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pharmacology final ( 1st sem) > B: 21-24 > Flashcards

B: 21-24 Flashcards

1
Q

Dyslipidemia drugs

A

Atorvastatin
Rosuvastatin
Simvastatin
Ezetimib
Fenofibrate
Colesevelam

Evolocumab, Alirocumab (PCSK9 Inhibitor= inhibits degredation of LDL-R )

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2
Q

Statins MOA

A

HMG-CoA reductase inhibitors which is the rate limiting step of endogenous cholesterol synthesis

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3
Q

Statins actions

A

Liver cholesterol ↓
LDL-R expression ↑ (liver compensation to clear LDL, vLDL remnants from blood)

HDL ↑ 5-15%
Plasma LDL ↓ (20-50% reduction)

VLDL synthesis by liver ↓
Plasma TG ↓

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4
Q

Atorvastatin
Rosuvastatin
Simvastatin

Difference

A

Atorvastatin: Active as given
Rosuvastatin: Active as given
Simvastatin: Prodrug

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5
Q

Atorvastatin
Rosuvastatin
Simvastatin

Metabolism

A

CYP450

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6
Q

Atorvastatin
Rosuvastatin
Simvastatin

Indications

A

Atherosclerotic vascular disease
Acute coronary syndrome
Reduced risk of cardiovascular disease
Reduced mortality in ischemi heart dieseas

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7
Q

Statins side effects

A

Hepatotoxicity
Myalgia
Rhabdonyolysis

increase creat kinase in 10%

allergy “statin intolerance”

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8
Q

Statins contraindications

A

Teratogenic
Liver diseas caution

food which inhibit CYP450 eg grapefruit increase hepatotoxicity risk and myopathy.

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9
Q

Colesevelam MOA

A

resin

Bile acid binding resin are

Large non absorbable polymers that bind bile acid and prevent their absorption in intestine –> increase BA in intestiine > GI side effect

this divert hepatic cholesterol to the synthesis of new bile >> decreasing cholesterol in tightly regulated pool

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10
Q

Bile acid sequestrans drug

A

Colesevelam

colestipol

cholestyramine

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11
Q

Colesevelam how to give and when?

A

Oral
With meals

Dont give togather with other drugs (warfarin, thiazide, digoxin, aspirin, statin) and vitamins (K, folate) (wait btw. 4 h)

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12
Q

Colesevelam indications

A

Primary hypercholesterolemia type IIA (LDL↑)
With Statins

pruritis

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13
Q

Colesevelam side effects

A

VLDL ↑
TG ↑

  • GI: bloat, constipation, diarrhea , Vit. ADEK malabsorption
  • Hyperglycemia
  • Gall stones
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14
Q

Sterol absorption inhibitors

A

Ezetimibe

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15
Q

Ezetimibe MOA

A

decrease intestinal absorption by
Block NPC1L1 in intestine
Reduce cholesterol absorption

Liver cholesterol ↓
LDL-R expression ↑
Plams LDL ↓ (20% reduction)

5% increase HDL

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16
Q

PCSK-9 inhibitors

A

Evolocumab, Alirocumab (PCSK9 Inhibitor= inhibits degredation of LDL-R )

Humanized monoclonal antibody against enzyme PCSK-9, which normally transport LDL-R to lysosomal degradation

  • decreases LDL-R recycling > increase in LDL-R > Decreased LDL
    se: Local rxn at site of injection, URT (flu-like symptoms)
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17
Q

Alirocumab, Evolocumab

indications

A

PCSK-9 inhibitors

  • familial hypercholestermeia
  • resistant hypercholesteremia
  • statin intolerance
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18
Q

Carbonic Anhydrase inhibitors

A

Acetazolamide

Brinzolamide
Dorzolamid
Methazolamid

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19
Q

Acetazolamide indicaitons

A
  • Diuretic use if edema+ metabolic alkalosis
  • Glaucoma (topical brinzolamid, dorzolamid)- decreases secretion of H2CO3 by ciliary epi into aquous humor > decreases IOP
  • Mountain sickness: decreases H2CO3 secretion into CSF pro by choroid plexus >> acidosis of CSF> Hyperventilation which protect against high alititude sickness
Innr ear disorder
Urinary alkalosis (alkalinization of urine --\> ppt Ca salt --\> renal stones
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20
Q

Acetazolamide side effects

A 
Metabolic acidosis
Renal stones (due to urine alkalinization)

Rapid tolerance ( 1 week application only)

Renal K+ wasting

paraesthesia

Hyperammonemia in cirhosis ( due to urine alkalinization prevents NH3 > NH4+ > hepatic encephalopathy)

self-limiting diuresis in 2-3 days

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21
Q

Loop diuretics MOA and names

A

Furosemide

Torsemide
Ethacrynic acid

Inhibition of Na/K/2Cl in the thick ascending limb

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22
Q

Inhibition of Na/K/2Cl in the thick ascending limb will cause

A

Loss of NaCl
Loss of luminal positive potential (Mg,Ca reab.↓)
K and H wasting
Hypokalemic metabolic alkalosis
XOX-2 ↑ → GFR ↑

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23
Q

Furosemide drug interactions

A

NSAID’s (Decreases efficacy )

Aminoglycosides (ototoxicity)

Lithium
Digoxin

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24
Q

How are they different?

furosemide

ethacrynic acid

A

Furosemide is a Sulfa drug
Ethacrynic acid is not a Sulfa drug

BOTH are loop diuretics

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25
Furosemide indications
- HF - pulmonary edema - other forms of edema - Severe hypercalcemia HTN Acute renal failure management
26
Furosemide side effects
Sulfa drug Hypovolemia Hypokalemic metabolic alkalosis Ototoxicity Hypocalcemia Hypomagnesemia Hyperuriceria
27
Thiazides diuretics MOA
Inhibition of Na/Cl transporter in the distal conv. tubule
28
Hydrochlorothiazide drug properties
Sulfa drug Oral 6-12 h
29
Hydrochlorothiazide drug interactions
Digoxin Avoid in DM NSAID (efficacy decreased due to inhibition of PG, which are important in maintaining GF) Gout ( due to hyperuricemia SE)
30
Hydrochlorothiazide indications
HTN mild HF Hypercalciurea w/stones. (Nephrolithiasis) Nephrogenic DI Osteoporosis
31
Hydrochlorothiazide side effects
Sulfa - Hypokalemic metabolic alkalosis - Hyponatremia - Hypercalcemia , Hyperuricemia , Hyperglycemia -hypomagnesmia Lithium levels ↑
32
Thiazides diuretic drugs
Hydrochlorothiazide Indapamide chlorothiazide(1957) -parenteral only chlorthalidone
33
Indapamide indications
HTN Can be combined with ACEi
34
Mannitol MOA How to give? Duration of action
Osmotic diuresis IV Short
35
Mannitol indications
* solute overload in * rhabdomyolysis, * hemolysis, * tumor lysis syndrome * Acute Glaucoma * brain edema w/coma * Intracranial HTN
36
Mannitol side effects
- hyponatremia followed by Pulmonary edema - hypernatremia as H2O excreted - headache - nausea, vomit Na imbalance Acute hypovolemia
37
ENaC inhibitor
Amiloride triamteren
38
Amiloride MOA How to give? Duration?
ENaC inhibitor oral ! 12-24 h
39
Amiloride indications
-Hypokalemia caused by other diuretics Nephrogenic DM Liddle's syndrome - usually in combo with thiazide (Na/Cl transporter inhibitor) - (book)
40
Amiloride side effects
Hyperkalemia
41
ADH antagonist
Tolvaptan Conivaptan
42
Tolvaptan MOA Receptor preferance How to give? Duration?
ADH antagonist V2-R antagonist parenteral !! 12-24 h
43
Tolvaptan indications
SIADH hyponatremia
44
Tolvaptan side effects
- infusion site rxn - demyelination if hyponatremia treated rapidly!! Polyuria Thirst Hypernatremia
45
Antihistamines H1-r blockers Types
1st gen: Diphenhydramine, Promethazine, Dimetindene 2nd gen: Cetirizine, Fexofenadine, loratidine 3rd gen: desloratidine, levo-citrizine
46
Antihistamines- 1st gen
Diphenhydramine Promethazine Dimetindene
47
Antihistamines- 2nd gen
Cetirizine (zyrtec) Fexofenadine loratidine (clarithine)
48
Antihistamines MOA
H1-R antagonists
49
Antihistamines- 1st gen How to give Duration Metabolism Molecule type
Oral, parenteral 4-12 h CYP450 Lipophilic
50
Diphenhydramine indications
IgE mediated allergies (hay fever, urticaria, ) Sedative Antiemetic Sleep aid Anti motion sickness Pregnancy nausea Acute extrapyramidal symp. (eg. due to antipscychotic)
51
Diphenhydramine side effects
Sedation Antimuscarinic : dry mouth, blurred vision) a-R inhibatory effect: orthostatic hypotension Interact with alcohol- Sedation: BZD , Alcohol
52
Promethazine special features
Less anti motion sickness effect More sedative More autonomic effect
53
Dimetindene special features
Treatment of allergic reactions Minimally cross BBB; milder SE
54
Antihistamines- 2nd gen What is special about them?
H1-R antag. at peripheral No autonomic or anti motion sickness effect
55
Cetirizine Fexofenadine loratidine How to give Duration Metabolism Molecule type
Oral 12-24 h CYP450 Less lipophilic
56
Cetirizine Fexofenadine Indications
IgE allergies ( hay fever, angioedema
57
Cetirizine Fexofenadine Side effects
Sedation Arrhythmias in overdose When interact with alcohol- Sedation
58
H2-r blockers
* cimetidine (+weak anti-androgenic effect) * ranitidine * famotidine * nizatidine
59
Histamine analogue name, moa
* beta-histine dihydrochloride: * weak H1 agonist * H3 antagonist
60
beta-histine indication
* vestibular vertigo * menieres syndrome (virtigo+hearing loss)
61
beta-histine MOA
* local vasodialation improves inner ear microcirculation * dose-depending inhibiting effect in CNS on spike-generation in vestibular nuclei neurons.
62
beta-histine CI
* peptic ulcer * never give histamine + antihistamine

pharmacology final ( 1st sem) (15 decks)

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