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phB Flashcards

1
Q

acetylsalicylic acid

A

antiplatelet agent, inh of TXA2 synthesis and inhibit the platelet aggregation

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2
Q

clopidogrel

A

P2Y12-R antagonist(ADP-R antagonist), antiplatelet agent

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3
Q

prasugrel

A

P2Y12-R antagonist(ADP-R antagonist), antiplatelet agent

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4
Q

ticagrelor

A

P2Y12-R antagonist(ADP-R antagonist), antiplatelet agent

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5
Q

abciximab

A

inhibitor or Gp 2b/3a receptor, antiplatelet agent

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6
Q

alteplase

A

tissue plasminogen activator’s activator, fibrinolytic agent

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7
Q

reteplase

A

tissue plasminogen activator’s activator, fibrinolytic agent

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8
Q

epinephrine

A

local antihemorrhagic drug

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9
Q

fibrin foam

A

local antihemorrhagic drug, activates intrinsic pathway of coagulation cascade, for soldiers to put on their wounds temporarily

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10
Q

vitamin K1

A

in green foods(cabbage, spinach), reduced vitamin K1 is needed to activate gamma glutamyl transferase enzyme, which converts factor 2,7,9,10, C, S to become a functional form

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11
Q

vitamin K2

A

from bacteria(cheese, milk..), reduced vitamin K2 is needed to activate gamma glutamyl transferase enzyme, which converts factor 2,7,9,10, C, S to become a functional form

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12
Q

ε(epsilon)-aminocaproic acid (EACA)

A

inhibits conversion of plasminogen to plasmin, systemic antihemorrhagic drugs(competitive antagonist at lysine binding sites of plasminogen→inhibits plasminogen)

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13
Q

heparin

A

activated antithrombin 3, which inactivates factor 10a and 2a(thrombin), chains longer than 18 monosaccharide so inactivates BOTH 10a and 2a

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14
Q

dalteparin(LMWH)

A

low molecular weight heparin, chains shorter than 18 monosaccharides, only inactivates factor 10a (10a:2a= 3:1 ratio)

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15
Q

warfarin

A

inhibitor of vitamin K epoxide reductase→blocks synthesis of factor 2,7,9,10,C,S , agent inhibiting synthesis of coagulation factors
***CI in pregnancy!!!

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16
Q

dabigatran-etexilate

A

direct thrombin(factor 2a) inhibitor, taken ORALLY, given in prodrug form thats why its bound to etexilate

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17
Q

rivaroxaban

A

direct factor 10a inhibitor (rivaroXaban→Xa inh), taken ORALLY

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18
Q

fondaparinux

A

inactivate only factor 10a, lowest molecule heparin, crosses placenta, theres no GAGs thats why it only inactivates factor 10a and NOT thrombin(factor2a)

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19
Q

iron hydroxide polymaltose

A

for anemias, iron supplement

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20
Q

vitamin B12

A

for anemias,

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21
Q

folic acid

A

for anemias, vitamin B9

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22
Q

epoetin-alpha(erythropoeitin)

A

for anemias, IV or SC

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23
Q

filgrastim

A

for anemias, recombinant G-CSF

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24
Q

digoxin

A

positive ionotropic drug for acute heart failure, cardiac glycosides, inhibits Na2+/K+ ATPase →↑Ca2+ ic

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25
Q

digitoxin

A

positive ionotropic drug for acute heart failure,cardiac glycosides, inhibits Na2+/K+ ATPase →↑Ca2+ ic

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26
Q

milrinone

A

positive ionotropic drug for acute heart failure, inhibits PDE3 which inhibits cAMP→ Ca2+↑

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27
Q

levosimendan

A

positive ionotropic drug for acute heart failure, increases Ca2+ sensitvity of troponin C→ stabilizes it in a conformation needed for contraction!!

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28
Q

dobutamine

A

positive ionotropic drug for acute heart failure, beta1 R agonists and stimulates cAMP and PKA→Ca2+↑

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29
Q

acetazolamide

A

acts on PCT, inhibits carbonic anhydrase

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30
Q

furosemide

A

loop diuretics, acts on asc loop of henle, inhibits Na/K/2Cl- co transporter

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31
Q

etacrynic acid

A

loop diuretics, acts on asc loop of henle, inhibits Na/K/2Cl- co transporter

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32
Q

hydrochlorothiazide

A

thiazide diuretics, inhibits Na/Cl- cotransporter in distal convoluted tubule, CI in diabetes

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33
Q

indapamide

A

thiazide LIKE diuretics, inhibits Na/Cl- cotransporter in distal convoluted tubule, ONLY USED IN HYPERTENSION!!

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34
Q

mannitol

A

osmotic diuretics, pulls H2O from nearby tissues like brain tissue or vitreous humor for cerebral edema or glaucoma!, ↑osmolarity of blood, IV!!

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35
Q

glycerol

A

osmotic diuretics, pulls H2O from nearby tissues like brain tissue or vitreous humor for cerebral edema or glaucoma!, ↑osmolarity of blood, IV!!!

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36
Q

spironolactone

A

aldosterone antagonists, potassium sparing diuretics

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37
Q

eplerenone

A

aldosterone antagonists, potassium sparing diuretics

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38
Q

amiloride

A

potassium sparing diuretics, inhibitors of ENaC channel used for Liddle syndrome,, amiLORI====LIDDLE sydnrome!!!

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39
Q

tolvaptan

A

ADH antagonist diuretics, acts on lower part of collecting tubule to inhibit effect of ADH→ increase water excretion by inhibiting aquaporin channel!→ can lead to SE: thirst, polyuria

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40
Q

simvastatin

A

statins, HMG-CoA reductase inhibitor, inhibits cholesterol synthesis, used for dyslipidemias, SIMVAAAA!

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41
Q

atorvastatin

A

statins, HMG-CoA reductase inhibitor, inhibits cholesterol synthesis, used for dyslipidemias

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42
Q

rosuvastatin

A

statins, HMG-CoA reductase inhibitor, inhibits cholesterol synthesis, used for dyslipidemias

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43
Q

fenofibrate

A

fibrates, used against dyslipidemia, PPARalpha agonist→increases activity of lipoprotein lipase, which yanks TG from VLDL and chylomicrons, SHOULD NOT BE USED WITH STATINS bc fibrates inhibits degradation of statins into inactive metabolites inside the liver

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44
Q

fenofibrate

A

fibrates, used against dyslipidemia, PPARalpha agonist→increases activity of lipoprotein lipase, which yanks TG from VLDL and chylomicrons, SHOULD NOT BE USED WITH STATINS bc fibrates inhibits degradation of statins into inactive metabolites inside the liver

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45
Q

cholesevelam

A

bile acid sequestrants, for dyslipidemia drugs, is a positively charged molecule which binds on bile acid inside GI tract and gets excreted via feces→ BA↓ into liver to reutilzed→ cholesterol synthesize more BA→ cholesterol DECREASE→ signals DNA to make up more LDL R on membrane of hepatocytes→LDL in blood DECREASE（EFFECT!!)

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46
Q

ezetemibe

A

cholesterol absorption inhibitors for dyslipidemia, in the small intestine,→ LDL↓↓↓ in the blood stream, OFTEN COMBINED WITH STATINS(SIMVASTATIN)

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47
Q

lidocaine

A

class 1B antiarrythmic drug, Na+ channel blocker(WEAK INHIBITION!!), alters repolarization phase(phase 0 only!), IV infusion, lease cardiotoxic

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48
Q

propafenone

A

class 1C antiarrythmic drug(STRONGEST), strong inhibition of Na+ channels and Na+ only!!!, PROARRYTHMIC as SE!

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49
Q

esmolol

A

class II, beta blocker, ↓cAMP so it inhibits L type VDCC from making calcium ions to come into the cell and cause the rise of AP from RMP to threshold potential, only used PARENTERAL,

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50
Q

amiodarone

A

class III antiarrythmic drugs, most efficient of all anti arrythmic drugs!!, strongest K+ channel blocker!! @ contractile cells,→affects phase 1+2+3 bc involved with K+ channels, IODINE in the structure → SE： hyperthyroidism!! can occur

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51
Q

sotalol

A

class III antiarrythmic drugs, K+ channel blocker!!→affects phase 1+2+3 bc involved with K+ channels

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52
Q

verapamil

A

class IV of antiarrhythmic drugs, direct inhibitor of L type VDCC of PACEMAKER CELLS only!!→slower conduction of SA and AV node, DONT USE IT WITH BETA BLOCKERS!!!

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53
Q

adenosine

A

class V antiarrythmic drugs(others group), acting on adenosine R of the heart cells and activates Gi protein, which alpha and beta subunit decrease cAMP formation and leads to less phosphorylation of channels, and gamma subunit activates K+ channels from opening and leads to hyperpolarization!!

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54
Q

magnesium(sulfate)

A

class V antiarrythmic drugs(others group), Calcium channel blocker!!!

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55
Q

digoxin

A

class V antiarrythmic drugs(others group), activates vagus nerve and activates AchR which activate Gi protein→same as adenosine function,, also Na+/K+ ATP ase blocker!!!!

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56
Q

nitroglycerin

A

antianginal drugs, one of nitrates, goes inside venous SMC and release their structure: NO→stimulates G.C. which converts GTP into cGMP and stimulates PKG which activates MLCP and inhibits the contraction of actin and myosin → venodilation→preload↓→ 02 demand and O2 supply decrease, DEVELOP TOLERANCE!!!, SHORT ACTING NITRATE EXAMPLE IS NITROGLYCERIN,
-FIRST PASS EFFECT → to avoid it, give sublingual pill or spray and NOT ORALLY

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57
Q

isosorbide-mononitrate

A

antianginal drugs, one of LONG ACTING nitrates, goes inside venous SMC and release their structure: NO→stimulates G.C. which converts GTP into cGMP and stimulates PKG which activates MLCP and inhibits the contraction of actin and myosin → venodilation→preload↓→ 02 demand and O2 supply decrease, DEVELOP TOLERANCE!!!(drug holiday)
-FIRST PASS EFFECT → to avoid it, give sublingual pill or spray and NOT ORALLY

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58
Q

trimetazidine

A

antianginal drugs, blocks beta oxidation of FA and enhances glucose oxidation→ requires less O2 in ischemic cells

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59
Q

ivabradine

A

antianginal drugs, inhibits funny current in SA node→ HR↓

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60
Q

beta blockers: antianginal drugs

A

antianginal drugs, ex: metoprolol(beta1R). atenolol(beta1 R). propanolol(beta 1+2 R), blocks the Receptors and inhibits the nodal cells and contractile cells from contraction→ O2 demand↓→ischemia will decrease!!(goal)

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61
Q

calcium channel blockers: antianginal

A
  1. non dihydropyridine CCBs(verapamil, diltiazem) and 2. DHP CCBs(amilodipine, nefidepine), blocks Ca2+ channels of nodal and contractile cells and arterial SMC and myocardium (see notes), decrease AFTERLOAD!!
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62
Q

vinpocetin

A

for microcirculation drugs, PDE-1 inhibitor taken parenteral
nootropic, inhibits platelet aggregation so increase cerebral perfusion
-used for cerebral microcirculation

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63
Q

nicergoline

A

for microcirculation drugs
-alpha 1R inhibitor, leads to vasodilation and increase arterial blood flow
-used for brain circulation problems, post-stroke, dementia
-CI in PREGNANCY!

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64
Q

cilostazol

A

PDE3 inhibitor for microcirculation drugs, decrease platelet aggregation and increase vasodilation
-used in pain, ache, ccramp
-CI in CHF

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65
Q

calcium-dobesilate

A
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65
Q

pentoxyfilline

A

for microcirculation drugs, parental admin
-methylated xanthine derivative for PDE competitive non selective inhibitro!!
-increase tissue perfusion, decrease platelet aggregation
-for atherosclerotic or diabetic peripheral perfusion disorders

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66
Q

cinnarizine

A

antihistamines

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67
Q

captopril

A

ACE inhibitors, antihypertensive drugs, blocks ACE which converts AT-1 into AT-2→ decrease AT-2 and increase bradykinin bc bradykinin is usually converted into an inactive metabolite by ACE but if its inhibited→ bradykinin↑

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68
Q

perindopril

A

ACE inhibitors, antihypertensive drugs, blocks ACE which converts AT-1 into AT-2→ decrease AT-2 and increase bradykinin bc bradykinin is usually converted into an inactive metabolite by ACE but if its inhibited→ bradykinin↑

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69
Q

enalapril

A

ACE inhibitors, antihypertensive drugs, blocks ACE which converts AT-1 into AT-2→ decrease AT-2 and increase bradykinin bc bradykinin is usually converted into an inactive metabolite by ACE but if its inhibited→ bradykinin↑

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70
Q

ramipril

A

ACE inhibitors, antihypertensive drugs, blocks ACE which converts AT-1 into AT-2→ decrease AT-2 and increase bradykinin bc bradykinin is usually converted into an inactive metabolite by ACE but if its inhibited→ bradykinin↑

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71
Q

losartan

A

AT-2 Receptor blockers for antihypertensive drugs, decreases BP in case of hypertension

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72
Q

valsartan

A

AT-2 Receptor blockers for antihypertensive drugs, decreases BP in case of hypertension

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73
Q

valsartan+sacubitril(ARNi)

A

AT-2 Receptor blockers for antihypertensive drugs, decreases BP in case of hypertension

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74
Q

irbesartan

A

AT-2 Receptor blockers for antihypertensive drugs, decreases BP in case of hypertension

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75
Q

spironolactone

A

aldosterone antagonists for antihypertensive drugs, inhibits aldosterone dependent Na+/K+ ATP ase and Na+ transporters, decreases BP, SE: GYNECOMASTIA

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76
Q

eplerenone

A

aldosterone antagonists for antihypertensive drugs, inhibits aldosterone dependent Na+/K+ ATP ase and Na+ transporters, decreases BP, SE: GYNECOMASTIA

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77
Q

verapamil

A

non-DHP CCB’s for antihypertensive drugs, ONLY present in Cardiac myocytes but it can also bind onto the DHP-Ca channels on arterial smc so has a little bit of vasodilatory effect, → contractility decreases which decrease BP

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78
Q

nifedipine

A

short acting DHP CCBlockers for antihypertensive drugs, they inhibit Ca channels on arterial SMC of the heart which vasodilates and BP will decrease in case of hypertension

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79
Q

nimodipine

A

short acting DHP CCBlockers for antihypertensive drugs, they inhibit Ca channels on arterial SMC of the heart which vasodilates and BP will decrease in case of hypertension

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80
Q

felodipine

A

moderate acting DHP CCBlockers for antihypertensive drugs, they inhibit Ca channels on arterial SMC of the heart which vasodilates and BP will decrease in case of hypertension

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81
Q

amlodipine

A

long acting DHP CCBlockers for antihypertensive drugs, they inhibit Ca channels on arterial SMC of the heart which vasodilates and BP will decrease in case of hypertension

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82
Q

dihydralazine

A

vasodilators for hypertension, induce release of NO from endothelial cells which stimulate G.C. from converting GTP into cGMP and activate MLCP which inhibits contraction of mm of ARTERIAL VASODILATION!! and decrease afterload, but can lead to orthostatic hypotension and LUPUS

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83
Q

bosentan

A

vasodilator for hypertension, endothelin R antagonists which inhibits vasoconstriction

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84
Q

sildenafil

A

vasodilator for hypertension, PDE5 inhibitors which enhance vasodilation of NO by inhibiting PDE5, DO NOT GIVE WIHT NITRATE bc it will cause severe hypotension!

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85
Q

glipizide

A

insulinotropic drugs for diabetes, one of SULFONYLUREAS, closes ATP sensitive K+ channel inside the pancreas→ depol of cell→ Ca2+ influx→ insulin release bc of stimulation of vesicle of insulin

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86
Q

glimepiride

A

insulinotropic drugs for diabetes, one of SULFONYLUREAS, closes ATP sensitive K+ channel inside the pancreas→ depol of cell→ Ca2+ influx→ insulin release bc of stimulation of vesicle of insulin

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87
Q

repaglinide

A

insulinotropic drugs for diabetes, one of NON-SULFONYLUREAS, closes ATP sensitive K+ channel inside the pancreas→ depol of cell→ Ca2+ influx→ insulin release bc of stimulation of vesicle of insulin
quick drug-only for mimicking postprandial insulin

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88
Q

metformin

A

drugs for T2DM, acts on AMPkinase which activates carbohydrate and fat metabolism,FIRST LINE DRUG choice in T2DM

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89
Q

vildagliptin

A

gliptins, DPP4 inhibitors for T2DM, increases insulin production and decrease glucose level

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90
Q

dapagliflozin

A

SGLT2 inhibitors for T2DM, (reversible inhibition), inhibits absorption of glucose in SGLT2 in proximal CT

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91
Q

acarbose

A

alpha glucosidase inhibitor for T2DM, inhibits splitting of di, oligo, polysaccharide→ results in decrease in carbohydrate absorption→ reduce postprandial hyperglycemia, used in OBESE patients, SE: diarrhea

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92
Q

levothyroxin

A

thyroid drugs for hypothyroidism treatment, T4!!!, 25-150 microgram, used for hypothyreosis, endemic goiter and substitute after thyroidectomy

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93
Q

thiamazole

A

inhibitors of peroxidase enzyme for hyperthyroidism treatment, used for graves disease, multinodular goiter

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94
Q

propylthiouracil

A

inhibitors of peroxidase enzyme AND 5’ deiodinase enzyme for hyperthyroidism treatment, used for graves disease, multinodular goiter, CAUSE THYROID STORM with high dose!!

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95
Q

iodine

A

high dose of iodine used for hyperthyroidism treatment(like negative feedback), also used for hypothyroidism treatment: iodine deficiency

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96
Q

octreotide

A

somatostatin analogue, inhibits release of GH and TSH, hypothalamic and pituitary hormones!!, used for glucagonoma, insuloinoma, upper GI bleeding since it can vasoconstrict!

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97
Q

bromocriptine

A

dopamine R agonist, used for Parkinson disease, stop of lactation, acromegaly(p.o)

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98
Q

desmopressin

A

man made form of vasopressin(ADH), increases water reabsorption in kidney tubule!!, used to replace a low level of vasopressin

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99
Q

oxytocin

A

hypothalamic hormones, effects: uterine contractions during childbirth and cause lactation!

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100
Q

hydrocortisone

A

short duration of action, =CORTISOL, glucocorticoids, used for HR replacement therapy

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101
Q

prednisolone

A

intermediate duration of action, glucocorticoids, for systemic antiinflammatory adn immunosuppressive effect

102
Q

methylprednisolone

A

intermediate duration of action, glucocorticoids, MINIMAL MINERALOCORTICOID ACtiON

103
Q

triamcinolone

A

intermediate duration of action, glucocorticoids, more toxic than others

104
Q

dexamethasone

A

LONG duration of action, glucocorticoids, used in cerebral edema

105
Q

fludrocortisone

A

mineralocorticoids, short duration of action, used for acute/chronic adrenocortical insufficiency or post-adrenalectomy, salt and water retention effect, excretes K+ and H+

106
Q

fluticasone

A

topically applied glucocorticoids, used ICS!!

107
Q

mometasone

A

topically applied glucocorticoids, used ICS!!

108
Q

budesonide

A

topically applied glucocorticoids, used ICS!!

109
Q

fluocinolone

A

topically applied glucocorticoids, TOPICALLY,

110
Q

metyrapone

A

reversible inhibitor of 11beta-hydroxylase enzyme, cant produce corticosterone and cortisol, used for overnight metyrapone stimulation test for diagnosis of adrenal insufficiency

111
Q

undecanoate

A

-testosterone, prodrug of testosterone, androgen R agonist, orally active,

112
Q

bicalutamide

A

androgen R antagonists, used for prostate cancer= prostate cancer needs testosterone to grow, but if bicalutamide competes with testosterone to bind onto the androgen Reptor, less testosterone will bind to androgen R so it will stimulate the cancer gene less → thats why used for prostate cancer

113
Q

finasteride

A

5alpha-reductase inhibitors for formation of dihydrotestosterone from testosterone, dihydrotestosterone causes prostate to grow so we dont want that in case of benigh prostatic hyperplasia→increase testosterone to decrease prostate size!

114
Q

goserelin

A

GnRH agonist, androgenic suppression with it by continuous therapy, used in prostate cancer

115
Q

degarelix

A

GnRH R antagonist on pituitary gland and block interaction with GnRH, binds to Receptor, reduce the release of LH and FSH from pituitary gland and reduce testosterole released from testes, used for prostate cancer bc we want to decrease testosterone level in case of cancer

116
Q

sildenafil

A

agent affecting sexual activity, phosphodiesterase 5 inhibitor!!, so it can amplify NO-cGMP signaling pathway and decrease Ca2+→ arterial smooth mm relaxation→ increase arterial inflow→ ERECTION!!!, used for erectile dysfunction and premature ejaculation

117
Q

nandrolone

A

androgen R agonist, synthetic testosterone used for hypogonadism in men after castration, or hereditary angioedema, illegally among athletes

118
Q

estradiol

A
119
Q

ethinylestradiol

A
120
Q

clomifen

A

SERM, (selective estrogen R modulator) stimulates ant pituitary to produce more LH!!, ovulation inducing agent by inducing negative feedback to increase LH level

121
Q

tamoxifen

A

SERM, (selective estrogen R modulator), used in palliative treatment of breast cancer in postmenopausal women, blocks estrogen activity in breast and stops growth of breast tumors that need estrogen to multiply

122
Q

raloxifene

A

SERM, (selective estrogen R modulator), prevention of postmenopausal osteoporosis!!, acts on bones!!

123
Q

anastrozole

A

aromatase inhibitor, used in breast cancer resistant to tamoxifen to reduce the amount of estrogen/estradiol

124
Q

goserelin

A

GnRH agonist, used for breast cancer and hormone sensitive prostate cancer

125
Q

degarelix

A

GnRH antagonists, used for breast cancer and hormone sensitive prostate cancer

126
Q

medroxyprogesterone-acetate

A

synthetic progestin-pregnans category, better oral bioavailability, inhibits ovulation by acting on progesterone R present in nucleus

127
Q

drospirenone

A

synthetic progestin-pregnans category, better oral bioavailability, inhibits ovulation by acting on progesterone R present in nucleus

128
Q

norethisterone

A

synthetic progestin-ESTRANS category, better oral bioavailability, inhibits ovulation by acting on progesterone R present in nucleus

129
Q

levonorgestrel

A

synthetic progestin-GONANS category, better oral bioavailability, inhibits ovulation by acting on progesterone R present in nucleus

130
Q

desogestrel

A

synthetic progestin-GONANS category, better oral bioavailability, inhibits ovulation by acting on progesterone R present in nucleus

131
Q

cyproterone-acetate

A

synthetic progestin-pregnans category, better oral bioavailability, inhibits ovulation by acting on progesterone R present in nucleus

132
Q

mifepristone

A

progesterone antagonists, estran, used for termination of early pregnancy

133
Q

ulipristal acetate

A

selective progestin receptor modulator (progesterone antagonist), morning after pill(prevents preganncy if no choice to inhibit implantation

134
Q

levonorgestrel+ethinylestradiol

A
135
Q

teriparatide

A

30 amino acid analogue of PTH, PTH analogues basically stimulates pathway of taking phosphates and calcium to make the bones, used for osteoporosis, NOT TAKEN ORALLY bc this is made of PROTEINS, so its gonna get digested

136
Q

cholecalciferol

A

increase calcium and Phosphate absorption from gut AND decrease ellimination of Ca and P from the kidneys, cholecalciferol=vitamin D3 (made upon exposure to sunlight!!)

137
Q

alendronate

A

non hormonal drugs for osteoporosis, one of bisphosphonates, ORALLY and used daily, osteoclasts eat them up and leads to apoptosis and inactivation of the osteoclasts,

138
Q

zoledronate

A

taken IV!!non hormonal drugs for osteoporosis, one of bisphosphonates, osteoclasts eat them up and leads to apoptosis and inactivation of the osteoclasts,

139
Q

denosumab

A

non hormonal drugs, when we stop this med, no advantages are maintained, effects ONLY during the treatment, MOA: RANK-L antibody!! it binds to RANK ligand which inhibits the binding of RANK ligand with RANK receptor on the osteoclasts→ inhibits bone resorption and enhances BONE FORMATION!!

140
Q

raloxifene

A

SERM(selective estrogen R modulators) used for osteoporosis, act on estrogen R(agonists in bones and Antagonists in other organs like endometrium or breasts), SAME EFFICACY AS ESTROGEN!!→ activates OPG which inhibits binding of RANK-ligand released from osteoblasts onto the RANK Receptor on the osteoclasts, which basically inhibits activation of osteoclasts so inhibits bone resorption

141
Q

dimenhydrinate

A

H1 Receptor antagonists and M1 R antagonist for central antiemetic effect at vestibular system, INHIBITS MOTION SICKNESS!!(H1 and M1 R related), which leads to vomiting

142
Q

droperidol

A

D2 R antagonists for area postrema(vomiting center)→inhibits vomiting!!, antiemetic drug, also PROKINETIC effect

143
Q

metoclopramide

A

D2 ANTAGONIST(@area postrema which inhibits vomiting) AND 5-HT4 R AGONIST!!, has prokinetic effect(helps with digestioin of stomach, used in gastric emptying), used for gastroparesis where food is still inside the stomach to empty the stomach,

144
Q

ondansetron

A

antagonists of 5-HT3!!Receptor in the GI tract which inhibits vomiting, taken orally, used for CHEMOTHERAPY!!

145
Q

palonosetron

A

antagonists of 5-HT3!!Receptor in the GI tract which inhibits vomiting, IV!!! only , used for CHEMOTHERAPY!!

146
Q

aprepitant

A

NK-1 R antagonists inAREA POSTREMA(vomiting center), SE: cyp3A4 inhibitor!!, taken orally

147
Q

cannabinoids

A

inhibits presynaptic release of dopamine, used for chemotherapy induced vomiting, inhibits vomiting, taken orally

148
Q

plant fibers

A

laxative, ex: plums or dried fruits, effective in 1-3 days, indigestable hydrophilic colloids that absorbs water in the intestinal lumen forming a bulky gel distending the colon and promotes peristalsis

149
Q

magnesium (sulfate)

A

for constipation(laxative), effective in 3-10hrs(fast), osmotically acitve and draws water into the intestinal lumen→higher volume in bowel→stimulates intestinal motility and empty bowel easier,USED IN PREGRANCY!!

MG OXIDE IS ANTACID!! neutralize HCL

150
Q

lactulose

A

for constipation(laxative)
effective in 3-10hrs(fast), osmotically acitve and draws water into the intestinal lumen→higher volume in bowel→stimulates intestinal motility and empty bowel easier, USED IN PREGRANCY!!
-converted into lactic acid by bacteria, which lowers pH and turns NH4+into NH3, decrease NH4+ from bowel

151
Q

parrafin oil

A

stool softener, effective in 6-12hrs, orally or rectally,
-softens hard stool(stool surfactant agent increasing penetration of water and lipid)→helps empty bowel

152
Q

sennoside

A

strong laxative(used in constipation), effective in 1-6hrs(v quick so stay close to toilet), direct stimulation myenteric neuronal depol→ colon contractions occur, ONLY SHORT TERM USE(2 weeks), SE: dark stool and urine,CONTRAINDICATED IN PREGNANCY

153
Q

bisacodyl

A

strong laxative(used in constipation), effective in 1-6hrs(v quick so stay close to toilet), direct stimulation myenteric neuronal depol→ colon contractions occur, ONLY SHORT TERM USE(2 weeks),
-absorbed→conjugated in liver→ enter colon w bile, used in acute or chronic constipation
SE: metabolic alkalosis (by overuse)

154
Q

diphenoxylate

A

anti-diarrheal drug, mu opioid R agonist, taken orally, inhibits propulsive peristalsis

155
Q

loperamide

A

anti-diarrheal drug, mu opioid R agonist, taken orally, inhibits propulsive peristalsis+increase sphincter tone+inhibits intestinal fluid secretioin
CANNNOT CROSS BBB

156
Q

active charcoal

A

anti-diarrheal drug, ORALLY, used for diarrhea and acute poisoning, prevents system absorption of pharmaceutical drugs or poison, ADSORBING them on the surface of the particles(attach)

157
Q

ursodeoxycholic acid

A

increase production of bile and emulsify the dietary fats and cholesterol of bile, used for biliary cirrhosis

158
Q

acetylcysteine

A

antidote of paracetamols toxic metabolite
-increase production of depleted antioxidant GLUTATHIONE which conjugates and detoxify paracetamol metabolite
-used in paracetamol/aspirin overdose

159
Q

silimarin

A

milk thistle extract
-used in LIVER AND BILIARY TRACT
-decrease level of ROS, inhibits lipid peroxidation
-for hepatotoxicity

160
Q

methotrexate

A

folic acid antagonists, antimetabolites for cancer chemotherapy, inhibits dehydrofolate reductase enzyme→ folic acid depletion→ inhibits purine and thymnidine synthesis thus DNA synthesis, cytotoxic action, IV or tablet, treat solid tumors , HEPATOTOXICITY!!

161
Q

pemetrexed

A

folic acid antagonists, antimetabolites for cancer chemotherapy, inhibits dehydrofolate reductase enzyme→ folic acid depletion→ inhibits purine and thymnidine synthesis thus DNA synthesis, cytotoxic action, IV or tablet, treat solid tumors, SE: HAND FOOT SYNDROME

162
Q

5-fluorouracil

A

pyrimidine analogue for antimetabolites cancer chemotherapy, inhibits thymidylate synthase converting dUMP to dTMP, LEUCOVORICIN enhances its effect but also adverse effects, taken IV!!, used for solid tumors(GI tumors), SE:GI and neurotoxic

163
Q

capecitabine

A

pyrimidine analogue for antimetabolites cancer chemotherapy, inhibits thymidylate synthase converting dUMP to dTMP, LEUCOVORICIN enhances its effect but also adverse effects, taken IV!!
-prodrug of 5-fluorouracil!! (ORALLY)

164
Q

6-mercaptopurine

A

purine analogue for antimetabolites cancer chemotherapy, metabolized by HGPRT(hypoxanthine guanine phosphoribosyl transferase)→inhibits several enzymes of de novo purine synthesis→block IMP, AMP GMP synthesis
-orally
-used for leukemia of child but myelotoxicity

165
Q

cytarabine

A

deoxycytidine analogues for antimetabolites cancer chemotherapy, converted by deoxycytidine kinase to Ara CMP→ to Ara CTP!!!→ inhibits DNA polymerase alpha and beta(inhibits S phase of cell cycle)
-taken IV
-NO ACTIVITY IN SOLID TUMOR
-neurotoxicity in high dose

166
Q

cyclophosphamide

A

alkylating agent for cancer chemotherapy
-breaks DNA double strand
-used for solid tumor
-SE: hemorrhagic cysitits (PREVENTED WITH MESNA)
-infertility, vomiting in high doses

167
Q

dacarbazine

A

alkylating agent for cancer chemotherapy
-breaks DNA double strand
-used for solid tumor
-similar to cyclophosphamide
-SE: myelosuppression, vomiting

168
Q

temozolomide

A

alkylating agent for cancer chemotherapy
-alkylation of DNA and RNA→ decrease DNA replication
-for BRAIN TUMOR!!!
-SE* myelosuppression and neurotoxicity

169
Q

cisplatin

A

platinum based alkylating agent for cancer chemotherapy
cross link bw DNA strands → decrease DNA replication
-for solid tumors
-very strong EMETIC EFFECT!!, NEPHROTOXICITY, OTOTOXICITY, NEUROTOXICITY

170
Q

oxaliplatin

A

platinum based alkylating agent for cancer chemotherapy
cross link bw DNA strands → decrease DNA replication
-for solid tumors (GI TUMOR!!!)
-NEUROTOXICITY!!

171
Q

dactinomycin

A

interfere with DNA transcription which decrease RNA synthesis, alkylating agent for cancer chemotherapy
-used for childhood tumors

172
Q

bleomycin

A

-alkylating agent for cancer chemotherapy
-induce formation of free radicals→ cell cycle arrest at G2 phase which leads to cell death
-for SOLID TUMORS
-SE: ***LUNG TOXICITY!!(pulmonary fibrosis etc)

173
Q

irinotecan

A

topoisomerase 1 inhibitor
-ssDNA breaks→ decrease DNA replication and increase DNA degradation
-IV!!
-used for solid tumors: colorectal or small cell lung cancer
-SE* myelosuppression, GI symptoms(diarrhea)

174
Q

etoposide

A

topoisomerase 2 inhibitor
-dsDNA breaks→ decrease DNA replication and increase DNA degradation
-for solid tumors
-SE* myelosuppression

175
Q

doxorubicin

A

topoisomerase 2 inhibitor
-dsDNA breaks→ decrease DNA replication and increase DNA degradation
-formation of free radicals which breaks DNA strands
-1st ANTHRACYCLINE which is produced naturally by strep peucetius
-for solid tumors
SE: myelosuppression and cardiotoxicity

176
Q

vincristine

A

inhibitor of microtubule
-binds to beta tubi¥ulin and inhibits beta tubulin polymerization into microtubules→ inhibits M phase
-for SOLID TUMORS
-neurotoxicity

177
Q

docetaxel

A

inhibitor of microtubule
-hyperstabilization of polymerized microtubules→ prevents mitotic spindles disassembly→ arrest in M phase
-used for BREAST CANCER
-SE* nail changes, hepatotoxicity

178
Q

aspart insulin

A

fast acting insulin analogues, onset is 20-30 min, proline at B28 position is replaced by other aa (aspargine in this case)→ no hexamer formation so its doesnt take time for insulin to become monomer and it can be rapidly used in blood circulation!!

179
Q

lispro insulin

A

fast acting insulin analogues, onset is 20-30 min, proline at B28 position is replaced by other aa (LYSINE in this case)→ no hexamer formation so its doesnt take time for insulin to become monomer and it can be rapidly used in blood circulation!!

180
Q

regular insulin

A
181
Q

NPH insulin

A

intermediate acting insulin, onset:4-5hrs(long),takes time for insulin to degrade from hexamer to monomer form to get into the blood circulation)

182
Q

glargine insulin

A

ULTRA LONG acting insulin, duration is up to 24hr(given once per day), addition of 2 arginine!! after B30-Thr

183
Q

liraglutide

A

GLP-1 agonist for parenteral antidiabetics, admin: SC
long acting
-used for obesity for weight loss
-se: DOES NOT CAUSE HYPOGLYCEMIA RISK

GLP-1 decrease plasma glucose level by INCREASING INSULIN LEVEL!!, decrease glucagon also by inhibiting alpha cells to produce glucagon

184
Q

terbutaline

A

SABA for COPD/asthma(short acting B2 R agonist)→acts on B2 R of bronchioles like NE/E does and then acts the same, activates　cAMP→↑PKA→ inhibits MLCK which leads to bronchodilation!!(bc in case of COPD/asthma theres bronchospasm so we want to vasodilate the bronchioles!)

185
Q

salbutamol

A

SABA for COPD/asthma(short acting B2 R agonist)→acts on B2 R of bronchioles like NE/E does and then acts the same, activates　cAMP→↑PKA→ inhibits MLCK which leads to bronchodilation!!(bc in case of COPD/asthma theres bronchospasm so we want to vasodilate the bronchioles!)

186
Q

fenoterol

A

SABA for COPD/asthma(short acting B2 R agonist)→acts on B2 R of bronchioles like NE/E does and then acts the same, activates　cAMP→↑PKA→ inhibits MLCK which leads to bronchodilation!!(bc in case of COPD/asthma theres bronchospasm so we want to vasodilate the bronchioles!)

187
Q

formoterol

A

LABA for COPD/asthma(long acting B2 R agonist)→acts on B2 R of bronchioles like NE/E does and then acts the same, activates　cAMP→↑PKA→ inhibits MLCK which leads to bronchodilation!!(bc in case of COPD/asthma theres bronchospasm so we want to vasodilate the bronchioles!)
** ALWAYS TAKE IT WITH INHALED CORTICOSTEROIDS!!!

188
Q

theophylline

A

inhibitor of PDE(phosphodiesterase) which inhibits cAMP, so basically activates cAMP which leads to smooth mm relaxation!!→ good for COPD for bronchodilation!

189
Q

ipratropium

A

SAMA(short acting Muscarinic3 R antagonists) for COPD/ASTHMA
-binds to Ach-R instead of Ach→blocks the contraction of smoooth mm cells which leads to bronchodilation of lung

190
Q

tiotropium

A

LAMA(long acting Muscarinic 3 R antagonists) for COPD/ASTHMA
-binds to Ach-R instead of Ach→blocks the contraction of smoooth mm cells which leads to bronchodilation of lungSAMA(short acting Muscarinic R antagonists) for COPD/ASTHMA

191
Q

montelukast

A

for asthma!!, inhibits bronchospasm bc it is LEUKOTRIEN R ANTAGONIST!!

192
Q

omalizumab

A

for severe allergic ASTHMA, taken SC
-anti-Ig-E antibody!! binds to IgE and inhibits binding to mast cell for the release of histamines and LT

193
Q

salmeterol

A

LABA for COPD/asthma(long acting B2 R agonist)→acts on B2 R of bronchioles like NE/E does and then acts the same, activates　cAMP→↑PKA→ inhibits MLCK which leads to bronchodilation!!(bc in case of COPD/asthma theres bronchospasm so we want to vasodilate the bronchioles!), ALWAYS TAKE IT WITH INHALED CORTICOSTEROIDS!!!

194
Q

prednisolone

A

corticosteroids, used in asthma/COPD(inhaled Corticosteroids)
-TAKEN ORALLY!! (ONLY in case of severe acute attacks or severe persistent asthma)

195
Q

methylprednisolone

A

corticosteroids, used in asthma/COPD(inhaled Corticosteroids)
-TAKEN IV!! (ONLY in case of severe acute attacks or severe persistent asthma)

196
Q

fluticasone

A

Inhaled Corticosteroids for COPD/asthma,
NO BRONCHODILATION,
only anti inflammatory effects!!

197
Q

budesonide

A

Inhaled Corticosteroids for COPD/asthma,
NO BRONCHODILATION,
only anti inflammatory effects!!!

198
Q

codeine

A

centrally acting Antitussive agent, Opioid
-↓sensitivity of cough centers in CNS to peripheral stimuli and decrease cough reflex
-decrease mucosal secretions
-acts on Mu Receptors(selective mu opioid R agonist)

199
Q

butamirate

A

centrally acting Antitussive agent,
-↓sensitivity of cough centers in CNS to peripheral stimuli and decrease cough reflex
-decrease mucosal secretions

200
Q

prenoxdiazine

A

peripherally acting Antitussive drug
-used for strong cough of bronchial origin
-act by ↓sensitivity of R and afferent neurons of pulmonary stretch R

201
Q

bromhexine

A

mucolytics(dissolves thick mucous), expectorants,
-degradations of mucopolysaccharides of mucous to eliminate those thick mucous stuck in the tubes!
-acts like a cutter!! of mucous

202
Q

acetylcysteine

A

mucolytics(dissolves thick mucous), expectorants
-cleaves disulfide bridges in mucous and reduces viscosity
used for CYSTIC FIBROSIS!!(where thick mucous will be blocking the airway)
-in case of paracetamol poisoning, HIGH DOSES ARE REQUIRED!!
→ increase production of depleted antioxidant glutathione which will conjugate and detoxify pracetamol metabolite

203
Q

ambroxol

A

secretolytic agents for productive cough which increases ciliary activity

204
Q

omeprazole

A

irreversible inhibitor of H+/K+ ATPase used for GERD/ peptic ulcer disease/zollinger ellison syndrome
-pro drug, lipophilic, weak bases
-taken 1hr before meal, 3-5days needed for development of max effect
-INHIBITS EFFECT OF CLOPIDOGREL!!(competes for metabolism by CYP2C19)

205
Q

pantoprazole

A

irreversible inhibitor of H+/K+ ATPase used for GERD/ peptic ulcer disease/zollinger ellison syndrome
-pro drug, lipophilic, weak bases
-taken 1hr before meal, 3-5days needed for development of max effect

206
Q

famotidine

A

H2-Receptor Antagonist, decrease gastric acid and pepsinogen secretion
-for GERD/peptic ulcer disease
-taken 1time daily at BEDTIME!!

207
Q

MgO(magnesium oxide)

A

ANTACID(neutralize acid in stomach)
-poor solubility, prolonged neutralizing effect

208
Q

Al2(OH)3 (aluminum hydroxide)

A

ANTACID(neutralize acid in stomach)
-Al(OH)3+ 3HCl= AlCl3 + H2O + CO2
-if absorbed and patient has impaired kidney function it can lead to ENCEPHALOPATHY

209
Q

methotrexate

A

antimetabolite
-competitive inhibitor of dihydrofolate reductase which cant convert DHF to THF→ depletes folic acids and cant make purine/pyrimidine synthesis needed for DNA production
-also anti inflammatory effect and inhibits B and T cell activation

210
Q

cyclophosphamide

A

alkylating agent for immunopharma
-derived from mustard gas
-prodrug which becomes ACROLEIN!!
-alkylating DNA of N7 guanine form cross links inside DNA chain or bw 2 chain and blocks both B and T cells

211
Q

azathioprine

A

antimetabolite which becomes 6-mercaptopurine, and acts like a PURINE analogue where its incorporated into DNA and inhibits DNA synthesis by breaking chromosome down!
-used for prophylaxis of renal transplant rejection or RA
-SE: liver toxicity, bone marrow suppression

212
Q

leflunomide

A

immunopharma
-inhibits dihydroorotate DH which blocks PYRIMIDINE synthesis!!→ inhibits T cell proliferation and AB production of B cells
-TETRAGENICITY!! SE
-used for RA or psoriatic arthritis

213
Q

mycophenolate-mofetil

A

antimetabolite,
-inhibits inosine monophosphate DH (reversibly)→ blocks de novo GMP synthesis→ selective inhibition of lymphocyte proliferation and blocks both T and B cell!!
-combine with CYCLOSPORINE OR TACROLIMUS for solid organ transplant rejection prophylaxis

214
Q

cyclosporine A

A

calcineurin inhibitor (binds to cyclophilin) which wont be able to activate(dephosphorylate) NFAT(Nuclear factor of activated T cell), so wont be able to produce IL-2!!/activate T cell
-metabolism by CYP3A4!!

215
Q

tacrolimus

A

calcineurin inhibitor (binds to FK-binding protein) which wont be able to activate(dephosphorylate) NFAT(Nuclear factor of activated T cell), so wont be able to produce IL-2!!/activate T cell
-more potent than cyclosporin A
-metabolism by CYP3A4!!

216
Q

sirolimus

A

also called RAPAMYCIN!!
-mTOR inhibitor!!
-binds to FK binding protein 12 and ihibits mTOR Kinase→ decrease response to IL-2 an decrease activation of T and B cell!
-orally

217
Q

tofacitinib

A

immunopharma
-JAK1 and JAK3 inhibitor→blocks IL2 production
-orally
-used for RA or psoriatic arthritis/COVID
-SE: airway infections

218
Q

sulfasalazine

A

prodrug converted into SULFAPYRIDINE AND 5-ASA(aminosalicylic acid)
-activated by colon bacteria
-sulfapyridine is resorbed in GI and active in RA
-5-ASA blocks NFkappaB and blocks cytokines(TNF-alpha or IL1,2,8)→ used for IBD treatment(UC, CD)

219
Q

Anti-thymocyte globulin(ATG)

A

polyclonal antibodies, isolated from rabbit/horse blood immunized by human thymocytes
-blocks and kill B and T cells in the body by binding onto the surface of the cells

220
Q

rituximab

A

immunopharma
-monoclonal AB attacks CD20 of B cell!!→ reduce function of these B cells
-used in non hodgkin lymphoma/RA/autoimmune hemolytic anemia

221
Q

infliximab

A

immunopharma
-monoclonal AB attacks TNF-alpha(cytokine)
-reduces inflammatory response
-used in IBD/RA/psoriasis arthritis
-IV once/2 months

222
Q

adalimumab

A

immunopharma
-monoclonal AB attacks TNF-alpha(cytokine)
-reduces inflammatory response
-used in IBD/RA/psoriasis arthritis
-SC once/2 weeks

223
Q

tocilizumab

A

immunopharma
-Anti-IL6 R antibody!!
-IV once/month
-used for RA/ juvenile idiopathic arthritis

224
Q

ustekinumab

A

immunopharma
-anti-12/23 antibody
-IL12 blockage→ no activation of Th1 cell
-IL23 block→ no activation of Th17 proinflammatory lymphocytes
-used in psoriasis

225
Q

dupilumab

A

immunopharma monoclonal AB
-anti-IL-4alphaR and IL 13R antibody
-blocks Th1 and Th2 mediated immune reactioon
-used for severe atopic dermatitis
-SE: oral herpes, conjuctivitis

226
Q

natalizumab

A

immunopharma monoclonal Ab
-anti alpha4 integrin AB
-inhibits docking and extravasation of T cells thru
-a4b1 VCAM1 interaction in CNS
-a4b7 MadCAM1 interaction in GI tract
-used for Multiple sclerosis
-RARELY PROGRESS TO PML(progressive multifocal leukoencephalopathy)

227
Q

abatacept

A

costimulation inhibitor, blocks binding of costimualtory CD28(of T cell) to CD80/86 of APC
-used for RA or psoriatic arthritis
-SE: headache, infections

228
Q

tamoxifen

A

hormonal agent for cancer therapy
-Antiestrogens(inhibition of Estrogen R)→ acts as SERM!!
-used for breast cancer
-SE: menopause symptoms

229
Q

anastrozole

A

hormonal agent for cancer therapy
-AROMATASE inhibitor (inhibits estrogen synthesis), reversible

230
Q

goserelin

A

hormonal agent for cancer therapy
-GnRH AGONIST!!(inhibits release of LH and FSH from pituitary)→ estrogen and androgen decreases
-used for prostate/breast cancer
-SE: menopause symptoms

231
Q

degarelix

A

hormonal agent for cancer therapy
-GnRH ANTAGONIST!
-used for advanced prostate cancer

232
Q

bicalutamide

A

hormonal agent for cancer therapy
-anti-androgen(androgen R antagonists)
-reduce hormone dependent growth of prostate cancer
-SE: male postmenopausal symptoms

233
Q

prednisolone

A

hormonal agent for cancer therapy
-GLUCOCORTICOIDS!!
-inhibits all phases of inflammation, induce apoptosis in lymphomas, appetite enhancer, decrease nausea/vomiting
-used for ALL/CLL/chemo and radiotherapy induced voimiting, decrease nausea

234
Q

octreotide

A

somatostatin analogues, inhibits secretion of GH (hormonal agent for cancer therapy)
-used in acromegaly, insulinoma, neuroendocrine tumors, gigantism to inhibit release of GH

235
Q

imatinib

A

small molecule signaling inhibitor
-BCR-ABL TK inhibitors
-used for CML, GIST
-SE* edema, vomiting, CARDIOTOXICITY!!!

236
Q

gefetinib

A

small molecule signaling inhibitor
-EGFR TK inhibitors
-for NSCLC
-SE: rashes, diarrhea. fatigue

237
Q

erlotinib

A

small molecule signaling inhibitor
-EGFR TK inhibitors
-NSCLC used for
-rashes, fatigue diarrhea

238
Q

lapatinib

A

small molecule signaling inhibitor
-EGFR 1 and 2 TK inhibitors
-for breast cancer(HER2 positive)
**CARDIOTOXICITY!!(imatibnib ex)

239
Q

ibrutinib

A

small molecule signaling inhibitor
-other TK inhibitors
-BRUTON TK inhibitor!!
-used for CLL
-pneumonia, fever, infections SE

240
Q

crizotinib

A

small molecule signaling inhibitor
-ALK TK inhibitor
-used for NSCLC
-SE* nausea, vomiting, edema

241
Q

sunitinib

A

small molecule signaling inhibitor
-multiTK inhibitor
-inhibts VEGFR and C-KIT inhibitor!!
-used for GIST and kidney cancer
-HAND FOOT SYNDROME!!
-edema, vomiting, diarrhea

242
Q

everolimus

A

small molecule signaling inhibitor
-serine threonine kinase inhibitor
-used for HER2 NEGATIVE breast cancer
-neuroendocrine tumor/kidney cancer indication
-SE+ anemia, thrombocytopenia, vomiting, diarrhea

243
Q

dabrafenib(+trametinib)

A

-used with TRAMETINIB
-small molecule signaling inhibitor
-BRAF Serine threonine kinase inhibitor
(trametinib is inhibitor of MEK1/2)
-for metastatic melanoma
-SE* fever, joint pain, hand foot syndrome, hair loss

244
Q

bortezomib

A

small molecule signaling inhibitor
-reversible inhibitor of 26S proteasome!!
-used for myeloma multiplex

245
Q

tretionin

A

TRANS RETINOL
-used for acute promyelocyte leukemia
-TETRAGENIC!!(CI In PREGNANCY)

246
Q

panitumumab

A

IgG2, monoclonal AB!! binding to EGFR (HER1)
-used for colorectal carcinoma with KRAS wild type
-SE* fatigue, skin symptoms, GI symptoms, myelosuppression but rare

247
Q

transtuzumab

A

HER2 MONOCLONAL AB
-used for HER2 positive breast/gastric cancer
-CARDIOTOXICITY!!!!
-TETRAGENIC!!!
-**can be conjugated to -emtansine!!(toxin)

248
Q

rituximab

A

monoclonal AB against CD20 of B cell!!
-for CLL/NHL
-SE+ immunosuppression + infections
-HBC reactivation as SE

249
Q

bevacizumab

A

monoclonal AB against anti-VEGF antibodies
-used for colorectal carcinoma and renal cell carcinoma
-SE: CARDIOTOXICITY!!!!!**(with transtzumab)
-bleeding, would healing and surgical complications, shouldnt be used in case of surgery post

250
Q

aldesleukin

A

IL2 recombinant version,
-recruits T and B and NK cells
-used for melanoma, renal cell carcinoma
-SE: cardiovascular, flu like symptoms,
CAPILLARY LEAK SYNDROME

251
Q

INF alpha

A

binds to specific receptor on celll membrane and induce transcription, inhibits cell growth
-used for HEP B AND C
-SE* musculoskeletal pain, flu like symptoms in children 100, rashes, fever

252
Q

pembrolizumab

A

anti-PD1 antibody for tumor cells
-monoclonal AB
-used for melanoma, NSCLC
-SE: autoimmune diseases

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