module 6 cardiovascular

Question 1

1. What is hypertension? How many times it needs to be elevated to count?
2. What is systolic and diastolic?
3. Hypertension is 95% of the time ………….. . What does that mean? The rest of the time it is ………… .
4. What are the 4 things we look for in secondary hypertension?

Answer 1

1. consistent arterial pressure of >130mmHg systolic over >80mmHg diastolic. 3 times
2. systolic is ejection (top number). Diastolic is filling (bottom number).
3. primary (idiopathic aka essential). It is of unknown cause. Secondary (something specific causing the blood pressure to be high. When issue is addressed the blood pressure lowers).
4. Renal, endocrine, cardiovascular, or neurological.

Question 2

1. Name the possible causes of primary hypertension (9):
2. What is RAAS job? How does it contribute to hypertension?
3. Name the female hormone that causes vasodilation. What is the significance of this?
4. How do problems with naturietic peptide contribute to hypertension?
5. What does sodium do to contribute to high blood pressure?
6. Why does inflammation contribute to hypertension?
7. Why does obesity contribute to hypertension, and what goes hand in hand with obesity?
8. smoking?

Answer 2

1. genetics (big risk), age, male, sodium, inflammation, obesity, insulin resistant, smoking, stress, naturietic peptide abnormalities
2. To raise blood pressure in response to low blood volume. If triggered in a pathogenic way causes too much blood volume.
3. Estrogen. Why women have less hypertension that men … at least until menopause.
4. naturietic peptide eliminates Na from blood. So if dysfunctional won’t counteract RAAS
5. Draws water towards it. Makes you drink more. More water = more volume = Higher BP
6. causes change in vessel structure (starting point for atherosclerosis).
7. Adipokines from adipose tissue cause insulin resistance linking with diabetes. Diabetes = hyperglycemia = epithelial damage= Reactive O2 species = inflammation = angiotensin 2 = vasoconstriction and triggers thirst = more fluid volume = hypertension
8. causes endothelial damage = inflammation etc….

Question 3

1. Does hypertension have symptoms?
2. What are treatments?
3. Name some hypertension drug categories/mechanisms:
4. Name 5 complications resulting from hypertension:
5. Describe malignant hypertension:

Answer 3

1. no
2. Low-sodium diet. Exercise. weight loss. medications (diuretics beta blockers etc.)
3. • Diuretics = lower blood volume (first choice)
     - ACE1 inhibitors (“pril” drugs) block angiotensin (vasodilation)
     - ARB2 inhibitors block angiotensin 2 receptor (vasodilation)
     - combo drugs that combine any of the above.
4. Stroke, kidney failure, Coronary artery disease/MI, Aortic aneurysm, and malignant hypertension
5. rapidly progressing hypertension w/ systolic >180 diastolic >120. Life threatening. Organ failure

Question 4

1. what is arteriole sclerosis?
2. What is atherosclerosis?
3. What is an atheroma?
4. Atherosclerosis has both modifiable and nonmodifiable risk factors. Name a few of each:
5. Go thru the chain of events in atherosclerosis genesis:

Answer 4

1. Damage to blood vessel. Narrowed lumen from stiffening or vessels
2. Arteriole sclerosis with presence of atheroma in large arteries.
3. Accumulation of cellular debris, lipids, calcium etc in walls of arteries.
4. Modifiable: smoking, diabetes, hyperlipidemia, inflammation.
   Nonmodifiable: genetics, sex, age
5. Chronic endothelial inflammation/injury = platelet recruitment and lipid leak = Macrophage eats lipid droplets becoming “foamy” = grouped together makes “Fatty streak” that releases cytokines = smooth muscle and fiberous connective tissue = Capsule formation = either stable, or not = can break loose and be a thrombus. Or can grow, invading lumen or vessel.

Question 5

1. What is coronary artery disease (CAD)? What is most common cause?
2. What is statin? Lowers LDL, VLDLs etc.
3. Name the nontraditional risk factors to coronary artery disease:

Answer 5

1. Any vascular disorder that narrows or occludes the coronary arteries leading to myocardial ischemia or myocardial infarct
   • Atherosclerosis is the most common cause
2. A class of drugs to treat CAD
3. • Markers of inflammation and thrombosis • Adipokines (doesn’t need to be obese)
   • Kidney disease
   • Air pollution and ionizing radiation
   • Medications
   • Microbiome (hpylori, chlamydia) - affect on lipid metabolism increasing atherosclerosis.

Question 6

1. What are symptoms of transient myocardial ischemia?
2. What are the 3 types of angina, why do they happen, and which 2 are involved with CAD?
3. Is unstable angina reversible? What will it lead to if not corrected?
4. How to treat stable angina?
5. How to treat emergency angina:
6. How do we establish that we’ve progressed from stable to unstable angina?

Answer 6

1. angina caused by temporary blood deprivation. Can be silent ischemia
2. variant (prinzmetal) angina due to vasospasm from autoimmune, Classic (aka stable or exertional) angina, and Unstable angina pain at rest.
3. Yes, but can easily become MI.
4. Prevent progression by eliminating modifiable risk factors. Nitroglycerin (vasodilator, but patient can build resistance).
5. rest/stop activity. Seat patient upright. nitroglycerine. check pulse/respiration. Give O2. 911.
6. longer than 20 min episodes, frequency and duration increases, and lower threshold of activity.

Question 7

1. What are the symptoms of MI?
2. If patient presents w/ MI symptoms, what do we do next (in the hospital)
3. What protein is present in blood serum in the case of MI?
4. What is treatment for MI?
5. What are complications of MI?

Answer 7

1. intense pain 30-60m, radiating to neck/jaw/shoulder/left arm. Epigastric pain. Nausea, vomiting, levine sign, diaphoresis, dyspnea, fatigue, malaise
2. ECG, serum enzyme and isoenzyme levels (Troponin or CK-MB), complete blood count and metabolic panel, lipid profile
3. troponin
4. First: beta blocker, O2, morphine, aspirin. After stable, may treat other associated issues (use of thrombolytics etc).

5. Sudden death
• Cardiogenic shock
• Congestive heart failure
• Rupture of necrotic heart tissue/cardiac tamponade (fluid in pericardial sac compressing heart).
• stroke

Question 8

1. What is heart failure?
2. Which side of heart most commonly fails? Why?
3. What is the difference between systolic and diastolic failure?
4. How does MI lead to heart failure?

Answer 8

1. when heart can’t pump effectively to meet body’s demand.
2. L. It pumps against greater pressure then the R side.
3. Systolic can’t eject blood out of heart (thin, weak heart muscle). Diastolic can’t fill the heart sufficiently so it lessens the ability to eject (thick, stiff heart muscle).
4. Causes dead tissues that can’t pump (systolic failure), nor stretch to fill (diastolic failure). Decreased contractility.

Question 9

1. What is congestive heart failure?
2. Do CHF patients show pulmonary symptoms? Why or why not?
3. What causes the blood pooling around the heart in L heart failure?
4. What are manifestations of CHF?

Answer 9

1. L heart failure when ventricular ejection is down.
2. The blood pooling associated w/ L heart failure backs blood up into pulmonary circuit causing pulmonary edema.
3. 4. Contractility is down, kidneys trigger RAAS to get BP up which increases afterload. Heart can’t eject sufficiently, so blood pools
4. Pulmonary issues like wheezing, dyspnea, frothy sputum (pink), fatigue, decreased urine, edema and pulmonary edema, cyanosis, tachycardia

Question 10

1. What is most common cause of R heart failure?
2. What are symptoms of R heart failure?
3. What type of diseases would cause R heart failure (aside from L heart failure)?

Answer 10

1. L heart failure putting too much pressure on R heart.,
2. less obvious systemic symptoms like liver/spleen enlargement, edema in feet, ascites (abdominal swelling)
3. Pulmonary diseases: Cystic fibrosis, Parenchyma, pulmonary hypertension

Question 11

1. What is high output heart failure?

2. What causes it?

Answer 11

1. inability of the heart to supply the body despite adequate blood volume and normal contractility. Basically it is working too hard for a reason not attributed to itself
2. Causes include anemia, hyperthyroidism, septicemia, and beriberi (vitamin B1 deficiency)

Question 12

1. What is Rheumatic fever?
2. What is Rheumatic heart disease, and what damage does it commonly cause?
3. How does rheumatic fever cause rheumatic heart disease?
4. How does rheumatic heart disease lead to infectious endocarditis?

Answer 12

1. the precursor to rheumatic heart disease. Delayed response to group A (beta-hemolytic) strep causes inflammation to heart.
2. Heart valves become permanently damaged by rheumatic fever. Most common cause for mitral valve stenosis
3. Body’s immune system attacks it’s own heart valves because their proteins are so similar to the “M” proteins released from rupturing streptococci capsules. Leads to inflammation of the heart tissues.
4. Inflammation of the hearts tissues slows blood flow and promotes microorganism infection. Most common are staph aureus and strep viridans

Question 13

1. What is endocarditis or myocarditis or pericarditis?
2. What is the diff between acute and sub-acute?
3. What are the visible characteristics of infective endocarditis?
4. How do bacteria that cause infective endocarditis enter the bllod stream?
5. Name a few key characteristic symptoms of infective endocarditis:

Answer 13

1. inflammation of the endocardium/myocardium/pericardium of heart. Can be acute or sub-acute.
2. acute: staph aureus
   sub-acute: strep viridans
3. Large, soft, friable, easily
   detached vegetations consisting of intermeshed bacteria and inflammatory cells. (look like cauliflower)
4. dental or surgical procedures, wounds, injections, catheters etc.
5. osler nodes (painful nodules on fingers and toes), janway lesions (lesions on palms and soles). There are other classic symptoms too (fever, etc).

Question 14

1. What happens in shock?
2. What are the main physical manifestations of shock?
3. Name the 5 types of shock and what causes them:

Answer 14

1. inadequate tissue perfusion, leads to impaired metabolism (impaired O2 use, impaired glucose use).
2. hypotension, tachycardia, fast breathing, weak, hot or cold, nauseated, dizzy, thirsty, confused.
3. Hypovolemic Shock: (bleeding out)
   Cardiogenic Shock: (decreased cardiac output) Vasogenic Shock: (loss of sympathetic tone) Anaphylactic Shock: (allergic reaction)
   Septic Shock: (infection)