NSG 530 ADVANCED PATHOPHYSIOLOGY 530
EXAM 1,2,3 WITH VERIFIED QUESTIONS AND
ANSWERS|| GUARANTEED PASS || LATEST
UPDATE 2025
What are the key characteristics of stable angina that set it apart from unstable
angina? - ANSWER--chest discomfort caused by myocardial ischemia =
brought on by exertion (predictable)
-ischemia without necrosis
-relieved by rest and/or NTG
-pathop - imbalance between myocardial requirements/demand and supply -
demand may be elevated when HR increases, LV wall stress
What are key characteristics of unstable angina that set it apart from stable
angina? - ANSWER--patho - atherosclerotic plaque that is prone to rupture
-signals that the atherosclerotic plaque has become a complicated lesion; sign
that MI is imminent
-management requires hospitalization and MONA (morphine, oxygen, NTG,
aspirin)
-unrelieved by rest/NTG
What does MONA stand for? - ANSWER-Morphine
Oxygen
Nitroglycerin
Aspirin
used in unstable Angina
,Factors contributing to risk of death during acute infarction - ANSWER--the
degree of LV dysfunction
-the degree of LV ischemia
-the potential for ventricular dysrhythmais
-the individual's age
Heart disease structure differences for women - ANSWER--smaller size,
increased stiffness (fibrosis, remodeling, etc.)
-more diffuse disease
-more plaque erosion versus rupture
-microemboli, rarefaction (drop out), disarray
Heart disease functional differences for women - ANSWER--endothelial
dysfunction
-smooth muscle dysfunction (raynauds, migraine, coronary artery spasm)
-inflammation: plasma markers and vasculitis (takayasu's, rheumatoid, SLE,
CNSV, giant cell)
Symptomatic differences for women in heart disease - ANSWER-women rate
angina pain as more intense, more often described pain as throbbing, sharp,
hot/burning, fearful, pressing
more often reported pain/discomfort in neck area
Primary (essential; idiopathic) HTN - ANSWER--90-95% of people with HTN,
unknown cause
-results from complicated interaction btwn genetics and the environment that
increases vascular tone (increase peripheral resistance) and blood volume, thus
causing sustained increase in BP
Factors associated with primary HTN - ANSWER-family hx
,advanced age
gender (men <50yo, women>50yo)
AA race
high dietary Na intake
glucose intolerance
sedinatry lifestyle
tobacco use
poor diet
secondary HTN - ANSWER-50-10% caused by underlying disease process that
raises peripheral vascular resistance or CO
-renal parenchymal disease, renovascular disease, primary aldosteronism,
obstructive sleep apnea, drug or alcohol induced
Isolated Systolic HTN - ANSWER-can be due to age-related aortic stiffening
Class I angina - ANSWER-new onset - severe or accelerated angina
class II angina - ANSWER-angina at rest, subacute (angina at rest within the
preceding month but not within the preceding 48 hours
class III angina - ANSWER-angina at rest, acute (angina at rest within the
preceding 48 hours)
What are the common complications of myocardial infarction? - ANSWER-
dysrhythmias
LV failure
RV infarction
Cardiogenic shock
, Papillary muscle rupture
Pericarditis
LV Aneurysm
dysrhythmias in relation to MI - ANSWER--disturbances of cardiac rhythm
-most common complication of MI
-caused by ischemia, hypoxia, ANS imbalances, lactic acidosis, electrolyte
abnormalities, alterations of impulse conduction pathways or conduction
defects, drug toxicity, hemodynamic abnormalities
-originate from atria, ventricles, nodal regions, or conduction tissues
What does a wide QRS indicate? - ANSWER-taking longer for the ventricles to
contract and they are probably not contracting in synchrony
increased risk for mortality even if they have a normal HR
ventricular remodeling - ANSWER-results in disruption of the normal
myocardial extracellular structure with resultant dilation of the myocardium and
causes progressive myocyte contractile dysfunction over time
cellular changes associated with ventricular remodeling - ANSWER--
hypertrophy (abnormal myocyte growth)
-intrinsic myocyte dysfunction
-alteractions in gene expression (proteins)
-cell loss
-extracellular matrix remodeling
-Ca handling (within the myocyte)
-mitochondrial dysfunction (the heart has a lot of mitochondria because a lot of
processes are ATP dependent)
hypertophied heart - ANSWER-diastolic heart failure (filling)
EXAM 1,2,3 WITH VERIFIED QUESTIONS AND
ANSWERS|| GUARANTEED PASS || LATEST
UPDATE 2025
What are the key characteristics of stable angina that set it apart from unstable
angina? - ANSWER--chest discomfort caused by myocardial ischemia =
brought on by exertion (predictable)
-ischemia without necrosis
-relieved by rest and/or NTG
-pathop - imbalance between myocardial requirements/demand and supply -
demand may be elevated when HR increases, LV wall stress
What are key characteristics of unstable angina that set it apart from stable
angina? - ANSWER--patho - atherosclerotic plaque that is prone to rupture
-signals that the atherosclerotic plaque has become a complicated lesion; sign
that MI is imminent
-management requires hospitalization and MONA (morphine, oxygen, NTG,
aspirin)
-unrelieved by rest/NTG
What does MONA stand for? - ANSWER-Morphine
Oxygen
Nitroglycerin
Aspirin
used in unstable Angina
,Factors contributing to risk of death during acute infarction - ANSWER--the
degree of LV dysfunction
-the degree of LV ischemia
-the potential for ventricular dysrhythmais
-the individual's age
Heart disease structure differences for women - ANSWER--smaller size,
increased stiffness (fibrosis, remodeling, etc.)
-more diffuse disease
-more plaque erosion versus rupture
-microemboli, rarefaction (drop out), disarray
Heart disease functional differences for women - ANSWER--endothelial
dysfunction
-smooth muscle dysfunction (raynauds, migraine, coronary artery spasm)
-inflammation: plasma markers and vasculitis (takayasu's, rheumatoid, SLE,
CNSV, giant cell)
Symptomatic differences for women in heart disease - ANSWER-women rate
angina pain as more intense, more often described pain as throbbing, sharp,
hot/burning, fearful, pressing
more often reported pain/discomfort in neck area
Primary (essential; idiopathic) HTN - ANSWER--90-95% of people with HTN,
unknown cause
-results from complicated interaction btwn genetics and the environment that
increases vascular tone (increase peripheral resistance) and blood volume, thus
causing sustained increase in BP
Factors associated with primary HTN - ANSWER-family hx
,advanced age
gender (men <50yo, women>50yo)
AA race
high dietary Na intake
glucose intolerance
sedinatry lifestyle
tobacco use
poor diet
secondary HTN - ANSWER-50-10% caused by underlying disease process that
raises peripheral vascular resistance or CO
-renal parenchymal disease, renovascular disease, primary aldosteronism,
obstructive sleep apnea, drug or alcohol induced
Isolated Systolic HTN - ANSWER-can be due to age-related aortic stiffening
Class I angina - ANSWER-new onset - severe or accelerated angina
class II angina - ANSWER-angina at rest, subacute (angina at rest within the
preceding month but not within the preceding 48 hours
class III angina - ANSWER-angina at rest, acute (angina at rest within the
preceding 48 hours)
What are the common complications of myocardial infarction? - ANSWER-
dysrhythmias
LV failure
RV infarction
Cardiogenic shock
, Papillary muscle rupture
Pericarditis
LV Aneurysm
dysrhythmias in relation to MI - ANSWER--disturbances of cardiac rhythm
-most common complication of MI
-caused by ischemia, hypoxia, ANS imbalances, lactic acidosis, electrolyte
abnormalities, alterations of impulse conduction pathways or conduction
defects, drug toxicity, hemodynamic abnormalities
-originate from atria, ventricles, nodal regions, or conduction tissues
What does a wide QRS indicate? - ANSWER-taking longer for the ventricles to
contract and they are probably not contracting in synchrony
increased risk for mortality even if they have a normal HR
ventricular remodeling - ANSWER-results in disruption of the normal
myocardial extracellular structure with resultant dilation of the myocardium and
causes progressive myocyte contractile dysfunction over time
cellular changes associated with ventricular remodeling - ANSWER--
hypertrophy (abnormal myocyte growth)
-intrinsic myocyte dysfunction
-alteractions in gene expression (proteins)
-cell loss
-extracellular matrix remodeling
-Ca handling (within the myocyte)
-mitochondrial dysfunction (the heart has a lot of mitochondria because a lot of
processes are ATP dependent)
hypertophied heart - ANSWER-diastolic heart failure (filling)
