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CPR I > Lecture 17+18 > Flashcards

Lecture 17+18 Flashcards

1
Q

Cholesterol ABC transporters

A

release free cholesterol into the blood from membranes undergoing turnover and from dying cells

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2
Q

macrophages and reverse cholesterol transport

A
  1. they uptake LDL with the LDL-R and uptake oxLDL by the SRs
  2. release free cholesterol by the ABCA1 transporter for HDL
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3
Q

what does LCAT do?

A

an enzyme synthesized in the liver and released into the blood.

needs to be activated by apo A-1

binds to HDL and uses a fatty acid from phosphatidylcholine (PC) of the HDL membrane to form
cholesteryl esters (CE) in the blood.

CE move immediately inside the HDL.

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4
Q

The two fates of mature HDL?

A

HDL can bind to the SR-B1 receptor and allow cholesteryl esters to flow into the liver, then can be filled up again by LCAT

HDL can interact with VLDL via the CETP (a hydrophobic channel is formed). Nonpolar lipids are exchanged

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5
Q

Functions of HDL

A
  1. transport excess cholesterol from tissues/ macrophages to the liver
    this can be done by SR-B1 or CETP
  2. prevent or reduce fatty streak formation caused by foam cells
  3. act as a circulating “reservoir” of apo C and apo E which are transferred to nascent chylomicrons and VLDL.
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6
Q

Tangier disease (hypolipidemia)

A

this occurs due to extremely low HDL levels caused by a defect of the ABAC1 transporter, thus less free cholesterol

features: 
orange colored tonsils in nearly all children (due to cholesterol) 
peripheral neuropathy 
premature MI 
enlargement of liver and spleen
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7
Q

Abetalipoproteinemia and Hypobetalipoproteinemia (hypolipidemias)

A

both show low CM, VLDL, and LDL levels

abetalipoproteinemia = MTP deficiency
TAG = below 19mg/dL
total cholesterol = below 50mg/dL

hypobetalipoproteinemia = apo B-48 and 100 deficiency

features: 
failure to thrive 
TAG accumulation 
retinitis pigmentosa 
peripheral neuropathy  
Acanthocytosis (RBC with spicules)
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8
Q

normal ranges for cholesterol in the blood?

A

normal LDL = 100-130mg/dL

normal HDL =

males: 50
females: 70

normal VLDL = 20-30

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9
Q

primary and secondary causes of dyslipidemia

A

primary:
genetic disorders

secondary: 
smoking
lifestyle
diet 
diabetes 
obesity 
etc.
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10
Q

Friedewald equation

A

LDL-C = total C – [(HDL-C) + (TAG / 5)]

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11
Q

Type 1: Familial Hyperchylomicronemia (rare)

A

seen to have abnormally high TAG levels due to high CM levels

normally CM are not present in a fasting serum, however they are present in those who have this disease. can be seen by creamy layer on top of serum

this can result from a LPL deficiency and/or a apo C-II deficiency (impacts CM clearance)

clinical features:

  1. onset is childhood
  2. lipemia retinalis
  3. heptosplenomegaly
  4. recurrent epigastric pain
  5. eruptive xanthomas
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12
Q

Type IIa: Familial Hypercholesterolemia (common)

A

seen to have high HDL, normal VLDL, and clear serum

higher risk of CVD and MI. Treatment is holistically and statins

heterozygous: adult onset
homozygous: childhood onset; chance of MI

this is due to a defective LDLr (AD)

clinical:
seen to have tendon xanthomas and xanthomas near eyelids
diminished clearance of LDL

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13
Q

Type IIb: Familial Combined Hyperlipidemia (common)

A

seen to have high LDL, VLDL, and lipemic serum

risk of CVD and MI. treated holistically along with statins

heterozygous show puberty onset

result from: overproduction of apo B-100, VLDL, or defective clearance of LDL

xanthomas are rare

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14
Q

Type III: Dysbetalipoproteinemia (rare)

A

high CM remnants and IDL, abnormal beta-VLDL

adult onset is seen with accelerated atherosclerosis

results from apo E deficiency

clinical:
seen to have palmar and tubereruptive xanthomas on elbows and knees

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15
Q

Type IV: Familial Hyperprebetalipoproteinemia (common)

A

High VLDL, normal LDL, and low HDL

plasma is lipemic

High VLDL level may result from LPL deficiency or VLDL overproduction. High VLDL lead to low HDL

high serum TAG’s lead to the risk of pancreatitis and CVD

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16
Q

Type V: Familial Mixed Hypertriacylglyerolemia

A

High CM and high VLDL

patients blood will be lipemic and a creamy layer will be seen on top.

17
Q

How to treat hypercholesterolemia?

A
  1. to stimulate LDL-R synthesis

2. increase LDL-R recycling

18
Q

PCSK9 inhibitor

A

PCSK9 inhibitors lead to increased recycling of the hepatic LDL receptors. This increases the amount of LDL receptors by reducing LDL-R degradation in
hepatocytes

19
Q

LDL-B

A

smaller and more dense than LDL-A
is oxidized to ox-LDL

LDL pattern B can result from saturated fatty acids, tans fats, and cleavage of TAG’s

higher risk of CVD

20
Q

Lp(a)

A

very similar to LDL, but it has a apo-A linked to apo B-100 by a disulfide bond.

competes for the binding of fibrin, thus may reduce the removal of clots and trigger stroke or MI

21
Q

How are prostanoids formed?

A

They are formed from arachidonic acid by COX

arachidonic acid comes from the membrane phospholipid; converted by phospholipase A2

22
Q

What are the prostanoids and what do they do?

A

PGE-2 = mediator of inflammation

PGF2 = induction of labor in pregnant uterus

PGI2 (prostacyclin) = inhibits platelet aggregation and vasodilation

TXA2 (thromboxane A2) = facilitates platelet aggregation and vasoconstriction (antagonist of PGI2)

23
Q

inhibitors of eicosanoid synthesis

A

cortisol inhibits phospholipase A2 and COX-2 (anti-inflammatory)

aspirin and NSAIDs inhibit COX 1 and 2; again anti-inflammatory

24
Q

How are leukotrienes synthesized

A

membrane phospholipid is converted to AA by phospholipase A2

AA is converted to leukotriene by lipoxygenase

synthesized in mast cells

25
Q

Effects of leukotrienes

A

mediate allergic and anaphylactic response

bronchoconstriction and airway obstruction (asthma)

inhibited by cortisol and lipoxygenase inhibitors

26
Q

What are the steps of hemostasis

A
  1. vascular spasm / vasoconstriction
  2. platelet plug formation / primary hemostasis
  3. blood coagulation / secondary hemostasis
  4. clot stabilization and resorption
27
Q

what occurs during vascular spasm

A

trauma to the vessel results in SM contraction due to the release of endothelin

transient effect

28
Q

platelet plug formation

A
  1. Exposure of subendothelial collagen
  2. Platelet adhesion via GPIA and GPIB (via vWF) to subendothelial collagen
  3. Platelet activation, shape change and degranulation (ADP release)
  4. ADP binds to neighboring platelets to increase intracellular calcium and decrease intracellular cAMP;
    Increased TXA2
  5. Platelets recruited to the site of injury
  6. Platelet aggregation via fibrinogen linking adjacent platelets via GPIIB/IIIA
29
Q

Bernard- Soulier syndrome

A

A defect in the GP-IB

defective platelet adhesion and aggregation

30
Q

What is vWF deficiency associated with

A

defect in primary and secondary hemostasis

defective formation of platelet plug and coagulation

31
Q

Thromboxane A2 formation

A
  1. membrane phospholipids to AA due to phospholipase A
  2. AA to PGG2
  3. PGG2 to PGH2
  4. PGH2 to TXA2 by thromboxane synthesis
32
Q

Glanzmann Thrombasthenia

A

a defect in gp-IIB and gp-IIIA

impaired aggregation of the platelets

33
Q

Bleeding test

A

increase in bleeding time / defective platelet aggregation may point to a defect in hemostasis

34
Q

extrinsic pathway to the formation of thrombin?

A
  1. Tissue injury leads to the release of tissue factor or factor III
  2. Factor VII is activated by tissue factor to Vlla
  3. Factor VIIa and tissue factor, with Ca and phospholipids, activate factor X
35
Q

intrinsic pathway of thrombin formation

A
  1. exposure of collagen leads to the activation of factor XII
  2. XIIa acts on XI to activate it
  3. XIa acts on IX to activate it
  4. thrombin activates factor VIII to VIIIa
  5. IXa and VIIIa and Ca and phospholipids activate X to Xa
36
Q

common pathway of thrombin formation

A
  1. thrombin acts on factor V to Va
  2. Xa combines with Va, phospholipids, and Ca to form the prothrombin to form thrombin
  3. Prothrombin complex splits prothrombin to form thrombin
  4. thrombin acts on fibrinogen to form fibrin
  5. thrombin activates factor XIII to XIIIa
  6. Fibrin monomers are covalently crosslinked by factor XIIIa to form cross-linked fibrin (Hard clot)
37
Q

Lab tests for the coagulation cascade?

A

prothrombin time (INR): tests the extrinsic pathway

aPTT: tests the intrinsic pathway

CPR I (13 decks)

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