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J Term 2 mix > MOD 6 > Flashcards

MOD 6 Flashcards

1
Q

What is an atherosclerosis

A

Thickening and hardening of the vessel walls due to an atheroma

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2
Q

What’s an atheroma

A

accumulation of intra and extracellular lipid in the intima and media of large-medium sized vessels

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3
Q

What’s an arteriosclerosis and name one cause

A

Thickening and hardening of vessel wall NOT due to an atheroma. E.g; calcification with age

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4
Q

What would you see histologically in an atherosclerosis

A
  1. Pale - fat

2. Asymmetrically narrowed lumen

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5
Q

Name the normal layers of an artery from lumen out

ESIMEA

A
  1. Endothelium
  2. Sub-endothelial CT
  3. Internal elastic lamina
  4. Muscular media
  5. external elastic lamina
  6. adventitia
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6
Q

Name the 5 steps leading up to an Atherosclerosis and which mechanism they fall under

A

Mechanism 1 = step 1: Chronic endothelial injury
-hemodynamic stress, hypertension, toxins, high LDLs

Mechanism 2 = Step 2,3,4
2. Endothelial dysfunction: platelet adhesion and release of PDGF, monocyte accumulation in the intima, T lymphocytes join the party

  1. Smooth muscle emigrates from media –> intima, narrowing the vessels
  2. Smooth muscle cells and macrophages engulf oxidized LDLs producing foam cells

Mechanism 3: step 5:
-smooth muscle cells proliferate in response to cytokines, GFs, collagen and ECM, and neovascularisation

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7
Q

Name the three stages in which plaques develop and their characteristics

A
  1. Fatty Streak: normal in adolescence, no disturbance to blood flow, yellow lipid deposits in the intima
  2. Simple Plaque: endothelium still intact but vessel lumen is impinged, plaque often occurs around the Ostia and are irregularly outlined, widely distributed and raised about 1 cm in diameter
  3. Complicated Plaque: endothelial surface has broken and released TF. Next steps can be hemorrhage, thrombosis and calcification
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8
Q

What can occur as a result of hemorrhage to a plaque? Name one example of a consequence

A

Thromboemboli/microemboli if the plaque ruptures.
(The plaque can also expand)
e.g cholesterol emboli could reach the kidneys and cause renal failure

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9
Q

What three could occur as a result of degeneration of surrounding elastic tissue and muscle due to an atherosclerosis

A

Weakening of the vessel walls, can cause dilation of the vessel (aneurysmal dilation), inflammation and arthritis

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10
Q

What could become exposed as a result of ulceration or erosion to the luminal surface of the plaque

A

Highly thrombogenic substances, encourages the formation of a superimposed thrombus

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11
Q

What is the clinical term for what progressive plaque growth causes

A

Critical Stenosis; critical narrowing of an artery

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12
Q

Name 4 early microscopic changes of an atherosclerosis

A
  1. foam cells
  2. lymphocytes
  3. smooth muscle cells
  4. extracellular lipid deposition
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13
Q

Name 6 late microscopic changes of an atherosclerosis

A
  1. fibrosis
  2. necrosis
  3. cholesterol clefts
  4. disruption of internal elastic lamina that could extend into the media
  5. ingrowth of blood vessels
  6. plaque rupture
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14
Q

Name 5 common sites for an atherosclerosis

A
  1. coronary arteries - ischemic damage
  2. carotid
  3. cerebral - stroke
  4. arteries of the legs
  5. abdominal aorta
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15
Q

Why do you get an edema when the heart weakens?

A

Blood is pumped less efficiently and can back up and increase pressure in the veins, fluid can then be pushed into any air spaces including the lungs and peripheral tissues

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16
Q

How much of the lumen has to be blocked for blood flow in an artery to be significantly reduced?

A

70-80%

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17
Q

What is a coronary thrombosis

A

formation of a blood clot inside a vessel of the heart, usually occurs over ruptured atheromatous plaques resulting in an MI

18
Q

What does a survived infarction look like, and why can it be dangerous?

A

White as there is old fibrous scarring, the scarring disrupts the electricity of the heart and can cause an arrhythmia - leading to sudden death

19
Q

Provide 6 things that can happen in a timeline of Cerebral Ischemia

A
  1. Atherosclerosis of carotid arteries
  2. Thrombus forms over a plaque
  3. Thromboembolism to cerebral arteries
  4. Transient ischemic attacks: brief episodes of neurological dysfunction
  5. Stroke
  6. Multi-infarct dementia: a major stroke, one of many causes of dementia
20
Q

What kind of necrosis can form as a result of a stroke, and what would it cause?

A

Liquefactive necrosis, may cause an absess filled with CSF

21
Q

What is an AAA, list one major risk factor and a current preventative step in place?

A

Abdominal Aortic Aneurysm

  • continuous smoking
  • ultrasound scans at 65
22
Q

Why can an AAA cause terrible abdominal pain?

A

Because the atheroma has gone on for decades and caused constant endothelial damage, resulting in chronic abdominal pain

23
Q

How does an AAA usually form, and what are some of its characteristics

A

Due to weakening of the large abdominal artery wall causing local dilation, almost always due to atherosclerosis,

  • can be 10-15 cm in diameter
  • lined/filled by thrombus
  • may rupture and produce an emboli
24
Q

What colour is dead muscle?

A

yellow

25
Q

What happens if you have a blockage to your superior mesenteric artery?

A

Lose blood supply to the …

a) intestine: causes malabsorption and intestinal infarction
b) bowel: will die within a day or so with no oxygen, when the mucosal lining starts dying the bacteria in the feces can enter the bloodstream causing septic shock

26
Q

Name 3 consequences as a result of peripheral vascular disease and what other disease it is particularly associated with?

A
  1. intermittent claudication
  2. ischemic rest pain
  3. gangrene

Diabetes

27
Q

What’s Leriche syndrome?

A

Atherosclerosis of the abdominal aorta as it bifurcates into the common iliac arteries

28
Q

Name 6 cells involved in atherogenesis

A
  1. macrophages
  2. lymphocytes
  3. smooth muscle cells
  4. platelets
  5. endothelial cells
  6. foam cells
29
Q

Name the 4 steps of a plaque rupture leading to a blood clot

A
  1. Plaque forms lining an artery, takes many years and is a silent disease
  2. Plaque grows
  3. plaque ruptures - causing the release of TF from the endothelium
  4. Blood clot forms as a result of coagulation activation
30
Q

What are the 3 roles of endothelial cells

A

Secrete collage, stimulate proliferation/migration of smooth muscle cells, alter permeability to lipoproteins

31
Q

What do platelets do other than form a platelet plug?

A

stimulate proliferation/migration of smooth muscle cells through releasing PDGF

32
Q

What are the 2 roles of smooth muscle cells

A

phagocytose oxidized LDLs to form foam cells, secrete collagen and ECM

33
Q

What are the 3 roles of macrophages

A

phagocytose oxidized LDLs to form foam cells, stimulate proliferation and migration of smooth muscle cells, secrete proteases that modify the matrix

34
Q

Name 8 risk factors for an atherosclerosis

A
  1. age (increases with age)
  2. premenopausal women are protected due to estrogen
  3. Familial hyperlipidemia and cholesterolemia
  4. smoking
  5. alcohol - an independent risk factor
  6. hypertension
  7. geography - less-developed nations
  8. diabetes
35
Q

What is the main defect in familial hyperlipidemia and 3 clinical signs

A

Abnormal lipoproteins

  1. corneal arcus
  2. tendon xanthoma
  3. xanthelasma
36
Q

What is the main defect in familial cholesterolemia

A

Defect in LDL receptor on hepatocytes, making it more difficult to take up oxidized LDLs so they remain in the circulation for longer

37
Q

What can hypertension form a strong link between

A

Ischemic heart disease and high diastolic and systolic BP

38
Q

Why is smoking a risk factor for atherosclerosis and ischemic heart disease?

A

It’s a procoagulant that inhibits prostacyclin

39
Q

Why is diabetes a risk factor for atherosclerosis

A

Amino acids react with glucose derivatives to form advanced glycation end products (AGE). AGE cross-links collagen in large vessels - leading to decreased endothelial elasticity (changing the protein properties of the vessel wall) and increased LDLs get trapped - more cholesterol in the intima

40
Q

What is the clinical relevance of LDLs

A

Have a very long half-life (and liver has less of an affinity for them) so they’re more susceptible to oxidative damage

41
Q

Why is aspirin not the best treatment for atherosclerosis

A

Since aspirin is a blood thinner you’re less likely to die of atherosclerosis but more likely to have a hemorrhagic stroke :(

J Term 2 mix (8 decks)

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