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Pharm 3 > Drugs of Unit 3 in random order > Flashcards

Drugs of Unit 3 in random order Flashcards

1
Q

Disopyramide

A

Tx: Arrythmias (Class Ia)

Mech: Na channel blocker

  • Even stronger antivagal effects (than quinidine)

SE:

  • Antimuscarinic effects (opposite of DUMBBELS)
    • Wouldn’t use w/ glaucoma pts
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1
Q

Sotalol

A

Tx: arrytmhias (Class III)

Mech: K+ channel blocker

Also a beta blocker

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1
Q

Heparin

A

Tx: Anticoagulant

Mech: Heparin binds to anti-thrombin (protease inhib) and increases its affinity for clotting factors by 1000x

Low doses: inhibits Xa, decreasing formation of thrombin

High doses: inhibits thrombin and irreversibly binds to IXa, XIa, and XIIa

Heparin inhibits clotting in vivo and in vitro

Activates lipoprotein lipases in blood

Where we get it: located in mast cells

Harvest it from cow lung and pig intestines

Strong neg charge

Not synthetic-each batch tested individually

Pharmacokinetics: IV or subQ

Too large to be absorbed in GI tract or pass placenta

Not risk free in pregnancy though

Immediate onset–T1/2=1 hour

Degradation via heparinase

Can bind to variety of proteins so dose response in unpredictable

_Toxicity: _

  • Generally non toxic
  • Major danger is bleeding
  • Overdose treated w/ protamine sulfate
    • Strong pos charge binds w/ strong neg of heparin
  • Long term use can lead to
    • Osteoporosis-act. osteoclasts
    • Thrombocytopenia-loss of platelets
      • HIT-heparin induced thrombocytopenia
    • Hypersensitivity-rare but we are injecting animal products
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2
Q

Isosorbide dinitrate

A

Tx: Angina

Slow release nitrate formulation

Can be given orally

Slow enough that effects occur before 1st pass metabolism

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2
Q

“-afils”

A

Sildenafil

Vardenafil

Tadalafil

Avanafil

Tx: ED

Mech:

  • Inhibits type 5 cGMP phosphodiesterase
  • Nitrates→NO→cGMP→smooth m relax
  • cGMP degraded to 5’GMP via type 5 cGMP phosphodiesterase
  • Relaxes arteries in corpus cavernosum→increase BF

SE:

  • Slight drop in BP
    • Do not use w/ alpha 1 blockers or nitrates
    • Too much drop in BP
  • Stroke
  • MI (may be due to activity)
  • Visual disturbances
    • Impaired blue/green color discrimination
    • NAION-some potential for damage to retina induced by cGMP PDE inhibitors

Metabolism: P450

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2
Q

Calcium chelators

A

Citric acid (in blood transfusion bags(

ADTA

EGTA

Tx: Anticoagulants

Mech: Chelate Ca

Remove Ca from clotting cascade (4 steps need Ca)

We don’t give these to people b/c Ca is involed w/ lots of mechanisms

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2
Q

Fondaparinux

A

Tx: Anticoagulant

Synthetic heparin like drug

T1/2=17 hrs

Acts only on Xa

Can cross placenta

Can’t bind protamine

Given SubQ

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2
Q

Warfarin

A

Tx: Anticoagulant

Mech:

  • Vit K analog–*Koagulation*
  • Inhibits enzyme that allows vit K to be recycled
    • Leads to vit K deficiency
  • Vit K is essential for factors 7, 9, 10 and prothrombin
  • Works indirectly-doesn’t directly block clotting cascade

Route: Oral

Pharmacokinetics:

  • Factor T1/2s (hrs)
    • VII–6
    • IX–24
    • X–40
    • II–60
  • So 5-6 T1/2s for 99% to be gone
    • 30-36 hrs
    • So initial onset is 24+ hours
  • Metabolism
    • P450
    • Lots of drug interactions
      • Phenytoin/barbituates vs grapefruit juice, etc.
    • Diet interactions
      • Lots of Vit K in green veggies

Toxicity:

  • Overdose-tx w/ Vit K
  • Hemorrhage
  • Can pass placenta-preg. category X
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2
Q

“-kinase”s

A

Streptokinase

Urokinase

Tx: Thrombolytic agent

(dissolve formed clots)

Mech:

  • Urine plasminogen activator=Enzyme activator
  • Plasminogen→plasmin
  • Plasmin:
    • hydrolyzes fibrin
    • degrades fibrinogen
    • degrades factors V and VII

Route: IV

SE: May prolong bleeding time

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2
Q

Deferoxamine

A

Tx: Acute iron OD

Mech: Iron chelator

De-Fer-oxamine

_De_toxes _Fer_rous overdose

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3
Q

Esmolol

A

Tx: arrythmias (Class II)

Mech: B1 blocker

More rapid onset of action

SE:

  • Bradycardia
  • Hypotension
  • B2 effects-asthma
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4
Q

Adenosine

A

Tx:

  • Arrythmias (Other class)
  • Atrial Tachycardia

Mech:

  • Binds to adenosine receptor
  • Decreases firing rate of AV node
  • Coronary vasodilator

Kinetics-Very short T1/2=10sec

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4
Q

Eptifibatide

A

Tx: Anticoagulant

Mech: Platelet inhibitor

Fibrinogen receptor blocker on platelet (GPIIB/IIIA receptor)

Clinical use: Decrease white thrombi

Used for coronary operation

Route: IV

SE: Thromobocytopenia

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4
Q

Gemfibrozil

A

Tx: Hyperlipidemia

Mech: Bind to PPAR-peroxisome proliferation acting receptor

Effects

  • Increase transcription of LPLase
  • Decrease VLDL
  • Decrease Trig.

SE:

  • GI upset-nausea, vomiting
  • Can displace warfarin from plasma binding sites
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6
Q

“Choles- or coles-“

A

Cholestyramine

Colestipol

Coleselevam

Tx: Hyperlipidemia

Mech: Irreversibly binds bile acids in gut→choles. excreted

Effects:

  • Decrease circulating cholesterol
  • Increase LDL receptor

Combine w/ statins for additional decrease in LPs

SE:

  • No systemic SE-too big to be absorbed
  • Can bind drugs
    • Digoxin
    • Oral anti-coagulants
  • Decrease absorption of fat soluble vitamins
  • GI upset-nausea
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7
Q

Tissue plasminogen activator (TPA)

A

Tx: Thrombolytic agent

(dissolve formed clots)

Mech:

  • Urine plasminogen activator=Enzyme activator
  • Plasminogen→plasmin
  • Plasmin:
    • hydrolyzes fibrin
    • degrades fibrinogen
    • degrades factors V and VII

Route: IV

SE: May prolong bleeding time

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8
Q

Diltiazem

A

Tx: Arrythmias except vent. arrythmias (class IV)

Mech: Ca channel blockers

Increase refractory period

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9
Q

Lidocaine

A

Tx: arrythmias (Class Ib)

*also LA

Mech: Na channel blocker

Route: Given IV

Kinetics: First pass effect

Toxicity: Low

SE:

  • Less likely to cause arrythmias but can enter CNS
    • Tremors
    • Seizures
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9
Q

Argatroban

A

Tx: Anticoagulant

Peptide from hirudin-diff structure, similar mech

Clinical use: when patient has HIT

Skin grafts and reattaching body parts

Route: Injection

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10
Q

Alprostadil

A

Tx: ED

Injectable prostaglandin (PGE1) leads to vasodilation when injected directly into penis

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11
Q

Mipomersen

A

Tx: hyperlipidemia

Antisense oligonucleotide

Mech: Binds to mRNA of ApoB

Prevents Apo from being synth

*(Apolipoprotein)*+cholesterol→VLDL

Must be given by injection

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12
Q

Ticlopidine

A

Tx: Anticoagulant

Mech: Platelet inhibitor

ADP receptor blocker on platelet

SE:

  • Neutropenia-loss of neutrophils
  • Agranulocytosis
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13
Q

Dabigatran

A

Tx: Anticoagulant

Mech: Direct thrombin inhibitor

Enzyme inhibitor

Route: Oral

Kinetics:

  • Prodrug
  • Onset w/in 1 hr
  • P450 inhibitor may impact

SE-hemorhhage

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15
Q

Glyceryl Trinitrate (nitroglycerin) (GTN)

A

Tx: Angina

Mech:

GTN→NO→Act. guanylate cyclase→cGMP→vasodilation

Rapidly dilates all blood vessels, including coronary art.

Route: Given sublingually–1st pass effect

Effects last 30-60min

Rapid tolerance so cannot take continuously

SE:

  • Hypotension
  • Skin flushing
  • Headache-opening blood vessels in brain, feel pulsing

*Nitroglycerin is unstable and explosive in some conditions

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16
Q

Icosapent

A

Tx: Hyperlipidemia

Mech: Inhibit enzyme responsible for Trig synth

Not clear though

18
Q

Anagrelide

A

Tx: Anticoagulant

Mech: Platelet inhibitor

Platelet count reducer

Decreases platelet formation, maturation, and #

19
Q

“-grel”s

A

Tx: Anticoagulant

Mech: Platelet inhibitor

ADP receptor blocker on platelet

Same as ticlopidine-diff is pharmacokinetics: rapid onset, shorter T1/2

21
Q

Digoxin

A

Tx: CHF

Class: Cardiac glycoside

  • Naturally occuring (foxglove and milk weed)
  • Produced as protection for plant

Route: orally

Kinetics: long T1/2

Mech:

  • When m stimulated, small influx of Ca→causes release of Ca into cell from SR→contraction
  • In order for m to relax after contraction, Ca must be removed (Na and Ca pumped out, K pumped in)
  • Digoxin inhibits NaK-ATPase
    • Na remains high in cell→prevents loss of Ca
    • High conc of Na inhibits the Na-Ca exchanger
  • Net result: Ca remains high
    • High Ca→greater contractility

Effects:

  • Increases duration of contractile response
  • Stimulates vagus n
  • Anti-arrythmic effects

SE:

  • Cardiac arrythmias
  • CNS effects
    • Yellow-green tinting of vision
    • Hallucinations
    • Activation of chemoreceptor trigger zone→severe nausea
  • Effects enhanced in hypokalemia
    • Cardiac glycosides bind and K site
    • If less K outside of cell, more effective

Digoxin poisoning treated w/ anti-digoxin anti-bodies

22
Q

“-rudin”s

A

Bivalirudin

Desirudin

Tx: Anticoagulant

Synthetic analogs of hirudin

Clinical use: when patient has HIT

Skin grafts and reattaching body parts

Route: Injection

23
Q

Dronedarone

A

Tx: arrytmhias (Class III)

Mech: K+ channel blocker

Analog of amiodarone

Fewer SE-less efficacious

25
Q

Metoprolol

A

Tx: arrythmias (Class II)

Mech: B1 blocker

More selective

SE:

  • Bradycardia
  • Hypotension
26
Q

Abciximab

A

Tx: Anticoagulant

Mech: Platelet inhibitor

Fibrinogen receptor blocker on platelet (GPIIB/IIIA receptor)

Monoclonal antibody

Clinical use: Decrease white thrombi

Used for coronary operation

Route: IV

SE: Thromobocytopenia

27
Q

Dobutamine

A

Tx: CHF

Class: Inotropic agents

Mech: Beta1 agonist

Effects: Increase force of contraction

28
Q

Vorapaxar

A

Tx: Anticoagulant

Mech: Platelet inhibitor

Thrombin receptor blocker on platelet

SE: Use carefully w/ pts w/ history of intracranial bleeding

29
Q

Olestra

A

Fake fat

SE: Butt leakage

30
Q

“-xaban”s

A

Tx: Anticoagulant

Mech: Factor Xa inhibitor

Think -xaban=_Ban_s factor Xa

Route: Oral

Kinetics: Rapid onset

SE: Bleeding after spinal tap or spinal injurty

31
Q

Fenofibrate

A

Tx: Hyperlipidemia

Mech: Bind to PPAR-peroxisome proliferation acting receptor

Effects

  • Increase transcription of LPLase
  • Decrease VLDL
  • Decrease Trig.

SE:

  • GI upset-nausea, vomiting
  • Can displace warfarin from plasma binding sites
33
Q

Verapamil

A

Tx: Arrythmias except vent. arrythmias (class IV)

Mech: Ca channel blockers

Increase refractory period

34
Q

Aminocaproic acid

A

Tx: Hemostatic agent (enhance clotting)

Mech: Inhibits plasminogen activation

Enzyme inhibitor

Binds to plasminogen in plasma

Route: Oral or injection

35
Q

Procainamide

A

Tx: All arrythmias (Class Ia)

  • Also LA

Mech: Na channel blocker

  • Like quinidine but does not get into CNS
  • Quinidine:*
  • Depresses all mm fxn
  • Anti-cholinergic effects (antivagal effects)
  • *Vagal innervation slows HR–Quinidine will speed it up

SE:

  • Lupus like syndrome in slow acetylators
37
Q

Omega 3 fatty acids

A

Tx: Hyperlipidemia

Mech: Inhibit enzyme responsible for Trig synth

Not clear though

38
Q

Quinidine

A

Tx: All arrythmias (Class Ia)

Mech: Na channel blocker

  • Depresses all mm fxn
  • Anti-cholinergic effects (antivagal effects)
  • *Vagal innervation slows HR–Quinidine will speed it up

SE:

  • GI
    • Nausea and vomiting
  • Anorexia
  • CNS
    • Tinnitus
    • Alterted color vision
40
Q

Iomitapide

A

Tx: Hyperlipidemia

Mech: Inh assembly of VLDL in liver

Apolipoprotein+cholesterol→(X)→VLDL

Enzyme for assembly is also a transporter

SE: hepatotoxicity

41
Q

Ezetimibe

A

Tx: Hyperlipidemia

Mech: Blocks cholesterol transport

SE: Flatulence

42
Q

Niacin

aka Vit B3

aka Nicotinic acid

A

Tx: Hyperlipidemia

Mech:

  • Inh. enzyme essential for VLDL synth
  • May also bind to receptor that decreases VLDL synth

Effects:

  • Decrease VLDL
  • Increase HDL–strongest increase of any drug

SE:

  • Cutaneous flushing and itching (prevented by aspirin)
  • Increase uric acid–>gout
  • Increase incidence of diabetes
43
Q

“-statin”s

A

Lovastatin

Bunch of other -statins whose diff is pharmacokinetics

Tx: Hyperlipidemia

Mech:

  • Lovastatin is prodrug
  • HMG CoA reductase inhibitor
    • Rate limiting step in cell synth of their own cholesterol
  • When cells can’t make own cholesterol→increase in LDL receptors→increase LDL uptake

Effects:

  • Decrease LDL (25%)
  • Decrease VLDL synth

SE:

  • Myositis (muscle pain)
    • At worst→rhabdomyolysis (muscle breakdown)
  • Liver toxicity
  • Teratogenic–preg. category X
  • Some memory loss

Kinetics-metab by P450

44
Q

Mexiletine

A

Tx: arrythmias (Class Ib)

Mech: Na channel blocker

Clinical use:

  • Emergency tx of ventricular arrythmias
  • Tx of ventricular tachycardia

Like lidocaine but can be given orally

46
Q

Angina definition and general tx methods

A

Not enough BF to heart

Causes chest pain (m becomes anoxic)

We usually have chest pain after we work out b/c we need more O2

But if at rest it is unstable angina

Tx by increasing BF or decreasing O2 demand

Tx:

  • Behavioral
    • Diet
    • Exercise
      • Creates collateral circulation (more blood vessels) in heart
    • Stop smoking
  • Drugs
47
Q

Amiodarone

A

Tx: arrytmhias (Class III)

DOC for cardiac arrest–most effective anti-arrythmic

Mech: K+ channel blocker

Acts like all 4 classes of anti-arrythmic

SE:

  • Potentially fatal pulmonary fibrosis
    • Replaces lung tissue w/ fiber composites
  • Liver damage
  • Corneal deposits-optic neuritis
  • Deposits in skin-blue/gray skin coloration
  • GI upset

*Iodine responsible for some deposits

48
Q

Cilostazol

A

Tx: Anticoagulant

Mech: Platelet inhibitor

Inhibits phosphodiesterase

Inh. enzyme that breaks down cAMP

Increased cAMP→Decrease platelet agg.

49
Q

Tranexamic acid

A

Tx: Hemostatic agent (enhance clotting)

Mech: Inhibits plasminogen activation

Enzyme inhibitor

Binds to plasminogen in plasma

51
Q

“-parin” drugs excluding heparin

A

Enoxaparin

Dalteparin

Tx: Anticoagulant

Low molecular wt heparins-Partially purified heparin

Longer T1/2=4 hrs

More effect on Xa than thrombin

Less osteoporosis and HIT

More predictable dose-response

(Smaller so don’t bind as readily to lots of proteins)

More expensive

Not readily reversed by protamine sulfate

SE: spinal hematoma in pts who have had spinal tap or anesth.

52
Q

Dipryridamole

A

Tx: Anticoagulant

Mech: Platelet inhibitor

Inhibits phosphodiesterase

Inh. enzyme that breaks down cAMP

Increased cAMP→Decrease platelet agg.

53
Q

Tirofiban

A

Tx: Anticoagulant

Mech: Platelet inhibitor

Fibrinogen receptor blocker on platelet (GPIIB/IIIA receptor)

Clinical use: Decrease white thrombi

Used for coronary operation

Route: IV

SE: Thromobocytopenia

54
Q

Hydroxyurea

A

Mech: Increase formation of fetal Hb (does not sickle)

SE: Mutagenic

Pregnancy category D

55
Q

Nifedipine

A

Tx: Arrythmias except vent. arrythmias (class IV)

Mech: Ca channel blockers

Increase refractory period

56
Q

Orlistat

A

Tx: Hyperlipidemia

Mech: Inh GI and pancreatic lipase

Decrease fat absorption from gut

SE: Loose stool

57
Q

Sitostanol

A

Tx: Hyperlipidemia

Mech: Looks like cholesterol–blocks uptake

58
Q

Hirudin

A

Tx: Anticoagulant–found in leech saliva

Mech: Directly inhibits thrombin

Enzyme inhibitor

60
Q

Aspirin

A

Tx: Anticoagulant

Mech: Platelet inhibitor

COX (enzyme) inhibitor

Inhibits TXA2 synth

Decreases platelet aggregation

61
Q

Propranolol

A

Tx: arrythmias (Class II)

Mech: B1 blocker

Decreases pacemaker firing rate

SE:

  • Bradycardia
  • Hypotension
  • B2 effects-asthma
62
Q

“Poetin” and “Pegin”

A

Epoietin alfa

Darbepoietin

Peginesatide

Tx: Anemia due to chronic renal failure or chemotherapy

Toxicities: Due to excess RBCs

  • Increase BP
  • Increase clotting
  • MI
  • Stoke

Pharm 3 (6 decks)

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