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Pathology-Alaa > Atherosclerosis > Flashcards

Atherosclerosis Flashcards

1
Q

what is this finding called?

A

corneal arcus

White, grey, or blue opaque ring in the corneal margin as a result of hypercholesterolemia.

Arcus senilis can be confused with the limbus sign, which reflects calcium rather than lipid deposits.

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2
Q

what is menhoraggia?

A

excessive heavy periods

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3
Q

(patient’s elbow.)

What is present?

How do these appear microscopically?

What condition is the patient likely to have?

What does this condition mean for the patient?

A
  • Xanthelasma
  • plaques or nodules composed of lipid laden histiocytes (macrophages) in the skin (expecially in eyelids) (Xanthelasma)
  • Familial Hypercholesterolemia
  • Increase risk of atherosclerosis.
  • due to high
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4
Q

what is this called?

A

xanthelasma

signs of Hyperlipidemia

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5
Q

Define Atherosclerosis

A

is the accumulation of intracellular and extracellular lipid in the intima and media of large and medium sized arteries

or

the thickening and hardening of arteries due to an atheroma!

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6
Q

Define Aretrioscelrosis

A

hardening of the walls of the arteries and arterioles usually as a result of hypertension or diabetes

(no due to atheroma)

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7
Q

**atherosclerosis does NOT effect veins and cappillaries

A

ok

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8
Q

what does an atheromatus plaque consist of?

roughly, how thick is it usually?

A

raised lesion w/ soft and yellow, grumous core of lipid (mainly cholestrol and CE) covered by a fibrous plaque!

1-2mm thick

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9
Q

what is an atheroma? what does it consist of?

A

the necrotic core of the atherosclerotic plaque!

  • dead cells
  • debris
  • cholstrol crystals
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10
Q

what r the 3 macroscopic feautures of atherosclerosis?

A
  • fatty streak
  • simple plaque
  • complicated plaque
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11
Q

Describe the appearence of a fatty streak

A
  • Lipid deposits in intima, yellowy and slightly raised
  • composed of foam cells.
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12
Q

flow through a stenosed tube or artery is not significantly affected until the lumen is reduced by_______%.

A

70-80%.

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13
Q

where does atheroscleosis occur?

where is it nost commonly seen?

A

elastic arteries= aorta, carotid, iliac

medium Muscular= coronory, popliteal

It is commoner in the abdominal aorta rather than the thoracic aorta.

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14
Q

what is Monkeyberg’s disease?

A

an uncommon disease where there is calcification of the Media of large arteries

monkey likes taking pics of calsified arteries!

🐒+📸

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15
Q

Arteriosclerosis

Atheroscleosis

Areterioloscleroisis

A
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16
Q

“athere” is Greek for porridge

A

why do u do this to me why?

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17
Q

what type of plaque is this?

describe its macroscopic feauture

A

Simple plaque

  • raised white and yellow
  • widely distributed
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18
Q

what type of plaque is this?

describe its macroscopic feauture

A

complicated plaque

there has been:

  • thrombosis into plaque
  • hemmorhage
  • aneurysm
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19
Q

describe the structure of the epithelium starting from inwards to out

A

(theres elastic tissue in the media as well, and depending on where the artery is, that will determine the amount of elastin there is) ex nearer the heart> the more there is, aorta)

20
Q

Arteriosclerosis

Atheroscleosis

Areterioloscleroisis

monkeybergs disease

A
21
Q

the plaque is the basic lesion of atheroscelrosis.

what r the 3 basic components of it?

A

Come Eat Lipids!

  • Cells= leucocytes, SMC
  • ECM= collagen, peptidoglycan, elastin
  • Lipids
22
Q

what is the earliest lesion in atherosclerosis?

how do they appear microscopiclaly

A

-fatty streak!

  • Lipid deposits in intima, yellowy and slightly raised
  • composed of foam cells, SMC, Extracellular lipid

(these r FLAT, bs there is no disturbance of BF yet)

23
Q

after the fatty streak has formed, what comes after that?

describe what there is miscroscopicallY?

A

fatty streaks grow to become plaques!

they impinge in the lumen of the artery and r partially circumfrential.

there is fibrosis, necrosis, cholestrol clefts, extension into media & growth on small vessel from adventitia

24
Q

what r some of the plaque complications?

A
  • -u think studying atheromas comes easy? Haha*
  • -ulceration*
  • -thrombosis*
  • -spasm*
  • -Aneurysm*
  • -Calcification*
  • -Embolism*
  • -Rupture of atherosclerotic artery*
25
Q

Clinical effects of atherosclerosis?

A

-Heart>> IHD, Arryhtmia, MI, angina, cardiac failure, chronic ischemic heart disease

-brain>> TIA, cerbral infarction, mutli-infarct dementia

-Kidney>> Hypertension, renal failure

-Legs>> gangrene, peripheral vascular disease

-Bowel>>bowel ischemia

26
Q

Risk factors of atheroscelrosis?

(modifiable and nonmodifiable)

A

(for more detail look at handout!)

nonmodifiable

Age

Gender -common in men than in women (but increases after the menopause as oestogen is protective,)

Genetic predisposition

modifiable

Hyperlipidaemia

Hypertension

Cigarette smoking

Geography

Obesity

Infection

27
Q

what is an Aneurysm?

A

dilations of the artery due to weaking of the arterial wall!

(they r almost always secondary to atherosclerosis!)

28
Q

describe the different shapes of aneurysms!

A
  • Saccular> shaped like a sac!
  • Fusiform> shaped like a spindle!
29
Q

where do u usually find saccular aneuryms?

A

in the abdominal aorta!

30
Q

dilation of the arteries r called?

veins?

A

aneurysm

Varices

31
Q

**genetic variations in the apopolipoprotein ___, r asscoaited with changes in LDL levels!

A

E

32
Q

how can cigarrette smoking increase risk of atheroscleross?

A
  • inflammation
  • dmage to BV

=increased predisobositon of thrombis

-Oxidation of lipids! (OxLDL)

REduced PG12

-nicotine makes platelets sticky

33
Q

how can hypertension cause atherosclerosis?

A

high pressure causes endothelial damage!

34
Q

apparently small amounts of alchohol can have protective effects from atherosclerosis -.-

A

wtf

35
Q

what types of infections can contribute to atherosclerisis?

A
  •  Chlamydia pneumoniae
  •  Helicobacter pylori
  •  Cytomegalovirus
36
Q

significance of Apo E lipoprotein

A

LDLreceptor on hepatocytes binds apoE & chylomicron remnant taken up by receptor mediated endocytosis

37
Q

Name and explain the 4 possible theories for the possible mechanisms of atherosclerosis!

A
  • Thrombogenic theory> plaques formed by repeated thrombi, lipid core dervied from thrombi
  • Insudation theory> endothelial injury, inflammation,

 increased permeability to lipid from plasma

  •  Monoclonal hypothesis>
  •  Reaction to injury hypothesis > atheroscelrosis is a chronic inflammatory response of the arterial wall initiated by injury

Thrombosis is Red mess

38
Q

what r the Cells Involved in atherosclerosis process?

A
  •  Endothelial cells
  • SMC
  • Platelets
  •  Macrophages
  •  Lymphocytes
  •  Neutrophils
39
Q

what is the role of SMC in atherosclerosis?

A

1) Take up LDL and other lipid to become foam cells

2)Form the roof of the plaque (fibrous cap) w/ synthesis of collagen and proteoglycans and ECM in it.

40
Q

role of macrophages in atherosclerosis

A
  •  Oxidise LDL by releasing FR
  • eat lipids to become foam cells
  •  Secrete proteases which modify matrix
  •  Stimulate proliferation and migration of smooth muscle cells
41
Q

role of lymphocytes

A
  • TNF may affect lipoprotein metabolism
  •  Stimulate proliferation and migration of smooth muscle cell
42
Q

role of neutrophils in atherosclerosis

A

 Secrete proteases leading to continued local damage and inflammation

43
Q

when do atherosclerosis symptoms appear?

A

atherosclerosis is a totally silent disease.

Symptoms eventually arise when plaques become complicated.

44
Q

Prevention of atherosclerosis

A
  • No smoking
  • Reduce fat intake
  • Treat hypertension
  • Not too much alcohol
  •  Regular exercise/weight control
  •  Stop smoking
  •  Modify diet
  •  Treat hypertension
  •  Treat diabetes
  •  Lipid lowering drugs -statins, and aspirin prophylaxis,
  • Anti-oxidants, such as vitamin E, may be protective.
45
Q

examples of lipid lowering drugs?

A

statins and anaphylaxis lowring drugs

46
Q

What do these holes indicate?

A

In the final step of atherosclerosis, the cells in the centre of the plaque DIE and necrosis. these dead cells release cholestrol and cholestrol crytal appear,

these crystals r removed suring tissue section and leave behind these hole Cholestrol clefts!

Pathology-Alaa (16 decks)

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