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Pathology > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Cardiovascular diseases involves…

A

The heart & blood vessels

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2
Q

Arteriosclerosis

A

Rigidity and often thickening of blood vessels
- due to deposition of fatty materials under the blood vessels

effects small blood vessels
full thickness

usually found in people with hypertension and diabetes

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3
Q

What happens if arterioscleriosis occurs within the blood vessels?

A

Obstructs blood flow - less blood supply to organs = ischemia

prolonged ischemia can caused cell death

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4
Q

Where does Medial Calcific sclerosis occur?

A

in medium size arteries, no obstruction to blood

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5
Q

What is atherosclerosis?

A

Chronic inflammatory disorder of intima of large and medium arteries characterised by the formation of fibr-fatty plaque AKA atheroma

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6
Q

What does atherosclerosis lead to?

A

Major cause of ischemic heart disease, myocardial infarction and hypertension

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7
Q

Cause of atherosclerosis

A

Modern lifestyle

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8
Q

How long does it take to produce clinical manifestations of atherosclerosis?

A

Primary atherosclerosis: decades
Transplant atherosclerosis:months - years
Re-stenosis after coronary bypass: months - years

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9
Q

What are the two main causes of atherosclerosis?

A

Exact causes is not known - however 2 main hypotheses:
1. Lipid hypothesis
2. Injury hypothesis (stronger opinion)

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10
Q

Causes of Atherosclerosis - Lipid hypothesis

A

high lipid level - deposited in the blood vessels
hypothesis is supported by people with diabetes have higher lipid levels.

Also people with Familiar hyperlipidemia have v high levels of LDL

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11
Q

Causes of Atherosclerosis - Injury hypothesis

A

blood vessels are first injured - becomes leaky which allows LDL to go in and get deposited

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12
Q

How can injury to blood vessels occur?

A

Hypertension
Oxidised LDL - MAIN cause
Infections
Smoking

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13
Q

Risk factors of Atherosclerosis - Uncontrollable

A

Sex (more common in men)
Herditary
Race (white)
Age (elderly)

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14
Q

Risk factors of Atherosclerosis - Controllable

A

Delay process of atherosclerosis
HBP - with medication
High Blood Cholesterol
Smoking
Physical activity
Obesity
Diabetes
Stress and Anger
Diet

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15
Q

What is the lipid hypothesis?

A

Infiltration of intima with lipid is the primary atherogenic event due to raised blood lipid levels

Increased cholesterol is associated with a higher incidence of heart disease

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16
Q

Triglyceride

A

saturated fat such as dairy products, animal fat, vegetable oils

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17
Q

What foods are higher in cholesterol?

A

Liver, kidneys, eggs and prawns are higher in dietary cholesterol than other foods.

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18
Q

What organs produce cholesterol

A

Liver and kidneys

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19
Q

Lipid Metabolism - describe

A

Eat food containing lipid (cholesterol + triglyceride)
Packaged in chylomicrons within the intestine
Through circulation it is brought to skeletal muscle and fatty tissue where triglyceride is released.
Chylomicron with remaining cholesterol, is taken to the liver where it is deposited.
Liver cell also produces triglycerides
Cholesterol and triglycerides are packaged together into vLDL
Circulate
When it reaches the level of the muscles and fatty tissues - triglycerides are released with the help of lipoprotein lipase.
After removal of triglyceride remaining cholesterol is now LDL instead of vLDL.
Cholesterol is deposited into cells - each cell has a receptor called LDL receptor (LDLr).
Once there is excess deposition in a cell - has to be removed by HDL - deposits into liver.
Liver converts excess lipids into bile acid

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20
Q

Very Low-Density Lipoprotein (VLDL)
- where is it made
- what does it contain
- function

A

Made in the liver
- Secreted into the bloodstream
- Contain triglyceride mainly but also cholesterol
Function: deliver TGs to body cells

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21
Q

Low density lipoprotein
- where is it made
- what does it contain
- function

A
  • Made in the Liver as VLDL
  • Arise from VLDL once it has lost a lot of its TG’s
  • Present in the bloodstream
  • Rich in cholesterol (contain 75% of cholesterol)
    Function: Deliver cholesterol to all body cells
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22
Q

High density lipoprotein
- where is it made
- what does it contain
- function

A

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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23
Q

Cholesterol levels in the blood - Total Cholesterol (TC)

A

5.0mMol/L or less
2 in 3 adults have a TC level of 5.0mMol/L or above

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24
Q

Cholesterol levels in the blood - Low-density lipoprotein (LDL) cholesterol after an overnight fast

A

3.0mMol/L or less

25
Q

Cholesterol levels in the blood - High density lipoprotein (HDL) cholesterol

A

1.2mmol/L or more

26
Q

Cholesterol levels in the blood - TC/HDL cholesterol ratio

A

4 or less

27
Q

Causes of hypercholesterolemia

A

Same as causes of hypertention and Heart attack

Being overweight
Heavy alcohol use
Lack of exercise, inactive lifestyle & diet

28
Q

What are the medical conditions associated with Hypercholesterolemia?

A

Diabetes
Hypothyroidism
Familial hypercholesterolemia
Polycystic ovary syndrome

29
Q

Causes of endothelial cell injury

A

Oxidised LDL
Hypoxia
Shear stress of blood flow
Hypertension
Cytokines e.g. TNF-a
Free radicals
Viral infection
Smoking
Homocysteine - high level

30
Q

Atherosclerosis: The response-to-injury hypothesis pathogenesis

A

Injury > increased permeability, LDL & monocyte migration
Accumulation of lipoproteins ) in intima platelet adhesion
Monocyte adhesion and converted into macrophage
Lipid accumulation in macrophages (foam cells) – inflammatory cytokines released
cytokine release allows smooth muscle to move into the intima
smooth muscle secretes fibres - forms thick cap

31
Q

Stages of Arteriosclerosis

A

Starts at 10-14 yrs

  1. Endothelial damage - entry of lipid into intimia
  2. Fatty streaks
  3. Advanced lesions
32
Q

Systemic distribution of atherosclerosis

A

Common sites:

LARGE VESSELS - Aorta, carotid artery, Iliac
artery

MEDIUM VESSELS - coronary artery, cerebral artery and limb vessels

SMALL BLOOD VESSELS AND VEINS ARE NOT INVOLVED

33
Q

What are the clinical manifestations of atherosclerosis?

A

Coronary heart disease
- stable angina, acute myocardial infarction, sudden death, unstable angina

Cerebrovascular disease
- stroke

Peripheral arterial disease
- intermittent claudication, gangrene

34
Q

What are the consequences of atheroma?

A
  1. Narrowing of lumen
  2. Plaques undergo changes
  3. Thrombus formation > ischemia > infarction
  4. Embolism: thrombus can break away to become emboli
  5. Atrophy of media > weakening of wall > aneurysm > rupture > thrombus
35
Q

Complications

A

Thrombosis
Rupture - haemorrhage
Aneurism
Fibrosis and calcification
Ischemia: Angina/infarction
Stroke, myocardial infarction, renal infarction
Intermittent claudication, gangrene

36
Q

What is used to make a diagnosis?

A
  1. Angiography - inserted into the femoral artery - moved into the aorta and when it reaches the coronary arteries, contract dye is injected to visualise it.
  2. Ultrasound
37
Q

What is the main contributor of atherosclerosis?

A

LDL, which carries cholesterol into the arterial wall, is oxidised by the endothelium and is a major contributor to atherosclerosis.

38
Q

What is angina pectoris?

A

Episodic chest pain caused by lack of oxygen to the myocardium due to atherosclerotic narrowing of coronary arteries

39
Q

What is angina pectoris precipitated and relieved by?

A

by exertion and is relieved by rest or vasodilators e.g. nitroglycerin

40
Q

How long does angina pectoris pain last?

A

10 minutes

41
Q

What is acute myocardial infarction?

A

An irreversible myocardial injury as a result of prolonged ischemia due to coronary artery atherosclerosis

42
Q

Which ventricle is most commonly involved in acute myocardial infarction?

A

Left ventricle (works harder)

43
Q

right ventricular infarction usually represents….

A

When right ventricular infarction occurs, it is almost always represents an extension of severe left ventricular infarction

44
Q

What is Transmural infarction?

A

It traverses the entire ventricular wall from endocardium to pericardial surface.

most common form of MI

45
Q

What is Subendocardial infarction?

A

limited to interior one-third of the wall of the left ventricle

46
Q

Coronary arteries percentage involvement in MI

A

Left CA - separated into two
1. Anterior descending (40-50%)
2. Left circumflex (15-20%)

Right CA (30-40%)

47
Q

What are the positions of left ventricular infarctions

A

Posterolateral infarct
Anterior infarct
A posterior infarct

48
Q

Posterolateral Infarct

A

following blockage of the left circumflex artery

49
Q

Anterior infarct

A

follows blockage of the left anterior descending branch of the left coronary artery

50
Q

Posterior infarct

A

results from blockage of the right coronary artery and involves the posterior wall.

51
Q

What are the clinical manifestations of an MI

A

Chest pain (typically radiating to the left arm or left side of the neck - more than 20 mins)
Shortness of breath
Nausea, vomiting, palpitations, sweating and anxiety
Fatigue

52
Q

What is a silent MI and what percentage of MI’s are silent?

A

MI without chest pan or other symptoms
1 quarter of all MI’s are silent

53
Q

Development of myocardial infarction during 24hrs microscopically

A
54
Q

Diagnosis of myocardial infarction

A

History

ECG: Q wave depression, ST segment elevation or depression

Laboratory: detection of cardiac proteins in serum

55
Q

What serums are detected to diagnose MI’s

A

Creatine Kinase MB: strongly positive at 12-16hrs and remain elevated 24hrs after infarct

Troponin I: strongly positive at 12-16hrs and remain elevated 4-6 days after infarct

Troponin T: strongly positive at 12-16hrs and remain positive more than 6 days after infarct

Lactate dehydrogenase: peaks at 3-4 days and remain elevated for up to 10 days.

56
Q

Treatment of heart attack

A

Oxygen, aspirin, and analgesia are usually administered as so glyceryl trinitrate.

Morphine is classically used if nitroglycerin is not effective due to its ability to dilate blood vessels.

Once the diagnosis of MI is confirmed, other pharmacologic agents are often given. These include beta-blockers, anticoagulation and possibly additional antiplatelet agents such as clopidogrel.

When these therapies are unsuccessful, Percutaneous coronary intervention (PCI) such as Angioplasty (mechanically widening a narrowed or obstructed blood vessel) or Coronary artery bypass graft surgery is needed.

57
Q

Angioplasty

A

where a narrowed section of a coronary artery is widened by using a balloon and a stent attached to a catheter

58
Q

Coronary artery bypass surgery

A

Arteries/veins from elsewhere in the patient’s body are grafted to the coronary arteries to bypass atherosclerotic narrowings and improve the blood supply to the coronary circulation supplying the myocardium.

59
Q

What are the complications of MI

A

Arrytheymia - most common cause of death in first several hours after infarction.

Myocardial failure can lead to congestive failure/or shock

Myocardial rupture - occurs in 1% of all cases within 3-5 days and may result in death from cardiac temponade (compression of heart by haemorrhage into pericardial space)

Rupture of papillary muscles

Mural thrombosis

Ventricular aneurysm

Pericaditis

Pathology (11 decks)

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