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Med Path Fall 2020 > CVD1 > Flashcards

CVD1 Flashcards

1
Q

CVD

A

Diseases of the heart and vessels that affect the efficient functioning of the cardiovascular system.

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2
Q

What is the leading cause of mortality in the US?

A

CVD #1 is heart disease. #2 is stroke.

Incidence increases with age

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3
Q

Primary forms of CVD

A

***Coronary heart disease (disease of blood vessels that supply the heart), stroke, heart failure, high blood pressure, congenital heart defects.

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4
Q

Main form of CVD

A

Coronary heart disease

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5
Q

Key risk factors of CVD

A

Hypertension, hyperlipidemia, smoking

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6
Q

The cardiovascular continuum

A
  1. HTN, hyperlipidemia, diabetes
  2. Atherosclerosis
  3. Coronary artery disease
  4. Myocardial infarction
  5. Heart failure
  6. Death

*Can start/stop at diff parts along this path

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7
Q

Cholesterol natural role in the body

A

Produced in the liver and uptaken through diet.

Membrane fluidity, myelin sheath, nerve conduction, steroid hormones, bile acids.

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8
Q

Triglyceride role

A

Storage of fat. Mobilized for energy production and storage.

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9
Q

How are cholesterol and triglycerides transported in the blood?

A

In the form of lipoproteins.

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10
Q

Where do these lipoproteins transport cholesterol/triglycerides?

  1. Chylomicrons
  2. VLDL
  3. LDL (bad)
  4. HDL (bad)
A
  1. Small intestine (diet) to liver
  2. Liver to tissue
  3. Tissue to liver
  4. Tissue to liver
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11
Q

On it’s way from peripheral tissues to liver, LDL can also

A

Get stuck in vascular intimacy and deposit triglycerides in vessels.

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12
Q

Another name for hyperlipidemia

A

Dyslipidemia

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13
Q

Requirements for hyperlipidemia

A

Excess lipids in the blood.
TG over 150 mg/dl
LDL over 100
HDL less than 40

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14
Q

How much HDL is protective against CVD?

How much HDL causes regression of atherosclerosis?

A

Greater than 60

Greater than 70

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15
Q

What is the key contributor to atherosclerosis?

A

Hyperlipidemia

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16
Q

Total cholesterol (TC) greater than ___ is an increase risk for CVD

A

160 mg/dl

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17
Q

2 forms of hyperlipidemia

A
  1. Primary (genetic) Less common, but more severe.
    Familial hypercholesterolemia (high LDL)
    Familial hypertriglyceridemia (high TG)
    Combined (high LDL and TG)
  2. Secondary. Polygenetic. More common, runs in families, multiple genes involved, environmental factors play a role. Ex: high fat diet and sedentary lifestyle.
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18
Q

Primary hyperlipidemia 3 examples

A 
Familial hypercholesterolemia (high LDL)
Familial hypertriglyceridemia (high TG) 
Combined (high LDL and TG)
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19
Q

Treatment of hyperlipidemia

A

Diet, exercise, lifestyle changes, medication

20
Q

3 ocular manifestations of hyperlipidemia?

A
  1. Arcus/lipid keratopathy
  2. Xanthelasma
  3. Lipemia retinalis
21
Q

Arcus

A

Lipid in the cornea stroma. Common in people over 50. Abnormal in people younger than 50.

22
Q

Xanthelasma

A

Accumulation of foam cells in the region of the nasal cants.

TG likely greater than 1,000 mg/dl. Normal is under 150. For sure need to evaluate. Ask family hx.

23
Q

Lipemia REtinalis

A

Tg levels higher than 2500 mg/dl. Normal is under 150.

Chunky blood and white vessels packed with lipids

24
Q

Guidelines on the management of blood cholesterol

A

Lifestyle therapy is the primary intervention. Heart-healthy. Statins if drugs needed.

25
Q

Atherosclerosis

  • What is it
  • Where is it located
  • Can lead to what
A

Chronic inflammatory disorder of the tunica intimacy (large and medium arteries) Small arteries cannot develop this.
Lead to ischemia, thrombosis, embolism, aneurysm.

26
Q

Most common chronic disease in the US

A

Atherosclerosis

responsible for 80% of CVD

27
Q

5 steps to pathogenesis of atherosclerosis

A
  1. Injury to intima (HTN, diabetes, smoking. Pre-existing)
  2. Insudation. LDL filters into the intima.
  3. Oxidation of lipids. Produces free radicals and elicits an immune response. M0 filter in.
  4. Foam cell accumulation due to M0 eating lipids and getting stuck.
  5. Fatty streaks gradually transform into fibrous plaques that continually undergo remodeling. This narrows lumen of vessels and can contribute to thrombus formation.
28
Q

What happens if plaque in atherosclerosis ruptures?

A

Foam cells that express tissue factor will be dispersed. This will activate PPS systems = clot inside vessel.

29
Q

Stable atherosclerotic plaque characteristics

A

Fibrous cap with lipid core. No activated M0

30
Q

Advanced atherosclerotic plaque characteristics

A

Smooth muscle cells die. Activated M0 degrade matrix in the fibrous cap.

31
Q

Unstable coronary artery disease characteristics

A

Thrombus (blood clot) forms and extends into the lumen and the plaque.

32
Q

How does flow rate change in atherosclerosis

A

As walls thicken due to plaques, this reduces blood flow.

33
Q

coronary heart disease

  1. What is it?
  2. Causes
  3. Clinical manifestations
  4. Risk factors.
A
  1. Narrowing of coronary arteries
  2. Atherosclerosis
  3. Angina, MI
  4. Smoking, hypertension, hyperlipidemia, diabetes.
34
Q

2 types of coronary heart disease

A
  1. Critical stenosis (70-75% obstruction)
    Symptomatic during increased activity.
  2. Greater than 90% stenosis.
    Symptomatic at rest.

^ both pay result in plaque distribution and 1. Healing or 2. Thrombus (plaque rupture)

Collateral development may occur.

35
Q

Angina Pectoris

  1. What is it
  2. Causes
  3. Symptoms
  4. What activates symptoms?
  5. Tx?
A
  1. Ischemia of myocardium. Pain and inflammation.
    NO PERMANENT DAMAGE.
  2. Coronary heart disease, aortic stenosis, HTN, coronary artery spasm
  3. Shortness of breath and crushing chest pain for 30 mins.
  4. Cold weather, exertion, heavy meals, stress (hormone levels may cause inadequate blood flow)
  5. Acute: Nitroglycerin. Vasodilator helps restore blood flow.
    Chronic: BB. Decreases HR and contractility.
36
Q

MI

  1. What is it
  2. Causes
  3. Common male symptoms
  4. Common female symptoms
  5. Clinical findings
  6. Types
A
  1. Myocardial death due to ischemia.
  2. Thrombosis is the main cause. Also coronary heart disease, embolism
  3. Radiating chest pain
  4. Shortness of breath, weakness, fatigue
  5. Autonomic symptoms, elevated blood indicators, ECG abnormalities
  6. Transmural, subendocardial
37
Q

Main difference between MI and angina pectoris

A

Angina does not cause permanent damage.

MI causes damage to myocardium.

38
Q

Autonomic symptoms of MI

A

Sympathetic: Tachycardia, sweating, pallor

Para: Brady, vomiting

39
Q

Elevated blood indicators in MI

A

Myoglobin in blood indicates damage to myocardium
Cardiac creatine kinase
Cardiac troponin

Timing of these in the blood indicates when MI occurred.

40
Q

Transmural MI

A

Occlusion of major coronary artery. Affects complete thickness of heart wall.

41
Q

Subendocardial MI

A

Particularly at risk area. Not entire thickness of heart wall.

42
Q

Another name for arrhythmia

A

Dysrhytmia

43
Q

Most important cause of death from MI?

A

Arrhythmia. Occurs in 85% of MI cases. Often reversible.

44
Q

6 complications from MI?

A
  1. Arrhythmia is most common. Most important cause of death after MI.
  2. Heart failure due to extensive damage to muscle or valve.
  3. Myocardial rupture. (associated with transmural MI) Rare. Pericardium tamponande (pericardium fills with blood, which swells and decreases CO)
  4. Pericarditis- inflam and necrosis of myocardium
  5. Fever due to endogenous pyrogens
  6. Mural thrombosis and embolism
45
Q

Coronary artery disease treatment through the skin

A

Percutaneous coronary intervention (PCI) through the skin.

  1. Angioplasty: uses balloon to dilate and rupture plaque.
  2. intracoronary stents. Prevent re-stenosis. Holds open area.
46
Q

CAD treatment through bypass graft

When is this done and what artery is grafted?

A

Used for multi vessel CHD. Mammary artery graft.

Med Path Fall 2020 (20 decks)

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