Exam 5 Mon 4.18 Heart patho PP Flashcards

1
Q

Info about True and false aneurysms

A
  • Local dilation or outpouching of a vessel wall or cardiac chamber
  • True aneurysms – all 3 layers of the arterial wall, weakening of the vessel
    • Fusiform aneurysms
    • Circumferential aneurysms
  • False aneurysms – extravascular hematoma
    • accular aneurysms
  • Aorta most susceptible, especially abdominal

Causes include atherosclerosis, hypertension
Can lead to aortic dissection or rupture

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2
Q

Cardiac aneurysm

A
  • ˜seen after MI, when noncontracting infarcted muscle is stretched
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3
Q

What is Aortic dissection?

A

– tear in the intima, blood enters wall of artery

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4
Q

Info about aortic aneurysms

A
  • Aortic aneurysm may be asymptomatic until rupture, then severe pain
  • Pain between shoulder blades or in abdomen, sometimes with hypotension – emergency
  • May cause difficulty swallowing or dyspnea
  • Aortic – ¾ of all aneurysms here
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5
Q

Very basic info about how aneurysms are diagnosed and treated

A
  • All are confirmed with ultrasonography (think she is talking about aortic?)
  • If slow-growing, may be treated conservatively
  • Surgical resection and graft placement, or stent
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6
Q

Basic explanation of ˜Atherosclerosis

A
  • Form of arteriosclerosis
  • Thickening and hardening caused by accumulation of lipid-laden macrophages in the arterial wall
  • Plaque development through all body arterioles
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7
Q

How the endothelium sustains Injury and inflammation in Atherosclerosis

A
  • †Endothelial cells cannot make normal amounts of antithrombic and vasodilating cytokines
  • †Inflamed cells express adhesion molecules that bind macrophages and immune cells (TNF-α, interferons, interleukins, C-reactive protein), further injuring vessel wall
  • Macrophage migration and adherence
  • Low density lipoprotein (LDL) oxidation (foam cell formation – lipid-laden macrophages)
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8
Q

What’s the deal with fatty streaks and Atherosclerosis?

A
  • accumulation of foam cells, which now recruit T cells and secrete toxic oxygen “free” radicals
  • †Now seeing fatty streaks in vessels of children
  • †Lipid-lowering treatments (diet, statin drugs) may reverse this process
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9
Q

What’s up with the Fibrous plaque in Atherosclerosis?

A
  • macrophages also release growth factors that stimulate smooth muscle cell proliferation, produce collagen, and migrate over the fatty streak, forming a fibrous plaque
  • •Fibrous plaque may calcify, protrude into vessel lumen, obstruct blood flow to distal tissues (especially during exercise)
  • Angina (cardiac) or intermittent claudication (peripheral)
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10
Q

What is complicated plaque in the progression of Atherosclerosis

A
  • unstable plaques may rupture without warning due to underlying inflammation, causes bleeding within the plaque (plaque hemorrhage) –
  • †Clotting cascade begins, forming a thrombus
  • Antithrombotic medicines are used to treat/prevent thrombi
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11
Q

Risk factors for Atherosclerosis and what it can lead to

A

Risk factors include:

  • hyperlipidemia/dyslipidemia
  • diabetes
  • smoking
  • hypertension

Result in:

  • inadequate perfusion
  • ischemia
  • necrosis – heart attack
  • stroke
  • peripheral vessel occlusion (wounds and amputations)
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12
Q

What are Arterial bruits?

A

auscultation of blood flow sounds

More detailed explanation:

Most commonly, a bruit is caused by abnormal narrowing of an artery. Listening for a bruit in the neck with a stethoscope is a simple way to screen for narrowing (stenosis) of the carotid artery, which can be a result of cholesterol plaque accumulation.

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13
Q

What is Coronary Artery Disease?

A
  • ˜Any vascular disorder that narrows or occludes the coronary arteries leading to myocardial ischemia
  • ˜Atherosclerosis is the most common cause
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14
Q

Major risk factors for Coronary Artery Disease (3)

A
  • Increased age
  • Family history
  • Male gender or female gender post menopause
  • These factors cannot be modified
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15
Q

Modifiable risk factors of Coronary Artery Disease (6)

A
  • Dyslipidemia
  • Hypertension
  • Cigarette smoking
  • Diabetes mellitus
  • Obesity/sedentary lifestyle
  • Atherogenic diet
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16
Q

Pathophysiology of Dyslipidemia

A
  • Lipids, phospholipids, cholesterol, and triglycerides all bind to carrier proteins
  • Lipids are needed for manufacture and repair of plasma membranes
  • Cholesterol needed for manufacture of bile acids and steroid hormones
  • Most body cells manufacture cholesterol
  • Chemical reactions in the liver produce
    • Very low density lipoproteins (VLDLs), triglyceride and protein
    • Low density lipoproteins (LDLs), cholesterol and protein
    • High density lipoproteins (HDLs), phospholipids and protein
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17
Q

Things that can lead to Dyslipidemia

A
  • Abnormalities are combination of genetics and diet
  • Familial factors – genetics of metabolism and processing lipids
  • Secondary factors include medications, diabetes, hypothyroidism, pancreatitis, nephrosis
18
Q

What is LDL

A
  • the “lousy” lipids - ↑ risk of coronary disease because LDLs are atherogenic
  • VLDLs are also lousy lipids
19
Q

What is HDL?

A
  • the “happy” lipids - ↑ levels of HDL are protective against atherogenesis, actually remove excess cholesterol from tissues
  • Exercise, weight loss, fish oil consumption, moderate alcohol can ↑ HDL levels
20
Q

things to know about hypertension as it relates to CAD

A
  • 2-3X ↑ risk of CAD
  • Overactivity of SNS and RAAS, both of which raise BP, contribute to this risk
21
Q

How smoking affects CAD

A

For both primary and second-hand smoke:

  • Nicotine stimulates catecholamines (epi and norepi) which ↑ HR and cause vascular constriction, increasing cardiac workload and O2 demand
  • Cigarette smoking also ↑ LDL and ↓ HDL, creates free O2 radicals, causing vessel inflammation and thrombosis
22
Q

How Diabetes mellitus is connected to CAD (6)

A

insulin resistance and diabetes contribute to:

  • endothelial damage
  • thickening of vessel walls
  • inflammation
  • thrombosis
  • glycation of vascular proteins
  • ↓ production of vasodilators
23
Q

The Obesity/CAD connection

A

65% of U.S. adults are overweight or obese – combined risk of CAD with dyslipidemia, hypertension, insulin resistance,HDLs

24
Q

Nontraditional risk factors for CAD that are still under investigation

A
  • Markers of inflammation and thrombosis
    • High density C-reactive protein, erythrocyte sedimentation rate, von Willebrand factor concentration, interleukin-6, interleukin-18, tumor necrosis factor, fibrinogen, and CD 40 ligand
  • Hyperhomocysteinemia – genetic lack of an enzyme that metabolizes the amino acid homocysteine, related to folate and vitamins B12 and B6
  • Adipokines - obesity hormones
  • Infection – may increase atherosclerosis
  • ˜Highly sensitive C-reactive protein (hs-CRP) may prove to be a predictor of cardiovascular risk; statin drugs reduce hs-CRP levels
    • Adipokines may also be predictors
    • Predictors can only quantify risk – people still need to work on modifiable factors
25
Q

Info about Myocardial ischemia and angina

A
  • ˜local, temporary deprivation of the coronary blood supply
  • Stable angina – blood vessels harden and cannot dilate when cardiac demand ↑
  • May have transient discomfort, jaw pain, L or R arm pain, or severe chest pain
  • Women may have no symptoms or just a feeling of unease or fatigue – different clinical presentation
  • may be reduced by rest or medications (such as short and long-acting nitroglycerines)
26
Q

What is Prinzmetal angina?

A
  • variant angina – occurs unpredictably, including while at rest or during sleep
  • May be related to SNS, vagal activity, or ↓ NO
  • Usually benign
27
Q

What is Silent ischemia/mental stress-induced angina?

A
  • May be totally asymptomatic or present as fatigue, dyspnea, feeling of unease
  • May be related to LV sympathetic innervation abnormality
  • Also seen in diabetes mellitus, or surgical denervation for coronary artery bypass grafting (CABG), transplantation, or after MI
28
Q

Points that were highlighted in PP about EKGs and ischemia

A
  • During ischemia, will see ST segment depression on EKG; stress testing done to provoke symptoms
  • ST segment and T wave correlate with ventricular contraction and relaxation
  • EKG can also identify the coronary artery involved, as each artery has a specific area of distribution
29
Q

Points highlighted about women and CAD (6)

A
  • ˜More women die from stroke and CAD than all cancers combined
  • ˜Much higher mortality rate than men
  • 2/3 of women who die from CAD had no prior symptoms
  • ˜Women have higher prevalence of modifiable risk factors than men
  • ˜Estrogen replacement does not reduce risk of CAD
  • ˜Statin drugs may not be effective and have higher incidence of side effects (muscle pain and liver damage)
30
Q

Lab Values norms– Lipid Panel

A
  • ˜Total cholesterol 100-199 mg/dL
  • ˜Triglycerides 0-149 mg/dL (from diet)
  • ˜HDL >39 mg/dL (“happy”)
  • ˜VLDL 5-40 mg/dL
    • est. as % of triglycerides – limited use
  • ˜LDL 0-99 mg/dL (“lousy”)
  • ˜Chol/HDL Radio 0.0 – 4.4 ratio units (risk of heart disease)
31
Q

What are the objectives of common cardiovascular meds?

A
  • Reduce risk of clotting
  • Treat hypertension
  • ↓serum cholesterol if >200 mg/dl
32
Q

major classes of common heart meds (6)

A
  • Diuretics
  • Beta blockers
  • Alpha-1 blockers
  • ACE inhibitors
  • Calcium channel blockers
  • Nitrates
33
Q

What do Diuretics do?

A
  • ↓blood volume by eliminating sodium and water
  • may also ↑ calcium reabsorption
34
Q

What do Beta blockers do?

A
  • relax blood vessels and heart muscle
  • HR reduced
  • may limit response to exercise
35
Q

What do Alpha-1 blockers do?

A

dilate blood vessels

36
Q

What do ACE inhibitors do?

A

interrupt the RAAS chain that constricts blood vessels

37
Q

What do Calcium channel blockers do?

A
  • blocks calcium from entering blood vessel walls
  • limits constriction
38
Q

What do Nitrates do?

A

dilate coronary arteries

39
Q

What is PTCA?

A
  • ˜percutaneous transluminal coronary angioplasty- “stents”
  • Works better than balloon angioplasty alone, lower rate of restenosis
40
Q

A couple of points about Coronary artery bypass graft (CABG)

A
  • May use saphenous vein or internal mammary artery
  • New procedures may require only partial sternotomy
41
Q

˜Guidelines for Physician Referral

A
  • Any signs of dyspnea, pain, palpitations (more than 6 in 1 minute or lasting for hours), fainting, lightheadedness extreme fatigue
  • Neurological instability or recent event may also trigger cardiac arrhythmias
  • Difference >40 mm Hg in pulse pressure

Key points, p. 284