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pathology > w23 cardiovascular pathology > Flashcards

w23 cardiovascular pathology Flashcards

1
Q

LO

A

To understand the pathogenesis and clinical consequences of atherosclerosis

To learn about myocardial infarction and its management.

to fix w lec notes slide 13,14, 15 16 18 make cards & 23 onwards - lol

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2
Q

rigidity (sclerosis)
and often thickening of blood vessel) is known as

A

Arteriosclerosis

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3
Q

Whats the diff bw arteriosclerosis and arteriolosclerosis

A

arteriosclerosis - rigid & thicken. BV
arteriOLOsclerosis - small BVs ; fully thick ; hypertension & diabetes
- kidneys affected

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4
Q

What is medial calcific sclerosis

A

Medium size arteries
Tunica media involved
No obstruction to blood
flow

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5
Q

Define Atherosclerosis

A

Chronic inflamm. disorder of intima of L & Medium arteries
characterised by fibrofatty plaque called atheroma

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6
Q

atherosclerosis is a disease of what sized arteries

A

large and medium

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7
Q

3 Major causes of atherosclerosis are

A

Major cause of ischemic heart disease, Myocardial infarction, hypertension

modern lifestyle ?

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8
Q

How long does primary atherosclerosis take to produce clinical manifestations?

A

Duration of dvpmt in decades (longest)

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9
Q

How long does TRANSPLANT atherosclerosis take to produce clinical manifestations?

A

Narrowing of arteries at the points of engraftment of transplanted organs - Duration of dvpmt in mths –years

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10
Q

How long does Re-stenosis after coronary bypass take to produce clinical manifestations?
(atherosclerosis)

A

duration of dvpmt in mths - yrs

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11
Q

name the 2 hypothesis for possible causes of atherosclerosis

A

lipid hypothesis
injury hypothesis

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12
Q

what is the lipid hypothesis for atherosclerosis

A

potential cause ; Lipid hypo:
- Diabetes
- Familial hyperlipidemia
- Hyperlipedemia due to life style
- Raised LDL in blood

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13
Q

whats injury hypothesis for atherosclerosis

A
  • Hypertension
    • Oxidised LDL
    • infections e.g .cytomegalovirus, herpes simplex viruses, enteroviruses, hepatitis A and chlamydia pneumoniae
      - Smoking
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14
Q

what is familial hypercholesterolemia

A

Familial Hypercholesterolemia (FH)is a genetic disease which results in the reduced clearance of atherogenic LDL-cholesterol (“bad cholesterol”) in the blood, and an increased risk of early heart disease.
Ppl w FH - elevated LDL cholesterol levels from birth
children with FH show an increased thickness of arteries compared to their non-FH siblings by age of 11,
showing the process of atherosclerosis development starts early in life.

As a result of their FH, the incidence of fatal or non-fatal myocardial infarction without treatment is about 50% by the age of 50 years in men and about 30% by the age of 60 years in women.

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15
Q

Name 4 uncontrollable risk factors of atherosclerosis

A

Sex (M > F)
Hereditary
Race
Age

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16
Q

Name some controllable RFactors for atherosclerosis

A

High blood pressure
High blood cholesterol
Smoking
Physical activity
Obesity
Diabetes
Stress and anger
Diet

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17
Q

Who discovered the lipid hypothesis for atherosclerosis

A

Rudolf Virchow 1856

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18
Q

what does the lipid hypothesis for atherosclerosis propose

A
  • proposes that infiltration of intima with lipid is the primary atherogenic event due to raised blood lipid levels
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19
Q
  • Increased cholesterol level is associated with a ________ ___________ of heart diseases
A

higher incidence of heart diseases

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20
Q

define sources of triglycerides

A

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

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21
Q

name sources of cholesterol

A

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

22
Q

describe composition of a fatty acid (2 things)

A

Fatty acid is composed of a hydrocarbon chain with one terminal carboxyl group (COOH).

23
Q

whats the diff bw unsaturated Facids & saturated FAs

A

Unsaturated fatty acids have one or more carbon-carbon double bonds, whereas saturated fatty acid has no double bond in its hydrocarbon chain.

24
Q

whats oleic acid (example of smthn not needed)

A

Oleic acid is an example of a monounsaturated fatty acid. The most common polyunsaturated fatty acids are linoleic and arachidonic. Arachidonic acid (C20) is of particular interest as the precursor of a family of molecules, known as eicosanoids (from Greek eikosi, “twenty”), that includes prostaglandins, thromboxanes, and leukotrienes.

25
Q

in lipid metabolism how many pathways of ‘frwd’ lipid transport move from liver > peripheral tissues

A

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

26
Q

Exogenous path

A
27
Q

endogenous path

A
28
Q

in depth q of two lipid metabolism paths

A
29
Q

name the 3 lipid types in the blood

A

very low density lipoprotein (VLDL)
low density lipoprotein
high density lipoprotein

30
Q

Describe Very low density lipoprotein (VLDL)
where made ? hwo it travels ? what it contains ? function?

A

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

31
Q

describe Low density lipoprotein (LDL)

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

32
Q

describe high density lipoprotein

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
33
Q

describe high density lipoprotein

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
34
Q

High risk for coronary diseases = high for VLDL high for LDL and is it high or low for HDL ?

A

low level risk for coronary diseases for HDL

35
Q

slide 13 to do

A
36
Q

name some lifestyle causes of hypercholesterolemia

A

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

37
Q

name some medical conditions that could contribute to causing hypercholesterolemia

A

Diabetes
● Hypothyroidism
● Familial hypercholesterolemia
(LDL receptor mutations and ApoB mutations have detected in bw 50- 80% cases of FH)
● Polycystic ovary syndrome

38
Q

description of physical characteristics of hypercholestrolemia

A

Xanthelasma palpebrarum, yellowish patches consisting of cholesterol deposits.

These are more common in people with familial hypercholesterolemia

39
Q

what age does arteriosclerosis start

A

10-14 young

40
Q

name the 3 stages of arteriosclerosis

A

endothelial damage
fatty streaks
advanced lesions

41
Q

describe what happens in the endothelial damage stage of arterosclerosis

A

lipid enters into intima

42
Q

describe what looks like in the fatty streaks stage of arteriosclerosis

A

pale yellow, smooth surface, defined border that protrude into the lumen containing macrophages filled with lipid

43
Q

describe composition of the advncd lesions stage of arteriosclerosis

A

fibro fatty plaques
(connective tissues, smooth muscle cells proliferation , accumulated lipids and lipid laden macrophages -foam cells, lymphocytes, lesion covered by fibrous cap)

44
Q

Name 3 clinical manifestations of atherosclerosis

A

CHeartDisease
Cerebrovascular disease
peripheral arterial disease

45
Q

Describe symptoms of coronary heart disease (rel. to atherosclerosis)

A

Stable angina, acute myocardial infarction, sudden death, unstable angina

46
Q

what clinical manifestation of atherosclerosis causes gangrene and intermittent claudication

A

peripheral arterial disease

47
Q

the 3rd clinical manifestation of atherosclerosis is cerebrovascular disease AKA ______

A

stroke

48
Q

what is gangrene

A

death of tissue in body
foul smellin discharge of black foot ; surface & subsurface discolouration

49
Q

5 consequences of atheroma are..

A

Narrowing of lumen
Plaques undergo changes:
ulceration
- fissuring
haemorrhage into plaque
- thrombus
3) Thrombus formation –> ischemia –> infarct
4) Embolism: thrombus can break away to become emboli

5) Atrophy of media –> weakening of wall –>
aneurysm (abnormal dilatation of a vessel wall–>
- rupture
- thrombus

50
Q

complications of atherosclerosis

A

Thrombosis, thrombo-embolism

Rupture – haemorrhage

Aneurism – fusiform, dissecting, berry etc.

Fibrosis and Calcification

Ischemia: Angina/infarction

Stroke, myocardial infarction, renal infarction

Intermittent claudication, gangrene etc.

51
Q

2 diagnostic methods for atherosclerosis

A

Angiography

Ultrasound

52
Q

what is angiography

A

guidewire w catheter inserted into femoral artery. It is moved into aorta and when it reaches opening of coronary arteries, contrast dye inj. to visualise the coronary arteries.

pathology (6 decks)

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