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56 Cards in this Set

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aspirin
antiplatelet

MOA: inhibits COX, platelets dont produce TXA2, cant activate eachother as well, and dont form the initial platelet plug. also, inhibits PGG2 and PGH2 formation. inhibits vasoconstriction?

USES:
1. prevent heart disease
2. acute MI - if pt has chest pain give them aspirin to prevent coagulation with ruptured plaque

NOTES:
inhibits circulating platelets for their lifetime (7-10 d)
NSAIDs
antiplatelet
dipyridamole
antiplatelet
dipyridamole [2 ways to prevent platelet activation]

USE: phrophylaxis of thromboembolic events

MOA: inhibits platelet activation by increasing platelet cAMP levels
2 methods:
a. blocking uptake of adenosine -> + A.C -> inc. cAMP
b. inhibits phosphodiesterase
inc'd cAMP inhibits platelet activation
CLOPIDOGREL
antiplatelet

MOA: blocks ADP receptor

USES: prevent thromboembolic events

similar: ticlopidine (clop)
abciximab
antiplatelet

MOA: blocks GP IIb/IIIa receptors (blocks activated receptors from binding fibrinogen)

USES: prevent thromboembolic events
WARFARIN
oral anticoagulant

MOA: inhibits epoxide reductase, preventing vitamin K from being converted to active form.
K+ is a necessary cofactor for the addition of a carboxyl group from glutamic acid to factors II, VII, IX, and X. w/o K+, inactive clotting factors are synthesized by liver

NOTES:
MUST BE MONITORED!!
-highly protein bound
-dose independent (highly ep on metabolism)
-green leafy veggies and cereals require extra warfarin. diets def. in vitamin K require less warfarin
-teratogenic - not for use in pregnancy (heparin better for pregnant women)
-antibiotics kill normal flora that make vitamin K and can lead to vitamin K deficiency and bleeding

actions are not immediate (vs. heparin). circulating factors are depleted enough in a week. can cause coagulation first b/c of depletion of protein C!!
monitor with INR=(PT/mean normal PT)^ISI. window b/t 2 and 3

risk factors for thromboembolic events: age, HTN, cerebrovascular and cardiovascular disease, DM, hyperlipidemia, smoking, drugs, INR < 2
risk factors for bleeding: age, hx of stroke or GI hemorrhage
HEPARIN
anticoagulant

used for prophylaxis AND after a thromboembolic event (works immediately)

MOA:
1. pentapeptide binds AT and increases accessibility to Active Site
2. binds Xa or IIa and inactivates it (like enoxaparin)
3. catalytic template - binds both AT and factor IIa, Xa, IXa, XIA, and XIIa. AT inactivates the factor, and heparin is ready to go again

NOTES:
antidote = protamine
monitor with PTT
MUST BE MONITORED
-binds many things
-liver failure will inc effects
-kidney failure will increase effects

S/E: HIT
heparin binds to platelet factor 4 and triggers immune response against these complexes. platelet FcR binds the complexes causing both thrombocytopenia and thrombosis. detect with platelet 4 antibody test.
Rx for HIT is DTI such as lepirudin or argatroban



drug of choice for pregnancy (doesnt cross placenta like warfarin)
ENOXAPARIN
LMWH (anticoagulant)

fragments of UFH
in contrast to heparin, it mainly inactivates Xa b/c the fragments are too short to bind Xa and AT
most frags donts have the pentapeptide to bind AT
most patients are not monitored, but you can monitor with anti-factor Xa test.

monitor: renal failure pts, large pts, small cachetic pts, women, those with tumors, pts with DIC, pts with bleeding or thrombi
may cross react with HIT antibody
lepirudin
direct thrombin inhibitor (from leeches)

use: heparin alternative, esp for HIT

no antidote
monitor with PTT (like heparin)
argatroban
direct thrombin inhibitor

ARGO LIKES LEACHES

monitor with PTT (like heparin)
streptokinase
plasminogen activator (fibrinolytic)

no intrinsic nzm activity. binds plasminogen and exposes active site. then SK-plasmin converts SK-plasminogen to more SK-plasmin.
USE:
1. acute MI

for strokes, use TPA (ALTEPASE) instead
urokinase
plasminogen activator (fibrinolytic)

directly converts plasminogen to plasmin - enzyme activity
(vs streptokinase-indirect)
USE:
1. acute MI

use TPA (altepase for strokes)
eta-aminocaproic acid
fibrinolysis inhibitor

USE: hemophiliacs (can make weak blood clot)
tranexamic acid
fibrinolysis inhibitor

USE: hemophiliacs (can make weak blood clot)
ALTEPASE
plasminogen activator (recombinant tPA)

fibrin selective - its activity is increased 100x when bound to fibrin, which decreases nonspecific fibrinolytic activity (it should just occur at the clot)
USE:
1. acute MI
2. pulmonary embolus, DVT, arterial thrombosis
3. acute nonhemorrhagic CVA (sometimes!)
antihemophilic factor
factor VIII
phytonadione
vitamin K
fondaparinux
fondaparinuX X X X
anticoagulant

Jane Fonda has hypercoagulation

pentasaccharide that binds factor Xa and inhibits it.

even smaller than lwmh
folic acid
needed to transfer methyl groups in purine and amino acid synthesis (folate cycle)
found in green leafy vegetables, liver, kidney, yeast

deficiency - megaloblastic anemia

measure levels with RBC-folate

prophylactic for pregnancy, alcoholism, dialysis, hemolytic anemia

drugs which inhibit folate abs: oral contraceptives, isoniazid, phenytoin

methotrexate and trimethorim block DHF reductase. these patients have "folate deficiency" but giving folate would be counterproductive.
vitamin B12
1. cofactor in methyl transfer from THF to methionine (eventually making SAM)

2. cofactor in isomerization of methyl-malonyl CoA to succinyl CoA (utilization of fatty acids)

found in meat, eggs, and dairy, stored in liver for YEARS

absorption: binds IF (from parietal cells) in stomach, absorbed in distal ileum

deficiency: there are NEUROLOGICAL SYMPTOMS!! (unlike folate) - paresthesias, weakness, ataxia. giving folate may mask!

Rx for def:
oral supplements if ileum and IF are intact
parenteral otherwise

labs to detect dficiency:
-vitamin B12 in serum
-MMA (will be HIGH!! in B12 deficiency)
iron
needed for hemoglobin (and cytochromes)

deficiency causes microcytic anemia with large RDW, low MCV, low MCHC

measure iron levels by plasma ferritin b/c it's in equilibrium with storage ferritin. transferrin is increased (increased TIBC)

oral supplements: give 325 mg Fe 3x/day (s/e - impractical)

S/E: constipation, nausea, black stool.

unable to tolerate: give parenterally. iron dextran (watch out for anaphylaxis)
S/E: pain at inj site, fever, H/A

Acute Iron toxicity:
-necrosis of gut!
Rx: bowel irrigation from both ends! also use activated charcoal and fe chelators

body has limited ability to excrete iron (intestinal cell sloughing?)
epoietin alfa
erythropoietin

USE: anemia

given SC or IV. given more often in dialysis pts. takes ~1 week to increase Hct

only give if epo is low... duh
to determine if bone marrow or kidney is problem, check the epo. if high, the marrow is the problem. must monitor Hb levels to prevent from getting too high. high Hb -> sludging -> clotting, htn, and seizures.

complications: seizures, clotting, hypertension

normal phys:
normally produced by peritubular system of kidney
acts on erythroid precursors in bone marrow
G-CSF
treat neutropenia

granulocyte CSF
stimulates neutrophil CFU
dose dep leukocytosis

use to treat CGD and others.
GM-CSF
granulocyte macrophage CSF
affects lots of CFU: macrophage, lymphocyte, RBC
dose dep leukocytosis
PROPYLTHIOURACIL
USE: hyperthyroidism
MOA (2):
1. blocks organification
2. blocks conversion of T4 to T3 (faster onset)
conjungation too?

notes: given 3x/day (vs methimazole 1/day)
METHIMAZOLE
USE: hyperthyroidism
MOA: blocks organification step

notes: give 1/day
slower onset of action b/c it blocks thyroids synthesis instead of conversion
IODIDE
low dose: hypothyroidism

high dose: hyperthyroidism

1. inhibits organification
2. inhibits endocytosis AND secretion
3. inhibits conversion of T4 to T3
great to use before surgery to shrink thyroid (also inhibits hyperplasia)
propanolol
use: thyroid storm
MOA:
1. blocks conversion of T4 to T3
2. blocks target organ effects of thyroxine (tachycardia, etc)

for thyroid storm, give corticosteroids, beta blockers, iodide and start slow onset antithyroid therapy such as methimazole
steroids
use: thyroid storm
blocks converstion of T4 to T3
thiocyanate
use: hyperthyroidism

moa: blocks iodide uptake
perchlorate
use: hyperthyroidism

moa: blocks iodide uptake (trapping)
ipodate
use: hyperthyroidism

those fucking ipods block t4 to t3

moa: blocks conv of T4 to T3
LEVOTHYROXINE
synthetic T4 for hypothyroidism
liothyronine
synthetic T3

preferred over T3 in myxedema coma b/c of its faster onset
CALCITONIN
dec bone ca reabs
inc kidney ca ecr
PTH
1. bone: inc. ca reabs
2. kidney: dec. ca excr. and inc. po4 excr.
3. inc 1,25-diOH-D3. inc ca and po4 abs in gut (ca-po4 cotransporter)
VITAMIN D
synthesis:
skin: calcitriol made
liver: -> 25-OH-D3
kidney: -> 1,25-diOH-D3
(kidney is last stop!)

vitamin D deficiency - give D3
in liver failure: give 25-OH D3
in kidney failure: give 1,25-di-OH D3
BISPHOSPHONATE
osteoporosis drug

moa: mimics pyrophosphate
incorporated into bone and stays there longer

S/E: take with lots of water b/c it can damage esophagus if it lodges there
CYCLOSPORINE
T cell blocker

uses: transplants, rheumatoid arthritis, psoriasis
MOA: suppresses lymphocyte proliferation
binds to cyclophilin, and cc complex inhibits calcineurin. NFAT cannot be dephosphorylated, and TCR signal does not trigger production of IL-2, IL-3, IL-4, and TNFalpha

S/E: narrow therapeutic index, hypertension and nephrotoxicity
drug interactions (CYP450)
must be monitored

forms: eyedrop, iv, oral
2 oral forms: sandimmune (soft gel) and neoral (microemulsion, better abs)
TACROLIMUS
T cell blocker

uses: transplants (liver and kidney)

moa: inhibits t cell proliferation. binds FK506, tacrolimus-FK506 complex inhibits calcineurin, NFAT cant be dephosphorylated, TCR signalling doesnt cause production of IL-2,3,4 and TNF alpha

s/e: nephrotoxicity, hypertension. neurotoxicity, diarrhea
drug interactions (CYP450)
must be monitored
SIROLIMUS
T cell blocker

moa: inhibits signalling pathway from IL-2 receptor to DNA synthesis
this means it inhibits prolif of t cells AND B CELLS* but not cytokine production (well?)

NOT CALCINEURIN INHIBITOR!

uses: acute rejection (with cylosporine and steroids)

s/e: leukopenia, thrombocytopenia, hypertriglyceridemia
less renal toxicity than cyclosporine and tacrolimus b/c of diff moa
PREDNISONE
corticosteroid

moa of immunosuppression:

1. blocks proliferation of activated T cells and B cells*
2. antiinflammatory - blocks production of inflammatory mediators
3. inhibits antibody production
4. increases neutrophils in blood (demargination-inhibits migration too)
5. decreaes lymphocytes in blood (movement out of vasculature)

use: organ transplantation and autoimmune disorders (combo therapy)

s/e: infections, growth deficiency, osteoporosis, diabetes, obesity, cushings

chronic use causes adrenal suppression. taper dose to prevent iatrogenic adrenal insufficiency. watch out during surgery.

IV form: METHYLPREDNISOLONE SODIUM SUCCINATE (give for liver failure pt)
AZATHIOPRINE
immunosuppressant
(cytotoxic drug)

moa: metabolized to 6MP (6-mercaptopurine) which antagonizes purine metabolism

prevents T cell proliferation (by preventing DNA synthesis)

notes: pharmacokinetic effect lasts minutes. pharmacodynamic effect lasts days

caution in renal and hepatic failure: hepatic dysfunction (will build up), renal problems (will build up) - decrease dose

drug interaction: allopurinol, which inhibits xanthine oxidase, which normally inactivates 6-MP. 6-MP stays active and has too much of an effect - pancytopenia

uses: PREVENTION of rejection in renal transplant
rheumatoid arthritis

s/e: bone marrow suppression and inc risk of neoplasia.
pancytopenia when given with allopurinol
CYCLOPHOSPHAMIDE
immunosuppressant
(cytotoxic)

moa: alkylating agent that interferes with DNA and RNA synthesis.

Uses: transplants

s/e: bone marrow suppression. GI, nausea, vomitting, cardiotoxicity, inc. risk of neoplasms, esp. bladder cancer
MYCOPHENOLATE MOFETIL
immunosuppressant
(cytotoxic drug)

prodrug of mycophenolic acid (MPA)
moa: inhibits inosine monophosphate dehydrogenase.
inhibits purine synthesis

decreases proliferation of T and B cells
decreasing B cell proliferation decreases antibody production

undergoes enterohepatic circulation, and inactive metabolites are converted back to MPA

use: transplants

s/e: (mild) GI and hematologic, inc. risk of infection
leflunomide
immunosuppressant
(cytotoxic drug)

moa: inhibits dihydroorotate DH, an enzyme in de novo PYRIMIDINE synthesis.

prevents T and B cell proliferation.

use: rheumatoid arthritis primarily (think LEFT knee)

s/e: mild. elevated liver function test, nausea, diarrhea, alopecia, and rash
MUROMONAB-CD3 (OKT3)
monoclonal antithymocyte antibody

purified monoclonal ab against CD3 antigen of T cells

use: reverse graft rejection by blocking function of t cells, which play a role in acute rejection
s/e: allergic reaction
LYMPHOCYTE IMMUNE GLOBULIN
ANTITHYMOCYTE GLOBULIN
immunosuppressant

moa: eliminates antigen reactive T cells in the blood or alters their function

purified, concentrated, POLYCLONAL sterile gamma globulin

administered IV only

use: transplantation (with azathioprine and corticosteroids in combo rx)

s/e: fever, chills, rash, itch (derm reactions)
DACLIZUMAB
immunosuppressant
humanized anti-CD25 antibody (anti - IL2 receptor) made from RECOMBINANT DNA

use: prophylaxis of acute rejection (with cyclosporine and corticosteroids)
moa: IL-2 mediates T cell activation. CD25 exp'd on activated T cells, and daclizumab inhibits IL-2 binding

s/e: GI effects, h/a, dizziness
similar: basiliximab
basiliximab
immunosuppressant

anti-CD25 antibody (an IL2 receptor) PRODUCED BY RECOMBINANT DNA

moa: IL-2 mediates T cell activation. CD25 exp'd on activated T cells, and daclizumab inhibits IL-2 binding

use: prophylaxis for rejection (with cyclosporine and corticosteroids)
similar: DACLIZUMAB

s/e: hypersensitivity
ETNACERPT
immunosuppressant
antibody that intercepts TNFalpha

prevent an eruption of rheumatoid arthritis by binding TNFalpha

monoclonal antibody from RECOMBINANT DNA against TNF-alpha, preventing it from binding TNF receptor.

normally, TNF causes induction of cytokines, leukocyte migration, neutrophil and eosinophil activation, induction of acute phase proteins in liver

use:
rheumatoid arhtritis (with methotrexate)

s/e: reactions at site of injection, upper resp infections, lupus-like syndrome
infliximab
similar to etnercept

monoclonal antibody from recombinant DNA

binds to TNF alpha

use: rheumatoid arthritis and crohn's disease
TRASTUZUMAB
breast cancer drug? wtf?
INTERFERON BETA-1b
immunostimulant:

use: reduce severity of multiple sclerosis attacks
INTERFERON GAMMA-1b
immunostimulant

use: prevent infections in chronic granulomatous disease
IL-2
immunostimulant:

moa: stimulate T helper and cytotoxic T cells

use: metastatic melanoma, renal cell carcinoma

s/e: highly toxic! severe hypertension, cardiotoxicity, pulmonary edema, renal toxicity
levamisole
levamisole (soul??)

synthetic immunostimulant - increases T cell mediated immunity. causes macrophages and T cells to secrete cytokines which suppress tumor growth.

use: hodgkin's disease, rheumatoid arthritis, colorectal cancer

moa: increase T cell mediated immunity