

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what is the most common cause of RCHF?

LCHF

what are some signs of RCHF and their pathogenesis?

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)

what are examples of ischemic heart disease (IHD)?

angina, chronic IHD, MI

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

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

what nerve innervates the carotid sinus?

glossopharyngeal

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

direct systemic vasoconstriction via increasing sympathetic output

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

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

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

NO elevation for any type of angina

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

NONE for any type of angina

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

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

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

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

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

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

what is described as chronic IHD?

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

RF for chronic IHD

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

complications of chronic IHD

leading cause of death worldwide progressive CHF > heart transplant

pathogenesis chronic IHD

long and slow - late manifestations of coronary atherosclerosis often appears post-infarction due to functional decompensation of hypertrophied non-infarcted myocardium

etiology chronic IHD

dec blood flow due to obstructive atherosclerotic lesions in CAs typically preceded by MI

sx chronic IHD

- enlarged, heavy heart with LV hypertrophy + dilation - obstructive coronary atherosclerosis - scars from healed infarcts

complications of MI by time frame

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

pathogenesis of an MI

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

biochemistry of an MI

cessation of aerobic metabolism within seconds > dec ATP production > accumulation of lactic acid

name the microscopic changes of an MI by time period

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

name the gross changes of an MI by time period

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

compare the following for an NSTEMI and STEMI: pain

pain at rest with both

compare the following for an NSTEMI and STEMI: troponin

troponin elevated for both

compare the following for an NSTEMI and STEMI: infarction type

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

compare the following for an NSTEMI and STEMI: ECG changes

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

list the most common arteries affected in an MI

LAD > RCA > circumflex