case study module 5

Question 1

Based on the information provided, what condition is Mr. C experiencing?

Answer 1

Mr. C is experiencing stable angina because he is experiencing episodes of excruciating pain radiating from the substernal area to the left shoulder and neck. His pain is also brought on when he begins to exercise and is only relieved once he rests. Also, once he rests, the pain subsides after roughly 10-15 minutes which supports the diagnosis of stable angina. He also smokes and is slightly obese, which are risk factors when it comes to stable angina. His pain was subsided after he was prescribed nitro-glycerine and normal levels of biomarkers and the ECG is normal

Question 2

what are the risk factors for this condition, as outlined in the case description

Answer 2

Age, obesity, and heavy smoker

Question 3

assuming that Mr. C’s condition is the result of a reduction in oxygen delivery to his heart muscle, describe the steps in the development of a common condition that he probably has that would result in occlusion of his coronary arteries?

Answer 3

Atherosclerosis

Damage = increases endothelial permeability to plasma proteins and lipids

Migration of monocytes into sub-endothelial layers

Monocytes differentiate to macrophages, ingest lipid and transform into lipid filled “foam cells”

Macrophages release ROS and other toxic substances that further damage tissue, as well as growth factors that cause secretion of extracellular matrix and proliferate (elastin, collagen, smooth muscle) that grows over plaque

Deposits often become calcified = plaques

Plaques protrude into vessel lumens, partially blocking blood flow

Question 4

What would be the concern if Mr. C’s condition arises even when he is not exercising? Explain the pathophysiology behind this development. (4)

Answer 4

Unstable angina because there would be pain while resting, not during exercise I.e. biomarkers are still low

Plaque develops a clot and the plaque is unstable and rupture, the clot partially blocks the blood flow

Question 5

identify one sign/symptom noted in the treatment of the above case that shows that this more serious plaques type of coronary disorder is not present in this case. (1)

Answer 5

Nitro-glycerine worked

Question 6

What is the significance of the normal levels of TnI and TnT, CK-MB and myoglobin? (I.e., what are these compounds called as a group?

Answer 6

TnI & TnT myoglobin biomarkers = proteins stored within cells

Increased level of these would indicate cell death

Normal = not an infarction

Angina = pain

STEMI = cell death

Question 7

Among other effects, beta-blockers decrease the force of contraction of the heart. What is the medical term for this characteristic? What hormones are beta blockers counteracting, and therefore what system are beta blockers “blocking”?

Answer 7

Inotropy = block the hormone (epinephrine) which causes the heart to beat faster

Beta blockers make the heart beat slower and less force which lowers blood pressure

Block the nervous system (sympathetic)

Question 8

Name and describe two patterns of damage to the heart that are possibly occurring if Mr. C’s pain was not relieved by nitro-glycerine, and his levels of the compounds in question 6 were seen to be elevated. (3)

Answer 8

Pain does not subside after nitro-glycerine that indicates a thrombi has developed and is partially or fully blocking the vessel which will restrict blood flow to areas “downstream” which would lead to decreased ATP and cell death would occur
STEMI or NONSTEMI

STEMI = damage to whole heart NSTEMI = subendocardial

Question 9

Describe the results of a test that could be done to determine which of these patterns is actually occurring. (1)

Answer 9

ECG test (ST elevation = STEMI)

Question 10

Based on the described symptoms, what is Mr. S. likely experiencing? Support your decision by explaining all pathologic manifestations based on your diagnosis. (5)

Answer 10

Breathing difficulty, legs and feet are swollen

Left and right side heart failure because he’s tired and weak which means there is a lack of blood supply to the body

Peripheral edema (swollen legs and feet) = right side heart failure

Difficulty breathing = left side heart failure

Question 11

His condition has worsened: from difficulties with breathing to peripheral edema. Explain the pathophysiology behind this development, beginning with the likely cause of the breathing difficulties. (5)

Answer 11

Left ventricle begins to fail > blood pressure in left ventricle increases > increased blood pressure in lungs (because blood has difficulty moving to left ventricle) > pulmonary edema = breathing difficulties & more difficult for blood to leave right ventricle to get into lungs (increased pressure in right ventricle) > increased venous pressure in body > peripheral edema

Question 12

What are the risk factors for his present condition?

Answer 12

Age, smoking, myocardial infarction

Question 13

ACE inhibitors act to decrease the body’s production of a certain compound. Name the compound.

Answer 13

Angiotensin I > Angiotensin II

ACE = angiotensin converting enzyme

Question 14

Describe the initial compensatory effects that are caused by the named compound (The named compound is the compound that ACE inhibitors decrease, not the ACE inhibitor).

Answer 14

Angiotensin II increases vasoconstriction in arteries which increases blood pressure and causes the release of aldosterone -> retention of sodium, water follows which increases blood volume

Question 15

Name and define the three terms involved with cardiac output

Answer 15

Preload: volume of blood in the ventricle at the end of diastole

Afterload: resistance to ejection of blood from the left ventricle

Contractility: force of contraction

Question 16

What changes in preload and afterload (i.e., increase? decrease?) will cause the heart to work harder, thus putting more stress on the heart? (2)

Answer 16

Heart would work harder if there was an increase in preload due to the frank starling law which means the stretch of the wall means theres a greater force of contraction

More stress if afterload increases because ventricle will have to work harder to accomplish the goal of ejecting blood into aorta

Question 17

Which of the above factors is most directly related to the Frank-Starling law of the heart? Explain your answer, using the definition of the Frank-Starling law. (5)

Answer 17

increase in stroke volume results in a more forceful contraction during systole

the more blood that is in the ventricles, the stronger the contraction will be (= greater stroke volume).

Preload is most related to frank law

the more stretched the ventricle wall, the greater the force of the contraction (up to a maximum value).

Question 18

Link the two compensatory effects described in 4b with the two terms named in 4d to show why compensation for decreased cardiac output would eventually increase the severity of Mr. S’s problem.

Answer 18

Vasoconstriction & increase in blood volume by angiotensin II

Angiotensin II causes vasoconstriction which leads to increased afterload & causes the release of aldosterone which increases blood volume (uptake more sodium, water follows increases blood volume)

Question 19

Based solely on having suffered a previous myocardial infarction, is Mr. S.’s heart failure most likely systolic or diastolic in nature? Explain your answer using the definitions of systolic and diastolic heart failures.

Answer 19

Systole heart failure

Systole is the inability of the heart to contract because of the infarct – there is scar tissue instead of muscle

Diastolic : decrease in the volume of left ventricle during diastole (prior to contraction)