Translational Physiology Block 3 Flashcards Preview

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Flashcards in Translational Physiology Block 3 Deck (64):
1

What are heart murmurs and arterial bruits?

Normal blood flow across normal heart valves is silent; murmurs are heard with turbulent flow (Reynold's number above 3000; increases in vessel diameter, pressure (velocity) and decreases in viscosity); grade I murmurs are barely audible (grade 6: loudest); with atherosclerosis (narrows vessel lumen and increases velocity) in arteries, an arterial murmur (bruit) is audible

2

Why is thallium scanning a good tool for assessing coronary blood flow?

in areas supplied by stenotic coronary vessels, the uptake is slower, and appear as defects on a thallium scan. Thallium scans are used to detect coronary artery disease during exercise stress tests (SPECT)

3

Describe the acute-phase response. What does enhanced erythrocyte sedimentation rate illustrate?

During the course of several hours, in response to inflammatory cytokines, the liver rapidly synthesizes and secretes into the circulatory system a number of proteins that aid in the host response to the threat (fibrinogen causes RBCs to cluster and effectively increases the density of RBCs); ESR is widely used by clinicians to assess the presence and severity of inflammation

4

What causes interstitial edema?

lack of muscle contraction during orthostasis; pulmonary hypertension or left-sided heart failure (pulmonary edema decreases lung compliance and compromises gas-exchange at the lung); right-sided heart failure (blood backs up in veins and increases capillary pressure; ascites in the liver); in proteinurea plasma colloid osmotic pressure decreases reducing the amount of reabsoprtion in the venular portion of the capillary (also seen in pregnancy when maternal plasma protein levels fall or with malnutrition); inflammation (histamine); reperfusion of ischemic tissue (with increased hydraulic conductivity and decreased reflection coefficient for plasma proteins) leads to edema; impairment of lymphatic drainage by either removal or lymph nodes or presence of a lymphatic neoplasm

5

What are the two vagal maneuvers?

valsalva: grunting (forced expiration against a closed airway) while lifting a heavy object raises the intrathoracic pressure. Opening of the airway allows intrathoracic pressure to fall; the increased transmural pressure stretches the aortic arch baroreceptors triggering bradycardia (or decreased heart rate); Digitalis compounds can be used to treat supraventricular tachycardias (atrial) because these drugs may increase vagal tone and decrease sympathetic tone (slowing conduction velocity at the AV node) (In patients with congestive heart failure increases myocardial contractility)

6

Describe the progression of early phase of myocardial infarction to late phase.

if blood flow is not restored in due time, ischemic tissue will become necrotic; The first electrical change associated with an acute myocardial infarction is peaking of the T waves, followed soon after by T-wave inversion (reversible if blood flow is restored); The next change, more characteristic of an acute myocardial infarction, is elevation of the ST segment. With irreversible cell death, the ECG typically shows the evolution of deep Q waves

7

What is the direction of the QRS complex vector in myocardial infarction?

Because action potentials cannot propagate into the infarcted area, the net vector of the remaining areas of ventricular depolarization points away from the infarcted area (reflected by a "deep" negative deflection on the ECG)

8

Describe atrial fibrillation.

loss of atrial contraction due to chaotic electrical activity

9

What are co-morbidities associated with atrial fibrillation?

atrial thrombosis and cerebral embolus (stroke)

10

What conditions compromise the myocardium (ventricles?)

ischemic heart disease (MI); prolonged hypertension (hypertrophy); mitral stenosis

11

Is atrial contraction important for patients with reduced ventricular function?

Yes; the loss of the atrial contraction may further reduce cardiac output just enough to send the patient into florid congestive heart failure or even shock (i.e., arterial pressure so low that it compromises perfusion of peripheral tissues (also crucial for patients with aortic stenosis and tachycardia)

12

How does blood flow during diastole? where it this phenomenon most apparent?

This sizeable diastolic component is largely the result of the high compliance of the vessel walls and the radial expansion of the vessels that occurs during ventricular ejection (Windkessel model); aorta and nearby arteries (carotid artery and renal artery)

13

Why does the myocardium hypertrophy?

Because cells of the adult heart are terminally differentiated, stimuli that might be mitogenic in other cells cannot elicit cell division in the heart but rather cause the cardiac myocytes to hypertrophy and increase muscle mass (muscles increase in width and length) (result of volume or pressure overload)

14

Describe how volume overload results in ventricular hypertrophy. pressure overload?

Volume overload leads to eccentric hypertrophy characterized by increases of myocyte length out of proportion to width; Pressure overload causes concentric hypertrophy with a relatively greater increase in myocyte width

15

What are mechanism of ventricular hypertrophy?

pathway: MAPK (zinc finger transcription factor GATA4; SRF; Sp1; TEF-1 family); catecholamines and angiotensin II activate MAPK; elevated intracellular calcium activates GATA4); alternate or additional branch: MLP and AP-1

16

What are features of ventricular hypertrophy?

Reduced levels of the mRNA encoding three critical proteins in the membrane of the SR: (1) the Ca 2+ release channel, (2) phospholamban, and (3) the SR Ca 2+ pump (SERCA2); Lower contractility/cross-sectional area

17

What are features of heart failure?

People whose hearts cannot sustain an adequate cardiac output become breathless (because blood backs up from the left side of the heart into the lungs) and have swollen feet and ankles (because blood backs up from the right side of the heart and promotes net filtration in systemic capillaries).

18

What cellular mechanism has been associated with heart failure?

In an animal model of hypertension-induced cardiac hypertrophy that leads to heart failure, the Cav1.2 channels exhibit an impaired ability to activate RYR2 through Ca 2+ -induced Ca 2+ release (depletion of calstabin 2 results in leaky RYR2 receptors and delayed afterdepolarizations and ventricular arrhythmias)

19

Does primary hypertension have a known cause?

No

20

What can cause secondary hypertension?

renal artery stenosis; tumor of adrenals

21

What must be ruled out when making a diagnosis of coronary artery disease? What is the crucial exam?

Physicians rule out gastroesophoageal reflux, hyperventilation, and costochondritis by ordering a stress test (with thallium scan)

22

What is the first sign of coronary artery disease?

For many patients with gradual narrowing of their coronal arteries by atherosclerotic plaque, the first sign of disease may be development of angina pectoris. Pain results when the metabolic demands of a region of myocardium exceed the ability of the compromised blood supply to satisfy those needs (when stressed)

23

What are therapies for coronary artery disease (angina)?

Nitrates induce vasodilation by releasing nitric oxide. The nitrates dilate peripheral veins, reducing venous return and thus preload to the heart; also dilate arteries and arterioles reducing blood pressure and afterload; finally, nitrates may increase coronary collateral flow to the involved region of myocardium; Beta blockers prevent the sympathetic nervous system from stimulating myocardial beta1 receptors, thereby reducing both heart rate and contractility and thus metabolic demand; Calcium channel blockers lessen the contractility of the heart muscle and vascular smooth muscle (reduce metabolic demands of the heart)

24

Does therapy change for patients with increasing frequency and severity of anginal attacks (when stressed)?

Yes; mechanical revascularization may be required (surgery or angioplasty)

25

Describe angioplasty. How is a stent different

physician advances a balloon-tipped catheter through a peripheral artery into the left ventricle and then loops the catheter back out the left ventricle to have a favorable angle for entering coronary vessels from the aorta. Inflation of the balloon at the site of obstruction flatten the plaque into the wall of the vessel and restores blood flow; a metal cage is retained.

26

What is the mechanism for recurrence of coronary obstruction following angioplasty? How is this treated or prevented?

may be due to proliferation of vascular smooth muscle cells; use of aggressive anticoagulation and cell cycle inhibitors

27

What is cirrhosis? What are complications associated with cirrhosis?

scarring of the liver; albumin, fibrinogen, and cholesterol levels fall; increased venous pressure increases capillary pressure and incidence of ascites (blood may be shuttled to other abdominal regions and dilation of those vessels can cause internal, life-threatening bleeding; since liver detoxifies, shuttling blood away from liver exposes bloodstream to toxins; may need shunting for therapy)

28

What is sepsis?

Sepsis occurs when chemicals released into the bloodstream to fight the infection trigger inflammatory responses throughout the body.

29

What are the criteria for diagnosis of essential hypertension?

Three readings over 140/90 over the course of several weeks

30

What are secondary causes of hypertension, how they are diagnosed, and what are the treatment options?

Pheochromocytoma, renovascular hypertension, various adrenocortical tumors, sleep apnea, Cushing’s disease, hyperthyroidism, excessive alcohol consumption, excess dietary salt, medications including oral contraceptives and over-the-counter decongestants or diet aids.

31

What are the nonpharmacologic treatments for hypertension? How effective are they?

Weight loss, low salt diet, reduced alcohol intake, exercise, relaxation therapy. Usually limited effectiveness except in mild or borderline hypertension, but important as adjuncts to pharmacotherapy. Alcohol reduction. Profitable to give nonpharmacologic therapy a trial during the initial observation period.

32

What pharmocologic therapies should be pursued after failure of nonpharmacologic intervention in treating hypertension (first regimen)?

start with a diuretic because of proven mortality and morbidity benefit and because if a second drug had to be added, then a diuretic can be added with almost any other agent. Thiazide diuretics lower blood pressure by reducing blood volume through an inhibition of Na+-Cl- cotransport in the distal convoluted tubule, thus reducing cardiac output, volume and vascular resistance. Disadvantages of thiazide diuretics are hypokalemia, hypercalcemia, hyperuricemia, reduced glucose tolerance, and adverse effects on blood lipids.

33

What is a good option for a second regimen for treating hypertension?

increasing the dose of thiazide, but this could increase the risk of adverse effects. A good choice would be to add a second drug, such as a B-adrenergic antagonist or an angiotensin converting enzyme inhibitor (ACEI) such as captopril or enalapril. This combination works synergistically, because thiazides (and also vasodilating drugs) cause a reflex activation of the sympathetic nervous system and increases in renin, both of which tend to limit the effectiveness of thiazides. B-Blockers prevent some of the effects of catecholamines and also lower renin levels by blocking B-adrenergic receptors in the kidney juxtaglomerular apparatus. Of the B-blockers, those that have selectivity for B1-adrenergic receptors may have advantages in terms of exercise tolerance and avoidance of bronchoconstriction; other options alpha 1 antagonist of calcium channel blocker

34

What classes of antihypertensive agents can be combined advantageously?

All classes combine advantageously with diuretics.

35

How does comorbidity of hypertension with diabetes affect prognosis? What are the possible pathophysiological mechanisms for this interaction?

Diabetes significantly worsens the prognosis for hypertension. Diabetes and hypertension affect some of the same target organs, but through different pathways, resulting in synergistic pathological effects in coronary arteries, the kidneys, and the retinal blood vessels.

36

Why are thiazide diuretics not suggested for treating patients with both diabetes and hypertension?

impair glucose tolerance

37

How does on treat patients (acutely) with papilledema or a blown pupil?

Blood pressure must be lowered immediately but in gradual fashion over a few hours (IV; labetalol is a combined alpha and beta blocker)

38

Describe progression to atherosclerosis.

atheroma, fibrous plaque, rupture of plaque leads to thrombus and myocardial infarct

39

What is flow-mediated brachial artery dilation and what is the significance of the test?

occlusion of the artery (or nitroglycerin) to test hyperemic blood flow; A flow mediated brachial artery dilation (FMD) lower than the mean for the individuals sex increases an individual’s risk for;

40

Describe fractional flow reserve.

It is not resting flow, but maximum achievable flow which determines the functional capacity (exercise tolerance) of a patient; FFR = ratio of hypermic flow in the stenotic vessel to hyperemic flow in the same vessel but in the absence of the stenosis (below 0.8 suggests the need for stenting

41

What are the most invasive cardiac imaging technologies?

OCT (optical coherence tomography) and intravascular ultrasound (IVUS)

42

What are the clinical hallmarks of heart failure?

elevated cardiac filling pressures and inadequate peripheral oxygen delivery

43

What is systolic heart failure? diastolic?

reduced ejection fraction; decreased compliance (little change in volume to large cardiac filling pressures)

44

What increases afterload?

aortic stenosis and hypertension

45

what impairs ventricular relaxation (left)?

Left ventricular hypertrophy, hypertrophic and restrictive cardiomyopathy, and myocardial ischemia (diastolic pathology)

46

what are obstructions of left ventricle filling?

Mitral stenosis and pericardial constriction or tamponade (diastolic pathology

47

What is the pathogenesis of congestive heart failure?

neurohormonal activation (renin-angiotensin, catecholamines, vasopressin)

48

What is the role of angiotensin II in heart failure?

vessel remodeling, increased aldosternone, vasopressin, and endothelin, platelet aggregation (thrombosis)

49

What is the determinant of oxygen demand in the heart?

heart rate

50

Describe angina.

squeezing, tightness, burning associated with nausea and vomiting + referred pain (liver and shoulder?)

51

What are blood tests for MI? Why are they not the best diagnostic tool?

creatine kinase and troponin (peak hours after onset)

52

What increases oxygen demand of the myocardium?

heart rate, wall tension, and contractility

53

What is cardiovascular shock?

tachycardia, decreased MAP (low systolic pressure and pulse pressure)

54

What are remnants of perturbations that arise following MI?

fibrous scarring (decreased compliance); myocardial remodeling; arrythmias (from re-entry loops and after-depolarizations)

55

Who are candidates for implantable defibrillators?

Patients with history of MI and ejection fractions below 35%

56

Which side of the heart fails first in heart failure?

left

57

For patients with right ventricular ischemia, what drugs are not suggested?

anything that reduces venous return (nitroglycerins and diuretics)

58

What is the S3 sound? S4?

rapid filling (congestive heart failure); atrial contraction with a decreased ventricular compliance

59

How is carotid ultrasound used in cardiology?

used for visualizing plaques and for measuring intima-media thickness

60

Describe the two types of plaques.

Stable: cholesterol plaque with a hard dense core; fibrous cap of smooth muscle (px has no symptoms at rest but is symptomatic when stressed); Unstable: no fibrous lip cap; inflammation; ruptures expose lip core, which activates platelets resulting in a thrombus that occludes the artery (px has symptom at rest)

61

What can cause ischemia?

occlusion, anemia, vasospasms, compression by tissue

62

What is PAD?

the presence of stenosis or occlusion in arteries of the peripheral limbs (lower extremity); Patient presentation: may be asymptomatic, intermittent claudication (discomfort, ache, cramping when stressed; stable at rest), functional impairment, pain at rest, ischemic ulceration (gangrene?); ankle-branchial index below .9

63

What are therapies for PAD?

Therapies: prevent heart failure (anti-platelets, statins, and ACE inhibitors); reduction of symptoms or limb preservation (angioplasty or surgery; limb may need to be amputated)

64

What are indicators for intervention for PAD?

intermittent claudication that is disabling and lifestyle limiting or critical limb ischemia, characterized by ischemia, rest pain, and/or refractory infection, poor pedal pulse