Patho Cardiovascular 2

56問 • 2年前

問題一覧

Chest pain caused by ischemia

Angina

Transient pain, caused by accumulation of lactic acid—> ischemic stretching of myocardium—> irritates myocardial nerve fibers

Stable Angina

Manifestation of pain vary as a result of afferent fibers that transmit pain enter spinal cord from C3-T4

Stable Angina

Occurs at rest, unpredictable, vasospasm caused by atherosclerosis related to decreased vagal activity, hyperactive SNS, decreased NO activity, altered Ca channel function —> benign or serious dysrththmia

Unstable (Prinzmetal) Angina

Non-chest pain ischemia. Presents as fatigue, dyspnea or feelings of unease. LV sympathetic innervation, DMII, post-cardiac surgery, mental stress

Silent Ischemia

Reversible Myocardial Ischemia, Forecasts Impending MI

Unstable Angina

Prolonged ischemia with irreversible damage to heart muscle, results from rupture of unstable plaque in coronary arteries—> thrombosis of vessel

Related to superficial plaque erosion—> transient thrombotic vessel occlusion—> vasoconstriction at site. Symptoms: new onset angina, angina at rest> 20 mins, increasing severity or frequency of previous angina. ST depression, T-wave inversion that goes away when pain stops. Normal Trops, CK-MB.

Unstable Angina

Thrombus breaks up before complete distal necrosis. ST depression and T-wave inversion, elevated cardiac biomarkers. Intervention needed promptly as dislodged is plaque is likely to cause thrombosis elsewhere.

NSTEMI

Infarction extends through myocardium creating severe cardiac dysfunction. Presents with ST elevation, elevated cardiac biomarkers.

STEMI

Hypoxia induces

Cellular injury

Hypoxia induces

Decreased glycogen stores = anaerobic metabolism

Hypoxia induces

Increased H+ and lactic acid

Hypoxia induces

Acidosis

Hypoxia induces

Decreased K, Ca, and Mag

Hypoxia induces

Decreased contractility

Hypoxia induces

Release of Catecholamines

Hypoxia induces

Hypoxia induces Norepinephrine—> increase serum glucose

Hypoxia induces

Angiotensin II—> peripheral vasoconstriction, fluid retention, coronary artery spasm

Hypoxia induces

Reperfusion injury

Hypoxia induces

Release of toxic O2 radicals, Ca influx, pH change—> cell death

Hypoxia induces

Inflammatory cells—> myocardial tissue injury

Temporary loss of comtractile function, last hours-days

Myocardial stunning

Myocyte hypertrophy, scarring and loss of function distant to area of infarction—> can be limited and reversed with quick restoration of coronary flow

Myocardial remodeling

Degradation of injured cell—> scar tissue. Decreased contractility, altered LV compliance, decreased stroke volume and EF, increased LV-end diastolic pressure and volume, SA node malfunction.

Myocardial repair

Dysrhythmia, Cardiogenic Shock, Pericarditis, Ventricular Aneurysm/Rupture, Papillary Muscle Rupture, Thromboembolism

MI Complications

Elevated Troponin (most specific indicator), CK-MB, LDH, and CRP. leukocytosis and hyperglycemia.

MI Lab Diagnosis

Inadequate perfusion to tissues and/or increased diastolic filling pressures

Heart Failure

Inability of heart to generate adequate CO to perfuse tissues, EF <40%, decreaed contractiliy, increaed preload, increased afterload

Left HFrEF (Systolic HF)

Pulmonary congestion despite normal stroke volume and CO. Decreased compliance in LV, abnormal relaxation of LV (lusittopy), associated with: changes in Ca transport from myocytes, autonomic and endothelial dysfunction

Left HFpEF (Diastolic HF)

LV doesn’t relax but empties (normal LV end-diastolic volume) but there is increased LV end-diastolic pressure—> increased LV pressure—> pulmonary edema—> pulmonary HTN

Left HFpEF (Diastolic HF)

Symptoms: dyspnea on exertion, fatigue, crackles, S4 gallop, LV hypertrophy, CXR congestion

Left HFpEF (Diastolic HF)

Inability to provide adequate blood to lungs at normal CVP. Often caused by LHF and Pulmonary HTN. Initially RV hypertrophy in attempt to compensate for increased pulmonary pressure but ultimately, diastolic and systolic dysfunction—> HF

Right HF

Symptoms: JVD, peripheral edema, hepatosplenomegaly (systemic symptoms)

Right HF

B-type natriuretic peptides (BNP)

Helpful in ruling out HF

Potent vasoconstrictors associated with poor HF prognosis

Endothelial hormones

Elevated in HF, contribute to myocardial hypertrophy and remodeling, and cardiac cachexia?

TNF-a and IL-6

Related to activation of SNS and RASS

Insulin Resistance

Hypertrophy and dilation of ventricle, Large Cells, Impaired Contractility

Ventricular Remodeling

Valve is narrow and blood flow forward is constricted—> increase workload of chamber

Stenosis

Valve leaflets don’t close completely, and blood continues to flow when the valve is supposed to be closed—> increases blood flow in chamber affected, increasing workload —> dilation—>hypertrophy

Regurgitation

Most common valve disease, decreases blood flow from LV—> body, results in LV hypertrophy. Causes: calcification of valve, bicuspid valve, inflammation from rheumatic heart disease.

Aortic Stenosis

Normal blood flow out of LV in systole but blood flow leaks back into LV during diastole resulting in LA dilation and Hypertrophy. Causes: bicuspid valve, degeneration, HTN, rheumatic heart disease, Marfan’s syndrome.

Aortic Regurgitation

Mist common rheumatic heart disease, scars leaflets, limits blood flow from LA—> LV. LA hypertrophy—> atrial dysrhythmias and pulmonary edema.

Mitral Stenosis

Primarily related to mitral valve prolapse. Results in back flow of blood from LV—> LA. LA hypertrophy—> LA dilation—> pulmonary HTN—> RV failure

Mitral Regurgitation

Most common valve disorder in the US. Associated with inherited tissue disorders and hyperthyroidism. Anterior and posterior cusps of MV billow up. Allow leaking into artium.

Mitral Valve Prolapse

Infection and inflammation of the endothelium, especially the valves. Staph A most common cause but also associated with other bacteria and viruses. Risks include: prosthetic valves, IV drug use, acquired heart disease, long term IV catheters

Endocarditis

Symptoms: formations of vegetations, emboli, fever, night sweats, malaise, murmur, regurgitation, HF.

Endocarditis

Treatment: Antibiotics, Valve repair/replacement, Prophylaxis

Endocarditis

Amount of blood in Pulmonary Circulation

Amount of blood in Heart

Amount of blood in Arteries

13%

Hypoxia induces Cellular Injury leading to:

Decreaed glycogen = anaerobic metabolism —> Increaed H+ Lactic Acid —> Acidosis —>HF

Hypoxia Induces Electrolyte Disturbances (Decreased K, Ca, Mg):

Decreased Contractility—> Release of Catecholamines—> Norepinephrine increases serum glucose—> Angiotensin II causes vasoconstriction, fluid retention, coronary artery spasm

Hypoxia Induces Reperfusion Injury:

Release of toxic oxygen radicals, calcium influx, pH change —> cell death. Inflammatory cells—> myocardial tissue injury

Patho Renal

Two Clean Queens · 100問 · 2年前

Patho Renal