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Fall Pharm > Final > Flashcards

Final Flashcards

1
Q

We get cholesterol from what 2 ways:

A

Diet or we make it ourselves

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2
Q

Cholesterol 3 part synthesis in cells:

A

1) Mevalonate from Acetyl-CoA
2) Conversion of mevalonate to squalene
3) Cyclization of squalene to cholesterol

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3
Q

Plaque formation

A

LDL becomes oxidized in the interstitium–>
Macrophages go into swallow up fatty build up–>
they become foam cells–>
foam cells crystalize, die then calcify –>
increased inflammation over time

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4
Q

4 main Lipoproteins:

A

Chylomicrons
VLDL
LDL
HDL

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5
Q

Chylomicrons:

A

Lipoproteins

  • Formed in intestine (dietary)
  • Carry triglycerides and cholesterol
  • Degraded by cells, final in liver
  • Transported to liver where they are converted to VLDL
  • Should not be in blood. only lymphatic system.
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6
Q

VLDL

A

Lipoprotein

  • Secreted by liver
  • Travel to peripheral tissues
  • Converted to LDL
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7
Q

LDL

A

Lipoprotein

  • Main transport mechanism throughout body
  • Transport to cells
  • Uptake through LDL-R
  • Excessive amounts will deposit into arteries
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8
Q

HDL

A

Lipoprotein

  • Takes extra cholesterol out from cells/lipoproteins, transports it to liver for degradation
  • Decreased levels associated with atherosclerosis
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9
Q

Total Cholesterol level

A

<200

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10
Q

LDL level

A

<130

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11
Q

HDL level

A

> 40-50

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12
Q

Triglycerides level

A

<120

the number one fat in our body

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13
Q

Cholesterol drug classes:

A
  • Statins (HMG-CoA Reductase Inhibitors)
  • Niacin
  • Fibrates
  • Binding Resins
  • Absorption Inhibitors
  • PCSK9 Inhibitors
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14
Q

Statins: MOA

A

-Inhibits HMG-CoA Reductase which decreases cellular cholesterol synthesis

  • Decreases LDL (-40%)
  • Increases LDL-R
  • Modest decreases in triglycerides
  • increase in HDL (+10%)
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15
Q

Statins: considerations

A
  • Better at night
  • Enhanced with food
  • 10-80mg
  • Restricted use in children, pregnant/lactating
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16
Q

Statins: toxicity

A
  • Elevated liver enzymes (asian descent)

- CK elevations (muscle pain/weakness)

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17
Q

Niacin: MOA

A
  • Blocks the production of VLDL
  • Decreases VLDL, LDL (-20%)
  • Increases HDL (+25%)
  • Decrease Triglycerides
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18
Q

Niacin: considerations/toxicity

A

2-6g daily

cutaneous vasodilation/flushing

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19
Q

Fibrates: MOA

A

-PPAR mediated lipolysis

  • Decrease VLDL
  • Modest decrease in LDL (-10%)
  • Increase HDL (+15%)
  • Decrease triglycerides
  • Increase lipolysis in liver
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20
Q

Fibrates: Toxicity

A 
Rare:
GI upset
arrhythmias
elevated liver enzymes
potentiation of coumarin
myopathy
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21
Q

Bile Acid Binding Resins: Drug names

A

Colestipol

Cholestyramine

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22
Q

Bile Acid Binding Resins: MOA

A
  • Surrounds dietary fat/biliary acids and prevents their reabsorption
  • Decrease total cholesterol
  • Isolated increases in LDL
  • may increase VLDL
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23
Q

Bile Acid Binding Resins:

considerations

A
  • usually given with statins
  • Granular preparation
  • 5-30g per day
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24
Q

Inhibitors of intestinal sterol absorption: Drug

A

Ezetimibe (Zetia)

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25
Q

Inhibitors of intestinal sterol absorption: MOA

A

Prevents reabsorption of dietary fat/biliary acids by inhibiting NPCT1

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26
Q

PCSK9

A

a protein that binds to LDL-R and will cause it to break down.

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27
Q

PCSK9 inhibitors: MOA

A

Monoclonal antibody binds to PCSK9 which prevents breakdown of LDL-R

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28
Q

PCSK9 inhibitors: considerations

A

New
Expensive
Injections 1-2x wk

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29
Q

autocoid groups

A 
histamine
serotonin
bradykinin
prostoglandin
leukotrienes
30
Q

Chronic inflammation mediators

A 
Interleukins
GM-CSF
TNF
Interferons
PDGF
31
Q

Cox-1

A 
"good" 
"housekeeping"
always on
Protects GI tract
Renal tract
Plt fx
32
Q

Cox-2

A

“bad”

induced during inflammation

33
Q

NSAIDS: MOA

A
  • Inhibition of COX (decreases inflammation)
  • Decreases sensitivity of vessels to bradykinin/histamine (reverse vasodilation in brain to relieve HA)
  • Inhibit plt aggregation (Cox-1)
34
Q

NSAIDS: precautions

A

all can cause GI upset, nephrotoxicity, and heptotoxicity

35
Q

ASA:

MOA

A

Irreversible block of Cox.

Cox1 > Cox2

36
Q

Celecoxib:
MOA
use
SE

A

Cox2 selective
use: arthritis
black box warning for cardiac events, sulfa allergy

37
Q

Ibuprofen:
MOA
SE

A

Cox1=Cox2

less GI upset than ASA

38
Q

Indomethacin:
MOA
Use
SE

A

Cox and Lox (may inhibit phospholipase A and C)
Use: arthritis, gout, patent ductus arteriosis
SE: GI upset 1/3 patients

39
Q

Acetaminophen:

MOA

A

Cox2

no anti-inflammatory effect

40
Q

Glucocorticoids:

Acute action

A

Suppress inflammation
Mobilize energy stores
Improve cognitive fx
Salt and water retention

41
Q

Glucocorticoids:

Chronic use problems

A

Immunosuppression
DM, obesity, muscle wasting
depression
HTN

42
Q

Glucocorticoids:

MOA

A

Blocks transcription/translation:

  • Suppresses pro-inflammation mediators.
  • Up regulate anti-inflammatory mediators.
43
Q

4 main proteins that are upregulated with glucocorticoids:

A
  • Annexin-1 (lipocortin-1)
  • Secretory leukoprotease inhibitor (SLPI)
  • IL-10
  • Inh-NFkB
44
Q

Secretory leukoprotease inhibitor (SLPI)

A

decrease inflammation by blocking protease

45
Q

IL-10

A

Immunosuppressive enzyme

46
Q

Inh-NFkB

A

protein that directly inhibits the NFkB

47
Q

Annexin-1 (lipocortin-1)

A
  • suppresses phospholipase A2

- Inhibits leukocyte response

48
Q

Methotrexate:

A

non-biologic DMARD

blocks adenosine production

49
Q

Cyclophosphamide:

A

non-biologic DMARD

B&T cell suppression

50
Q

Cyclosporine:

A

non-biologic DMARD

Inhibition of interleukins

51
Q

Abatacept (Orencia)

A

Biologic DMARD

Blocks Tcell activation

52
Q

Rituximab (Rituxan)

A

Biologic DMARD

Depletes B-lymphocytes

53
Q

Adalimumab (humira)

A

Biologic DMARD

Anti-TNF-alpha

54
Q

Hierarchical system

A

stimulus travels down neuron, sends neurotransmitter, causes excitatory or inhibitory action

55
Q

Diffuse system

A

Release Neurotransmitter throughout brian

56
Q

A-beta fibers

A

touch and pressure

57
Q

A Delta fibers

A

sharp fast pain/heat

58
Q

C fibers

A

slow dull pain

noxious chemical/ heath

59
Q

Mu receptors

A

Most of the effects from this receptor

60
Q

Delta and kappa receptors

A

less side effects but can cause dysphoric reactions

61
Q

Full agonist of Mu receptors:

A

Morphine

fentanyl

62
Q

Partial agonist of Mu receptors:

A

codeine

oxycodone

63
Q

Morphine metabolism

A

More active after phase 2

64
Q

Heroin metabolism

A

tissue esterases to morphine

65
Q

2 main metabolic pathways for opioids:

A

CYP3A4

CYP2D6

66
Q

Opioids: MOA

A
  • Reduce neurotransmitter release (glutamate, ACh, NE, serotonin, substance P)
  • Hyperpolarize postsynaptic neurons
67
Q

3 classes of opioids:

A

phenanthrenes
phenylheptylamines
phenylpiperidines

68
Q

Strong agonist Phenanthrenes: drugs

A

Morphine
Dilaudid
Heroin

Codeine, oxycodone

69
Q

Strong agonist Phenylheptylamines: drugs

A

Methadone:
(half life 25-50hrs, CYP3A4)

Propoxyphene (Darvon)

70
Q

Strong agonist Phenylpiperidine: drugs

A

Fentanyl
Meperidine (demerol)

Loperamide (diarrhea)

71
Q

Meperidine (demerol)

A

antimuscarinic effects (tachycardia)
(-) inotorpe
seizures

Fall Pharm (8 decks)

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