Exam 5 Mon 4.18 Heart patho PP Flashcards Preview

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Flashcards in Exam 5 Mon 4.18 Heart patho PP Deck (41)
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Info about True and false aneurysms

  • 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



Cardiac aneurysm 

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


What is Aortic dissection?

– tear in the intima, blood enters wall of artery





Info about aortic aneurysms

  • 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


Very basic info about how aneurysms are diagnosed and treated

  • 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


Basic explanation of ˜Atherosclerosis

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


How the endothelium sustains Injury and inflammation in Atherosclerosis

  • †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)


What's the deal with fatty streaks and Atherosclerosis?

  • 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


What's up with the Fibrous plaque in Atherosclerosis?

  • 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)


What is complicated plaque in the progression of Atherosclerosis

  • 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


Risk factors for Atherosclerosis and what it can lead to

Risk factors include:

  • hyperlipidemia/dyslipidemia
  • diabetes
  • smoking
  • hypertension

Result in:

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


What are Arterial bruits?

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.


What is Coronary Artery Disease?

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


Major risk factors for Coronary Artery Disease (3)

•Increased age

•Family history

•Male gender or female gender post menopause

•These factors cannot be modified


Modifiable risk factors of Coronary Artery Disease (6)



•Cigarette smoking

•Diabetes mellitus

•Obesity/sedentary lifestyle

•Atherogenic diet


Pathophysiology of Dyslipidemia

  • 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


Things that can lead to Dyslipidemia

•Abnormalities are combination of genetics and diet

•Familial factors – genetics of metabolism and processing lipids

•Secondary factors include medications, diabetes, hypothyroidism, pancreatitis, nephrosis


What is LDL

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



What is HDL? 

•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


things to know about hypertension as it relates to CAD

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


How smoking affects CAD

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


How Diabetes mellitus is connected to CAD (6)

insulin resistance and diabetes contribute to:

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


The Obesity/CAD connection

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


Nontraditional risk factors for CAD that are still under investigation

  • 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


Info about Myocardial ischemia and angina

  • ˜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)


What is Prinzmetal angina?

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


What is Silent ischemia/mental stress-induced angina?


  • 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


Points that were highlighted in PP about EKGs and ischemia 

  • 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 


Points highlighted about women and CAD (6)

  • ˜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)


Lab Values norms– Lipid Panel

  • ˜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)