ADVANCED PATHOPHYSIOLOGY UTMB 5355
EXAM 4 2026 KEY DISEASE PROCESSES AND
MECHANISMS REVIEW A+
◉ Prinzmetal Angina. Answer: Chest pain that may occur at REST,
typically at NIGHT, usually caused by VASOSPASM, may or may not
be associated with atherosclerosis.
◉ Acute Coronary Syndrome. Answer: Broad term which
emcompasses three diagnoses:
Unstable angina, Non ST Elevation Myocardial Infarction, ST
elevation infarction
◉ Unstable Angina. Answer: -Chest pain that is PROLONGED or
RECURRENT at REST, or chest pain that is INCREASING in SEVERITY
or FREQUENCY
-Caused by a labile (unstable) thrombus that is does NOT occlude
blood flow for any longer than 20 minutes
-PERFUSION IS RESTORED BEFORE MYOCARDIAL NECROSIS
OCCURS
-Can progress to a heart attack
,◉ Non ST Elevation Myocardial Infarction (NSTEMI). Answer: -
Myocardial infarction resulting from a thrombus that has occluded
coronary artery flow for MORE THAN 20 MINUTES
-Results in myocardial necrosis in the myocardium directly below
the endocardium (innermost layer of ventricles farthest from blood
supplied by coronary arteries, which lie on outside of heart)
-Does NOT involve full thickness of the ventricular wall
-Also called subendocardial infarct
-EKG: ST depression (hence the name NON ST elevation), or T wave
inversion
◉ ST Elevation Myocardial Infarction
(ST elevation = Serious Trouble). Answer: -Myocardial infarction
resulting from THROMBUS PERMANENTLY LODGING IN VESSEL
-Includes ENTIRE THICKNESS of VENTRICULAR WALL
(TRANSMURAL INFARCT)
-ST elevation on EKG
◉ Myocardial Infarction Patho. Answer: 1. After 10 seconds of
occluded blood flow, myoctyes become cyanotic.
2. Oxygen reserves are used up.
3. Glycogen (storage unit for glucose) decreases.
,4. Glycolysis (breakdown of glucose by enzymes, releasing energy) is
not able to supply all the needed energy to the heart, leading to less
ATP production.
5. Hydrogen ions & lactic acid accumulate from the anaerobic
metabolism (anaerobic metabolism is the creation of energy through
the combustion of carbohydrates in the absence of oxygen).
6. Myocardial cells deprived of nutrients lose contractility and result
in a diminished contraction.
7. Ischemic cells release catecholamines (fight/flight hormones),
further stressing the heart & increasing risk for arrythmias & heart
failure.
***8. Norepinehrine (a catecholamine) decreases insulin secretion
and hyperglycemia occurs (body tries to get more sugar in blood to
fuel heart). This can be seen by 72 hours post MI and is associated
with increased mortality.***
9. Angiotensin II is released causing vasoconstriction, thereby
increasing afterload (contraction) and myocardial work load.
◉ How long can cardiac cells remain viable in a severely hypoxic
(heart attack) state?. Answer: 20 minutes.
After 20 minutes, coagulative necrosis occurs.
◉ Reperfusion Injury. Answer: -Caused when blood flow is restored
, -Triggers release of TOXIC OXYGEN RADICALS from when myocytes
were deprived of oxygen, CALCIUM INFLUX, and PH CHANGES (this
causes persistently open mitochondrial permeability and
contributes to cell death)
◉ Troponins. Answer: -Detected in 2-4 hours of onset of pain
-Peak in 24 hours
-Disappear in 7-10 days
◉ Complications of MI. Answer: -Cardiac dysrhythmias: PVCS are
most common. Most common cause of death is V-Fib and is
associated with cardiogenic shock.
- Left ventricular failure and pulmonary edema: Usually occurs
within first 24 hours.
-Cardiogenic Shock: Results from a large infarct. High mortality.
Associated with V-Fib.
- Ventricular free wall rupture: Occurs in 4-7 days. Associated with
thrombosis of the LAD (left anterior descending) coronary artery.
Results in cardiac tamponade from hemorrhage into the pericardial
space. Cardiac tamponade is compression of the heart due to fluid
collecting in the sac surrounding the heart.
EXAM 4 2026 KEY DISEASE PROCESSES AND
MECHANISMS REVIEW A+
◉ Prinzmetal Angina. Answer: Chest pain that may occur at REST,
typically at NIGHT, usually caused by VASOSPASM, may or may not
be associated with atherosclerosis.
◉ Acute Coronary Syndrome. Answer: Broad term which
emcompasses three diagnoses:
Unstable angina, Non ST Elevation Myocardial Infarction, ST
elevation infarction
◉ Unstable Angina. Answer: -Chest pain that is PROLONGED or
RECURRENT at REST, or chest pain that is INCREASING in SEVERITY
or FREQUENCY
-Caused by a labile (unstable) thrombus that is does NOT occlude
blood flow for any longer than 20 minutes
-PERFUSION IS RESTORED BEFORE MYOCARDIAL NECROSIS
OCCURS
-Can progress to a heart attack
,◉ Non ST Elevation Myocardial Infarction (NSTEMI). Answer: -
Myocardial infarction resulting from a thrombus that has occluded
coronary artery flow for MORE THAN 20 MINUTES
-Results in myocardial necrosis in the myocardium directly below
the endocardium (innermost layer of ventricles farthest from blood
supplied by coronary arteries, which lie on outside of heart)
-Does NOT involve full thickness of the ventricular wall
-Also called subendocardial infarct
-EKG: ST depression (hence the name NON ST elevation), or T wave
inversion
◉ ST Elevation Myocardial Infarction
(ST elevation = Serious Trouble). Answer: -Myocardial infarction
resulting from THROMBUS PERMANENTLY LODGING IN VESSEL
-Includes ENTIRE THICKNESS of VENTRICULAR WALL
(TRANSMURAL INFARCT)
-ST elevation on EKG
◉ Myocardial Infarction Patho. Answer: 1. After 10 seconds of
occluded blood flow, myoctyes become cyanotic.
2. Oxygen reserves are used up.
3. Glycogen (storage unit for glucose) decreases.
,4. Glycolysis (breakdown of glucose by enzymes, releasing energy) is
not able to supply all the needed energy to the heart, leading to less
ATP production.
5. Hydrogen ions & lactic acid accumulate from the anaerobic
metabolism (anaerobic metabolism is the creation of energy through
the combustion of carbohydrates in the absence of oxygen).
6. Myocardial cells deprived of nutrients lose contractility and result
in a diminished contraction.
7. Ischemic cells release catecholamines (fight/flight hormones),
further stressing the heart & increasing risk for arrythmias & heart
failure.
***8. Norepinehrine (a catecholamine) decreases insulin secretion
and hyperglycemia occurs (body tries to get more sugar in blood to
fuel heart). This can be seen by 72 hours post MI and is associated
with increased mortality.***
9. Angiotensin II is released causing vasoconstriction, thereby
increasing afterload (contraction) and myocardial work load.
◉ How long can cardiac cells remain viable in a severely hypoxic
(heart attack) state?. Answer: 20 minutes.
After 20 minutes, coagulative necrosis occurs.
◉ Reperfusion Injury. Answer: -Caused when blood flow is restored
, -Triggers release of TOXIC OXYGEN RADICALS from when myocytes
were deprived of oxygen, CALCIUM INFLUX, and PH CHANGES (this
causes persistently open mitochondrial permeability and
contributes to cell death)
◉ Troponins. Answer: -Detected in 2-4 hours of onset of pain
-Peak in 24 hours
-Disappear in 7-10 days
◉ Complications of MI. Answer: -Cardiac dysrhythmias: PVCS are
most common. Most common cause of death is V-Fib and is
associated with cardiogenic shock.
- Left ventricular failure and pulmonary edema: Usually occurs
within first 24 hours.
-Cardiogenic Shock: Results from a large infarct. High mortality.
Associated with V-Fib.
- Ventricular free wall rupture: Occurs in 4-7 days. Associated with
thrombosis of the LAD (left anterior descending) coronary artery.
Results in cardiac tamponade from hemorrhage into the pericardial
space. Cardiac tamponade is compression of the heart due to fluid
collecting in the sac surrounding the heart.
