Oct. 2, 2019 Flashcards

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1
Q

Define HYPERLIPIDEMIA

A

Elevated levels of LIPIDS (fats) in the B

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2
Q

3 examples of LIPIDS

A
  • CHOLESTEROL
  • TRIGLYCERIDE
  • PHOSPHOLIPIDS
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3
Q

Roughly what % of the population of HYPERLIPIDEMIA?

A

About 40%

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4
Q

Are LIPIDS soluble?

A

No, insoluble

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5
Q

How are LIPIDS transported through the B?

A

By CARRIER PROTEINS

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6
Q

What is an example of a CARRIER PROTEIN?

A

APOPROTEIN

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7
Q

LIPID + APOPROTEIN = ?

A

LIPOPROTEIN

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8
Q

What determines the types of LIPOPROTEIN?

A

The density

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9
Q

3 examples of LIPOPROTEINS

A
  • VLDL
  • LDL
  • HDL
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10
Q

T or F:

LIPIDS are heavier the PROTEINS

A

F, other way around

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11
Q

Role of CHYLOMICRON?

A

Transports LIPIDS from GI tract into B

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12
Q

Which is worse for your health:

LDL or HDL

A

LDL

L = lousy

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13
Q

What does ATHEROS (a greek word) translate into?

A

Describing something soft or paste-like

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14
Q

SCLER = ?

A

Hardening

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15
Q

Define ATHEROSCLEROSIS

A

Deposit of “paste” (PLAQUE) in INTIMA of vessel (not in LUMEN)

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16
Q

What is an ATHEROMA?

A

A FIBROFATTY LESION in INTIMA of ARTERIES

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17
Q

T or F:

ATHEROMA is a BENIGN NEOPLASM

A

F, not a tumor despite the “OMA”

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18
Q

An ATHEROMA is a space-occupying-?

A

LESION

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19
Q

What are the 3 progressive lesions that develop during ATHERSCLEROSIS?

A

1) FATTY STREAK
2) FIBROUS ATHEROMATOUS PLAQUE
3) COMPLICATED LESION

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20
Q

What is a FATTY STREAK made up of?

A

MACROPHAGES, FOAM CELLS, SM CELLS

21
Q

What is a FIBROUS ATHERMATOUS PLAQUE made up of?

A

MACROPHAGES, FOAM CELLS, SM CELLS, accumulation of LIPIDS, scar tissue, Ca2+

22
Q

What is CALCIFICATION and why does it happen?

A

Build-up of Ca2+ as a result of CELL death

23
Q

What happens with a COMPLICATED LESION?

A

Hemorrhaging/bleeding into PLAQUE

24
Q

Explain the effect MACROPHAGES have on SM CELLS? Why?

A

MACROPHAGES release GF which stim SM CELLS to proliferate and move into the INTIMA

25
Q

What are FOAM CELLS?

A

LIPOPROTEINS that have been engulfed by MACROPHAGES

26
Q

What do FOAM CELLS release?

A

FREE RADICALS

27
Q

What effect do FREE RADICALS have in the vessel?

Specific to ATHERO, not just the usual “disruption of DNA blah blah blah”

A

They kill CELLS, which releases Ca2+ and cause CALCIFICATION

28
Q

The origin of ATHEROSCLEROSIS is..?

A

…insidious, subtle changes to ENDOTHELIUM

29
Q

What does CRP indicate?

A

Serum marker for INFLM and elevated levels indicate ATHS

30
Q

3 risk factors of ATHS

A
  • HYPERLIPIDEMIA
  • HTN
  • Smoking
31
Q

When do MNFTS appear?

A

Decades later

32
Q

Provide a quick overview of the role of MACROPHAGES int the formation of PLAQUE, starting with the introduction of MONOCYTES in the ENDOTHELIUM

A
  • MONOCYTES bind to ENDOTHELIUM
  • Pass to INTIMA
  • Transform into MACROPHAGE
  • Engulf LIPIDS and release FREE RADICALS (oxidize LDL)
  • Release GF which stim the growth and proliferation of SM CELLS, which enter the INTIMA
  • ATHEROMA
33
Q

Which is the #1 area for ATHS?

A

Abdominal aorta and iliac arteries

34
Q

Which is the #2 area for ATHS?

A

Proximal coronary artery

35
Q

Which is the #3 area for ATHS?

A

Thoracic aorta, femoral and popliteal arteries

36
Q

Define HYPERTENSION

A

Persistently elevated BP

37
Q

Is HTN common?

A

Yes, approx 22-25% of the population have HHTN

38
Q

? x ? = BP

A

PERIPHERAL RESISTANCE, CARDIAC OUTPUT

39
Q

What are the 4 major controls of BP?

A

1) BARORECEPTORS
2) RAAS
3) Volume reg
4) Vascular autoreg

40
Q

SYSTOLE = ?

A

Pumping phase

41
Q

DIASTOLE = ?

A

Filling phase

42
Q

When is BP highest (referring to circadian rhythm)?

A

Highest in the morning

43
Q

When is BP the lowest (referring to circadian rhythm)?

A

Between 2-5am

44
Q

S/D for a normal BP?

A

120/80

45
Q

S/D for a high normal BP?

A

S = 120-139, D = 80-89

46
Q

S/D for STAGE 1 HTN (aka MILD HTN)?

A

S = 140-159, D = 90-99

47
Q

S/D for STAGE 2 HTN (aka MODERATE HTN)?

A

S = 160-179, D = 100-109

48
Q

S/D for STAGE 3 HTN (aka SEVERE HTN)?

A

S = greater than 180, D = greater than 110