Cardio - Stuff Missed Flashcards
How do ACE inhibitors cause renal failure?
ACE inhibitors dilate efferent tubules, thus decreasing GFR and renal perfusion.
- For patients who depend on efferent arteriole constriction to maintain renal perfusion (pts with renal artery stenosi), ACE inhibitors can cause ARF
Discuss ACE inhibitors and aldosterone
block release of aldosterone resulting in decreased Na reabsoprtion and increase K retention in distal and collecting tubules
- responsible for hyperkalemia often seen with ACE inhibitor therapy
Cyclooxygenase 2 (COX-2)
- molecular weight of 72kd
- inducible enzyme that is normally undetectable in most tissue except in case of inflammation
“Coffee ground emeisis”
suggests upper GI bleed
- coffee ground color caused by oxidation of heme
- patients may lose a lot of blood and may experence hypvolemic shock
Hypovolemic shock
- when patient loses > 10% of blood volume
- sympathetic NS constricts arteriole and venous beds and stimulate heart
- arteriole constriction - increases total peripheral resistance and maintain organ pressure
- venous constriction - increases blood return to heart to maintain preload
Discuss IV fluid infusions and preload
IV infusions increase intravascular volume by varying degrees of solute composistion
- Preload increase increases mycocardial sarcomere lendgth and increases stroke volume and cardiac outpute
Most common cause of mitral stenosis
Rheumatic dever
Infective endocarditis
- results in larger, more friable vegetations
- destruction of valve leaflet, may cause regurgitation
- embolization of vegetations can cause stroke or septic infarct resulting in brain abscess
Degenerative calcific deposits
develop in mitral valve annulus in women > 60
- found in ppl with myxomatous, floppy mitral valve or elevated left ventricular pressure
Fibrinous pericarditis
- result of prolonged rheumatoid arthritis
- rarely involve the endocardium or heart valves
Reperfusion injury
- when after blood flow is returned to ischemic tissue, cells within damaged tissue die secondary to: - oxygen free radial generation - mitochondrial damage - inflammation
Mechanisms of reperfusion injury
- Oxygen free radical generation by parenchymal cells
- Severe, irreversible mitochondrial damage described as “ mitochondrial permeability transition”
- Inflammation - attracts circulating neutrophils that cause additional injury
- Activation of complement pathway, causing cell injury and further inflammation
Explanation of rise in serum creatinine kinase after thrombus extraction
- Result of reperfusion injury
- When heart, brain, or skeletal muscle are injured, enzyme creatinine kinase leaks across cell membrane and into circulation
Risk factors for intimal tears leading to aortic dissections
- Hypertension
Smoking (risk factor for which vascular diseases)
- ATHEROSCLEROSIS –> aortic aneurysm
2. BUERGER’S DISEASE (Thormboangitis obliterans)
If LAD is occluded by atherosclerotic plauque, what is the preferred vein for grafting?
Left internal mammary artery - preferred vseel
If mutiple coronary arteries/vessels are occluded, what is the preferred vein for grafting?
Great saphenous vein - longest vein in body
Great saphenous vein
- superficial vein that originate on medial side of foot, courses anterior to medial malleolus, and then travels up medial aspect of leg thigh
- drains into femoral vein within femoral triangle, inferior lateral to pubercle triangle
How soon after ischemia do the cardiomyocytes lose contractility?
60 seconds after ischemia
- due to cessation aerobic glycolysis
- ATP decreases rapidly due to high myocardial demand
Myocardial studding
if ischemia lasts less than 30 minues
- restoration of blood leads to REVERSIBLE contractile dysfunction
- contractility returns to normal within days or hours
What happens to cardiomyocytes after more than 30 minutes of ischemia?
IRREVERSIBLE injury
Most reliable indicator of the severity of mitral stenosis
S2 to opening snap interval (A2-OS interval)
- ## the shorter the interval, the more severe the stenosis
Xanthelasmas
- yellowish macules/papules found on medial eyelids
- dermal accumulations of cholesterol and triglucerides
- associated with primary and secondary hyperlipidema or dyslipidemia
- LDL receptor abnormality is most common cause
Normal variant cardiac anomaly in adult patients?
Patent foramen ovale (present in 20 - 30% adults
- remains functionally closed, but in situations of increased right atrial pressure may cause right atrial shunt