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
2
Q
Cardiac aneurysm
A
- seen after MI, when noncontracting infarcted muscle is stretched
3
Q
What is Aortic dissection?
A
– tear in the intima, blood enters wall of artery
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
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
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
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)
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
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)
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
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)
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.
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
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
15
Q
Modifiable risk factors of Coronary Artery Disease (6)
A
- Dyslipidemia
- Hypertension
- Cigarette smoking
- Diabetes mellitus
- Obesity/sedentary lifestyle
- Atherogenic diet
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
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
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)
26
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
27
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
28
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
29
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)
30
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)
31
What are the objectives of common cardiovascular meds?
* Reduce risk of clotting
* Treat hypertension
* ↓serum cholesterol if \>200 mg/dl
32
major classes of common heart meds (6)
* Diuretics
* Beta blockers
* Alpha-1 blockers
* ACE inhibitors
* Calcium channel blockers
* Nitrates
33
What do Diuretics do?
* ↓blood volume by eliminating sodium and water
* may also ↑ calcium reabsorption
34
What do Beta blockers do?
* relax blood vessels and heart muscle
* HR reduced
* may limit response to exercise
35
What do Alpha-1 blockers do?
dilate blood vessels
36
What do ACE inhibitors do?
interrupt the RAAS chain that constricts blood vessels
37
What do Calcium channel blockers do?
* blocks calcium from entering blood vessel walls
* limits constriction
38
What do Nitrates do?
dilate coronary arteries
39
What is PTCA?
* percutaneous transluminal coronary angioplasty- “stents”
* Works better than balloon angioplasty alone, lower rate of restenosis
40
A couple of points about Coronary artery bypass graft (CABG)
* May use saphenous vein or internal mammary artery
* New procedures may require only partial sternotomy
41
Guidelines for Physician Referral
* 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
