Cardiovascular Pathology 1 Flashcards

1
Q

Cardiovascular disease causes 1/3 deaths reported each year in the US. What are the leading risk factors for cardiovascular disease? [3]

A
  • Hypertension
  • High cholesterol
  • Smoking
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2
Q

List some general signs and symptoms of cardiovascular disease.

A
  • Weakness
  • Fatigue
  • Weight change
  • Poor excercise tolerance
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3
Q

List some system-specific cardiovascular signs and symptoms.

(e.g. integumentary, respiratory, cardiovascular…)

A
  • Integumentary: pressure ulcers, loss of body hair, cyanosis (lips, nail bed).
  • Central nervous system: headaches, impaired vision, light-headedness or syncope (fainting).
  • Respiratory: laboured breathing, dyspenia (shortness of breath), productive cough.
  • Cardiovascular: chest, shoulder, neck, jaw, or arm pain or discomfort (angina), palpitations, peripheral oedema, intermittent claudication (leg pain).
  • Genitourinary: frequent urination, nocturia, concentrated urine, decreased urinary output.
  • Musculoskeletal: muscular fatigue, myalgias, chest, shoulder, neck, jaw, or arm pain or discomfort, peripheral oedema, intermittent claudication (leg pain).
  • Gastrointestinal: nausea and vomiting, abdominal distension (caused by ascites), abdominal pain (abdominal angina).
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4
Q

What are the cardinal (most common) signs and symptoms of cardiovascular disease?

A
  • Chest, neck, or arm pain or discomfort
  • Palpitations
  • Dyspenia (shortness of breath)
  • Syncope (fainting)
  • Fatigue
  • Cough
  • Cynosis
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5
Q

Define ischemia.

A

Ischemia is an inadequate blood supply to an organ or part of the body due to obstruction of blood flow.

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6
Q

Define infarction.

A

Infarction is the obstruction of the blood supply to an organ or region of tissue, typically by a thrombus or embolus, causing local death of the tissue.

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7
Q

Outline how coronary arteries play a role in cardiovascular disease.

A

Coronary arteries carry oxygenated blood to the myocardium. When these arteries become narrowed or blocked the areas of the heart supplied by these arteries do not recieve enough oxygen and become ischemic and injured, and infarction may result.

Major disorders due to this are collectively known as ischemic heart disease, coronary heart disease (CHD), or CAD.

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8
Q

Outline arteriosclerosis.

A

Arteriosclerosis represents a group of diseases characterised by thickening and loss of elasticity of the arterial walls, often referred to as hardening of the arteries. Arteriosclerosis can be divided into three types:

  1. atherosclerosis: plaques of fatty deposits form under the tunica intima of the arteries.
  2. Mönckeberg arteriosclerosis (medial calcific sclerosis): involves the tunica media of arteries with destruction of muscle and elastic fibres and formation of calcium deposits.
  3. Arteriosclerosis: characterised by the thickening of the arteriole walls.

All three forms of disease can be present in one person, but in different blood vessels.

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9
Q

Describe atherosclerosis.

A

Atherosclerosis is defined as the thickening of the arterial wall through the accumulation of lipids, macrophages, T lymphocytes, smooth muscle cells, extracellular matrix, calcium, and necrotic debris. It can affect medium/large sized arteries in a condition known as cardiovascular disease (CVD).

When the coronary arteries of the heart are affected it is known as coronary artery disease (CAD) or coronary heart disease (CHD).

When arteries to the brain are affected, cerebrovascular disease develops. Atherosclerosis of arteries in other areas can lead to peripheral vascular disease (PVD), aneurysm, and intestinal infarction.

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10
Q

Define aneurysm.

A

An aneurysm is an excessive localised swelling of the wall of an artery.

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11
Q

List some modifiable and non-modifiable risk factors of CAD.

A

Modifiable:

  • Definite: cigarette smoking, elevated total serum cholesterol (>200 mg/dL), hypertension.
  • Likely: Obesity, physical inactivity, impaired glucose metabolism (diabetes), low levels of HDL cholesterol, hormonal status (menopausal/postmenopausal).
  • Maybe: Psychologic factors and emotional stress, discriminatory medicine (women treated less seriously than men), oxidative stress, moderate alcohol consumption, sleep disorders, poor nutrition.
  • *Non-modifiable**:
  • Increasing age
  • Family history of CVD
  • Ethnicity (highest among black people)
  • Infections (bacterial and viral)
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12
Q

What are the differences in terms of duration of progression between primary atherosclerosis, re-stenosis after coronary bypass, and transplant atherosclerosis?

A
  • Primary atherosclerosis: develops over decades.
  • Transplant atherosclerosis: narrowing of arteries at the points of engraftment of transplanted organs, takes months-years.
  • Re-stenosis after coronary bypass: duration of development in months-years.
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13
Q

What is the difference between the injury and lipid hypothesis for atherosclerosis? Briefly explain each.

A

The injury hypothesis proposes that the main cause for atherosclerosis is due to injury from hypertension, oxidised LDLs, infections, and smoking.

Whereas the lipid hypothesis proposes that the main atherogenic event is due to lipid accumulation in the tunica intima of arteries due to raised levels of lipids (triglycerides and cholesterol).

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14
Q

Outline lipid metabolism and describe the differences in the units that transport cholesterol and/or triglycerides.

A

In lipid metabolism, there are two major pathways of “forward” lipid transport in which lipids move from the liver to the peripheral tissues.

  1. Exogenous pathway: Lipids from the gut are packaged in the form of chylomicrons. After being metabolized by lipoprotein lipases (LPLs), chylomicron remnants remain and are taken up by the liver.
  2. Endogenous pathway: Triglycerides and cholesterol are packaged into VLDL by the liver, exported into the bloodstream where they are catabolized by LPLs. The products are IDL, which can then be further metabolized by hepatic lipase to yield LDL. LDL can be taken up by peripheral tissue, or taken up by the liver and converted to excretable bile acids, or modified by free radicals in the arterial walls leading to atherosclerosis.

Triglycerides and cholesterol are transported by lipoproteins:

  • Very Low Density Lipoprotein (VLDL)
    • Made in the liver
    • Secreted into the bloodstream
    • Contain triglycerides (TGs) mainly but also cholesterol
    • Function: deliver TGs to body cells
  • Low Density Lipoprotein (LDL)
    • Made in the Liver as VLDL
    • Arise from VLDL once it has lost a lot of its triglycerides
    • Present in the bloodstream
    • Rich in cholesterol (contain 75% of cholesterol)
    • Function: Deliver cholesterol to all body cells
  • High Density Lipoprotein (HDL)
    • Made in the Liver and Small Intestine
    • Secreted into the bloodstream
    • Function: pick up cholesterol from body cells and take it back to the liver = “reverse cholesterol transport”
    • Potential to help reverse heart disease
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15
Q

Define hypercholesterolaemia. What are desirable blood cholesterol levels?

A

Hypercholesterolaemia is high blood cholesterol.

Desirable levels of cholesterol:

Total cholesterol (TC) - 5.0 mMol/L or less.

Low-density lipoprotein (LDL) cholesterol after an overnight fast: 3.0 mmol/L or less.

High-density lipoprotein (HDL) cholesterol: 1.2 mmol/L or more.

TC/HDL cholesterol ratio: 4 or less. That is, your total cholesterol divided by your HDL cholesterol. This reflects the fact that for any given TC level, the more HDL, the better.

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16
Q

What are the causes of hypercholesterolaemia and what conditions can lead to it?

A

Causes: being overweight, heavy alcohol consumption, lack of exercise, inactive lifestyle, poor diet (fatty).

Conditions: Diabetes, hypothyroidism, familial hyercholesterolaemia, polycystic ovary syndrome.

17
Q

Outline the response-to-injury hypothesis.

A

Th response-to-injury hypothesis proposes that the primary event causing atherosclerosis is due to endothelium damage: produced by hypercholesterolaemia, mechanical injury, hypertension, immune mechanisms, toxins, and viruses. Hyperlipidaemia may also initiate endothelial injury and promote foam cell formation.

18
Q

Outline the steps in plaque and foam cell formation.

A
  1. Lipid/Injury hypothesis for primary event
  2. Mitogenic factors are released from platelets such as platelet derived growth factor (PDGF), fibroblast growth factor, epidermal growth factor and transforming growth factor-β.
  3. These factors induces proliferation and migration of smooth muscle into the intima with the production of connective tissue matrix proteins (collagen, elastin, glycosaminoglycans and proteoglycans)
  4. The activated mononuclear phagocytes in the lesions release chemo-attractant cytokines, proinflammatory mediators including cytokines, and small lipid molecules such leukotrienes and prostaglandins, as well as reactive oxygen species (ROS).
  5. The oxidation of low density lipoprotein (LDL) by macrophages and endothelial cells has may deleterious effects. The oxidised LDL is chemotactic for circulating monocytes, causes them to adhere endothelium, stimulate the release of growth factors and cytokines and is cytotoxic to smooth muscles and endothelium
  6. Monocytes and smooth muscle cells engulf lipid and contribute to the deposition of lipid into the lesion. Monocyte conversion into lipid laden foam cells is mediated by β-VDL receptor and scavenger receptor, which recognise modified LDL.
  7. Repeat from step 4.
19
Q

What are the different stages in atherosclerosis?

A
  1. Damage to the endothelium: oxidised LDL, bacteraemia, physical damage from hypertension -> cholesterol and platelets enter intima.
  2. Fatty streaks: consists of foam cells (WBCs coated in LDLs, smooth muscle cells, and platelets).
  3. Plaques: can take decades to form, platelets release chemicals that causes proliferation, which obstructs blood flow.
20
Q

Name some of the manifestations of arteriosclerosis.

A
  • Coronary heart disease (CHD)
    • Angina (stable/unstable), acute MI, sudden death
  • Cerebrovascular disease
    • stroke
  • Peripheral arterial disease
    • intermittent claudication, gangrene
21
Q

Outline the systemic distribution of atherosclerosis.

A
  • Large vessels: aorta, carotid artery, iliac artery
  • Medium vessels: coronary artery, cerebral artery, limb vessels

Small blood vessels and veins are not affected.

22
Q

What are the complications that can arise from arteriosclerosis?

A
  • Thrombosis
  • Rupture - haemorrhage
  • Aneurysm
  • Fibrosis and calcification
  • Ischemia/infarction
  • Stroke, MI, renal infarction
  • Intermittent claudication
23
Q

How is coronary artery disease (CAD) diagnosed?

A
  • People over 20 years of age need to have their cholesterol measured every 5 years
  • Angiography: x-ray examination of the artieries with a dye injection, limited as it can’t detect unstable sites for rupture
  • Ultrasound
  • Ultrafast CT (not widely used)
  • Magnetic resonance angiography (MRA) (not widely used)
24
Q

What is hypertension?

A

High blood pressure (HBP), a pressure of 140/90 mm Hg or more.

25
Q

Outline blood pressure classification.

A
26
Q

What is blood pressure?

A

Blood pressure is the force exerted against the walls of the arteries and arterioles. Diastolic pressure is the pressure in these vessels when the heart is relaxed between beats, and systolic pressure is the pressure exerted in the arteries when the heart contracts.

27
Q

Outline primary and secondary hypertension.

A
  • Primary hypertension: accounts for 90-95% of all cases of hypertension.
  • Secondary hypertension: accounts for only 5-10% of hypertension cases and results from an identifiable cause.
28
Q

Define labile hypertension.

A

labile blood pressure is blood pressure that abnormally increases and decreases frequently.

29
Q

Define malignant hypertension.

A

A syndrome of markedly elevated blood pressure (diastolic presure >125 mmHg) with target organ damage (e.g. retinal haemorrhage, papilledema, heart failure, stroke).

30
Q

Define isolated systolic hypertension.

A

The elevation of systolic blood pressure independantly of change in the diastolic blood pressure.

31
Q

Outline the differences between benign and malignant hypertension. [5]

A
  1. Benign is usually primary, whereas malignant hypertension can be primary or secondary.
  2. Benign hypertension hapens in middle-aged to elderly people, whereas malignant occurs in the young to middle-aged population.
  3. Benign is common, and malignant is uncommon.
  4. Benign has a slow formation (years), malignant is rapid (months).
  5. Benign has a slow BP rise (DBP 90-120 mm Hg) whereas malignant has a very rapid rise in BP (>120 mm Hg DBP).
32
Q

What are some causes for secondary hypertension?

A
  • Renal disease
    • Chronic renal failure
    • Renal artery stenosis
    • Glomerulonephritis
  • Endocrine disease
    • Adneral tumour
    • Cushing syndrome
  • Pre-eclampisa
  • Drugs
    • Oral contraceeptives
    • Corticostreoids
33
Q

How can hypertension be controlled?

A
  • Healthy diet
  • Exercise for an hour 4-5 times a week
  • Control your weight
  • Limit alcohol intake (<2 drinks/day)
  • Low salt intake
  • Do not smoke
  • Relax
  • Medications
  • Regularly check BP
34
Q

What drugs can be used to treat hypertension?

A
  • Diuretics
  • ACE inhibitors
  • Angiotensin receptor blockers
  • Calcium antagonists
35
Q

What can untreated hypertension lead to?

A
  • Stroke
  • Dementia
  • Heart failure
  • Kidney failure
  • Hypertensive retinopathy
  • Pooor circulation
  • Premature death