Cardio Pathology Flashcards
what is defined as systemic HTN?
persistent systolic 130+ and/or diastolic 80+
what is the most common secondary cause of systemic HTN?
kidney pathology
what are types of complications of systemic HTN?
heart
kidneys (CKD due to hypertensive nepropathy)
vessels
eyes
explain the pathogenesis of systemic HTN
multifactoral:
- genetics
- activation of SNS
- activation of renin-angiotension-aldosterone system
what can cause increased BP?
BP = CO x TPR
inc CO: inc HR (exercise, anxiety), inc contractility, inc preload (filling), dec afterload
what is defined at pulmonary HTN?
elevation of 20-25+ in pulmonary artery pressure at rest
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
what are some complications of pulmonary HTN?
arteriosclerosis
medial hypertrophy
intimal fibrosis of PAs
describe the pathogenesis of pulmonary HTN
inc pulmonary vasculature resistance > inc RV pressure > RV hypertrophy > RHF
what are the main causes of RHF?
LHF**
pulmonary HTN/pulmonary etiology
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
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)
what is CHF?
cardiac pump dysfunction > heart congestion > dec CO > low perfusion
left and right sided
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
describe the etiology of LCHF
ischemic causes:
IHD
HTN
Atrial and mitral valve dz
myocardial dz
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)
what is a sign that could be seen microscopically due to pulmonary edema present with LCHF?
HF cells in the lung (hemosideran laden macrophages)
what are some complications of LCHF?
a fib
RCHF
thrombosis/stroke
hypoxic encephalopathy
what is cor pulmonale?
RCHF due to a pulmonary etiology
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
