phB Flashcards
acetylsalicylic acid
antiplatelet agent, inh of TXA2 synthesis and inhibit the platelet aggregation
clopidogrel
P2Y12-R antagonist(ADP-R antagonist), antiplatelet agent
prasugrel
P2Y12-R antagonist(ADP-R antagonist), antiplatelet agent
ticagrelor
P2Y12-R antagonist(ADP-R antagonist), antiplatelet agent
abciximab
inhibitor or Gp 2b/3a receptor, antiplatelet agent
alteplase
tissue plasminogen activator’s activator, fibrinolytic agent
reteplase
tissue plasminogen activator’s activator, fibrinolytic agent
epinephrine
local antihemorrhagic drug
fibrin foam
local antihemorrhagic drug, activates intrinsic pathway of coagulation cascade, for soldiers to put on their wounds temporarily
vitamin K1
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
vitamin K2
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
ε(epsilon)-aminocaproic acid (EACA)
inhibits conversion of plasminogen to plasmin, systemic antihemorrhagic drugs(competitive antagonist at lysine binding sites of plasminogen→inhibits plasminogen)
heparin
activated antithrombin 3, which inactivates factor 10a and 2a(thrombin), chains longer than 18 monosaccharide so inactivates BOTH 10a and 2a
dalteparin(LMWH)
low molecular weight heparin, chains shorter than 18 monosaccharides, only inactivates factor 10a (10a:2a= 3:1 ratio)
warfarin
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!!!
dabigatran-etexilate
direct thrombin(factor 2a) inhibitor, taken ORALLY, given in prodrug form thats why its bound to etexilate
rivaroxaban
direct factor 10a inhibitor (rivaroXaban→Xa inh), taken ORALLY
fondaparinux
inactivate only factor 10a, lowest molecule heparin, crosses placenta, theres no GAGs thats why it only inactivates factor 10a and NOT thrombin(factor2a)
iron hydroxide polymaltose
for anemias, iron supplement
vitamin B12
for anemias,
folic acid
for anemias, vitamin B9
epoetin-alpha(erythropoeitin)
for anemias, IV or SC
filgrastim
for anemias, recombinant G-CSF
digoxin
positive ionotropic drug for acute heart failure, cardiac glycosides, inhibits Na2+/K+ ATPase →↑Ca2+ ic
digitoxin
positive ionotropic drug for acute heart failure,cardiac glycosides, inhibits Na2+/K+ ATPase →↑Ca2+ ic
milrinone
positive ionotropic drug for acute heart failure, inhibits PDE3 which inhibits cAMP→ Ca2+↑
levosimendan
positive ionotropic drug for acute heart failure, increases Ca2+ sensitvity of troponin C→ stabilizes it in a conformation needed for contraction!!
dobutamine
positive ionotropic drug for acute heart failure, beta1 R agonists and stimulates cAMP and PKA→Ca2+↑
acetazolamide
acts on PCT, inhibits carbonic anhydrase
furosemide
loop diuretics, acts on asc loop of henle, inhibits Na/K/2Cl- co transporter
etacrynic acid
loop diuretics, acts on asc loop of henle, inhibits Na/K/2Cl- co transporter
hydrochlorothiazide
thiazide diuretics, inhibits Na/Cl- cotransporter in distal convoluted tubule, CI in diabetes
indapamide
thiazide LIKE diuretics, inhibits Na/Cl- cotransporter in distal convoluted tubule, ONLY USED IN HYPERTENSION!!
mannitol
osmotic diuretics, pulls H2O from nearby tissues like brain tissue or vitreous humor for cerebral edema or glaucoma!, ↑osmolarity of blood, IV!!
glycerol
osmotic diuretics, pulls H2O from nearby tissues like brain tissue or vitreous humor for cerebral edema or glaucoma!, ↑osmolarity of blood, IV!!!
spironolactone
aldosterone antagonists, potassium sparing diuretics
eplerenone
aldosterone antagonists, potassium sparing diuretics
amiloride
potassium sparing diuretics, inhibitors of ENaC channel used for Liddle syndrome,, amiLORI====LIDDLE sydnrome!!!
tolvaptan
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
simvastatin
statins, HMG-CoA reductase inhibitor, inhibits cholesterol synthesis, used for dyslipidemias, SIMVAAAA!
atorvastatin
statins, HMG-CoA reductase inhibitor, inhibits cholesterol synthesis, used for dyslipidemias
rosuvastatin
statins, HMG-CoA reductase inhibitor, inhibits cholesterol synthesis, used for dyslipidemias
fenofibrate
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
fenofibrate
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
cholesevelam
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!!)
ezetemibe
cholesterol absorption inhibitors for dyslipidemia, in the small intestine,→ LDL↓↓↓ in the blood stream, OFTEN COMBINED WITH STATINS(SIMVASTATIN)
lidocaine
class 1B antiarrythmic drug, Na+ channel blocker(WEAK INHIBITION!!), alters repolarization phase(phase 0 only!), IV infusion, lease cardiotoxic
propafenone
class 1C antiarrythmic drug(STRONGEST), strong inhibition of Na+ channels and Na+ only!!!, PROARRYTHMIC as SE!
esmolol
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,
amiodarone
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
sotalol
class III antiarrythmic drugs, K+ channel blocker!!→affects phase 1+2+3 bc involved with K+ channels
verapamil
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!!!
adenosine
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!!
magnesium(sulfate)
class V antiarrythmic drugs(others group), Calcium channel blocker!!!
digoxin
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!!!!
nitroglycerin
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
isosorbide-mononitrate
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
trimetazidine
antianginal drugs, blocks beta oxidation of FA and enhances glucose oxidation→ requires less O2 in ischemic cells
ivabradine
antianginal drugs, inhibits funny current in SA node→ HR↓
beta blockers: antianginal drugs
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)
calcium channel blockers: antianginal
- 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!!
vinpocetin
for microcirculation drugs, PDE-1 inhibitor taken parenteral
nootropic, inhibits platelet aggregation so increase cerebral perfusion
-used for cerebral microcirculation
nicergoline
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!
cilostazol
PDE3 inhibitor for microcirculation drugs, decrease platelet aggregation and increase vasodilation
-used in pain, ache, ccramp
-CI in CHF
calcium-dobesilate
pentoxyfilline
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
cinnarizine
antihistamines
captopril
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↑
perindopril
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↑
enalapril
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↑
ramipril
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↑
losartan
AT-2 Receptor blockers for antihypertensive drugs, decreases BP in case of hypertension
valsartan
AT-2 Receptor blockers for antihypertensive drugs, decreases BP in case of hypertension
valsartan+sacubitril(ARNi)
AT-2 Receptor blockers for antihypertensive drugs, decreases BP in case of hypertension
irbesartan
AT-2 Receptor blockers for antihypertensive drugs, decreases BP in case of hypertension
spironolactone
aldosterone antagonists for antihypertensive drugs, inhibits aldosterone dependent Na+/K+ ATP ase and Na+ transporters, decreases BP, SE: GYNECOMASTIA
eplerenone
aldosterone antagonists for antihypertensive drugs, inhibits aldosterone dependent Na+/K+ ATP ase and Na+ transporters, decreases BP, SE: GYNECOMASTIA
verapamil
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
nifedipine
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
nimodipine
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
felodipine
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
amlodipine
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
dihydralazine
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
bosentan
vasodilator for hypertension, endothelin R antagonists which inhibits vasoconstriction
sildenafil
vasodilator for hypertension, PDE5 inhibitors which enhance vasodilation of NO by inhibiting PDE5, DO NOT GIVE WIHT NITRATE bc it will cause severe hypotension!
glipizide
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
glimepiride
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
repaglinide
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
metformin
drugs for T2DM, acts on AMPkinase which activates carbohydrate and fat metabolism,FIRST LINE DRUG choice in T2DM
vildagliptin
gliptins, DPP4 inhibitors for T2DM, increases insulin production and decrease glucose level
dapagliflozin
SGLT2 inhibitors for T2DM, (reversible inhibition), inhibits absorption of glucose in SGLT2 in proximal CT
acarbose
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
levothyroxin
thyroid drugs for hypothyroidism treatment, T4!!!, 25-150 microgram, used for hypothyreosis, endemic goiter and substitute after thyroidectomy
thiamazole
inhibitors of peroxidase enzyme for hyperthyroidism treatment, used for graves disease, multinodular goiter
propylthiouracil
inhibitors of peroxidase enzyme AND 5’ deiodinase enzyme for hyperthyroidism treatment, used for graves disease, multinodular goiter, CAUSE THYROID STORM with high dose!!
iodine
high dose of iodine used for hyperthyroidism treatment(like negative feedback), also used for hypothyroidism treatment: iodine deficiency
octreotide
somatostatin analogue, inhibits release of GH and TSH, hypothalamic and pituitary hormones!!, used for glucagonoma, insuloinoma, upper GI bleeding since it can vasoconstrict!
bromocriptine
dopamine R agonist, used for Parkinson disease, stop of lactation, acromegaly(p.o)
desmopressin
man made form of vasopressin(ADH), increases water reabsorption in kidney tubule!!, used to replace a low level of vasopressin
oxytocin
hypothalamic hormones, effects: uterine contractions during childbirth and cause lactation!
hydrocortisone
short duration of action, =CORTISOL, glucocorticoids, used for HR replacement therapy
prednisolone
intermediate duration of action, glucocorticoids, for systemic antiinflammatory adn immunosuppressive effect
methylprednisolone
intermediate duration of action, glucocorticoids, MINIMAL MINERALOCORTICOID ACtiON
triamcinolone
intermediate duration of action, glucocorticoids, more toxic than others
dexamethasone
LONG duration of action, glucocorticoids, used in cerebral edema
fludrocortisone
mineralocorticoids, short duration of action, used for acute/chronic adrenocortical insufficiency or post-adrenalectomy, salt and water retention effect, excretes K+ and H+
fluticasone
topically applied glucocorticoids, used ICS!!
mometasone
topically applied glucocorticoids, used ICS!!
budesonide
topically applied glucocorticoids, used ICS!!
fluocinolone
topically applied glucocorticoids, TOPICALLY,
metyrapone
reversible inhibitor of 11beta-hydroxylase enzyme, cant produce corticosterone and cortisol, used for overnight metyrapone stimulation test for diagnosis of adrenal insufficiency
undecanoate
-testosterone, prodrug of testosterone, androgen R agonist, orally active,
bicalutamide
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
finasteride
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!
goserelin
GnRH agonist, androgenic suppression with it by continuous therapy, used in prostate cancer
degarelix
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
sildenafil
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
nandrolone
androgen R agonist, synthetic testosterone used for hypogonadism in men after castration, or hereditary angioedema, illegally among athletes
estradiol
ethinylestradiol
clomifen
SERM, (selective estrogen R modulator) stimulates ant pituitary to produce more LH!!, ovulation inducing agent by inducing negative feedback to increase LH level
tamoxifen
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
raloxifene
SERM, (selective estrogen R modulator), prevention of postmenopausal osteoporosis!!, acts on bones!!
anastrozole
aromatase inhibitor, used in breast cancer resistant to tamoxifen to reduce the amount of estrogen/estradiol
goserelin
GnRH agonist, used for breast cancer and hormone sensitive prostate cancer
degarelix
GnRH antagonists, used for breast cancer and hormone sensitive prostate cancer
medroxyprogesterone-acetate
synthetic progestin-pregnans category, better oral bioavailability, inhibits ovulation by acting on progesterone R present in nucleus
drospirenone
synthetic progestin-pregnans category, better oral bioavailability, inhibits ovulation by acting on progesterone R present in nucleus
norethisterone
synthetic progestin-ESTRANS category, better oral bioavailability, inhibits ovulation by acting on progesterone R present in nucleus
levonorgestrel
synthetic progestin-GONANS category, better oral bioavailability, inhibits ovulation by acting on progesterone R present in nucleus
desogestrel
synthetic progestin-GONANS category, better oral bioavailability, inhibits ovulation by acting on progesterone R present in nucleus
cyproterone-acetate
synthetic progestin-pregnans category, better oral bioavailability, inhibits ovulation by acting on progesterone R present in nucleus
mifepristone
progesterone antagonists, estran, used for termination of early pregnancy
ulipristal acetate
selective progestin receptor modulator (progesterone antagonist), morning after pill(prevents preganncy if no choice to inhibit implantation
levonorgestrel+ethinylestradiol
teriparatide
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
cholecalciferol
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!!)
alendronate
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,
zoledronate
taken IV!!non hormonal drugs for osteoporosis, one of bisphosphonates, osteoclasts eat them up and leads to apoptosis and inactivation of the osteoclasts,
denosumab
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!!
raloxifene
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
dimenhydrinate
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
droperidol
D2 R antagonists for area postrema(vomiting center)→inhibits vomiting!!, antiemetic drug, also PROKINETIC effect
metoclopramide
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,
ondansetron
antagonists of 5-HT3!!Receptor in the GI tract which inhibits vomiting, taken orally, used for CHEMOTHERAPY!!
palonosetron
antagonists of 5-HT3!!Receptor in the GI tract which inhibits vomiting, IV!!! only , used for CHEMOTHERAPY!!
aprepitant
NK-1 R antagonists inAREA POSTREMA(vomiting center), SE: cyp3A4 inhibitor!!, taken orally
cannabinoids
inhibits presynaptic release of dopamine, used for chemotherapy induced vomiting, inhibits vomiting, taken orally
plant fibers
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
magnesium (sulfate)
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
lactulose
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
parrafin oil
stool softener, effective in 6-12hrs, orally or rectally,
-softens hard stool(stool surfactant agent increasing penetration of water and lipid)→helps empty bowel
sennoside
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
bisacodyl
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)
diphenoxylate
anti-diarrheal drug, mu opioid R agonist, taken orally, inhibits propulsive peristalsis
loperamide
anti-diarrheal drug, mu opioid R agonist, taken orally, inhibits propulsive peristalsis+increase sphincter tone+inhibits intestinal fluid secretioin
CANNNOT CROSS BBB
active charcoal
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)
ursodeoxycholic acid
increase production of bile and emulsify the dietary fats and cholesterol of bile, used for biliary cirrhosis
acetylcysteine
antidote of paracetamols toxic metabolite
-increase production of depleted antioxidant GLUTATHIONE which conjugates and detoxify paracetamol metabolite
-used in paracetamol/aspirin overdose
silimarin
milk thistle extract
-used in LIVER AND BILIARY TRACT
-decrease level of ROS, inhibits lipid peroxidation
-for hepatotoxicity
methotrexate
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!!
pemetrexed
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
5-fluorouracil
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
capecitabine
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)
6-mercaptopurine
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
cytarabine
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
cyclophosphamide
alkylating agent for cancer chemotherapy
-breaks DNA double strand
-used for solid tumor
-SE: hemorrhagic cysitits (PREVENTED WITH MESNA)
-infertility, vomiting in high doses
dacarbazine
alkylating agent for cancer chemotherapy
-breaks DNA double strand
-used for solid tumor
-similar to cyclophosphamide
-SE: myelosuppression, vomiting
temozolomide
alkylating agent for cancer chemotherapy
-alkylation of DNA and RNA→ decrease DNA replication
-for BRAIN TUMOR!!!
-SE* myelosuppression and neurotoxicity
cisplatin
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
oxaliplatin
platinum based alkylating agent for cancer chemotherapy
cross link bw DNA strands → decrease DNA replication
-for solid tumors (GI TUMOR!!!)
-NEUROTOXICITY!!
dactinomycin
interfere with DNA transcription which decrease RNA synthesis, alkylating agent for cancer chemotherapy
-used for childhood tumors
bleomycin
-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)
irinotecan
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)
etoposide
topoisomerase 2 inhibitor
-dsDNA breaks→ decrease DNA replication and increase DNA degradation
-for solid tumors
-SE* myelosuppression
doxorubicin
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
vincristine
inhibitor of microtubule
-binds to beta tubi¥ulin and inhibits beta tubulin polymerization into microtubules→ inhibits M phase
-for SOLID TUMORS
-neurotoxicity
docetaxel
inhibitor of microtubule
-hyperstabilization of polymerized microtubules→ prevents mitotic spindles disassembly→ arrest in M phase
-used for BREAST CANCER
-SE* nail changes, hepatotoxicity
aspart insulin
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!!
lispro insulin
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!!
regular insulin
NPH insulin
intermediate acting insulin, onset:4-5hrs(long),takes time for insulin to degrade from hexamer to monomer form to get into the blood circulation)
glargine insulin
ULTRA LONG acting insulin, duration is up to 24hr(given once per day), addition of 2 arginine!! after B30-Thr
liraglutide
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
terbutaline
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!)
salbutamol
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!)
fenoterol
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!)
formoterol
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!!!
theophylline
inhibitor of PDE(phosphodiesterase) which inhibits cAMP, so basically activates cAMP which leads to smooth mm relaxation!!→ good for COPD for bronchodilation!
ipratropium
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
tiotropium
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
montelukast
for asthma!!, inhibits bronchospasm bc it is LEUKOTRIEN R ANTAGONIST!!
omalizumab
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
salmeterol
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!!!
prednisolone
corticosteroids, used in asthma/COPD(inhaled Corticosteroids)
-TAKEN ORALLY!! (ONLY in case of severe acute attacks or severe persistent asthma)
methylprednisolone
corticosteroids, used in asthma/COPD(inhaled Corticosteroids)
-TAKEN IV!! (ONLY in case of severe acute attacks or severe persistent asthma)
fluticasone
Inhaled Corticosteroids for COPD/asthma,
NO BRONCHODILATION,
only anti inflammatory effects!!
budesonide
Inhaled Corticosteroids for COPD/asthma,
NO BRONCHODILATION,
only anti inflammatory effects!!!
codeine
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)
butamirate
centrally acting Antitussive agent,
-↓sensitivity of cough centers in CNS to peripheral stimuli and decrease cough reflex
-decrease mucosal secretions
prenoxdiazine
peripherally acting Antitussive drug
-used for strong cough of bronchial origin
-act by ↓sensitivity of R and afferent neurons of pulmonary stretch R
bromhexine
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
acetylcysteine
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
ambroxol
secretolytic agents for productive cough which increases ciliary activity
omeprazole
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)
pantoprazole
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
famotidine
H2-Receptor Antagonist, decrease gastric acid and pepsinogen secretion
-for GERD/peptic ulcer disease
-taken 1time daily at BEDTIME!!
MgO(magnesium oxide)
ANTACID(neutralize acid in stomach)
-poor solubility, prolonged neutralizing effect
Al2(OH)3 (aluminum hydroxide)
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
methotrexate
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
cyclophosphamide
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
azathioprine
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
leflunomide
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
mycophenolate-mofetil
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
cyclosporine 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!!
tacrolimus
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!!
sirolimus
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
tofacitinib
immunopharma
-JAK1 and JAK3 inhibitor→blocks IL2 production
-orally
-used for RA or psoriatic arthritis/COVID
-SE: airway infections
sulfasalazine
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)
Anti-thymocyte globulin(ATG)
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
rituximab
immunopharma
-monoclonal AB attacks CD20 of B cell!!→ reduce function of these B cells
-used in non hodgkin lymphoma/RA/autoimmune hemolytic anemia
infliximab
immunopharma
-monoclonal AB attacks TNF-alpha(cytokine)
-reduces inflammatory response
-used in IBD/RA/psoriasis arthritis
-IV once/2 months
adalimumab
immunopharma
-monoclonal AB attacks TNF-alpha(cytokine)
-reduces inflammatory response
-used in IBD/RA/psoriasis arthritis
-SC once/2 weeks
tocilizumab
immunopharma
-Anti-IL6 R antibody!!
-IV once/month
-used for RA/ juvenile idiopathic arthritis
ustekinumab
immunopharma
-anti-12/23 antibody
-IL12 blockage→ no activation of Th1 cell
-IL23 block→ no activation of Th17 proinflammatory lymphocytes
-used in psoriasis
dupilumab
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
natalizumab
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)
abatacept
costimulation inhibitor, blocks binding of costimualtory CD28(of T cell) to CD80/86 of APC
-used for RA or psoriatic arthritis
-SE: headache, infections
tamoxifen
hormonal agent for cancer therapy
-Antiestrogens(inhibition of Estrogen R)→ acts as SERM!!
-used for breast cancer
-SE: menopause symptoms
anastrozole
hormonal agent for cancer therapy
-AROMATASE inhibitor (inhibits estrogen synthesis), reversible
goserelin
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
degarelix
hormonal agent for cancer therapy
-GnRH ANTAGONIST!
-used for advanced prostate cancer
bicalutamide
hormonal agent for cancer therapy
-anti-androgen(androgen R antagonists)
-reduce hormone dependent growth of prostate cancer
-SE: male postmenopausal symptoms
prednisolone
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
octreotide
somatostatin analogues, inhibits secretion of GH (hormonal agent for cancer therapy)
-used in acromegaly, insulinoma, neuroendocrine tumors, gigantism to inhibit release of GH
imatinib
small molecule signaling inhibitor
-BCR-ABL TK inhibitors
-used for CML, GIST
-SE* edema, vomiting, CARDIOTOXICITY!!!
gefetinib
small molecule signaling inhibitor
-EGFR TK inhibitors
-for NSCLC
-SE: rashes, diarrhea. fatigue
erlotinib
small molecule signaling inhibitor
-EGFR TK inhibitors
-NSCLC used for
-rashes, fatigue diarrhea
lapatinib
small molecule signaling inhibitor
-EGFR 1 and 2 TK inhibitors
-for breast cancer(HER2 positive)
**CARDIOTOXICITY!!(imatibnib ex)
ibrutinib
small molecule signaling inhibitor
-other TK inhibitors
-BRUTON TK inhibitor!!
-used for CLL
-pneumonia, fever, infections SE
crizotinib
small molecule signaling inhibitor
-ALK TK inhibitor
-used for NSCLC
-SE* nausea, vomiting, edema
sunitinib
small molecule signaling inhibitor
-multiTK inhibitor
-inhibts VEGFR and C-KIT inhibitor!!
-used for GIST and kidney cancer
-HAND FOOT SYNDROME!!
-edema, vomiting, diarrhea
everolimus
small molecule signaling inhibitor
-serine threonine kinase inhibitor
-used for HER2 NEGATIVE breast cancer
-neuroendocrine tumor/kidney cancer indication
-SE+ anemia, thrombocytopenia, vomiting, diarrhea
dabrafenib(+trametinib)
-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
bortezomib
small molecule signaling inhibitor
-reversible inhibitor of 26S proteasome!!
-used for myeloma multiplex
tretionin
TRANS RETINOL
-used for acute promyelocyte leukemia
-TETRAGENIC!!(CI In PREGNANCY)
panitumumab
IgG2, monoclonal AB!! binding to EGFR (HER1)
-used for colorectal carcinoma with KRAS wild type
-SE* fatigue, skin symptoms, GI symptoms, myelosuppression but rare
transtuzumab
HER2 MONOCLONAL AB
-used for HER2 positive breast/gastric cancer
-CARDIOTOXICITY!!!!
-TETRAGENIC!!!
-**can be conjugated to -emtansine!!(toxin)
rituximab
monoclonal AB against CD20 of B cell!!
-for CLL/NHL
-SE+ immunosuppression + infections
-HBC reactivation as SE
bevacizumab
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
aldesleukin
IL2 recombinant version,
-recruits T and B and NK cells
-used for melanoma, renal cell carcinoma
-SE: cardiovascular, flu like symptoms,
CAPILLARY LEAK SYNDROME
INF alpha
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
pembrolizumab
anti-PD1 antibody for tumor cells
-monoclonal AB
-used for melanoma, NSCLC
-SE: autoimmune diseases
