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gen-path 2 > CV lecture 1- Arteriosclerosis and Hypertension > Flashcards

CV lecture 1- Arteriosclerosis and Hypertension Flashcards

1
Q

____________ is responsible for more morbidity and mortality than any other category of disease

A

vascular disease

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2
Q

name the 2 principal mechanisms of vascular disease

A

1) Narrowing or obstruction of vascular lumina

2) Weakening of vascular walls, leading to dilation and/or rupture

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3
Q

atherosclerosis is characterized by _________, which are A fatty deposit in the inner lining (intima) of an artery

A

atheromas

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4
Q

ahterosclerosis effects the _________ and _________ arteriolies

A

medium and large

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5
Q

what condition is classified by: medial calcification without luminal narrowing or intimal disruption

A

Mönckeberg’s medial calcific sclerosis

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6
Q

what are the 2 types of atherosclerosis? (describe both types)

A

1) hyaline type: thickening of basement membrane

2) hyperplastic (proliferative) type: fibrocellular intimal thickening

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7
Q

malignant hypertension and scleroderma both cause what type of atherosclerotic formation?

A

hyperplastic

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8
Q

hyaline type athrosclorosis is caused by _________ and ________

A

hypertension and diabetes mellitus

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9
Q

Atheromas protrude into the ______ of the vessel

A

lumen

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10
Q

how can atheromas cause injury to the body?

A

1) can enlarge and obstruct blood flow
2) May weaken the underlying media of the artery (aneurysm)
3) Plaques can rupture, resulting in catastrophic vessel thrombosis

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11
Q

what regions of the world have a high prevalence for atherosclerosis? which regions have a low prevalence?

A

High Prevelance – United States, Western Europe

Low Prevelance – Africa, Far East

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12
Q

name the Non-modifiable (“constitutional”) modifiers for risk of atherosclerosis

A

Genetics (family history) – most important in this group

Increasing age

Male gender

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13
Q

what are the major modifiable risk factors for atherosclerosis?

A

Hypercholesterolemia – high LDL, low HDL

Diabetes Mellitus

Hypertension

Cigarette smoking

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14
Q

what modifiable risk factor will increase your risk for Atherosclerosis by 200%?

A

smoking one pack of cigarettes a day

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15
Q

what are the steps involved in the “Response-to-injury” hypothesis for atherosclerosis?

A

1) endothelial cell injury
2) accumulation of lipoproteins
3) monocyte adhesion

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16
Q

what are the common sites for atheroma formations?

A
  1. Major arterial branch points
  2. Abdominal aorta
  3. Coronary arteries
  4. Popliteal arteries
  5. Carotid arteries
  6. Cerebral arteries
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17
Q

atheroma plaques contain what substances?

A

plaques contain collagen, lipid, myofibroblasts, macrophages, neovascularization.

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18
Q

during atheroma formation, a fibrous cap, composed of __________ and ________, develops over a central core of lipid/cellular debris with cholesterol

A

smooth muscle cells (myofibroblasts) and collagen

19
Q

Progressive changes in atheroma plaques include:

hint: theres 6 of them

A

1) ulceration
2) fissure formation
3) thrombosis
4) embolization (thrombus or debris from the central core)
5) calcification
6) hemorrhage into the plaque from neovascularization

20
Q

Fatty streaks appear in atherosclerosis involving __________, and is independent of geography, gender, race and environment

A

children

21
Q

T/F: Fatty streaks will form in almost any location, regardless of if that location is prone to atheroma formation

A

True

22
Q

T/F: fatty streaks signal the start of atheromas formation

A

False

not all atheroma formations will start as fatty streaks
- its a possible step in formation, but not always present

23
Q

what complications are associated with atherosclerosis?

theres 5

A 
Ischemic heart disease (MI)
Cerebral infarct (stroke)
Gangrene
Renal artery stenosis (narrowing)
Aortic aneurysm (dilation/bulge)
24
Q

what is mild hypertension?

what is mild to severe hypertension?

A

Mild: BP between 140/90 - 159/104 mmHg

Moderate – severe: BP greater than 160/106 mmHg

25
Q

Hypertension affects approximately _____% of the US population

A

25%

26
Q

the “peak death rate” for Myocardial infarctions (heart attacks) was ______% in the 1960s

A

54%

27
Q

what is the current death rate for all atherosclerosis-related complications ?

A

50%

28
Q

___________ hypertension Accounts for 90% or more of all hypertension

A

essential hypertension

29
Q

Contributing factors for hypertension include:

A 
genetics
stress
obesity
increased salt intake
inactivity
cigarette smoking
30
Q

what are the symptoms of low, and moderate, hypertension?

A

NO SYMPTOMS

31
Q

name the symptoms of severe hypertension:

A

Headache
Fatigue
Dizziness
Palpitations

32
Q

what is “essential hypertension”

A

hypertension that has no identifiable cause

33
Q

what are the FOUR factors involved in the pathogenesis of ESSENTIAL hypertension?

A

a) Peripheral vascular resistance (vasoconstriction)
b) hereditary factors
c) Reduced sodium excretion → salt and water retention→ increased plasma volume and cardiac output
d) environmental factors

34
Q

what are the COMPLICATIONS of hypertension?

theres 6 of them

A

1) Concentric left ventricular hypertrophy (LVH)
2) LVH + ventricular dilation
3) Atherosclerosis and arteriolosclerosis
4) Retinal injury
5) Nephrosclerosis
6) Dissecting hematoma of the aorta

35
Q

which complication of hypertension, if “decompensated”, can lead to coronary heart failure (CHF)?

A

LVH + ventricular dilation

LVH = left ventricular hypertrophy

36
Q

what occurs during decompensated hypertensive heart disease?

A
  • hypertrophy no longer adequate to provide normal cardiac output due to decreased myocardial contractility
  • results in left ventricle dilation and gradual onset of CHF
37
Q

what are the characteristics of “Concentric Hypertrophy”?

A
  • Thickening of the left ventricular wall at the expense of the left ventricular chamber
  • little or no increase in the outside cardiac dimensions.

(heart increases muscle mass at the expense of chamber volume)

38
Q

name the characteristics of Accelerated (Malignant) Hypertension:

A
  • Relatively rapid onset
  • Often superimposed on previous hypertension
  • Very high systolic and diastolic pressures
39
Q

the complications of accelerated (malignant) hypertension include:

A 
cerebral edema
papilledema
encephalopathy
renal failure
cerebral hemorrhage
40
Q

the thickness of what structure will determine if it is a vulnerable plaque or a stable plaque?

A

the fibrous cap

  • it surrounds the lipid core of the plaque

thick cap = stable
thin cap = vulnerable

41
Q

what are the PRE-clinical phases of plaque formation?

A

1) normal artery
2) fatty streak (may not be part of progression)
3) Fibrofatty plaque
4) Advanced/vulnerable plaque

42
Q

what differentiates a foam cell from a macrophage?

A

foam cells are macrophages that have become engorged with lipoproteins (cholesterol)

43
Q

during atherosclerosis progression, what happens once monocytes adhere to the lipoprotein deposits?

A
  • migration into intima

- differentiation into macrophages and “foam cells” (macrophages that have ingested lipid)

44
Q

what are the lipoproteins that adhere to the vessel walls following endothelial injury?

A

LDL and cholesterol

gen-path 2 (7 decks)

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