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CBE > Week 3 CBE > Flashcards

Week 3 CBE Flashcards

1
Q

what are lipoproteins

A

Protein-and-lipid substances in the blood that carry cholesterol and triglycerides.

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2
Q

3 pathways of lipid/lipoprotein transport

A
  1. Exogenous: GI to peripheral and liver
  2. Endogenous: Liver to Peripheral
  3. Reverse cholesterol transport: Peripheral back to liver
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3
Q

lipoprotein examples

A

chylomicrons, VLDL, IDL, LDL, HDL

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4
Q

exogenous lipid pathways

A

From small intestine transported to:
1. liver
2. peripheral tissues

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5
Q

How lipoprotein facilitates the exogenous lipid pathway - enzymes

A

Chylomicron
Chylomicrons get broken down by an enzyme (LPL)
FFA is given to peripheral tissue
Cholesterol (triglycerides) is given to the liver.

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6
Q

endogenous lipid pathways

A

From liver to:
1. muscle/adipose,
2. back to liver

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7
Q

How lipoprotein facilitates the endogenous lipid pathway- enzymes

A

VLDL is assembled in the liver and sent to circulation.

VLDL is broken down by LPL:
1. triglycerides (NEFA and glycerol) -> muscle & adipose.

Losing triglycerides: VLDL turns to IDL.
IDL has 2 destinies
1. IDL is taken by the liver
2. IDL turns to LDL and transport cholesterol to peripheral tissue

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8
Q

How did VLDL turn to IDL (intermediate density lipoprotein)

A

By losing triglycerides

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9
Q

IDL turn to LDL (significance & enzyme)

A

If IDL is not returned to liver, it will be processed by hepatic lipase (HPL) and turn to LDL.

LDL is very cholesterol-rich, bad cholesterol.

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10
Q

What enzymes facilitates reverse cholesterol transport

A

LCAT (Lecithin-Cholesterol Acyltransferase)
—Adds cholesterol to HDL

ABC-A1 (ATP binding cassette A1 transporter)
—transport free chol. from peripheral tissue to HDL

SRB-1 = scavenger receptor B type 1
—receptor on liver that accepts HDL - cholesterol

CETP = cholesterol-ester transfer protein
—convert HDL to VLDL

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11
Q

What lipoproteins are involved in reverse cholesterol transport

A

HDL
VLDL

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12
Q

Pathways of reverse cholesterol transport

A

HDL: main function - collect free cholesterol

ABC-A1 transports free cholesterol from peripheral tissue to HDL.

LCAT: when activated it esterifies free cholesterol to become a more hydrophobic cholesterol ester, thus transported inwards in the HDL particle.

2 Destinies for HDL:

  1. SRB-1 on liver accepts HDL.
  2. HDL gets converted (by CETP) to VLDL and goes into endogenous lipid pathway.
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13
Q

Where is HDL synthesized?

A

GI and liver

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14
Q

How is HDL transport disrupted?

A

CETP turns HDL into VLDL -> endogenous lipid pathway

(high VLDL means lower HDL levels)

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15
Q

what lipoproteins are triglyceride rich?

what lipoproteins are cholesterol rich?

A

Triglyceride rich: VLDL - endogenous pathway (trig to muscle..)
and chylomicron (trig to muscle, remnant to liver)

Cholesterol rich: HDL and LDL (LDL gives cholesterol and HDL collects cholesterol)

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16
Q

ApoA1 functions

A

HDL

  1. activates LCAT that is circulating (esterification).
  2. binds SRB-1
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17
Q

ApoB100

A

Mainly functions for LDL
Binds LDL receptor for faster cellular uptake (a major risk factor for atherosclerosis)

Facilitate formation of VLDL in liver.

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18
Q

ApoE

A

Mainly functions as ligand of liver receptor
- uptake of chylomicron remnants
- uptake of VLDL remnants, IDL.

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19
Q

ApoB48

A

structural component necessary for the assembly and secretion of chylomicrons

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20
Q

Which cells synthesise cholesterol

A

All nucleated cells:
Mitochondria -> Acetyl-CoA -> cholesterol

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21
Q

How do cells uptake cholesterol

A

LDL deliver cholesterol to peripheral tissues:

LDL-Receptor is expressed to uptake cholesterol from plasma.

Receptor expression will decrease if high intracellular cholesterol.

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22
Q

LCAT

A

HDL has this enzyme to collect free cholesterol

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23
Q

ABC-A1

A

Lipid transporter, from peripheral tissue to HDL

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24
Q

CETP

A

Disrupts HDL(exchange trig with HDL’s cholesterol), converts it to VLDL.

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25
Q

Lab measurement of lipid levels

A

Measure concentration of lipoproteins and apolipoproteins.

26
Q

Routine clinical measure of lipid levels

A

Total cholesterol levels

HDL-C levels

Triglycerides

27
Q

How is LDL-C calculated

A

Total - HDL-C - VLDL-C

28
Q

What drug is used for reducing cholesterol

A

statin

29
Q

Fatty streaks formation (early stage of atherosclerosis)

A
  1. When LDL penetrates the endothelial layer of the arteries
  2. O free-radicals oxidise LDL, these oxidised LDLs are consumed by monocytes.
  3. monocytes become foam cells.
  4. The streak of yellow foam cells are fatty streaks
30
Q

Oxygen free radicals are produced by?

A
  • Glycation reactions (diabetes)
  • smoking toxin
31
Q

Significance of fatty streaks

A

Fatty streaks are often detected during autopsies or imaging studies, predicting atherosclerosis.

32
Q

3 Steps of atherosclerosis

A
  1. Macrophages uptake oxidised LDL. Becoming foam cells
  2. Macrophages stimulate SMC (smooth muscle cells) to become fibroblasts and migrate and form a fibrous cap. Cholesterol will pool beneath fibrous cap
  3. If plaque ruptures, a blood clot will form
33
Q

Difference between angina and myocardial infarction

A

Angina: temporary decreased blood flow to heart

MI: cardiac muscle is damaged from blocked blood blow.

34
Q

what is CRP and hsCRP

A

C-reactive protein
A marker for inflammation.

high sensitivity CRP: inflammation in heart disease.

35
Q

What is troponin - heart disease

A

Regulates muscle contraction.
Specificity: cardiac troponin isoforms can be detected using immunoassays.

36
Q

Whyis troponin used for measurements (3 reasons)

A

1.Elevation in response to myocardial damage.
2. Specific to cardiac muscles.
3. Very sensitive to cardiac damage

37
Q

Threshold for troponin indication of MI

A

Need to be above 99th percentile of the reference population.

38
Q

Heart failure diagnosis - alternatives from imaging

A

Imaging (expensive)

Biochemical diagnosis: Natriuretic Peptide

39
Q

NP in heart failure

A

During heart failure, heart ventricles dilate. Myocytes stretch and release NP.
Atrium releases ANP and ventricles release BNP

40
Q

what do ANP and BNP do - why do myocytes release them (2 reasons)

A
  1. Vasodilation, reduce work for the muscle
  2. promote natriuresis (blood volume)
41
Q

BNP and measurement of it

A

BNP is released by the heart ventricle

After cleavage:
Nt-pro BNP and BNP.
Nt-proBNP is more stable

42
Q

Complications of BNP measurement

A

It has a relatively poor specificity: but it is sensitive

BNP levels can rise due to aging, and many other factors

43
Q

How is BNP measurements used despite poor specificity

A

Normal levels of BNP can be used to rule out heart failure.

44
Q

Complications of cardiac troponin measurements

A

Even though sensitive and high specificity, it doesn’t differentiate the mechanisms of heart injury.

45
Q

Classic:
symptoms of BNP
symptoms of troponin

A
  1. breathless (failure of the heart to pump)
  2. chest pain (obstructed blood flow to cardiac muscles)
46
Q

regulate Hydrogen Ion level (Chemical: buffering and ion exchange. Physiological)

A
  • Buffering with Haem - (Hb-)+(H+) -> HbH
  • Buffering with bicarbonate (HCO3-)
  • Phosphate buffer
  • K+ exchange with H+, intra. K+ goes out, H+ goes in.
  • Physiological
    Lungs remove CO2 (fast), H+ is also used.
    Kidney excrete H+ (slow)
47
Q

Metabolic alka/acidosis and potassium levels

A

To maintain charge balance to some degree
K+ and H+ will exchange:
Metabolic acidosis: Due to H+ accumulation, K+ will be exchanged out
Metabolic alkalosis: Due to low levels of H+, K+ will be exchanged to let intracellular H+ out.

48
Q

Respiratory acidosis and compensatory mechanism (chemical and physiological)

A

carbon dioxide retention -due to-
respiratory defects, CNS disease.

Increased carbon dioxide –> increase H+ conc
Respiratory acidosis

Compensatory:
1. buffering -> Increased bicarbonate (HCO3-)
2. increased kidney excretion H+

49
Q

acute/chronic/acute-on-chronic respiratory acidosis differences

A

chronic will: H+ level isn’t very very high.

–have a higher bicarbonate than acute- as it is always trying to compensate for the high H+.
kidneys increase bicarbonate reabsorption

acute on chronic: very high H+ and very high bicarbonate.

50
Q

chronic respiratory acidosis (physiological compensatory mechanism)

A

Increase renal bicarbonate reabsorption to compensate for sustained high levels of H+ in circulation.

51
Q

Metabolic Acidosis 2 causes and Anion gap

A

Metabolic acidosis: 2 causes
Increased H+
Decreased HCO3-

High anion gap:
Increased unmeasured -ve acids
- diabetic ketoacidosis: ketoacids
- lactic acidosis: lactic acid
- renal failure: decreased H+ excretion
- toxins (ethylene glycol): oxalic acid

Normal anion gap:
Decreased bicarbonate, this is compensated by Cl- reabsorption.
Diarrhea.

52
Q

High anion gap, normal anion gap

A
  1. Increased unmeasured -ve acids (gap between measured)
  2. Increased loss of HCO3- (compensated by Cl- reabsorption)
53
Q

Anion gap

A

Blood is neutral:
cation = anion
but we calculate it with measured cation - measured anion
there is a gap, because there are unmeasured anions
This gap increases, when unmeasured anions increase.

54
Q

Respiratory alkalosis and compensatory mechanism (physiological and buffer)

A

Decreased carbon dioxide -due to respiratory problems
Decreased H+
Respiratory alkalosis.

Compensatory:
1. Reduced H+ excretion,
2. reduced kidney bicarbonate generation.
3. Buffer -> reduce bicarbonate

55
Q

Causes of Metabolic acidosis

A
  • Diabetic Ketoacidosis (DKA): increased H+ production.
  • Severe diarrhea: Loss of HCO3-
  • Renal failure: Decreased H+ excretion.
    poison…
56
Q

Metabolic acidosis

A

High H+, lactic acidosis, DKA

Compensatory:
low CO2, as lung is over-functioning.
H+ will return to normal.

57
Q

Metabolic acidosis effects

A

Increased plasma K+.

Chronic acidosis can lead to bone decalcification
- bone decalcifies to produce phosphate as a buffer.

58
Q

Metabolic alkalosis cause

A

elevated bicarbonate

-abnormal renal absorption
-K+ deficiency, overall increased renal reabsorption
including bicarbonate

59
Q

Metabolic alkalosis is due to
(biochemical)

A

Elevated bicarbonate -> decreases H+

60
Q

Metabolic alkalosis compensatory responses

A
  • Release of H+ from buffers
  • Increased renal bicarbonate excretion despite intial bicarbonate reabsorption.
61
Q

predisposition of fatty streaks

A
  • High LDL concentration
  • damage to arterial wall (hypertension, oxidation/glycation)

CBE (16 decks)

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