CV Pt2 🏠 Hub 🩸 S1: CAD 💔 S2: Angina/MI 💧 S3: HF 📈 S4: HTN 🩹 S5: Valvular 💊 S6: Meds 🏆 S7: Final

🩸

Section 1: Coronary Artery Disease & Atherosclerosis

Endothelium and atherosclerosis

Endothelium injury: plaque formation and perfusion loss.

Cell Factory Focus: Coronary Endothelial Cell (Highway Crew) + Hepatocyte (Cholesterol Factory)

🏭 Meet the Cell Factories of Section 1

🛣 Coronary Endothelial Cell

"Highway Maintenance Crew"

  • Location: Lines every coronary artery
  • Job: Keep highway smooth, slippery, open
  • Produces: Nitric oxide (NO) → relaxes wall, prevents clots
  • When damaged: Surface cracks → atherosclerosis begins!
  • Damaged by: HTN shear stress, smoking, high LDL, diabetes
🧬 Hepatocyte (Liver Cell)

"Cholesterol Factory"

  • Location: Liver
  • Job: Produces most cholesterol in body
  • Key enzyme: HMG-CoA reductase (master switch)
  • LDL = BAD trucks (dump cholesterol INTO walls)
  • HDL = GOOD trucks (REMOVE cholesterol FROM walls)
🔍 Diagram 1: Normal Artery Wall — The Healthy Highway
TUNICA ADVENTITIA (Protective outer shell) TUNICA MEDIA — Smooth Muscle Cells "Traffic Controllers" — constrict/relax to change diameter TUNICA INTIMA — Endothelial Cells "Highway Maintenance Crew" — smooth, slippery surface NO NO NO NO NO LUMEN (Wide open!) Red blood cells flowing freely ✅ Healthy Endothelium Produces: • Nitric Oxide (NO) = vasodilator • Prostacyclin = prevents platelet sticking • Tissue plasminogen activator = dissolves tiny clots • Smooth surface = no platelet activation NORMAL FLOW
Baseline: A healthy coronary artery with intact endothelium producing nitric oxide. The lumen is wide open and blood flows freely.

💥 1A. Atherosclerosis — The 6-Stage Cellular Battlefield

Stage 1: Endothelial Wounding — HTN Shear Stress Tears the Highway
TUNICA MEDIA (Smooth Muscle) GAP! GAP! LUMEN (Blood flowing) ↓ ↓ ↓ HTN SHEAR STRESS ↓ ↓ ↓ Like a FIRE HOSE hitting a wall! ⚠ DAMAGE AGENTS: 💨 Smoking toxins ↑ High blood pressure ↑ High blood glucose ↑ LDL cholesterol 👨 Stress hormones ALL damage the endothelial cells! 💊 DRUG TARGET: Antihypertensives → ↓ shear ❌ less NO ❌ less NO ❌ less NO
Hypertension creates shear force that tears gaps in the endothelial lining. Smoking, diabetes, and high LDL worsen the damage. Antihypertensives reduce this shear stress.
Stage 2: LDL Invasion — Bad Trucks Burrow Through the Cracks
TUNICA MEDIA SUBENDOTHELIAL SPACE LUMEN (Blood) LDL LDL LDL LDL LDL LDL LDL ox-LDL ox-LDL ox-LDL ⚠ ALARM! ⚠ ALARM! 💊 DRUG TARGET: STATINS Block HMG-CoA reductase in the liver factory → FEWER LDL trucks on road = FEWER trucks to burrow! 🔬 WHAT HAPPENS: 1. LDL squeezes through gaps 2. Gets trapped in the wall 3. Becomes OXIDIZED (toxic!) 4. Triggers inflammatory alarm
LDL particles burrow through endothelial gaps, become oxidized and toxic in the wall. Statins reduce LDL production at the liver factory to cut off supply.
Stage 3: Foam Cell Formation — Cleanup Workers Get Overwhelmed
TUNICA MEDIA ⭐ FATTY STREAK FORMING ⭐ FOAM FOAM FOAM FOAM FOAM FOAM LUMEN Mono Mono Monocyte → Macrophage Macrophage + ox-LDL → FOAM CELL ↑ Lumen narrowing 🔬 THE PROCESS: 1. Monocytes arrive from blood 2. Transform into macrophages 3. Eat oxidized LDL (too much!) 4. Become bloated FOAM CELLS 5. Pile up → FATTY STREAK = First visible sign of disease! 🎯 Memory Trick: "Macrophages eat too much junk food (LDL) → get FAT → FOAM cells = FAT cells!"
Monocytes migrate into the wall, become macrophages, eat oxidized LDL, and bloat into foam cells. The pile-up creates a fatty streak — the first visible sign of atherosclerosis.
Stage 4: Fibrous Plaque — Smooth Muscle Builds a Bandage Over the Mess
TUNICA MEDIA (depleted of smooth muscle cells) SM cells migrate ↑ SM migrate ↑ LIPID CORE (foam cells + cholesterol debris) FIBROUS CAP (Collagen from smooth muscle cells) ENDOTHELIUM (stretched, thin over plaque) NARROWED LUMEN ← 50-75% blocked → Blood flow restricted but not stopped 🔬 PLAQUE ANATOMY: • Fibrous cap = hard protective shell • Lipid core = soft, unstable center • Thin cap = VULNERABLE plaque • Thick cap = STABLE plaque Vulnerable = rupture risk = MI! 🚑 Clinical Impact: At this stage, patient may experience STABLE ANGINA: chest pain with exertion, relieved by rest or NTG
Smooth muscle cells create a fibrous cap over the lipid core. The plaque narrows the lumen 50-75%, causing stable angina with exertion.
Stage 5: Plaque Rupture & Thrombus — Platelets, Fibrin, and the Clot
EXPOSED LIPID CORE (cholesterol debris) ⚡ RUPTURE ⚡ PLT PLT PLT PLT PLT THROMBUS (Blood Clot) SEVERELY NARROWED / BLOCKED LUMEN ⚠ Blood flow critically reduced or STOPPED! Heart muscle cells downstream = DYING (MI!) 💊 PLATELET RECEPTORS & DRUG TARGETS: ① COX-1 Enzyme Makes TXA2 → platelet clumping 💊 ASPIRIN blocks COX-1! → Less TXA2 → less clumping ② P2Y12 Receptor ADP docks here → recruits more PLTs 💊 CLOPIDOGREL blocks P2Y12! → Less ADP signal → fewer recruits ③ GPIIb/IIIa Receptor Fibrinogen bridges PLTs together 💊 ABCIXIMAB blocks GPIIb/IIIa! → No bridges → PLTs can't clump ④ Fibrin Mesh (red lines) Thrombin → Fibrinogen → Fibrin 💊 HEPARIN blocks thrombin! → No fibrin → weak clot
Plaque rupture exposes the lipid core. Platelets activate via COX-1, P2Y12, and GPIIb/IIIa receptors. Fibrin mesh strengthens the clot. Each receptor is a drug target: Aspirin (COX-1), Clopidogrel (P2Y12), Abciximab (GPIIb/IIIa), Heparin (thrombin/fibrin).
🔬 Platelet Close-Up: Normal Activation vs Drug-Blocked
⚠ NORMAL (No Drugs) Platelet fully activates & clumps! PLATELET (Activated!) COX-1 ✅ → TXA2 produced! → Amplifies clumping P2Y12 ADP ADP docks ✅ → Recruits more PLTs! GPIIb/IIIa Fibrinogen Bridges to next PLT ✅ → Strong clump forms! RESULT: Full activation → THROMBUS! Clot grows → blocks artery → MI risk! 💊 WITH DRUGS Platelet activation BLOCKED! PLATELET (Stays inactive!) COX-1 ❌ ASPIRIN blocks! No TXA2 → no clumping signal P2Y12 CLOPIDOGREL blocks! ADP can't dock → no recruitment GPIIb/IIIa ABCIXIMAB blocks! No bridges → no clumping RESULT: Activation blocked → NO clot! Artery stays open → blood flows! VS 💡 ANTIPLATELET SUMMARY: Aspirin = COX-1 blocker • Clopidogrel (Plavix) = P2Y12 blocker • Abciximab (ReoPro) = GPIIb/IIIa blocker • Heparin = Thrombin/Fibrin blocker
LEFT: Normal platelet with all receptors active → full clot formation. RIGHT: Antiplatelet drugs block each receptor → platelet stays inactive, no dangerous clot. This is the key to preventing MI after stent placement!
🧬 Hepatocyte (Liver Cell): Normal vs Statin Therapy
⚠ NORMAL (No Statin) Liver factory at FULL production! HEPATOCYTE (Liver Cell = Cholesterol Factory) HMG-CoA Reductase ✅ "Master Switch" = ACTIVE! ↓ Produces cholesterol! Cholesterol → LDL trucks LDL LDL LDL LDL MANY bad trucks on the road! ↑↑ LDL in blood → ↑↑ plaque formation! 💊 WITH STATIN Production switch turned OFF! HEPATOCYTE (Liver Cell = Production SLOWED) HMG-CoA Reductase ❌ BLOCKED by STATIN! ↓ Much less cholesterol produced ↑ More LDL receptors on surface! Liver PULLS LDL FROM blood → LDL FEW bad trucks left on road! Common Statins: Atorvastatin (Lipitor) Simvastatin (Zocor) ↓↓ LDL in blood → ↓↓ plaque growth! VS
LEFT: Without statins, the liver churns out LDL trucks that dump cholesterol into artery walls. RIGHT: Statins block HMG-CoA reductase, liver produces less cholesterol AND pulls more LDL from blood. Suffix clue: all statins end in "-statin."
💊 Master Drug Map: Where EVERY Drug Acts on the Atherosclerosis Timeline
ATHEROSCLEROSIS TIMELINE →→→ 1. Endothelial Damage 2. LDL Invasion 3. Foam Cells/Plaque 4. Narrowing/Angina 5. Rupture/Thrombus ☠ MI! 💊 ANTIHYPERTENSIVES → ↓ Shear stress on wall • ACE-I (lisinopril) • ARBs (losartan) • CCBs (amlodipine) • Beta-blockers (metoprolol) • Diuretics (HCTZ) 💊 STATINS → ↓ LDL production • Atorvastatin (Lipitor) • Simvastatin (Zocor) • Rosuvastatin (Crestor) Block HMG-CoA reductase 💊 STATINS also → Anti-inflammatory → Stabilize plaque → ↓ foam cell formation (Pleiotropic effects) 💊 VASODILATORS → Open narrowed arteries • Nitroglycerin (NTG) Dilates coronary aa. • CCBs (diltiazem) ↓ vasospasm • Beta-blockers ↓ O2 demand 💊 ANTIPLATELETS + ANTICOAGULANTS • Aspirin (COX-1 blocker) • Clopidogrel (P2Y12 blocker) • Abciximab (GPIIb/IIIa) • Heparin (thrombin blocker) • Warfarin (factor blocker) → Prevent / dissolve clots 💡 KEY INSIGHT: Patients with CAD are on MULTIPLE medications because EACH drug targets a DIFFERENT stage! Statin (↓LDL) + ACE-I (↓BP) + Aspirin (↓clots) + NTG PRN (open arteries) = comprehensive CAD management 🎯 NCLEX Memory: "SABA" — Statin + ACE-I (or ARB) + Beta-blocker + Aspirin = Standard CAD combo If the question asks what to expect a newly diagnosed CAD patient to be prescribed → think SABA!
Every drug class has a specific target on the atherosclerosis timeline. Understanding WHERE each drug acts helps you remember WHY it is prescribed. SABA = Statin + ACE-I + Beta-blocker + Aspirin.

📈 1B. Risk Factors for CAD

✅ Modifiable (CAN Change)
  • Atherosclerosis (treat early!)
  • Elevated cholesterol (diet + statins)
  • Cigarette smoking (cessation = #1!)
  • Hypertension (meds + lifestyle)
  • Obesity (diet + exercise)
  • Physical inactivity
  • Diabetes / impaired glucose
  • Stress
❌ Non-Modifiable (CANNOT Change)
  • Age (risk ↑ with age)
  • Gender (men higher risk; women ↑ after menopause)
  • Family history of heart disease

🎯 NCLEX: "CAN change it? = Modifiable. CANNOT? = Non-modifiable."

💡 Collateral Circulation — Backup Supply Routes

🎯 Memory: "Old roads = MORE detours. New roads = NO detours. Sudden blockage + no detour = DEAD END!"

⚠️ Critical Narrowing Thresholds

Left Main Artery

≥ 50%

Significant! (feeds BOTH LAD + Circumflex)

Any Major Branch

≥ 75%

Significant! (LAD, Circumflex, or RCA)

💥 Coronary Artery Territory Map — Which Artery Feeds What?
ANTERIOR (LAD territory) LATERAL/ POSTERIOR (Circumflex) INFERIOR (RCA territory) LAD "Widow Maker" Circumflex RCA LAD blocked = Anterior/Septal MI Circumflex blocked = Posterior/Lateral MI RCA blocked = Inferior MI
Know which artery supplies which territory — NCLEX will ask which MI type results from which artery blockage!

🚑 1C. Data Collection (LPN Scope)

☝ LPNs COLLECT DATA and REPORT! RNs ASSESS and DIAGNOSE!

💡 Be the eyes and ears at the bedside. Collect data, document it, REPORT abnormal findings immediately!

💊 1D. Interventions for CAD

Goal: Alter the atherosclerotic progression!

1. Lifestyle Modifications

2. Medications (See Master Drug Map above!)

3. Surgical Procedures

🎯 NGN Clinical Judgment: Recognize Cues for CAD

NCLEX wants you to identify which information is RELEVANT:

🧠 Ask: "Risk factors AND symptoms consistent with CAD?" → YES = cues recognized!

📝

Quiz 1: CAD & Atherosclerosis

15 Questions • 80% to Pass • Review Rationales After Submission • Flashcards If <80%

🎯 Test-Taking Strategy

  • Risk factors: Modifiable vs. non-modifiable
  • Atherosclerosis: Remember the 5 cellular stages
  • Drug suffixes: -pril=ACE-I, -sartan=ARB, -olol=BB, -statin=cholesterol
  • LPN scope: Collect data, report, reinforce teaching, do NOT diagnose
Question 1 of 15
The LPN is reinforcing teaching about CAD. The client asks, "What causes the blockage?" Which response best describes the cellular process of atherosclerosis?
  • A. "Blood cells clump together and form a permanent blockage."
  • B. "Heart muscle grows too large and presses against artery walls."
  • C. "Cholesterol sneaks through damaged artery walls, immune cells try to clean it up but get overwhelmed, forming plaque that narrows the artery."
  • D. "Calcium deposits from bones build up inside artery walls."
✅ C. Atherosclerosis begins when endothelial cells are damaged, allowing LDL to penetrate. Macrophages eat the LDL, become foam cells, form fatty streaks, then smooth muscle creates a fibrous cap = plaque. Cell Factory: highway crew damaged → bad trucks sneak in → cleanup workers overwhelmed.
LPN: Reinforce teaching provided by the RN.
Question 2 of 15
The LPN collects data on a client with suspected CAD. Select ALL findings to document and report. (SATA)
✅ A, B, D, E. Report: chest pain (ischemia cue), dyspnea, syncope, excessive fatigue. BP 118/76 and HR 72 are normal. Recognize Cues: Any symptom suggesting the heart isn't getting enough O₂ is relevant!
LPN Scope: Collect data and REPORT. RNs assess and diagnose.
Question 3 of 15
Which are modifiable risk factors for CAD? (SATA)
✅ A, C, D, F. Modifiable: smoking, HTN, obesity, inactivity (patient CAN change). Non-modifiable: family history, age (CANNOT change).
NCLEX Tip: "Can the patient change it? YES=modifiable, NO=non-modifiable."
Question 4 of 15
In the Cell Factory analogy, which cell is the "Highway Maintenance Crew" whose damage initiates atherosclerosis?
  • A. Cardiomyocyte
  • B. Coronary endothelial cell
  • C. Hepatocyte
  • D. Juxtaglomerular cell
✅ B. The coronary endothelial cell lines coronary arteries, keeps the surface smooth, and produces nitric oxide. Damage from HTN/smoking/LDL creates gaps → atherosclerosis begins. Cardiomyocyte=Pump Worker, Hepatocyte=Cholesterol Factory, JG cell=BP Sensor.
Question 5 of 15
A 45-year-old has a sudden MI. Why is a younger client at greater risk of death from sudden coronary occlusion?
  • A. Younger clients have weaker heart muscle
  • B. Younger clients have higher cholesterol levels
  • C. Younger clients have not developed collateral circulation
  • D. Younger clients have faster heart rates
✅ C. Collateral circulation (backup supply routes) takes years to develop. Older clients have backup pathways; younger clients have no detours. Memory: "Old roads=MORE detours. New roads=NO detours."
Question 6 of 15
Left main artery narrowing is significant at:
  • A. 25%
  • B. 50%
  • C. 75%
  • D. 90%
✅ B. Left main: ≥50% = significant (feeds BOTH LAD + Circumflex). Major branch: ≥75% = significant. The left main threshold is lower because blockage threatens a huge portion of the LV.
Question 7 of 15
Which statement best describes LDL cholesterol's role in atherosclerosis?
  • A. LDL penetrates damaged endothelium, deposits cholesterol, leading to foam cells and plaque
  • B. LDL removes cholesterol from walls and transports it to the liver
  • C. LDL strengthens endothelial lining with essential nutrients
  • D. LDL dissolves existing plaque and improves flow
✅ A. LDL="Bad trucks" dump cholesterol INTO walls. Once trapped, LDL oxidizes, macrophages eat it → foam cells → plaque. HDL="Good trucks" REMOVE cholesterol FROM walls. Goal: ↓LDL + ↑HDL.
Question 8 of 15
Which client statement shows effective discharge teaching for CAD?
  • A. "I can keep smoking if I take my cholesterol medication."
  • B. "My father had heart disease, so nothing can prevent mine."
  • C. "Only diet matters; exercise doesn't help."
  • D. "I will stop smoking, follow a low-fat diet, and walk 30 minutes daily."
✅ D. Shows understanding of multiple modifiable risk factor changes: smoking cessation + dietary modification + exercise. A=dangerous (smoking+meds not safe). B=fatalism ignoring modifiable factors. C=ignores exercise.
LPN: Reinforce teaching provided by RN.
Question 9 of 15
Place atherosclerosis steps in correct order (1-5):

A. Smooth muscle cells form fibrous cap
B. Endothelial cells damaged by risk factors
C. Plaque ruptures, thrombus forms
D. LDL penetrates damaged wall
E. Macrophages become foam cells forming fatty streaks
✅ B, D, E, A, C
1. B Endothelial damage (highway cracks) → 2. D LDL invasion (bad trucks sneak in) → 3. E Foam cells (cleanup workers overwhelmed) → 4. A Fibrous cap (bandage over mess) → 5. C Rupture + thrombus (clot blocks road → MI!)
Memory: Damage → Invasion → Overwhelm → Cover → Rupture
Question 10 of 15
Which lipid value is most concerning for atherosclerosis?
  • A. HDL 65 mg/dL
  • B. Total cholesterol 180 mg/dL
  • C. LDL 190 mg/dL
  • D. Triglycerides 140 mg/dL
✅ C. LDL 190=very high (bad trucks flooding the road). HDL 65=good (protective). Total 180=desirable (<200). Triglycerides 140=normal (<150). LPN: REPORT elevated LDL to RN/PHCP.
Question 11 of 15
A client asks what a stent does. Which response is most accurate?
  • A. "Replaces the damaged artery section with artificial tube."
  • B. "Holds the artery open and prevents restenosis."
  • C. "Dissolves the plaque buildup."
  • D. "Creates a bypass route around the blockage."
✅ B. A stent is scaffolding that holds the artery open and prevents restenosis. Does NOT dissolve plaque (=thrombolytics), replace artery (=graft), or bypass (=CABG). Post-stent: antiplatelet therapy (aspirin + clopidogrel).
Question 12 of 15
Which enzyme in the hepatocyte is the "master production switch" for cholesterol? (Statin target)
  • A. ACE (angiotensin-converting enzyme)
  • B. COX-1 (cyclooxygenase)
  • C. HMG-CoA reductase
  • D. Monoamine oxidase (MAO)
✅ C. HMG-CoA reductase controls cholesterol production in the liver factory. Statins block this enzyme → less cholesterol → liver pulls more LDL from blood → blood LDL drops. ACE=BP regulation. COX-1=platelet TXA2. MAO=neurotransmitters.
Question 13 of 15 (NGN Recognize Cues)
Which combination of findings should the LPN recognize as cues suggesting CAD?
  • A. Temp 99.2°F, sore throat, nasal congestion
  • B. BP 118/72, pulse 74, clear lungs
  • C. Weight 145 lbs, fasting glucose 92 mg/dL, non-smoker
  • D. Substernal chest tightness with exertion, LDL 210, 30-year smoking history, father had MI at 50
✅ D. Recognize Cues: CLUSTER of relevant findings: substernal chest tightness (classic angina), LDL 210 (very high), 30-year smoking (modifiable risk), family hx MI (non-modifiable). A=infection. B=normal vitals. C=low-risk.
Clinical Judgment: Look for the cluster pointing to the same problem!
Question 14 of 15
LAD artery obstruction causes which type of MI?
  • A. Anterior or septal MI
  • B. Inferior wall MI
  • C. Posterior or lateral wall MI
  • D. Right ventricular MI
✅ A. LAD=Anterior/Septal MI ("Widow Maker"). Circumflex=Lateral/Posterior MI. RCA=Inferior MI. LAD blockage affects the largest LV territory.
Question 15 of 15
Which interventions should the LPN anticipate for a newly diagnosed CAD client? (SATA)
✅ A, B, C, E. LPNs: administer prescribed meds, reinforce diet teaching, monitor/report labs, reinforce smoking cessation. NOT: independently prescribe (PHCP role) or diagnose (RN/PHCP role).
LPN Scope: COLLECT DATA + REPORT + REINFORCE. Never prescribe or diagnose.

📊 Quiz 1 Results

📃 Flashcard Remediation — Review Before Retaking

Click a card to flip it. Detailed explanations on the back.

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