Patho NSG 533 Exam 3 Questions and
answers 2025
(5) .Non-modifiable .risk .factors .for .CAD .- .ANS✓✓-(1) .Age .
(2) .Gender
(3) .Ethnicity
(4) .Family .history
(5) .Genetic .predisposition
(6) .Traditional .modifiable .risk .factors .for .CAD .- .ANS✓✓-(1) .Dyslipidemia
.(abnormal .serum .lipoproteins)
(2) .HTN .(endothelial .injury .and .myocardial .hypertrophy)
(3) .Cigarette .Smoking .(endothelial .injury .and .oxygen .radicals)
(4) .Diabetes .(endothelial .injury .and .vessel .wall .damage)
(5) .Obesity/Sedentary .Lifestyle .(strongest .link .to .CAD)
(6) .Atherogenic .Diet .(high .in .salt, .fat, .trans .fat, .carbs)
(10) .Novel .risk .factors .for .CAD .- .ANS✓✓-(1) .Markers .of .Inflammation, .ischemia
.and .thrombosis .(c-reactive .protein, .troponin, .fibrinogen)
(2) .Adipokines .(adiponectin, .leptin)
(3) .CKD .(as .GFR .declines, .risk .for .CAD .increases)
(4) .Air .Pollution .and .Ionizing .Radiation
(5) .Medications .(NSAIDS .increase .risk .for .CAD)
(6) .Coronary .Artery .Calcification .and .Carotid .Artery .Wall .Thickness
(7) .Microbiome .(diet/lifestyle)
(8) .Elevated .Fibrinogen .(inflammatory .marker)
(9) .Elevated .LDL .particle .number .(cholesterol .concentration .within .particles)
(10) .Small, .dense .LDLs .(vs. .large .fluffy .lipoprotein)
Lipids .- .ANS✓✓-Refers .to .cholesterol .in .particular. .Required .by .most .cells .for
.manufacture/repair .of .plasma .membranes. .
High .dietary .intake .of .cholesterol .and .fats .results .in .high .levels .of .LDL .in .the
.bloodstream, .which .can .lead .to .Atherosclerosis .and .contribute .to .CAD
Lipoproteins .- .ANS✓✓-Refers .to .lipids, .phospholipids, .cholesterol, .and
.triglycerides .bound .to .carrier .proteins.
- .LDL .(low-density .lipoprotein): .contain .mostly .cholesterol .and .protein.
- .HDL .(high-density .lipoprotein): .mainly .phospholipids .and .protein
- .VLDL .(very-low-density .lipoprotein): .mainly .triglyceride .and .protein
,Atherosclerosis .- .ANS✓✓-- .Progressive, .multifactorial .disease .process .that
.generally .begins .in .childhood; .clinical .manifestations .occur .in .middle .to .late
.adulthood, .that .results .in .the .variable .composition .of .lesions
- .High .dietary .intake .of .cholesterol .and .fats .results .in .high .levels .of .LDL .in .the
.bloodstream. .LDL .oxidation, .migration .into .the .vessel .wall, .and .phagocytosis
.by .macrophages .result .in .fatty .deposits .called .plaques .to .form .on .the .inner
.walls .of .the .arteries
Describe .the .relationship .between .HDL .(high-density .lipoprotein), .LDL .(low-
density .lipoprotein), .VLDL .(very-low-density .lipoprotein), .and .CAD .- .ANS✓✓-
Low .levels .of .HDL .pose .risk .for .CAD. .HDL .is .responsible .for .returning
.excessive .cholesterol .to .the .liver .for .elimination .or .conversion .to .cholesterol-
containing .steroids. .HDL .can .also .remove .excessive .cholesterol .through .the
.arterial .wall. .It .can .protect .LDL .from .oxidation, .preserve .endothelial .function,
.and .promote .anti-inflammatory .and .antithrombotic .effects. .VLDL .pose .risk .for
.CAD, .especially .in .combination .with .other .risk .factors .such .as .diabetes
Total .Cholesterol .risk .levels .for .CAD .(dyslipidemia .criteria) .- .ANS✓✓-<200 .=
.desirable
200-239 .= .borderline
≥240 .= .high
LDL .risk .levels .for .CAD .(dyslipidemia .criteria) .- .ANS✓✓-<100 .= .optimal .
100-129 .= .near .optimal
130-159 .= .borderline
160-189 .= .high
≥190 .= .very .high
HDL .risk .levels .for .CAD .(dyslipidemia .criteria) .- .ANS✓✓-<40 .= .low
≥60 .= .high
Triglyceride .risk .levels .for .CAD .(dyslipidemia .criteria) .- .ANS✓✓-<150 .=
.desirable .
150-199 .= .borderline
200-499 .= .high
≥500 .= .very .high
Atherosclerotic .plaque/lesion .- .ANS✓✓-- .Likely .to .develop .following
.endothelial .injury; .areas .of .increased .shear .wall .stress .are
especially .vulnerable
Fatty .streak .→ .Fibrous-fatty .plaque .→ .Advanced .complicated .lesion
Fatty .streak .(early .damage .to .vessel .wall) .- .ANS✓✓-- .Focal .thickening .of .the
.intima
, - .Increase .in .smooth .muscle .cells .and .extracellular .matrix
- .Smooth .muscle .cells .migrate .and .proliferate .into .the .intima
- .Lipid .deposits .accumulate
- .Macrophages .and .T-lymphocytes .(early .damage .to .vessel .wall)
Fibrous-fatty .plaque .(evolves .from .fatty .streak) .- .ANS✓✓-- .Accumulation .of
.connective .tissue
- .Increased .number .of .smooth .muscle .cells .laden .with .lipids
- .Deeper .extracellular .lipid .pool
- .Results .in .further .endothelial .cell .dysfunction, .necrosis .of .underlying .vessel
.tissue, .and .narrowing .of .the .lumen .as .the .lesion .protrudes .out .from .the .vessel
.wall
Advanced .complicated .lesion .- .ANS✓✓-- .Smooth .muscle .cells, .numerous
.macrophages, .T-cells ., .often .associated .with .lipid .core .and .necrotic .material
- .Covered .by .a .fibrous .cap .(smooth .muscle .cells .surrounded .by .CT .matrix)
- .Thick .cap .- .provides .stability .to .the .lesion
- .Thin, .non-uniform .cap, .macrophage-rich .- .lesion .is .unstable
- .Thrombosis, .hemorrhage, .and/or .calcification
Response .to .Injury .Hypothesis .- .ANS✓✓-(1) .Endothelial .cell .dysfunction
(2) .Macrophage .involvement
(3) .Smooth .Muscle .cell .involvement
(4) .Hyperlipidemia
Describe .the .response-to-injury .hypothesis .for .the .development .of
.atherosclerotic .lesions .- .ANS✓✓-- .Various .sources .or .risk .factors .may .induce
.some .form .of .endothelial .dysfunction/changes .including .alterations .in
.permeability, .adhesive .characteristics, .and .growth-stimulatory .characteristics
- .These .changes/alterations .lead .to .monocyte-endothelial .attachment,
.adherence, .and .transmigration
- .Monocytes .then .enter .the .sub-endothelium, .become .activated .as
.macrophages, .and .be .joined .by .T-cells
- .Macrophages .and .T .lymphocytes .compose .the .first .lesion .of .atherosclerosis .-
.the .fatty .streak
- .Activation .of .these .cells .can .result .in .the .formation .of .molecules .that .attract
.smooth .muscle .cells .to .migrate .and .replicate .within .the .lesion
answers 2025
(5) .Non-modifiable .risk .factors .for .CAD .- .ANS✓✓-(1) .Age .
(2) .Gender
(3) .Ethnicity
(4) .Family .history
(5) .Genetic .predisposition
(6) .Traditional .modifiable .risk .factors .for .CAD .- .ANS✓✓-(1) .Dyslipidemia
.(abnormal .serum .lipoproteins)
(2) .HTN .(endothelial .injury .and .myocardial .hypertrophy)
(3) .Cigarette .Smoking .(endothelial .injury .and .oxygen .radicals)
(4) .Diabetes .(endothelial .injury .and .vessel .wall .damage)
(5) .Obesity/Sedentary .Lifestyle .(strongest .link .to .CAD)
(6) .Atherogenic .Diet .(high .in .salt, .fat, .trans .fat, .carbs)
(10) .Novel .risk .factors .for .CAD .- .ANS✓✓-(1) .Markers .of .Inflammation, .ischemia
.and .thrombosis .(c-reactive .protein, .troponin, .fibrinogen)
(2) .Adipokines .(adiponectin, .leptin)
(3) .CKD .(as .GFR .declines, .risk .for .CAD .increases)
(4) .Air .Pollution .and .Ionizing .Radiation
(5) .Medications .(NSAIDS .increase .risk .for .CAD)
(6) .Coronary .Artery .Calcification .and .Carotid .Artery .Wall .Thickness
(7) .Microbiome .(diet/lifestyle)
(8) .Elevated .Fibrinogen .(inflammatory .marker)
(9) .Elevated .LDL .particle .number .(cholesterol .concentration .within .particles)
(10) .Small, .dense .LDLs .(vs. .large .fluffy .lipoprotein)
Lipids .- .ANS✓✓-Refers .to .cholesterol .in .particular. .Required .by .most .cells .for
.manufacture/repair .of .plasma .membranes. .
High .dietary .intake .of .cholesterol .and .fats .results .in .high .levels .of .LDL .in .the
.bloodstream, .which .can .lead .to .Atherosclerosis .and .contribute .to .CAD
Lipoproteins .- .ANS✓✓-Refers .to .lipids, .phospholipids, .cholesterol, .and
.triglycerides .bound .to .carrier .proteins.
- .LDL .(low-density .lipoprotein): .contain .mostly .cholesterol .and .protein.
- .HDL .(high-density .lipoprotein): .mainly .phospholipids .and .protein
- .VLDL .(very-low-density .lipoprotein): .mainly .triglyceride .and .protein
,Atherosclerosis .- .ANS✓✓-- .Progressive, .multifactorial .disease .process .that
.generally .begins .in .childhood; .clinical .manifestations .occur .in .middle .to .late
.adulthood, .that .results .in .the .variable .composition .of .lesions
- .High .dietary .intake .of .cholesterol .and .fats .results .in .high .levels .of .LDL .in .the
.bloodstream. .LDL .oxidation, .migration .into .the .vessel .wall, .and .phagocytosis
.by .macrophages .result .in .fatty .deposits .called .plaques .to .form .on .the .inner
.walls .of .the .arteries
Describe .the .relationship .between .HDL .(high-density .lipoprotein), .LDL .(low-
density .lipoprotein), .VLDL .(very-low-density .lipoprotein), .and .CAD .- .ANS✓✓-
Low .levels .of .HDL .pose .risk .for .CAD. .HDL .is .responsible .for .returning
.excessive .cholesterol .to .the .liver .for .elimination .or .conversion .to .cholesterol-
containing .steroids. .HDL .can .also .remove .excessive .cholesterol .through .the
.arterial .wall. .It .can .protect .LDL .from .oxidation, .preserve .endothelial .function,
.and .promote .anti-inflammatory .and .antithrombotic .effects. .VLDL .pose .risk .for
.CAD, .especially .in .combination .with .other .risk .factors .such .as .diabetes
Total .Cholesterol .risk .levels .for .CAD .(dyslipidemia .criteria) .- .ANS✓✓-<200 .=
.desirable
200-239 .= .borderline
≥240 .= .high
LDL .risk .levels .for .CAD .(dyslipidemia .criteria) .- .ANS✓✓-<100 .= .optimal .
100-129 .= .near .optimal
130-159 .= .borderline
160-189 .= .high
≥190 .= .very .high
HDL .risk .levels .for .CAD .(dyslipidemia .criteria) .- .ANS✓✓-<40 .= .low
≥60 .= .high
Triglyceride .risk .levels .for .CAD .(dyslipidemia .criteria) .- .ANS✓✓-<150 .=
.desirable .
150-199 .= .borderline
200-499 .= .high
≥500 .= .very .high
Atherosclerotic .plaque/lesion .- .ANS✓✓-- .Likely .to .develop .following
.endothelial .injury; .areas .of .increased .shear .wall .stress .are
especially .vulnerable
Fatty .streak .→ .Fibrous-fatty .plaque .→ .Advanced .complicated .lesion
Fatty .streak .(early .damage .to .vessel .wall) .- .ANS✓✓-- .Focal .thickening .of .the
.intima
, - .Increase .in .smooth .muscle .cells .and .extracellular .matrix
- .Smooth .muscle .cells .migrate .and .proliferate .into .the .intima
- .Lipid .deposits .accumulate
- .Macrophages .and .T-lymphocytes .(early .damage .to .vessel .wall)
Fibrous-fatty .plaque .(evolves .from .fatty .streak) .- .ANS✓✓-- .Accumulation .of
.connective .tissue
- .Increased .number .of .smooth .muscle .cells .laden .with .lipids
- .Deeper .extracellular .lipid .pool
- .Results .in .further .endothelial .cell .dysfunction, .necrosis .of .underlying .vessel
.tissue, .and .narrowing .of .the .lumen .as .the .lesion .protrudes .out .from .the .vessel
.wall
Advanced .complicated .lesion .- .ANS✓✓-- .Smooth .muscle .cells, .numerous
.macrophages, .T-cells ., .often .associated .with .lipid .core .and .necrotic .material
- .Covered .by .a .fibrous .cap .(smooth .muscle .cells .surrounded .by .CT .matrix)
- .Thick .cap .- .provides .stability .to .the .lesion
- .Thin, .non-uniform .cap, .macrophage-rich .- .lesion .is .unstable
- .Thrombosis, .hemorrhage, .and/or .calcification
Response .to .Injury .Hypothesis .- .ANS✓✓-(1) .Endothelial .cell .dysfunction
(2) .Macrophage .involvement
(3) .Smooth .Muscle .cell .involvement
(4) .Hyperlipidemia
Describe .the .response-to-injury .hypothesis .for .the .development .of
.atherosclerotic .lesions .- .ANS✓✓-- .Various .sources .or .risk .factors .may .induce
.some .form .of .endothelial .dysfunction/changes .including .alterations .in
.permeability, .adhesive .characteristics, .and .growth-stimulatory .characteristics
- .These .changes/alterations .lead .to .monocyte-endothelial .attachment,
.adherence, .and .transmigration
- .Monocytes .then .enter .the .sub-endothelium, .become .activated .as
.macrophages, .and .be .joined .by .T-cells
- .Macrophages .and .T .lymphocytes .compose .the .first .lesion .of .atherosclerosis .-
.the .fatty .streak
- .Activation .of .these .cells .can .result .in .the .formation .of .molecules .that .attract
.smooth .muscle .cells .to .migrate .and .replicate .within .the .lesion
