Oct. 2, 2019 Flashcards

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
What are FOAM CELLS?
LIPOPROTEINS that have been engulfed by MACROPHAGES
26
What do FOAM CELLS release?
FREE RADICALS
27
What effect do FREE RADICALS have in the vessel? | Specific to ATHERO, not just the usual "disruption of DNA blah blah blah"
They kill CELLS, which releases Ca2+ and cause CALCIFICATION
28
The origin of ATHEROSCLEROSIS is..?
...insidious, subtle changes to ENDOTHELIUM
29
What does CRP indicate?
Serum marker for INFLM and elevated levels indicate ATHS
30
3 risk factors of ATHS
- HYPERLIPIDEMIA - HTN - Smoking
31
When do MNFTS appear?
Decades later
32
Provide a quick overview of the role of MACROPHAGES int the formation of PLAQUE, starting with the introduction of MONOCYTES in the ENDOTHELIUM
- 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
Which is the #1 area for ATHS?
Abdominal aorta and iliac arteries
34
Which is the #2 area for ATHS?
Proximal coronary artery
35
Which is the #3 area for ATHS?
Thoracic aorta, femoral and popliteal arteries
36
Define HYPERTENSION
*Persistently* elevated BP
37
Is HTN common?
Yes, approx 22-25% of the population have HHTN
38
? x ? = BP
PERIPHERAL RESISTANCE, CARDIAC OUTPUT
39
What are the 4 major controls of BP?
1) BARORECEPTORS 2) RAAS 3) Volume reg 4) Vascular autoreg
40
SYSTOLE = ?
Pumping phase
41
DIASTOLE = ?
Filling phase
42
When is BP highest (referring to circadian rhythm)?
Highest in the morning
43
When is BP the lowest (referring to circadian rhythm)?
Between 2-5am
44
S/D for a normal BP?
120/80
45
S/D for a high normal BP?
S = 120-139, D = 80-89
46
S/D for STAGE 1 HTN (aka MILD HTN)?
S = 140-159, D = 90-99
47
S/D for STAGE 2 HTN (aka MODERATE HTN)?
S = 160-179, D = 100-109
48
S/D for STAGE 3 HTN (aka SEVERE HTN)?
S = greater than 180, D = greater than 110