Everything needs a Medication Flashcards
low potency first generation neuroleptics
chlopromazine, thioridazine
high potency first generation neuroleptics
trifluoperazine, fluphenazine, haloperidol
antispychotic MOA
block D2 receptors
Side effects of first gen neuroleptics
acute dystonia first, akasthisa, parkinson, tardive
atypical antpsychotics MOA
partial D2 antagonists and have varying effects on other neurotransmitters. Tend to decreased positive and negative symptoms
olanzapine SE
obestity
clozapine SE
agranulocytosis- moniter WBC weekly
risperidone SE
hyperprolactinemia
lithium SE
tremor, nephrogenic DI, hypothyroid, Ebsteins anomaly
why does lithium cause DI
it impairs the principle cells in the collecting tubule causing no water to be reabsorbed. Otherwise, it is reabsorbed in the PCT with Na
buspirone- MOA, uses
partial agonist of serotonin receptors, slow onset of action but used for GAD. Does not cause addiction, tolerance, or sedation. Does not interact with alcohol
SSRI MOA and SE
can induce mania in patients with bipolar disorder, can have SIADH and sexual dysfunction, it is a serotonin repute inhibitor because it blocks the SERT. Can have some GI distress
SNRI MOA and SE
inhibit SERT and NEt transporters to increase SE and NE in the synapse. Increase BP and stimulant effects and sedation and nausea
fluoxetine use
bulimia
venlafaxine use
social anxiety, panic disorder, PTSD, OCD
serotonin syndrome
increase in serotonin with clonus hyperrflexia, hypertonia, tremor and seize, hyperthermia, diaphoresis, diarrhea, and agitation
treatment for serotonin syndrome
cyproheptadine- antihistamine with anti SE properties
TCA- MOA and SE
block reuptake of NE and SE. It can cause sedation from alpha 1 effects and postural hypotension and atropine like side effects (ALICE), can prolong QT interval. Can have confusion and hallucination in elderly
TCA overdose
convulsions, coma, cardiotoxic from Na blockade in the heart leading to arrhythmia. treat with sodium bicarb.
MOAI MOA and SE
nonselective MAO inhibition and increase levels of neurotransmitters like NE, DA and Se. can have hypertensive crisis after ingestion of tyramine. CNS stimulation.
how long do you have to wait before starting antidepressants after starting and MAOI
2 week washout period to prevent serotonin syndrome
bupropion MOA
increased DA nd NE. for smoking cession.
what patients are contraindicated for bupropion
anorexic and bulimic patients have seizures
mirtazapine MOA
alpha 2 agonist which increases NE and SE. H1 antagonist. Sedation and increased appetite and weight gain.
who do you use mirtazapine in
old anorexic people who have insomnia
trazadone
block SE, alpha 1, and H1 receptors. weakly inhibits SE uptake. Used for insomnia and high doses can have antidepressant effect.
trazadone side effect
priapism
varenicline
nicotinic receptor partial agonist- used for smoking cessation. can have sleep disturbance
fluoxetine, paroxetine, sertaline, citopram
SSRi
venlafaxine, desvenlafaxine, duloxetine, levomulnacipran, milnacipran
SNRI
amitrytiline, notripyline, imipramine, desipramine, clomipramine, doxepinm amoxapine
TCA
trancyclopromine, phenelzeine, isocarboxazid
MOAI- nonselective
selegine
selective for MAO B which is for parkinsons
cyclosporine MOA
calcinuerin inhibitor- prevents IL2 transcription
cyclosporine toxicity
nephrotoxic so can have increased risk and damage with p450 inhibitors
tacrolimus MOA
prevents IL2 transcription and calcineuin inhibitor
tacrolimus SE
increased risk of diabetes and neurotoxic and nephrotoxic
sirolimus MOA
prevents response of IL2- MTOR inhibitor
sirolimus SE
not nephrotoxic but can cause pancytopenia
daclizumab and basiliximab MOA
monoclonal block of IL2-
azathioprine MOA
precursor of 6MP stops lymphocyte proliferation by blocking nucleotide synthesis
azothioprine SE
degrades by xanthine oxidase which is blocked by allopurinol. It messes with purine synthesis
mycophenolate MOA
reversibly inhibits IMP dehydrogenase to prevent the purine synthesis in B and T cells
mycophenoplate SE
can cause invasive CNS lymphoma or infection
corticosteroids MOA
inhibit NFKB suppress B and T cell function by decreasing transcription of many cytokines. Induce apoptosis of T lymphocytes
corticosteroid SE
Cushing from long term use
aldesleukin
IL2- used for RCC and melanoma
epoetin alfa
increased risk of HTN and clots but used for anemia from CKD. Anemias especially in renal failure
filgrastim
recovery of bone marrow
sargramostim
recovery of bone marryo
IFN alpha use
chronic heaptitis B and C. Kaposi sarcoma and malignant melanoma
IFN beta use
multiple sclerosis
IFN gamma use
chronic granulomatous disease
romiplostin and eltrobopag
thrombocytopenia
oprelvekin
IL11- thrombocytopenia
alemtuzumab target, use
CD52- CLL
bevacizumab- target and use
VEGF- colon cancer and renal cell carcinoma
cetuximab- target and use
EGFR-colon cancer and HEENT
rituximab target and use
CD20 B cell marker-B cell Hodgekin lymphoma, CLL, RA, ITP,
trastuzumab target and use
Her2neu used for breast cancer
adalimumab- target and use
soluble TNF alpha- IBD, RA, AS, and psoriasis- can reactivate TB because TNF alpha is what keeps TB sequestered
etancerpt– use and target
decoy TNF alpha receptor-IBD, RA, AS, and psoriasis
eculizumab- use and target
completment proein C5- paroxysmal nocturnal hemoglobinuria
natalizumab use and target
alpha 4 integrin- MS and crohn- risk of PML
abciximab use and target
platelet glycoprotein IIB/IIIa- antiplatelet agent for prevention of ischemic complications in patients undergoing percutaneous intervention- IIb multipled by IIIa is equal to absiximab
denosumab use and target
RANKL- osteoporosis inhibits osteoclast maturation and mimics osteoprotergin- effects clasts not blasts
omalizumab use and target
IGE- allergic asthma prevents allergic response
palivizumab use and target
RSV F protein- RSV prophylaxis for high risk infants
ranibizumab and bevacuzimab
VEGF for neovascular age related macular degeneration
Dala dala sturctural analog that binds penicillin binding proteins and blocks transpeptidase cross linkingg of peptidoglycan in cell wall
PCN
what does PCN cover
gram posiitive and used for gram negative cocci and spirochetes, penicillinase senstive
adverse reactions to PCN
hypersensitivity reactions and direct coombs positive hemolytic anemia
what is the resistance mechanism to PCN
cleaves the beta lactam ring, and penicillinase in bacteria
what is the mechanism of action for amoxicillin, ampicillin, and aminopenicillin
daladlala analog and PBP blocker
amoxicillin, ampicillin, and aminopenicillin clinical use
Hib, h pylori, ecoli, listeria, proteus, salmonella, shigella
amoxicillin, ampicillin, and aminopenicillin- adverse effects
hypersensitivity reactions rash, and psuedomembranous colitis
amoxicillin, ampicillin, and aminopenicillin- mechanism of resistance
penicillinase in bacteria that cleave the beta lactam ring
MOA of dicloxacillin, naficillin, oxacilin
narrow spectrum but works the same as PCN- bulky R group which blocks access of beta lactase to beta lactic ring
dicloxacillin, naficillin, oxacilin- clinical use
staph aureus, MRSA and resistant because of altered penicillin binding protein target site
dicloxacillin, nficillin, oxacilin- adverse effects
hypersensitivity reactions, interstitial nephritis
piperacillin and ticarcilin MOA
extended spectrum PCN MOA
piperacillin and ticarcilin- clinical use
pseudomonas and gram negative rods
piperacillin and ticarcilin- adverse effects
hypersensitivity reaction
amoxicillin- is it oral or IV
oral bioavailability
what are the beta lactase inhibitors
clavulinic acid, sulbactam, tazobactam,
what is the MOA of cephalosporins
beta lactase drugs that inhibit cell wall synthesis but are less susceptible to penicilinases
first generation cephalosporins
cefazolin, cephalexin
what do first generation cephalosporins cover
proteus, kleb, cefazolin can prevent staph aureus
what are the second generation cephalosporins
cefaclor, cefotaxime, ceftazidime
what do the second generation ceph cover
enterobacter, hib, neusseria, seratia, ecoli, kleb,
what are the third generation ceph
ceftriaxone, cefotaxime, ceftazidime- resistant to other beta lactams
what do the third gen ceph cover
ceftriazone cover meningitis, gonorrhea, disseminated lyme, ceftazidime- psudomonas
what are fourth generation cep
cefepime
what do the fourth gen ceph cover
gram negative with increased pseudomonas activity and other gram positive organisms
what are the fifth gen ceph
ceftaroline
what do fifth gen ceph cover
broad gram positive and gram negative coverage MRSA and does not cover pseudomonas
what are the adverse effects of cephalosporins
hypersensitive reactions, autoimmune hemolytic anemia, disulfiram like reaction, vitamin K deficiency, exhibit cross reactivity with PCN, and increased nephrotoxicity
what is the mechanism of resistance for cephalosporins
structural changes to penicillin binding proteins
penems MOA
beta lactamase resistant carbapenenm alswyas given with dilation to decreased inactivation in the renal tubules
penems use
gram positive cocci, gram negative rods, anaerobes- wide spectrum limit use to life threatening infections or after other drugs have failed. Meropenum has decreased risk of seuzres
penems adverse reactions
GI distress, skin rash and seizures
which carbapenem is used for pseudomonas
ertapenem
aztreonam MOA
less susceptible to beta lactase, prevents peptidoglycancross linking by binding to penicillin binding protein 3. Synergistic with aminoglycosides
aztreonam clinical use
gram negative rods
aztreonam adverse effects
non-toxic sometimes GI upset
vancomycin MOA
inhibits cell wall peptidoglycan formation by binding data data portion of cell wall precursors.
vancomycin clinical use
gram postivie bugs, serious multi drug resistant like MRSA, diff, enterococcus, staph pi, can be used orally for cdiff
vancomycin adverse effects
nephrotoxic, ototoxic, thrombophlebitits, diffuse flushing can pretreat with antihistamines
vancomycin resistance
occurs if there is a modification of dala dala to dala dlac
what are the 30s inhibitors
aminoglycosides and tetracyclines
what are the 50s inhibitos
chloramphenicol, clindamycin, erythromycin, linezolid
what are the aminoglycosides
gentamycin, neomycin, amikacin, tobramycin, streptomycin
what are the amino glycoside MOA
irreversible inhibition of initiation complex through binding of 30S submit. Causes misreading of mRNA and blocks translocation. Requires O2 for uptake and ineffectie against anaerobes
what is the use of aminoglycosides
severe gam negative rods, beta lactam antibiotics
what is neomycin used for
bowel surgery
what are the adverse effects of aminoglycosides
nephrotoxic, neuromuscular blcok, ototoxicity, teratogen
what is the mechanism of resistance to aminoglycosides
bacterial transferase enzumes inactivate the drug by acetylation, phopshorylation, or adenylation
what is the MOA of tetracyclines
bind to 30S and prevent attachment of aminoacyltTNA. limited CNS penetration. Doxycylcine is eliminated fecally and can be used with renal failure
what can you not eat with tetracyclines
milk and magnesium and iron containing prep
what is the clinical use of tetracyclines
borrelia burgdorferi, mycoplasma pneumoniae, ability ot acculate intracelluluar for rickettsia, chlamydia, and acne
what are the adverse effects of tetracylcines
GI distress, discolored teeth and inhibition of bone growth in children, photosensitivity,
tetracycline resistance
decreased uptake, or increased efflux out of the bacterial ells by plasmid encoded transport pumps
choloramphenicol MOA
blcoks peptidyltransferase at 50S ribosomal subunit
choloramphenicol clinical use
memingitis, rocky mountain spotted fever,
choloramphenicol adverse effects
anemia, aplastic anemia, grey baby syndome
choloramphenicol resistance
plasmid encoded acetyltrasnferase inactivates the drug
clindamycin MOA
blocks peptide transfer at 50S ribosomal subunit
clindamycin clinical use
anaerobic infections in aspiration pneumo, lung abscesses, and oral infections and invasive group A strep
clindamycin adverse effects
pseudomembranous colitis fever, diarrhea
linezolid MOA
inhibit protein synthesis by binding to 50S subunit and preventing formation of initiation complex
linezolid clinical use
gram positive MRSA and VRE
linezolid adverse effects
bone marrow suppression and peripheral neuropathy, and serotonin syndrome
linezolid mechanism of resistance
point mutation of ribosomal RNA
what are the macrolides
azithromycin, clarithromycin, erythromycin
macrolide MOA
inhibit portein sun by binding the 23S until of 50S
macrolide clinical use
atypical penumonia, STI, gram positive cocci, pertusis
macrolide adverse effects
GI motility, arryhtmia, prolonged QT, actue cholestatic hepatitis, rash, eosinophilia, increased serum concentration of thyophilline, oral anticoagulants
do any macrocodes do anything to P450
clarithromycin and erythromycin inhibit P450
macrolide mechanism of resistance
methylation of 23S rRNA binding site prevents binding of the drug
what are the sulfonamides
sulfamethoxazole, and sulfadiazine
what is the MOA of sulfonamides
inhibit dihydropteroate synths thus inhibiting folate synthesis, bacteriostatic combined with TMP
sulfonamides clinical use
gram positive and gram negative- nocardia, chlamydia, SMX for simple UTI
sulfonamides adverse effects
HSN reaction, G6PD deficienct, nephrotoxic, photosensitive, kernictursi, displace other drugs from albumin
sulfonamides resistance
altered enzyme, decreased uptake or altered PABA
dapsone MOA
similar to sulfonamides with inhibiting dihydropeteroate synthase and inhibit folate synthesis
dapsone clinical use
leprosy, PJP
dapsone adverse effects
hemolysis with G6PD
TMP MOA
inhibits bacterial dihydropfolate reductase
TMP clinical use
combination with sulfonamides SMX for sequential block of folate synthesis. Como use for uTI< shigella, salmonella, PJP, and toxoplasmosis prophylaxis
TMP adverse effects
megaloblastic anemia, leukopenia, granulocytopenia
nitrofuritan MOA
stop bacterial ribosomes, UTI, sad in pre, does not over proteus
polymyxin MOA
cationic detergent tend to be topical and use for resistat gram negative it is neurotoxic and nephrotoxic
what are the FQ/ what do they end it
floxacin
FQ MOA
inhibit prokaryotic enzymes topoisomerase II and IV.
what is the clinical use of FQ
gram negative rods of urinary tract infections and GI tract so pseudomonas, neisseria,
adverse effect of Fq
GI upset, superinfectiosn ,skin rash, cramps and mylgias. long QT fronte to tendon rupture and increased risk if they are taking prednisone
resistance to FQ
chomosome encoded mutation in DNA gyrase or plasmid or efflux pump
daptomycin MOA
lipopetide that disrupts cell membrane of gram positive cocci
daptomycin clinical use
staph skin infections MRSA, VRE, bacteria, endocarditis,
adverse effects of daptomycin
myopathy, rhabdomyolysis
what is daptomycin contraindicated in
it binds surfactant so its not used in pneumonia
metronidazole MOA
forms toxic free radical metabolies in the bacterial cell that damages the DNA
Metronidazole clinical use
giardia, entamoeba, trichomonas, gardernerall, anaerobes used with PPI and clarithromycin for h pylori triple therapy
treatment of anaerobes above the diaphragm
clinda
treatment of anaerobes below the diaphragm
metronidazole
adverse effect of metronidazole
disulfrram raction (flushing tachy and hypotension) with alcohol, headache, metallic taste
rifampin MOA, adverse effects and resistance
inhibits DNA dependent RNA polymerase,there can be hepatotoxicity, induce P450 system and orange body fluid, and resistant bed on if there is altered binding to RNA polymerase
isoniazid-MOA, adverse effects and resistance
it decreases the synthesis of mycelia acids, bacterial catalase peroxidase needed to convert INH to active metabolite, there is decreased mycelia acid. It can be used as solo prophylaxis against TB. Can also be used in mono therapy against latent TB. It is hepatotoxic and inhibits P450, and drug induced SLE, have to give B6 to the patients- resistance is the mutation in KatG which codes for the mycelia acid
pyrazinamide-MOA, adverse effects and resistance
mechanism is uncertain, it is a prodrug, works best at acidic pH, hyperuriciemia, hepatotoxic
ethambutol-MOA, adverse effects and resistance
decreased carbohydrate polymerization of mycobacterium cell wall by blocking arabinosyltransferase. It causes optic neuropathy and red green color blind
streptomycin-MOA, adverse effects and resistance
interferes with the 30S subunit and its is second line for TB. it causes tinnitus, vertigo, ataxia, nephrotoxicity
prophylaxis for endocarditis and undergoing dental procedure
amoxicillin
prophylaxis for exposure to gonorhea
ceftriaxone
prophylaxis for recurrent UTI
tmp SMX
prophylaxis for exposure to meningitis
cegtriazone, ciprofloxacin, rifampin
prophylaxis for pregnant woman carrying group B strep
intrapartum PCN G
prophylaxis for prevention of gondola conjunctivitis of the newborn
erythromycin
prophylaxis for prevention of post surgical infection by staph aureis
cefazolin
prophylaxis for strep pharnygitis prior rheumatic fever
PCN
prophylaxis for exposure to syphilis
PCN
treatment of MRSA
vanc, daptomycin, linezolid, tigecycline, ceftaroline
VRE treatment
linezolid and streptogrammin (pristin)
amphotericin B-MOA, adverse effects and resistance
binds ergosterol, pores then are formed, fever chills, hypotension, nephrotoxic, anemia, phlebitis, decreased nephrotoxic, it is all from the similarity to the cholesterol
nystatin-MOA, adverse effects and resistance
it is only used topically, it binds ergosterol and pores are formed in the cell, swish in swallow for oral thrush or topical
flucytosine-MOA, adverse effects and resistance
inhibits DNA and RNA biosythesis by coversion to 5FY by cytosine deaminase- bone marrow suppression
azoles-MOA, adverse effects and resistance
inhibits fung sterol synthesis by inhibiting the P450 enzyme that converts lanosterol to ergosterol- local and less serious myoses- it inhibits testosterone so gives gynecomastia, liver dysfunction from inhibition of cytochrome P450
terbinafine-MOA, adverse effects and resistance
inhibits the final enzyme squalene epoxidase- dermatophytes- GI upset, headaches, hepatotoxic, taste disturbance
echinocandins-MOA, adverse effects and resistance-ALL END IN FUNGIN
inhibit cell wall synthesis by inhibiting synthesis of beta glucan- used for invasive aspergillosis or candida-GI upset, flushing, and histamine
griseofulvin-MOA, adverse effects and resistance
interfere with microtubule function and disrupts mitosis, and deposits in keratin containing tissues- oral treatment for superficial dermatophyte infections. It is teratogenic, carcinogenic, confusion, headaches,increased cytochrome P450, and warfarin metabolism
what do you use to treat mites or louse
permethrin blocks the Na channels leading to neurotoxic, and malthion (ACH) and lindane (GABA)
chloroquine-MOA, adverse effects and resistance
blocks detoxification of heme to hemozoin. Heme accumulates and is toxic to plasmodia- it treats plasmodium falciparum, resistance is due to membrane pump, if its life threatening its better to use quinine- retinopathy, pruritis
antihelminthic therapy
mebendazole, pyrantel pamoate, ivermectin, diethycarbamazine, praziquantal
oseltamivir, zanamivir-MOA, adverse effects and resistance and what it treats
inhibit the release of virus from infected cells and spreads within the respiratory tract, Also slows mucosal penetration by the virus in the respiratory tract- inhibit neuraminidase and it is for flu- it is only good in the first 48 hours, and it is resistance against it so only use it in high risk patients
acyclovir, famciclovir, valacyclovir-MOA, adverse effects and resistance and what it treats
guanosine analogs, monophosphorylated by HSV/VZV thymidine kinase, and not phosphorylated in uninfected cells, few adverse effects. Triphosphate formed by cellular enzymes. Preferentially inhibit viral DNA polymerase by chain termination. Incorporated into cellular DNA. HSV and VZV and weak activity against EBV. No activity against CMV. Used for HSV induced mucocutanou and genital lesions as well as encephalitis. Prophylaxis in immunocompromised patients. No effect on latent forms of HSV and VZV. Valacyclovir has more oral availability because of its prodrug. Famciclovir is used for HSV encephalitis and herpes zoster. It can cause obstructive crystal neuropathy, and acute renal failure if not well hydrated- resistance is with mutated thymidine kinase
ganciclovir-MOA, adverse effects and resistance and what it treats
5’ monophosphate formed by CMV viral kinase guanosine analog- triphosphate cellular kinases- inhibits viral DNA polymerase- CMV especially in immunocompromised.- bone marrow suppression with leukopenia and neutropenia and thrombocytopenia- renal toxicity is also seen- combined with TMP SMX gets even more bone marrow suppression
valganciclovir how is it different from ganciclovir
it is a prodrug form so it has increased bioavailability
foscarnet-MOA, adverse effects and resistance and what it treats
viral DNA/RNA polymerase inhibitor and HIV reverse transcriptase inhibitor and binds pyrophosphate binding site of the enzyme- CMV retinitis in immunocompromiezed when ganciclovir fails. It is nephotroxic and can cause electrolyte abnormalities with increased seizures. It is resistant if the viral DNA polymerase is mutated
cidofovir-MOA, adverse effects and resistance and what it treats
it preferentially inhibits viral DNA polymerase. does not require phosphorylation. CMV retinitis and it is only in immunocompromised patients that are acyclovir resistant HSV- has long half life and and is nephrotoxic and you administer fluids with it
NRTIs-MOA, adverse effects and resistance and what it treats
competitively inhibit nucleotide binding to reverse transcriptase and terminate the DNA chain. It can cause bone marrow suppression and peripheral neuropathy, and lactic acidosis, anemia, and pancreatitis,
which HIV drug is contraindicated if the patient has HLA B5701 mutation
abacavir- hypersensitivity reaction
which drug is used for general prophylaxis for HIV and pregnancy to decrease transmission
zidovudine
NNRTI-MOA, adverse effects and resistance and what it treats
bind to reverse transcriptase at site different than NRTI, and it does not require phosphorylation to be avtive or compete with nucleotide- rash, hepatotoxic,
efaverintz
vivid dreams and CNS symptoms
what NNRTIs are not able to be used during pregnancy
efavirenze and delaviridine
what is the common lingo for NNRTI
vir somewhere in the name
protease inhibitors–MOA, adverse effects and resistance and what it treats
assembly of visions of HIV protease (pol) genre which cleaves the polypeptide produces of HIV mRNA into their functional parts, so protease inhibitors prevent maturation of new viruses- can cause GI tolerance, hyperglycemia, lipodystrophy, cushing like, nephropathy, hematuria,
what medication is contraindicated in with protease inhibitors
rifampin because it can decrease the amount in the blood
what is the ending of all protease inhibitors
navir ending
can boost other drug concentrations by inhibiting cytochrome p450- which of the protease inhibitors is this
ritonavir
integrase inhibitors-MOA, adverse effects and resistance and what it treats
inhibits the HIV viral genome integration into host cell chromosome by reversibly inhibiting HIV integrase- increase creatine kinase
what do integrase inhibitors end in
tegravir
enfuvirtide- MOA, and toxicity
binds gp41 and inhibits entry into the HIV and there is skin reaction at injection site
maraviroc- MOA
bins CCR5 on the surface of T cells and monocytes to inhibit the interaction with p120 and it is only used if CCR5
interferon- MOA
glycoproteins normally synthesized by virus infected cells, exhibiting a wide range of antiviral and antitumoral properties. had proline synthesis
what is interferon alpha used for
chornic HCV and HBV, kaposi sarcoma, hairy cell leukemia, condyloma acuminatum, RCC, and malignant melanoma
what is interferon beta used for
multiple sclerosis
what is interferon gamma used for
chronic granulomatous disease
ribavirin- MOA and use and adverse effects
inhibit synthesis of guanine nucelotides by competitively inhibiting inosine monophosphate dehydrogenase- Chronic HCV, RSV and adverse effect of hemolytic anemia and severe teratogen
sofosbuvir- MOA and use and adverse effects
inhibits HCV RNA dependent RNA polymerase and acts as a chain terminator- chronic HCV in comnination with ribavirn and peg interferon alpha- feature and headache and nausea but not used alone
simeprevir- MOA and use and adverse effects
HCV protease inhibitor prevents viral replication- chronic HCV in combination with ledipasvir. do not use as mono therapy, photosensitive, rash,
chlorohexidine infection control what does it do
denature proteins and disrupts cell membranes non sporadical.
iodine and iodophors infection control what does it do
halogenation of DNA, RNA, and proteins may be sporadical
antimicrobials to avoid in pregnancy and what does it cause- sulfonamides
kernicterus
antimicrobials to avoid in pregnancy and what does it cause- aminoglycosides
ototoxic
antimicrobials to avoid in pregnancy and what does it cause- FQ
cartilage damage
antimicrobials to avoid in pregnancy and what does it cause-clarithromycin
embryotoxic
antimicrobials to avoid in pregnancy and what does it cause- tetracyclines
discolored teeth and inhibition of bone growth
antimicrobials to avoid in pregnancy and what does it cause- ribavirin
teratogenic
antimicrobials to avoid in pregnancy and what does it cause- griseofulvin
teratogenic
antimicrobials to avoid in pregnancy and what does it cause- chloramphenicol
gray baby syndrome
tyramine
normally degraded by MAO. Increased levels of tyramine in patients taking MAO inhibitors, and if they ingest tyramine, they will have excess tyramine enter the presynaptic vesicles and displaces other NT so it increases active presynaptic NT and increased infusion of NT into the synaptic cleft. Increased sympathetic stimulation It can result in a hypertensive crisis
bethanechol
activates the bowel and bladder smooth muscle- used for postoperative ileum and urinary retention. Can have HR and increased secretion
carbachol
it is like acetylcholine- constricts pupil and relieves intraocular pressure in open-angle glaucoma
methacholine
It stimulates muscarine receptors in airway when inhaled. Challenge for diagnosis of astham
pilocarpine
contracts ciliary muscle of the eye for open angle glaucoma, it constricts the pupillary sphincter for close agle- potent stimulater of sweat, tears, and saliva
what are the acetlycholinesterase used for AD
donepezil, galantamine, rivastigmine they all increase the amount of acetylcholine
edrophonium
used for MG but is short acting so can be used to test to see for dosage. it is an acetylcholinesterase
neostigmine
increase acetylcholine has no CNS penetration. It is good for post operative ileum, neurogenic ileum, and urinary retention , MG, and reversal of NMJ blockade
physostigmine
increase Ach, it is good for atropine overdose. it does cross the BBB
pyridostigmine
- increase ACh, and it is used for treat myasthenia gravis and it does not penetrate the PNS
which Ache do cross the BBB
physostigmine
what patients do you need to watch out for with cholinomimetic agents
COPD exacerbation, asthma, and peptic ulcers
farmer that has diarrhea, urination, mitosis, bronchospasm, bradycardia, excitation of skeletal muscle, and CNS, and lacrimation, sweating, and salivation- wha t was the farmer poisoned with and what treats it
Organophosphate poisoning and treat with atropine for competitive inhibition and pralidoxime is for regeneration of AchE
atropine, homatropine, tropicamide
eye- produce mydriasis and cycloplegia-muscarinic antagonist
benztropine
parkinsons and acute dystonia-muscarinic antagonist
glycopyrrolate
GI and respiratory- parenteral for preoperative use to reduce airway secretion. Oral drooling an peptic ulcer-muscarinic antagonist
hyoscyamine, and dicyclomine
GI- antispasmodics for IBS- muscarinic antagonist
ipratropium, tiotripium
COPD and asthma, blocks PNS stimulation by the vagus to stop muscarinic stimulation
oxybutynin, solifenacin, darfenicin
reduce bladder spams and urger urinary incontinence-muscarinic antagonist
scopolamine
CNS, motion sickness- some effect can be blurry vision, dry mouth, urinary retention, and constipation
atropine
muscarinic antagonist used to treat bradycardia, ophthalmic applications, and organophosphate poisoning. In the eye it causes dilation, decreases secretions, acid secretion decreases, decreased gut motility, decreased urgency
what are the side effects of muscarinic antagonists
hot as a hare, dry as a bone, red as a beat, blind as a bat, mad as a hatter
how can you naturally get atropine poisoning
jimson weed- mydriasis due to plant alkaloids
elderly with acute delirium what drugs might be causing it
atropine, diphenhydramine, doxcline, chlorophenamine, neuroepileptics, TCA, amantidine
albuterol and salmetrerol- activation of G receptors, an applications
B2>B1- acute asthma or COPD
dobutamine
B1>B2 and a- it is a positive ionotrope, and increase CO, decreased LV pressure. positive chronotrope to increased HR and increased myocardial consumption can worsen myocardial ischemia- Use in heart failure and has a move inotropic than chronotropic effect. Severe HF or LV issue or cardio shock
dopamine
D1=D2>B>a- unstable bradycardia. HF, shock, inotropic and chronotropic effects at lower doses due to beta effects, vasoconstriction at high doses due to alpha effects
epinephrine
B>a- anaphylaxis, asthma, open angle glaucome- alpha effects predominate at high doses significantly stronger effect at beta2 receptor than NE
fenoldopam
d1- postoperative hypertension, HTN crisis, vasodilator of the coronary, peripheral, renal and splanchnic, promotes nature’s, can cause hypotension and tachycardia
isoproterenol
B1=B2- increased cardiac contractility and decreased vascular resistance and decrease MAP- can worsen ischemia
midodrine
a1- autonomic insufficiency and postural hypotension- may exacerbate HTN laying down
NE
a1>a2>B1- hypotension, septic shock
phenylephrine
a1>a2- Gq to IP3 and increase Ca and protein kinase C- hypotension vasoconstrictor, ocular procedures (dilation or mydriasis)- rhinitis as a decongestant
amphetamine
indirect general agonist, reuptake inhibitor, releases stored catecholamines- narcolepsy, obesity, ADHD
cocaine
indirect general agonist, reputake inhibitor- causes vasoconstriction and local anesthesia- never give beta blockers if cocaine intoxication in suspected because can lead to unopposed alpha 1 activation and extreme hypotension
ephedrine
indirect general agonist, releases stored catecholamines- nasal decongestion, urinary incontinence, hypotension
NE vs isoproterenol
NE increases systolic and diastolic BP as a result of alpha 1 mediated vasoconstriction. increased mean arterial presses and reflex bradycardia,Isoproterenol is no longer used has little alpha effect but causes beta2 mediated vasodilation, resulting in decreased MAP and increased HR through B1 and relax activity
clonidine and guanfacine- applications and adverse effects
hypertensive urgency used in ADHD, Tourettes- It can cause CNS depression, bradycardia, hypotension, respiratory depression, miosis
alpha methyldopa- applications and adverse effects
hypertension in pregnancy- it can cause direct Coombs and positive hemolysis and SLE like syndrome
phenoxybenzamine- applications and adverse effects
pheochromocytoma to prevent catecholamine crisis- non selective alpha blocker, stop HTN from pheochromocytoma- can cause orthostatic hypotension and reflex tachycardia- alpha blocker irreversible
phentolamine- applications and adverse effects
give to patients on Mao inhibitors who eat tyramine containing food- can cause orthostatic hypotension and reflex tachycardia- it is a reversible alpha blocker
alpha1 selective blockers end in what
osin
prazosin, terazosin, doxasocin, tamsulosin- applications and adverse effects
treats urinary symptoms of BPH, PTSD< and hypertension besides tamsulosin. It can cause first dose orthostatic hypotension, dizziness and headache from the decreased brain perfusion.
why is tamsulosin different than other selective alpha 1 blockers
it is specific for prostate ones
the osins cause orthostatic hypotension from
the decreased venous return, decreased CO, decreased BP causing the increase in sympathetic tone
what are the beta 1 selective blockers and what is it used for
acebutolol, atenolol, betazolol, esmolol, metoprolol- it is used for CHF, HTN
how does naming indicate which are beta 1 selective
A to M is the start of the names
which are non selective and whats the receptors and whats the naming
B1 and B2- nadolol, pindolol, propranolol, timolol- N to z
which are nonselective a and B antagonist and what are the naming
carvediol, labetalol- slightly different suffixes instead of olol
nebivolol
combines cardiac selective B1 blockade with stimulation of B3 receptors which activate NO synthase in the vasculature-
why are beta blockers used in angina
decrease HR and contractility, results in decreased O2 consumption
why are beta blockers used in MI
decreased mortality from arrythmia
why are beta blockers used in SVT and which are used
metoprolol, esmolol- decreased AV conduction velocity- class II antiarrythmics
why are beta blockers used in HTN
decreased cardiac output, decreased renting section due to Beta1 blockade on JGA cells
why are beta blockers used in HF and which drugs
decreased mortality and bisoprolol, varvediol, metoprolol
why are beta blockers used in glaucoma and what drug
decreased secretion of aqueous humor- timolol
why are beta blockers used in vatical bleeding and what drugs
decreased hepatic venous pressure gradient and portal hypertension
what are the adverse effects of beta blockers
erectile dysfnction, cardiovascular adverse effects like bradycardia, AV block, HF, and seizures, sedation, sleep alterations, dyslipidemia, and asthma and COPD exacerbations
what can beta blocker not be used concurrently with
cocaine because of unopposed beta blockade
what drugs to give with HF
beta blocker, ACE inhibitor, and angio II block,and aldosterone antagonist like spirolactone
tetrodoxin- source of toxin, action, symptoms, and treatment
pufferfish, highly potent toxin binds fast voltage gated Na channels in cardiac/nerve tissue, preventing depolarization- nausea, diarrhea, paresthesias, weakness, dizziness, loss of reflexes- primarily supportive
ciguatoxin- source of toxin, action, symptoms, and treatment
from reef fish like snapper, barracuda, snapper, and moray eel- opens NA channels causing depolarization- symptoms mimic cholinergic posioning- primarily supportive
histamine Scombroid posioning– source of toxin, action, symptoms, and treatment
spoiled dark meat fish such as tuna, mahi, mackerel, and bonito- bacterial histidine decarboxylase converts histidine to histamine frequently misdiagnosed as fish allergy- mimics anaphylaxis, bring sensation of mouth, facail flushing, erythema, itching, urticaria, may go to angioedema, hypotension, and bronchospasm, treatment is antihistamines, albuterol, and epinephrine if needed
what is the treatment for acetaminophen toxicity
NAC that replenishes the glutathione
what is the treatment for ache inhibitors and organophosphates tox
atropine>pralidozime
what is the treatment for amphetamines tox
ammonium chloride to acidify urine
what is the treatment for antimuscarinic toxicty and anticholergic agents
physostigmine, control hyperthermia
what is the treatment for arsenic tox
dimercaprol succimer
what is the treatment for benzodiazepines tox
flumazenil
what is the treatment for beta blocker tox
saline ,atropine glucagon
what is the treatment for CO tox
hyperbaric O2
what is the treatment for copper tox
pencillamine trientine
what is the treatment for cyanide tox
nitrite+thiosulfate, hydroxycolbalamin
what is the treatment for digitalis tox
anti dig fab fragments
what is the treatment for gold tox
penicllamine, dimercaprol, succimer
what is the treatment for heparin tox
protamine sulfate
what is the treatment for iron tox
deferozamine, deferasirox, deferiprone
what is the treatment for lead tox
EDTA, dimercaprol, succimer, penicillamine
what is the treatment for mercury tox
dimercaprol, succimer
what is the treatment for methanol and ethylene glycol tox
fomepizole or ethanol
what is the treatment for methemoglobin
methylene blue and vitamin C
what is the treatment for opioids
naloxone
what is the treatment for salicylate tox
alkalinize urine- bicarb
what is the treatment for TCA tox
bicarb
what is the treatment for warfarin
vitamin K and FFP
drug reactions causing: coronary vasospasm
cocaine, sumatriptan, ergot alkaloids
drug reactions causing: cutaneous flushing
vancomycin, adenosine, niacin, Ca channel blocker, echinocandins
drug reactions causing: dilated cardiomyopathy
anthracyclines (doxyrubacin and donarubicin) prevent with dexrazocane
drug reactions causing: torsades des pointes
antiarrythmics (class I1 and II), macrolides, antipsychotics, haloperidol, antiemetics like ondansetron
adenoctorical insufficiency drug reactions
withdrawal of long term steroids
drug reactions: hot flashes
tamoxifen and clomiphene
drug reactions: hyperglycemia
tacrolimus, protease inhibitors, niacin, HCTZ, corticosteroids
drug reactions: hypothyroid
lithium, amioderone, sulfonamides
drug reactions: acute cholestatic hepatitis, jaundice
erythromycin
drug reactions: diarrhea
acmprosate, acarbose, cholinesterase inhibitors, colchicine, erythromycin, ezetimibe, metformin, misoprostol, orlistat, pramlinitide, quinidine, SSRI
drug reactions: focal massive hepatic necrosis
halothane, amnita phalloidea, valproic acid, acerominophin- tender liver, increased LFT fever anorexia, rash, arthralgia,
drug reactions: hepatitis
rifampin, isoniazid, pyrazinamide, sttins, fibrates
drug reactions: pancreatitis
didanosine, corticosteoriids, alcohol, vampiric acid, drugs, azothiprine, diuretics, furosemide and HCTZ
drug reactions: pill induced esophagitits
tetracyclines, bisphophonates, potassium cholride
drug reactions: pseudomembranous colitis
clindamycin, ampicillin, cephalosporins
drug reactions: agranulocytosis
clozapine, carbamazepine, proylthiouracil, methimazole, colchicine, ganciclovir
drug reactions: aplastic anemia
carbamazepine, methimazole, NSAIDs, benzen, chloramphenicol, propylthiouracil-
drug reactions: direct Coombs- positive hemolytic anemia
methyldopa, PCN
drug reactions: Grey baby
chloramphenicol
drug reactions: hemolysis of G6Pd
isoniazid, sulfonamides, dapsone, primaquine, aspirin, ibuprofen, nitrofurantoin
drug reactions: megaloblastic anemia
phenytoin, methotrexate, sulfa drugs
drug reactions: thrombocytopenia
heparin
drug reactions: thrombotic complications
OCPs, hormone replacement therapy
drug reactions: fat redistribution
protease inhibitors, glucocorticoids
drug reactions: gingival hyperplasia
phenytoin, Ca channel blockers, cyclosporine
drug reactions: hyperuricemia (gout)
pyrazinamide, thiazides, furosemide, niacin, cyclosporine
drug reactions: myopathy
fibrates, niacin, colchicine, hydroxychloroquine, interferon alpha, penicillamine,statines, glucocoriticoids
drug reactions: osteoporosis
corticosteroids, heparin
drug reactions: photosensitivity
sulfomanides, amiodarone, tetracyclines, 5-FU
drug reactions: Stevens-Johnson Syndrome
anti-epileptic drugs like lamotrigine, allopurinol, sulfa drugs, penicillin
drug reactions: SLE-like syndrome
sulfa drugs, hydralazine, isoniazid, procainamide, phenytoin, etanercept
drug reactions: teeth discoloration
tetracyclines
drug reactions: tendentious and tendon rupture, and cartilage damage
FQ
drug reactions: cinchonism
quinidine, quinine
drug reactions: Parkinson-like syndrome
antipsychotics, reserpine, metoclopramide
drug reactions: seizures
isoniazid (B6 deficiency), bupropion, imipenem/cisplatin, tramadol, enflurane
drug reactions: tradeoff dyskinesia
antipsychotics, metoclopramide
drug reactions: diabetes insipidus
lithium, demeclocyline
drug reactions: Fanconi syndrome- secreted everything from the PCT
tenofovir, ifosfamide
drug reactions: hemorrhagic cystitis
cyclophosphamide, ifosfamide- treat with mensa before treating
drug reactions: interstitial nephritis
methcilin, NSAIDs, furosemide
drug reactions: SIADH
carbamazepine, cyclophosphamide, SSRI
drug reactions: dry cough
ACE inhibitors
drug reactions: pulmonary fibrosis
methotrexate, nitrofurantoin, carmustine, bleomycin, busulfan, amioderone
drug reactions: antimuscarinic
atropine, TCA,H1 blocker, atipsychotics
drug reactions: disulfiram reactions
metronidazole, certain cephalosporins, griseofulvin, procarbazine, first generation sulfonylureas
drug reactions: nephrotoxicity
aminoglycosides, vancomycin, loop diuretics, cisplatin, Cisplatin toxicity will respond to amifostine
Cytochrome P450 inducer
chronic alcohol use, st johns wart, phenyltoin, phenobarbitl, nevirapine, rifampin, griseofulvin, carbamazepine- Guiness Coronas, and PBRS induce Chronic Alcholism
Cytochrome P450 inhibitors
Ciprofloxacine, ritonavir, amnioderone, cimetidine, ketoconazole, acute alcohol, macrolides, isoniazid, grapefruit, ompeprazole, sulfonamides- CRACK AMIGOS
sulfa drugs
sulfonamide, sulfasalazine, probenacid, furosemide, acetazolamide, celecoxib, thiazides, sulfonylureas
what do patients with sulfa allergies present with
fever, UTI, SHS, hemoyltic anemia, thrombocytopenia, agranulocytosis, urticaria- range from mild to life threatening
azol
ergosterol syntehsis inhibitor
bendazole
antiparasitic/antihelminthic
cillin
peptidoglycan synthesis inhibitor
cycline
protein synthesis inhibitor
ivir
neuraminidase inhibitors
navir
protease inhibitor
ovir
DNA polymerase inhibitor
thromycin
macrolide antibiotic
ane
inhaled general anesthetic
azine
typical antipsychotic
barbital
barbituate
caine
local anesthetic
etine
SSRI
ipramide, triptyline
TCA
triptan
5HT agonists
zepam, zolam
benzodiazepine
chol
cholinergic agonist
curium, curonium
nondepolarizing paralytic
olol
beta blocker
stigmine
AChE inhibitor
terol
beta 2 agonist
zosin
alpha 1 antagonist
afil
PDE5 inhibitor
dipine
dihydropyridine Ca channel blocker
pril
ACE inhibitor
sartan
ARB
statin
HMG COA reductase inhibitor
xaban
direct factor Xa inhibitor
dronate
bisphosphonate
glitazone
PPAR gamma activator- down regulates receptor transcription
prazole
proton pump inhibitor
prost
prostaglandin analog
tidine
H2 antagonist
tropin
pituitary hormone
ximab
chimeric monoclonal antibody
zumab
humanized monoclonal antibody
SA node location
near the SVC and RA wall
AV node location
near the coronary sinus and tricuspid valve
what supplies the nodes in a right dominant heart
right circumflex artery
what supplies the nodes in a left dominant heart
the left circumflex artery
enlargment of what part of the heart can cause dysphagia and hoarsness
the left atrium can enlarge causing compression of the recurrent laryngeal nerve or the esophagus
what is Fick’s principle
rate of O2 consumed/ arterial O- pulmonary O
what happens to diastole when HR increases
it shortens which means less O2 to the heart
how do you calculate resistance
R=8viscosityL/pi r4
how do you calculate resistance in parallel
1/rt=1/r1+1/r2….
how do you calculate resistance in series
rt=r1+r2+r3
what vessels have the largest cross sectional area
capillaries
what is the force of contraction directly proportional to
EDV
what decrease the contractility
MI damage, beta blockers, CCB (non dihydro), dilated cardiomyopathy
what accounts for the total peripheral resistance
arterioles
what accounts for the blood storage capacity
venous system
normal heart split
it is pul being delayed because of inspiration increasing the venous return
wide split
RBBB or pulmonary stenosis causes a longer split with inspiration
fixed split
L to R shunt increases the blood volume on the R side all the time so its always split
paradoxical split
aortic valve is delayed during normal expiration which leads to increased split during expiration but closer split on inspiration. It is from LBBB or aortic stenosis
Phase 0 of myocardial AP and pacemaker AP
Na channels open in myocardium and Ca channels open in AP of SA node
Phase 1 in myocardium and pacemaker AP
inactivation of NA channels and K begin to open- only in myocardium
Phase 2 in myocardium and pacemaker AP
plateau phase with CA and it balances the K efflux and opens Ca is released from the SR- myocardium only
Phase 3 in myocardium and pacemaker AP
rapid repole with massive K efflux due to opening of voltage gated K channels and Ca channels closing in myocardium. In SA node its basically the same with K coming in and Ca being closed
Phase 4 in myocardium and pacemaker AP
high K permeability leading to resting potential in myocardium. In SA there is slow spontaneous Na flow through funny channels leading to the depole and the rising +values to threshold
speed of conduction after the SA node
purkinje>atria>ventricles>AV node
IF its positive in I and II leads then what
normal
if AVR is positie then
abnormal
HTN treatment
thiazides, ACE, ARB, dihydropyridine CCB
HTN with HF treatment
diuretics, ACE, ARB, beta blocker, aldosterone antagonists
HTN with DM treatment
ACE inhibitors, ARB, CCB, thiazides, beta blockers- ace inhibitors/ARB are protective against diabetic neprhopathy
HTN in pregnancy treatment
hydralazine, labetalol, methyldopa, nifedipine
dihydropyradines act on what and are which ones
all end in dipine
nondihydropyridines are which ones
diltiazam, and verapamil
what is the MOA of CCB
block voltage dependent L type channels of cardiac and smooth muscle- decreased smooth muscle contractility-
which CCBs work stronger on the vascular smooth muscle
amlodipine, nifedine>diltiazam>verapamil
which CCB work stronger on heart
verapamil> diltiazam>amlodipine-nigedipine
clinical use of CCB
hypertension, agnina, raynaus
use of nimodipine
subarachnoid hemorhage
clevedipine use
hypertensive emergency and urgency
what are the nondihydropyradines used for
HTN, angina, a fib or flutter
what are the adverse effects of non-dihydropyradines
cardiac depression, AV block, hyperprolactinmeia, constipation
what are the adverse effects of dihydropyradines
peripheral edema, flushing, diziness, gingival hyperplasia
what can happen if using verapamil and beta blockers
can cause a combination negative chronotropic effect, effect yielding severe bradycardia and hypotension
hydralazine MOA, clinical use, and adverse effects
increased cGMP, smooth muscle relaxation, increase vasodilation of arteries > veins and after load is reduced. Severe hypertension, HF, safe to use during pregnancy, coadminstered with beta blocker because of tachycardia. Compensatory tachycardia, fluid retention, headache, angina, lupus like syndrome
what drugs are used for hypertensive emergency
clevidipine, fenoldopam, labetalol, nicardipine, nitriprusside
nitroprusside what are the mechanisms and adverse effects
short acting but increased cyclic GMP, direct release of NO can cause cyanide toxicity
fenoldopam- mechanisms and adverse effects
dopamine D1 receptor agonist- cornary, peripheral, renal, and splanchnic, and vasodilation. decreased BP. increased nantruresis, post op for anti hypertension, Cau cause hypotension and tachycardia.
what does nitroprusside do to the heart
decreased LV, and after load so SV is maintained can be used in hypertensive heart failure
nitrate dosing
do not dose overnight because there is a tolerance
nitrate moa, clinical use, adverse effects
vasodilate by increased NO in vascular smooth muscle, and increase in cGMP and smooth muscle relaxation. Delate the veins>arteries and decrease preload. Angina, acute coronary syndrome, pulmonary edema- reflex tachycardia, hypotension, fishing headache- development of tolerance during the work week- tachy and dizzy and headache with re-exposure. decrease GTP and increase GMP and so decrease activation of myosin light chain kinase so diaphoresis of MLC so vascular relaxation
ranolazine- MOA, clinical use, adverse effects
inhibits the late phase of sodium current reducing diastolic wall tension and oxygen consumption, does not affect heart rate or contractility. Angina refractory to other medical therapies. Constipation, dizziness, headache, nausea, QT prolongation
what does HMG-Coa reducatse do to LDL, HDL, triglycerides
decreased LDL, increased HDL, decreased TAG
what is the MOA of statins
inhibit conversion of HMG oa to mevalonate a cholesterol precursos, and decreased mortality in CAD patients, increased LDL receptor recycling
what is the adverse effects of statins
hepatotoxic, increased LFT, myopathy with fibrates, and increased CK
what are the bile acid resins and what do they do to LDL, HDL, triglycerides
cholestyramine, colestipol, colsesvelam- decreased LDL, increased HDL, increased TAG
what is the MOA of the bile acid resins
prevent intestinal reabsorption of bile acids, liver must use cholesterol to make more- can help to get rid of gall stones
what are the adverse effects of bile acid resins
GI upset, decreased absorption, fat soluble vitamins decrease
what does ezetimibe do to LDL, HDL, triglycerides
decreased LDL only
what is the mOA of ezetimibe
prevent cholesterol absorption at small intestine brush border so stop cholesterol absorption through the intestine
what is the side effect of ezetimibe
increase in LFT and diarrhea
fibrates do what to LDL, HDL, triglycerides
decrease LDL, increase HDL, really decrease TAG
fibrates MOA
upregulate LPK and increase TG clearance. Activates PPAR alpha to induces HDL synthesis. Inhibit cholesterol 7 alpha hydroxylase so decayers cholesterol solubility
fibrates are used for what
good for TAG pancreatitis and because it lowers TAGs it increases gallstones
what are the adverse effects of TAGs
myopathy, increased risk of statins, cholesterol gallstones
niacin do what to LDL, HDL, triglycerides
decrease LDL, increase HDL, decrease TG
niacin MOA
inhibits lipolysis in adipose tissues reduces hepatic VLDL synthesis
niacin adverse effect
red flushed face which is by decreased NSAIDs, hyperglycemia, hyperuriciemia
why is there increased flushing from niacin
increased prostaglandins
why do fibrates increase the risk of myopathy with statins
fibrates inpair hepatic clearance of statins and increased blood levels of statin. also increase risk with niacin, and ezetimide
what does fish oil do
antagonize VLDL
digoxin MOA
stops Na/K ATPase so increase Na in the cell so increase Ca in the cell so increase contraction
clinical use of digoxin
HP, atrial fib, decrease conviction of AV node and depression of SA node
what are the adverse effects of digoxin
nausea, vomitting diarrhea, yellow vision .arrhymias, av block- can lead to hyperkalemia, renal failure, hypokalemia, drugs that displace digoxin from tissue binding sites and decrease clearance
what are the class IA antiarrythmics, MOA, clinical use, and adverse effects
quinidine, procainamide, disopyramide- increased AP duration, and increased refractory period. Can have cinchonism headache, tinitis, SLE, heart failure, thrombocytopenia, increased QT and torsades
what are the class IB antiarrythmics, MOA, clinical use, and adverse effects
lidocaine, mexiletine- decreased AP duration, preferentially affects ischemic or depolarized purkinje and ventricular tissue. Can be from acute centricualr arrhythmias, digitalis induces arrhythmias, post MI. CNS stimulation, depression, cardiovascular depression
what are the class IC antiarrythmics, MOA, clinical use, and adverse effects
flecainamide, propafenone- strongest binding, terminate tachycardia angina- significantly prolongs ERP in AV node and accessory bypass tracts. No effect of ERP in purkinge and ventricular tissue. minimal effect on AP duration. Used for SVT, including atrial fibrillation. Proarrythmic especially post-MI- contraindicated in strugural and ischemic heart disease
NA channel by strength
1C>1A>1B- so increased HR and to increased NA blockade- 1 C mose use dependent due to slow dissociative. 1B is the fastest to dissociate
Class II antiarryhtmics MOA, clinical use, and adverse effects
metoprolol, propanolol, esmolol, atenolol, timolol, carvediol- decrease SA and AV nodal activity by decrease cAMP, decreased Ca currents. Suppress abnormal pacemakers by decreased slope of phase 4. Ave node particualrly sensitive to increase PR interval. Impotence exacerbation of COPD and asthma, cardiovascular effects of bradycardia and heart block, HP, sedation, sleep alternations, mast hypoglycemia-
what can cause dyslipidemia
metoprolol
prinzmetal angina can be aggravated by which beta blocker
propanolol
how do you treat a beta blocker overdose
glucagona
what are the class III antiarryhtmics , MOA, clinical use, and adverse effects
amiodorone, ibutilide, dofetilide, sotalol- K blocker through atrial fib, atrial flutter, ventricular tachycardia-
adverse effects of sotalol
torsades des pointes excesssive beta blockage
adverse effects of ibutilide
torsades
adverse effects of amnioderone
pulmonary fibrosis, hepatotoxic, hypothyroid, hyperthyroid, hapten cuasing corneal deposits, blue grey skin deposits leading to phodermatitis, neurologic effects- bradycardia, heart block, HF
what do you check when starting amnioderone
PFT, LFT, TFT
what are the class IV antiarrythmics, MOA, clinical use, and adverse effects
verapamil, diltiazam- decreased conduction velocity, preven nodal arrythmias, rate control of fib. constipation, flushing, emema, vurdiovacualr effects- HF, AV block, sinus dpression
where in the SA nodal AP does class Iv antiarryhtmics work
phase 4 depolarization
adenosine MOA and what does it do
increase K out of cells, hyper polarize the cells and decrase intracellular CA. Drug of choice on diagnosing termination of certain forms of SVT. very short acting- blunted by theophylline and caffeine both are receptor antagnoists- flushing, hypotension, chest pain, sense of impending doom, bronchospasm- see a pause of EKG
what does Mg do to arryhtias
effective against torsades and K is also used to treat for decreased ectopic pacemakers- for hypokalemia
what should you check levels of with arryhtmias
K and Mg
Propyluracil and methimazole- MOA
block thyroid peroxidase and inhibit the oxidation of iodide and organification of iodine, inhibit thyroid hormone synthesis. Propyluracil also blocks the 5 deiodinase and decrease peripheral conversion of t4 to t3
Propyluracil and methimazole- clinical use
hyperthyroidism
Propyluracil and methimazole- adverse effets
skin rash, agranulocytosis, aplastic anemia, hepatotoxic
what can methimazole cause during pregnancy
cutis aplasia
levothyroxine and triiodothyronine which goes with which
levothyroxine- T4
triidothyronine T3
what are the side effects of levothyroxine and triiodothyronine
tachycardia, heat intolerance, tremor, arrhythmias
convivaptan and tolvaptan
it is block ADH at V2- SIADH treatment
desmopressin
central DI
GH as a drug
for turner or GH deficiency
oxytocin use as drug
stimulates labor, uterine contractions, milk let down, controls uterine hemorrhage
somatostatin as drug
acromegaly, carcinoid syndrome, gastrinoma, glucagonoma, esophageal varices- can stop bleeding out and GnRH release
demeclocylcine MOA
ADH antagonist- from tetracycline family
demeclocylcine clinical use
SIADH
demeclocylcine side effects
neprhogenic DI, photosensitivity, abnormal bone and teeth
glucocorticoids- MOA
metabolic carabolic anti-inflammatory, and immunosuppressive effects mediated with response elements, inhibit phospholipase A2, inhibition of transcription factors such as NfKB
glucocorticoids- clinical use
adrenal insufficiency, inflammation, immunosuppression, asthma
glucocorticoids- adverse effects
iatrogenic cushing, adrenocrotical atrophy, peptic ulcers, steroid diabets, steroid psychosis, cataracts. adrena insufficiency when the drug is quickly removed
fludrocortisone MOA
synthetic analog of aldosterone with little glucocorticoid effects
fludrocortisone clinical effects
mineralocorticoids replacement in 1 degree adrenal insufficiency
fludrocortisone adverse effects
similar cushing, edema, exacerbation of heart failure, hyperpigmentation
cinacalcet MOA
sensitizes Ca sensing receptor in parathyroid gland to circulating Ca and decreae PTH
cinacalcet clincal use
first or second hyperparathyroidism
cinacalcet adverse effects
hypocalcemia
H2 blockers- name
dine
H2 blockers- MOA and use
reversible block of hiatime H3 receptors and decreased H section by parietal cells- used for peptic ulcers, gastritis, mild refluc
adverse effects of H2 blockers-
cimetidine is a potente hihibitor of P450 and it is antiandrogenic effe can cross the BBB and placenta.
PPI- name
prazole
PPI- MOA and use
irreverisly inhibits the H/K ATPASe in stomach pareital cels os it blocks the final common pathyway for gastric acid secretion
ppi adverse effects
increased risk of diff infection, pneumonia, decreased serum Mg
aluminum hydroxide- adverse effeccts
constipation, hypophosphatemia and proximal msucle weakness, osteodystrophy, and seizures
calcium carbonate adverse effects
hypercalcemia, milk alkali, and increased rebound acid secretion can decrease effectiveness of tetracyclines
magnesium hydroxide adverse effects
diarrhea, hyporeflexia, hypotension, cardiac arrest
bismuth, sulcrafate
bind to ulcer base to provide physical protection and allow bicarb secretion to reestablish pH gradient in the mucous layer
misoprostol
PGE1 analo- increase poductio and secretion of gastric mucous carrier and reduce acid production. prevents NSAID induced peptic ulcers- induces labor and diarrhea- abortifactan
octreotide
long acting somatitsiin analog inhibits the secretion of various splanchnic vasodilatory hormones acute parcel bleeds, acromegaly, VIPoma, carcinoid tumors, nausea, cramps, steatorrhea, increased cholestsis from CCK inhibitorn
osmotic laxatives- which
magnesium hydroxide, magnesium citrate, polyethylen glycol, lactulose
MOA of osmotic laxatives
proived osmotic load to draw water into GI lumen. Constipation and the use and it can be used for hepatic encephalopathy
sulfasalazine
a combination of antibacterial and amsnosalcillic acid which his anti inflammatory- activated by colonic bacteria used for UC and crohn, can cause malaise , nausea, sulfonamide toxicity, and oligospermia
loperamide
agonist of the mu opiod receptor to slow gut motility
ondansetron
%ht receptor antagonist and decrease vagal stimulation. powerful central acting anti-emetic. Control vomiting, and chemo- can cause headache, constipatin ,QT prolongation
metoclopramide
D2 recptor antagonist increased resting tone contractility and LES tone, motility does not influence colonic transport time. Diabeticc and post surgery gastroparesis, antiemetic. Increased parkinson effects, tadive dyskinesia, restlessness, drowsiness, fatigue, depression, diahrrea, can interact with digoxin and diabetic agetns.
orlistat
inhibits gastric pancreatic lipase which decreases the breakdown and absorption of dietary fats. It cause weight loss, steatorrhea, decreased absorption of ADEK
ursodiol
nontoxinc bile acid to increase bile acid secretion and decrease cholesterol secretion and absorption. Primary biliary cirrhosis, gallstone prevention or dissolution
heparin MOA
it lowers the activity of thrombin and factor Xa and has a short half life and potentiates action of ATIII
what are the low molecular weight heparins
enoxaparin, dalteparin, fondaparinux
what does LMWH act on
it acts more on Xa- can bind ATIII but once active in Xa to stop thrombin to prothrombin
HIT
development of IgG antibodies against heparin bound platelet factor 4, an antibody PF4 complex activates platelets and thrombosis and thrombocytopenia form- direct thrombin inhibitors like argatroban
bivalirudin- MOA
it directly inhibits activity of free and clot associated thrombin.
warfarin MOA
interferes with gamma carboxylation of vitamin K dependent clotting factors II, VII, Ix, X and protein C and S. Metabolism by polymorphisms in the gene for vitamin K epoxide reductase complex. Has effect on extrinsic pathway and increased PT.
wafarin dverse effects
skin and tissue necroses, drug drug interactions. and protein C and S have shorter half lies, and this leads to early transient hypercoagulbility with warfarin use. Skin and tissue necrosis within the first few days of large doses due to small vessel microthrombi
which one, heparin or warfarin should be given in pregnancy
heparin because its polar and water soluble
apixaban and rivaroxaban- MOA- Xa in the name
bind to and directly inhibit factor Xa.
alteplase, reteplase, streptokinase, tenecteplase-MOA
directly inhibit conversion of plasminogen to plasmic which cleaves thrombin and fibrin clots. Increased Pt and PTT but no change in the platelet count.
adverse effects or who do you not use thrombolytics in
risk of inter cranial hemorrhage and asymetric pupils, irregular breathing, decreased consciousness and bleeding and active surgery, severe HTN.
what do you treat toxicity of thrombolytics with
aminocaproic acid
clopidogrel, prasigrel, ticagrelor, ticlodipine- MOA- gre in the name
inhibit platelt aggregation by irrversible blocking ACP receptors to prevent the expression of IIb/IIIa o platelets. this prevents platelet aggregation
cilostazol and dypyridamole MOA
PGIII inhibitior so increased CAMP in the platelets leading to decreased aggregation and vasodialtion so good for PAD and intermittent claudication
abciximab, eptifibatide, tirofiban MOA
bind BpII/IIIa on activated platelets, preventing aggregation is made from Fab fragments
when do the microtubule inhibitors work in the cell cycle
M phase
azothioprine and 6-MP- MOA
purine thiol analongs to decrease de novo purine synthesis and activated by HGPRT.
azothioprine and 6MP clinical use
preventing organ rejection, RA, IBD, SLE
what increases the toxicity of azothioprine and 6MP
its from xanthine oxidase and this increased toxicity with allopurinol or febuxostat
cladribine- MOA
purine analog and mucltiple mechanisms like inhibitors or DNA polymerase and DNA strand breaks
cladribine clinical use
hairy cell leukemia
cytarabine- arabinofuranosyl cytidine- MOA
pyrimidine analog and inhibit of DNA polymerase
cytarabine- arabinofuranosyl cytidine- adverse effects
pancytopenia
5-FU MOA
purimidine analog bioactivated 5-FdUMP which covalentlly complexes folic acid. This complex inhibits thymbdilate synthase
5-FU has what effect with leucovorin
it is enhanced by it
methotrexate MOA
folic acid analog that competitively inhibits dihydrofolate reductase and decreased DNA synthesis. Can have mouth ulcers
methotrexate has what effect with leucovorin
it is decreased effect with it. It is the rescue
bleomycin MOA
induce free radical formation and breaks in DNA strands
bleomycin adverse effects
pulmonary fibrosis and skin hyperpigmentation
dactinomycin MOa
intercalates DNA
what are the uses of dactomycin
used for childhood tumors
doxarubicin and daunorubicin MOA
generate free radicals and intercalate DNA and breaks in DNA and decreased replication
doxarubicin and daunorubicin adverse effects
cardiotoxicity, dilated cardiomyopathy. use ironchelator to prevent the cardiotoxicity
busulfan MOA
cross links DNA
busulfan adverse effects
severe myelosuppression and pulmonary fibrosis and hyperpigmentation
cyclophosphamide, ifofamide MOA
cross like DNA at guanine N7 require bioactivation by liver that screws up the DNA replication
cyclophosphamide, ifofamide- adverse effects
hemorrhagic cystitis blocked by mensa or NAC
carmustine, iomustine, semustine, treptozocin- MOA
require bioactivation and crosses the BBB- cross links the DNA
carmustine, iomustine, semustine, treptozocin- adverse effects
CNS toxicity
paclitaxel and other taxols- MOA
hyperstabalize polymerized microtibules in the M phase so that mitotic spindle cannot break down so anaphase cannot occur
paclitaxel and taxols- adverse effects
hypersensitivity
vincristine, vinblastine- MOA
vinca alkaloids that bind beta tubular and inhibit its polymerization into microtubules and prevent mitotic spindle formation so M phase arrest
vincristine, vinblastine adverse effect
neurotoxicity wit hareflexia, peripheral neuritis, constipation like paralytic ileus
cisplatin, carboplatin MOA
Cross link DNA
cisplatin, carboplatin adverse effects
can cause hearing loss form damage to organ of Corti. and there is nephrotoxicity and can be prevented with amifostine and chloride diuresis
etoposide and teniposide MOA
inhibits topoisomerase II and increased DNA degradation
etoposide and teniposide adverse effects
myelosuppression and alopecia
podophyllin MOA
used in genital warts has the same Moa and block DNA too 2
irinotecan and topotecan MOA
inhibit topoisomerase I and prevent DNA unwinding and replication
irinotecan and topotecan adverse effects
severe myelosuppression and diarrhea
hydroxyurea MOA
inhibits ribonucelotide reductase and decrease DNA synthesis so S phase
hydroxyurea other use
increased fetal hemoglobin which is protective against sickling
prednisone and prednisolone MOA
bdinind to intracytopalsmic steroid receptor to block gene transcription
prednisone and prednisolone adverse effects
cushing like, weight gain, central obesity, muscle breakdown, cataracts, acne, osteoporosis, hypertension, PUD, hyperglycemia, psychosis
bevacizumab MOA
monoclonal antibody against VEGF inhibits angiogenesis
bevacizumab adverse effects
hemorrhage, blood clots, impaired wound healing
erlotinib mOA
EGFR tyrosine kinase
erlotinib adverse effects
rash
cetuximab MOA
monoclonal antibody against EGFR
cetuximab adverse effect
rash, elevated LFT, diarrhea
imatinib MOA
tyrosine kinase inhibitor of BCR-ABL and c-kit.
imatinib uses
CML and GI stromal tumor
imatinib adverse effects
fluid retention
retuximab MOA
monoclonal antibody against Cd20 which is found on most B cell neoplasms
retuximab clinical use
non-hodgekin lymphoma, CLL, ITP, RA
retuximab adverse effects
increased risk of progressive multifocal leukoencepthalopathy
tamoxifn/raloxifene MOA
selective estrogen receptor modulators- receptor antagonists in breast and agonists in bone. Block he binding of estrogens to the ER positive cells.
adverse effects of tamoxifen
partial agonist in endometrium which increases the risk of endometrial cancer hot flashes
adverse effects of raloxifene
no increase in endometrial carcinoma because it is an estrogen receptor antagonist in endometrial tissue but it helps prevent breast cancer and treat with/prevent osteoporosis
trastuzumab MOA
monoclonal antibody against HER-2 a tyrosine kinase receptor. Helps kill cancer cells that overexposes HEr2, and through inhibitor of HER2 initiated cellular signaling and antibody dependent cytotoxicity
what are the adverse effects of trastuzumab
ardiotoxic
vemurafenib MOA
small molecule inhibitor of BRAF oncogene and positive for melanoma- mutation BRAF inhibiton
vemurafenib clinical use
melanoma
epinephrine and brimonide
decreased aqueous humor and synthesis via vasscondstriction- adverse effects of a1 do not sued in closed angle glucaoma
timolol, betaxolol, carteolol
decreased aqueous humor and no pupillary or vision changes
acetazolamide
decreasd aqueous humor synthesis veal inhibitor of carbonic anhydrase also hits the PCT
polocarpine and carbachol- direct cholinomemetics
increased outflow of quakes tumor via contraction of ciliary muscle and opening of trabecular meshwork- mitosis and contraction or pupillary sphincter and cylclospasm
indirect cholinomimetics of M3- its physostigmine and echothiphate
use pilocaripin in emergenices- but increases the outflow of aqueous humor via contraction of ciliary muscles and opening of traveler network
bimatoprost and iatoprost
increase the outflow of aqueous humor
adverse effects of bimatoprost and iatoprost
darkens iris and eyelash growth
opiod analgesics MOA
act as agonist at opiod receptors to modulate synaptic transition open K channels and close Ca channels- decreased synaptic transmission inhibit release of ACh, NE, and 5-HT, glutamate, and substance P
what are the opioids used in diarrhea
loperamide and diphenoxylate
what are the adverse effects of opiods
addiction, respiratory depression, constiaption, mioisis, additive CNS depression with other drugs tolerance does not develop to mitosis and constipation. toxicity treat with naloxone
what happens if there is morphine tolerance
active metabolites can cause build up and deterioration-called morphine 6 gloconamide
pentazocine MOA
kappa opiod receptor agonist and mu receptor antagonist
pentazocine adverse effects
can cause opioid withdrawal symptoms if patient is also taking full opiod antagonist competition for opiod receptors
butorphanol MOA
kappa receptor agonist with mu receptor partial agonist produces adalgesia
tramadol MOA
very weak opioid agents but also inhibitors 5HT and NE repute so it can be used to treat chronic pain, but it can cause serotonin syndrome
ethosuxamide MOA and use
it blocks the T type Ca channels and it causes GI , fatigue, urticaria, SJS, and it can be used for abssence seizure
Benzos
increased frequency of GAB channel opening- sedation, tolerance, dependency, and respiratory depression
phenobarbitol
increased GABA opening for longer- it has sedation, tolerance, dependence and induction of P450-
phenyotin
blcoks NA channel with zero order kinetics
phenytoin adverse effects
neurologic nystagmus, diplopia, ataia, sedation, peripheral neuropathy, hirsuitism, gingival hyperplasia, DRESS, DLE, megaloblastic anemia, P450 induction
carbamazepine
blocks NA channels- diplopia, blood dyscrasia, treatment, SIASH, SJS, induce cytoP450
valporic acid
increaed NA channel inactivation and increased GABa- GI distress, pancreatitis, neural tube, tremor, weight gain, contraindicated inpregnanacy
vigabatrin
increased GAB inactivation
gabapentin
inhibit CA channels and designed by GABA analot- sedation and ataia- it is perioheral neuropathy and postherpetic neuralgia
topiramate
blcoks NA channels and increased GABA action- sedation, mental dulling, kidney stones, and weight loss. migraine prevention
lamtotrigine
blcoks voltage gated NA channels can cause SJS
levetiracetam
may modular GABA or glutamate
tiagabine
increase GABA uptake
what is the alternate use of phenobarbitol
it is used to increase output of conjugated bilirubin in Criggler Najjar II
zolpedemi, zaleporn, eszopilon
act as BZ1 subtype of GABA receptor effects revers by flmazenil and it sleep cycle affected as compared with benzodiazepine hypnotics. It is used for insomnia- it has ataxia headaches and confsion- short duration because of rapid metabolism by liver enzymes. Can only modedest day after psychomotor depression and few amnesic effects decreased dependence and not as bad on old people
ramelteon
is a melatonin agonist better for geriatric because no adverse effects
anesthetics what happens if lipid solubility is increased
more potent because it crosses the BBB better so MAC is lower
anesthetic what happens if the inhaled has a higher partition or decreased blood solubility
faster induction/onset
which inhales anesthetic is hepatotoxic
halothane
which inhaled anesthetic is nephrotoxic
methoxyflurane
which inhaled anesthetic is proconvilsant
enflurane
what are the parameter changes with inhaled anesthetics
myocardial depression, respiratory depression, nausea, increased cerebral blood flow, decreased cerebral metabolic demand
malignant hyperthermia
life threatening condition in which inhaled anesthetics or succinylcholine induce fever and severe muscle contractions. Sucesptibility is often inherited as autosomal dominant with variable penetrance. Mutations in voltage sensitive ryandine receptor to cause increased CA release from SR. treat with dantrolene a ryanodine receptor antagonist
barbituates IV- thiopental-what does it do to blood flow
it decreases cerebral blood flow
midazolam- barb for anesthesia- what does it do to blood flow
it decreases repertory depression, decrease BP, anterograde amnesia
ketamine- what MOA and what does it do to blood flow
PCP analog so block NMDA receptor and causes cardio tim and increased cerebral blood flow
propofol- MOA what does it do to blood flow
it is for sedation and it potentiates GABA.
which are the ester local anesthetics
procaine, cocaine, tetracaine, and benzocaine- this is for allergic reactions
which are the amide LAs
lidocaine, mepivacaine, bupivacian- amides
MOA of LA
it is for block of NA channels and it can penetrate the membrane to prevent depolarization.
what order does LA unnerve the fibers- types
small diameter fibers>large diameter
order of loss of fibers of LA
it is pain, temperature, touch, pressure
which LA is cardiotoxic
bupivacaine
what LA can cause methylglobulinemia
its benzocaine
succinylcholine
strong Ach receptor agnost and produces sustained depolariation to prevent the muscle contraction
what is the phase I of the reversal of the succinylcholine block
it is no antidote block is potentates by cholinesteraseinhibitors
what is the phase II of the reversal of the succinylcholine block
it can be reversed because there are some Ach receptors- desnsitized
what are the complications with succinylcholine
hypercalcemia, heperkalemia, malignant hyperthermia
nondepoalizing NMJ blcokers- curare
all compete for ACh receptors- neostigmine can revere it.
dantrolene
prevents release of Ca from SR form skeletal muscle by binding to ryanodine receptor. malignant hyperthermia reatmuc. Neuroleptic malign syndrome
baclofen
activates GABA receptors the spinal cord levels- inducing skeletal muscle relaxation- muscle spasms- can be used for MS and acute low back pain with muscle spasms
cyclobenzaprine
centally acting skeletal muscle relaxant. related to TCA and similar anticholinergic side effects- muscle sparsms
dopamine agonists
ropinerole and pramipexole- direct stimulation of dopamine receptors
amantadine
increase dopamine availability- can cause lived reticularis
levodopa
- increase blocks, peripheral conversion of L dopa to dopamine by inhibiting dopa decarboxylase and reduce side effects of peripheral L dopa conversion into dopamine
entacapone, tolcapone
prevent peripheral L dopa degradation in 3-O methyldoma by inhibiting COMT- COMT inhibitors help prevent peripheral breakdown of L dopa used for its on off effects
selegine
blocks onversion of dopamine into DOPAc by selectively inhibiting MAO-B
tolcapone
lbcoks conversion of dopamine to 3-OMD by inhibiting central COMT
benztropine
antimuscarinic that improves tremor but little effect on bradykinesia
riluzole
used for ALS for increased survival and decreased glutamate excitiotixicity via unclear mechanism
triptans
5HT agonist that inhibits trigeminal nerve activation and prevents vasoactive peptide release and induce vasoconstriction. coronary vasospasm
what are synthetic prostaglandins used for
pulmonary HTN, and Raynauds, inhibit platelet aggregation, adhesion to vase endothlium, and vasodialte and increased vascular permeability, and stimulater leukocyte chemotaxis
aceotminophen MOA
it reversibly inhibits COS and mostly in CNS inactivates peripherally
acetominophen adverse effects
overdose produces heaptic necosis NAPQI the metabolite depletes glutathione and forms toxic byproducts in the liver.
what does NAC do
it regenerates glutatione
aspirin MOA
NSAID that irreversibly inhibits COX and by covalent acetylation and decreased synthesis of TXA2 and prostaglading and increased BT and no effect on PT and PTT effects last until new platelets are produced
what is the aspirin adverse effects
gastric ulcers, tinnitus from CNVIII, chronic acan lead to renal failure, interstitial nephritis
what is the metabolic pH change from ASA
it is respiratory alkalosis early then goes to mexed metabolic acidosis and respiratory alkalosis
celecoxib MOA
reveribly inhibtis specifically the cos isfoomr 2 which is found in inflammatory cel and vascular endothelium and mediates inflammation nan pain spacres COX1 an maintain gastric mucosa so less corrosive effect
adverse effects of celecoxib
thrmobosis and sulfa allergy
NSAID MOA
reversibley inhibit COZ and block prostaglandin synthesis
adverse effects of NSAIDs
interstitial nephritis, gastric ulcer, renal ischemia from prostaglandin dilation of the afferent arteriole
what are the NSAIDs
ibuprofen, naproxen, indometicin, ketorolac, diclofenac, meloxicam, piroxicam
leflunomide MOA
reversible inhiits dihydroorate dyhydrogenase to prevent pyrimiden synthes inad prevent T cell proliferation
leflunomide used for
RA and psoriatic arthritis
adverse effects of leflunomide
diarrhea, HTN, hepatotoxic, and teratogenicity
bisphosphinates MOA
pyrophosphate analogs, bind hydroxyapetitis in blone to prevent clast activity
bisphosphinates adverse effects
esophagitis, osteonecrosis of the jaw and atypical stress fracture
teriparatide MOA
recombinant PTH analog given subcutaneously daily to increase blast activity
teriparatide adverse effects
transiet hypercalcemia- used before bisphosphinates before starting
what are the acute gout drugs
NSAIDS, glucocorticoids, colchicine
what are the chronic gout drugs
allourinaol, febuxostate, pegloticase, probenacid
allopurinol
competitive inhibitor of xanthine oxidase to decreased conversion. sued in lymphoma and leukemia to prevent tumor lysis syndrome and increased concentration os azothiprine and ^MP from decreased metabolism
febuxostats
inhhibits xanthine oxidase
pegloticase
recombinant fricassee that catalyzes metabolism of uric acid to allantoin which is more water soluble
probenacid
inhiits resorbiton of uric acid in proximal convoluted tubules for uric acid calculi
colchicine
binds and stabalizes tubulin to inhibit microtubules polymerization, impairing neutrophil chemotzis and degranulation acute and prophylactic use
colchicine side effects
GI mucosa is disrupted leading to diarrhea nausea, and abdominal pain and vomiting
lubar punitive goes through what ligament
the ligament flavum
what has to be checked before starting TNF alpha inhibitors
TB test
etanercept
it is a fusion protein that is the receptor for TNF alpha so its used for RA, psoriasis, AS
infliximab and adalimumab
it is an anti-TNFalpha monoclonal antibody used for IBD, RA, AS, and psoriasis
rasburicase
recombinat fricassee that catalyzes metabolism of uric acid to allantoin, and prevention of tumor lysis syndrome
what are the first generation antihistamines
diphenhydramine, dimenhydrinate, hydroxyzine, chlorpheiramine
what are the adverse effects of first generation antihistamines
sedation, antimuscarinic anti alpha adrenergic
what are the side effects of first generation antihistamines on old people
cholinergic seide effects like blurry vision, glaucoma, delrium, retention, alpha 1 falls, serotinergic weight gain ,and appetitie stimulation
second generation antihistamines- what are they
loratadine, fexofenadine, desloratadine, cetirizine
second generation antihistamines adverse effects
far less sedating than first generation because of decreased entry into the CNS
what is guaifensin
expectorant thins respiratory secretions does not suppress cough reflex
what is N-acetylcysteine
mucolytic liquifies mucus in COPD patients by disrupting disulfide bonds used as an antidote for acetaminophen overdose
dextromethrophan
antitussive antagonizes NMDA gluatate receptors and codein analog. Mild opiod effect in excess. Can have contraption or serotonin syndrome
what is the adverse effects of dextromethrophan
constipation, sedation if high and serotonin syndrome
pseudo ephedrine and phenylephrine
alpha adrenergic agonist used as nasal decongestants. short term for nasal congestion.
adverse effects of pseudo ephedrine and phenylephrine
hypertension, can also cause CNS stimulation/anxiety and pseudoephedrine
bosentan MOA
compeittive antagonism of endothelin 1 receptors and decreased pulmonary vascular resistance.
bosentan side effects
hepatotixic, moniter LFP and decreased arterial pulmonary pressure and lessens RVH
sildalafil
inhibits cGMP PDE5 and prolongs vasodilatory effects of NO
epoprostenol and iloprost
PGi3 prostacyclin with direct vasodilatory effecton pulmonary and systemic arterial vascular bests. inhibits platelet aggregation
Beta 2 agonists- albuterol, salmeterol, formoterol-MOA
increased cAMP by Gs
albuterol
relaxes the bronchial smooth muscle by short acting beta 2 and used for acute
salmetrerol and formoterol
long acting for prophylaxis adverse effects of armor and arrythmia
inhaled corticosteroids like flutixaon and budesonide
inhibit the syndrther os all xytokines and inactivate NF-KB the transcription factor that induces TNF alpha and other inflammatory agents. first line for chronic asthma
ipratropium
blocks muscarinic receptors compeititvely and it prevents bronchoconstriciton also used for COPS
tiotropium
it is a long term inhibitor of muscarinic receptors prevents bronchoconstriction
montelukast and zafrilukast
block leukotriene receptors epxiaclly good for aspirin induced asthma- receptor blocker in LOX pathway
zileuton
5 lox pathway inhibits blocks conversion of arachadoinc acid to leukotrienes hepatotoxic
omalizumab
binds mostyl unbound serum IgE and blocks binding to FcERI used in allergic asthma with increased IgE levels resistant to inhaled steroids and long acting beta 2 agonists
theophylline
bronchi dilation by inhibiting phosphodiesterase increased cAMP and decreased CAMP hydrolysis. Usage limited for narrow TI cardio and neurotoxic metabolized by cytochrome P450 and blocks action of adenosine
methacholine
muscarinic 3 agonist and bronchial challenge test to induce and activate asthma in suceptible patients
mannitol MOA
osmotic diuretic and increased tubular fluid osmolarity and increased urine flow and decreased intraocular pressure and intracranial pressure
why do you use mannitol and what are the adverse effects
used for drug overdose, elevated inter cranial pressure or intraocular pressure, and causes pulmonary edema, and dehydration, contraindicated in anuria, HF
acetazolamide MOA
carbonic anhydrase inhibitor causing self-limited NaHCO3 diuresis and decreased total body HCO3 stores. works at PCT to alkalinize the urine works at the PCT
acetazolamide clinical use and adverse effects
used for glaucoma, urinary alkalization, metabolic alkalosis, altitude sickness, and pseudotumore cerebra and closed angle glaucoma. Adverse effects are proximal renal tubular acidosis, paresthesias, NH3 toxicity, sulfa allergy, somnolence, alkaline urine, metabolic acidosis, dehydration and decreased K and Na
loop diuretics which ones are they and their MOA
sulfonamide Loop diuretics, inhibit cotransport ssystem of NA/K/Cl of thick ascending limb. Abolism hypertonicity of the medulla and prevent concentration of the urine. stimulate PGE release and vasodilatory effect, and inhibited by nSAIDs and increased Ca excretion- furosemide, bumetanide, torsemide
loops clinical use and adverse effects
used for edematous states, HF ,cirrhosis, nephrotic syndrome, pulmonary edema, and hypertension, and hypercalcemia. it is ototoxic, hypokalemia, dehydration, allergy like sulfa drugs, metabolic alkalosis, nephritis, and gout
ethacrynic acid MOA
nonsulfonamide inhibitor to the same thing as loops
ethacrynic acid clinical use and adverse effects
diuresis in pateints allergic to sulfa drugs and similar to furosemide but more ototoxic
which are the thiazide diuretics
hydrocholorthiazide, chlorthalidone, metolazone, imatomapide
what is the MOA of thiazides
it inhibits NaCLe reabsorption at the DCT and it decreases the diluting capacity of the nephron and decreases Ca excretion. can cause stones but increased Ca leads to decreased fractures
thiazide clinical use
HTN (first line), HF, idiopathic hypercalciuria, nephrogenic DI, and osteoporosis
adverse effects of thiazide diuretics
hypokalemia, metabolic alkalosis, hyponatremia, hyperglycemia, hyperlipidemia, hyperuricemia, hypercalcimia, sulfa allergy
what happens to the electrolytes with thiazide diuretics
INCREASED CA, INCREASED URIC ACID, INCREASED glucose, increased cholesterol, increased TG, decreased Na, decreased K and decreased Mg
what are the potassium sparing diuretics
spirolactone, eplernone, trimeterene, amiloride
Moa of K sparing diuretics
spirolactone and eplerenone are competitive aldosterone receptor antagonists in the cortical collecting tubule. Triameterene and amiloride act at the same part of the tubule by blocking Na channels in the cortical collecting tubule.
what is the clinical use of the K sparing diuretics
hyperaldosteronism, K depleteion, HF, hepatic ascites, nephrogenic DI,regression of fibrosis and remodeliing in HF
what K sparing diuretics is specific usual for hepatic ascites
spirolactone
what K sparing diuretics is specific usual for nephrogenic DI
amiloride
what are the adverse effects of potassium sparing diuretics
hyperkalemia, arrthmyias from this, endocrine effects like gynecomastia and anti androgen for spirolactone
what happens to urine NaCl with diruetics
increased with all diuretics
what happens to urine K with diuretics
it increases with loops and thiazides
what diuretics decrease urine pH
carbonic anhydrase inhibitors like acetazolamide
what diuretics increase blood Ph
loops, thiazides cause alklemia through volume contraction, and K loss, low K state
what diuretics increase urine Ca so decrease serum Ca
loops
what diuretics decrease urine Ca so increase serum Ca
thiazides
what is common ending for ACE inhibitors
it is pril
what is the MOA of Ace inhibitors
inhibit ACE conversion to ATII and so decrease GFr by preventing the constriction of efferent arterioles. increased Rening from loss of feedback. There is a decreased GFr from the dilation of the efferent arteriole. Prevents inactivation of bradykinin
what is the clinical use of ACE inhibitors
hypertesnion,HF< protenuria, diabetic neprhopathy, heart remodelling prevention. slows GBM thickening in the diabetic patient
what are the adverse effects of ACE inhibitors
cough ,angioedema, teratogen (detal renal malformation), increased creatinine from decreased GFR, hyperkalemia, hypotension,
why can’t you use Ace inhibitors with bilateral renal artery stenossi
used with caution in bilateral renal artery stenosis because ACE inhibitors with further decrease in GFr can lead to renal failure See rigns of renal stenosis if patient has TIA or coronary atheroscelosis, so decreased RPF and decreased GFR, and increased renin so constricted efferent arteriole to increase GFr, and this is blocked by the perils because they stop the feedback
angiotensin II receptor blockers end in what and MOA
losartan, candesartan, and valsartan. selectively block binding of ATII or AT1 receptors effects are similar to ace inhibitors but ARBs do not increase bradykinin
artans clinical use and adverse effects
- clinical use- hypertension, HF, proteinuria, diabetic neprhopathy with intolerance to ACE inhibitors from cough and angioedema.
- adverse effects0 hyperkalemia, and decreased GFR, hypotension, and teratogenic
aliskiren MOA
direct renin inhibitor, blocks conversion of angiotensinogen to antiotensin I
aliskiren clinical use and adverse effects
- clincial use- hypertension
- adverse effects- hyperkalemia, decreased GFR, hypotension, contraindicated in patients taking ACE inhibitors or arbs
leuprolide MOA
GnRH analog with agonist properties when used n pulsatile fashion antagonist hwhen used in continuous fashion to down regulate GnRH and decrease Lh and FSh
leuprolide clinical use
uterine fibroids, endometriosis, precocious puberty, prostate cancer, infertility. Pulsatile is for infertility the others are continuous use for suppression
what are the synthetic estrogens
ethinyl estradiol, DES, and mestranol
estrogens MOA
bind estrogen receptors
estrogens use
hypogonadism, ovarian failure, menstrual abnormalities, hormone replacement therapy in postmenopausal women, use in men with androgen-depent prostate cancer
estrogens adverse effects
increased risk of endometrial cancer, bleeding in postmenopausal women, and increased risk of clear cell if DES in utero, and increased risk of thrombi
what is estrogen contraindicated in
ER positive breast cancer and history of DVT
selective estrogen reecptor modulators- which ones
clomiphene, tamoxifen, raloxifene
clomiphen
antagonist at estrogen receptors in the hypothalamus. Prevents normal feedback inhibition increased release of LH and FSH from pituitary which stimulates ovulation. Used to treat infertility due to involution from PCOS. May cause hot flashes, ovarian enlargement, multiple simultaneous pregnancies, visual disturbances
tamoxifen
antagonist at breast, uterus; agonist at the bone and uterus. Increased risk of thromboembolic events and endometrial cancer. Used to treat and prevent recurrence of ER/PR positive breast cancer
raloxifene
antagonist breast, uterus, increased risk of thromboembolic events but not increased risk of endometrial cancer. It is used to treat osteoporosis as ell
what are the aromatase inhibitors
anastozole, letrozole, exemestane
anastozole, letrozole, exemestane- MOA
inhibit peripheral conversion of androgens to estrogen
anastozole, letrozole, exemestane- clinical use
Er+ breast cancer in postmenopausal women
HRT
used for relief or prevention of menopausal symptoms- hot flashes and vaginal atrophy and osteoporosis and it increases estrogen and decrease osteoclast activity.
what does estrogen do in the bone
it decreases osteoclast activity and increases osteoblast activity
what happens with unopposed estrogen replacement therapy
increased risk of endometrial cancer, so progesterone is added. Possible increased cardiovascular risk
what are the synthetic progestins
levonogestrel, medroxyprogesterone, etongestrel, norethindron, megrestrol, and RU486, and mifepristol
what are the MOA of progestins
bind the progesterone receptors to decrease growth, increased vascularization of the nedometrium and thickened cervical mucus
what is the clinical use of progestins
contraception (forms in crude pill, intrauterine device, implant, depot injection), and endometrial cancer, abnormal uterine bleeding
progestin challenge
prsence with withdrawal beleeding excluded anatomic defeats (ashram syndrome) and chronic anovulation without estrogen
what is the mOA of the mini pull and IUD
thickens the cervical mucus
what is the progestin shot or implant MOA
it decreases the GnRH and it decreases ovulation
what is the MOA of combined contraception
progestins and ethinyl estradiol in a pill, patch or ring. Estrogens and progestins inhibit the LH/FSH and prevent estrogen surge. if there is no LH surge then there is no ovulation
what does the progestin part of the OCP do
it is to thicken tehe cervical mucus and limit the access of sperm to the uterus.. Progestin also inhibit endometrial prolideration making the endometrium less suitable to implantation
what are the contraindications for OCPs
smokers>35 and increased risk of cardiovascular events, patients with increased risk of cardiovascular disease and including history of venous thromboembolism, CAD, and migraine, breast cancer
copper IUD MOA
produces local inflammatory reaction toxic to sperm and ova, preventing fertilization and implantation and is hormone free
copper IUD clinical use
long-acting reversible contraception most effective emergency contraception
copperIUD and adverse effects
heavier or longer menses, dysmenorrhea, and risk of PID with insertion so it is contraindicated in active pelvic infection
terbutaline, ritodrine
beta 2 agonists that relax the uterus and used to decreased contraction frequency in women in labor- called tocolytics
danazol MOA and use
synthetic androgen that acts as partial agonist at androgen receptors the use is endometriosis, and hereditary angioedema
what are the adverse effects of danazol
weight gain, edema, acnes, hirsutism, masculinization, decreased HDL, and hepatotoxic
testosterone and methyltestosterone- MOA
agonists at the androgen receptors
testosterone and methyltestosterone- clinical use
treat hypogonadism and promote the development of secondary sex characteristics and stimulater anabolism to promote recovery after burn or injury
testosterone and methyltestosterone- adverse effects
causes masculinization in females and decreased intratesticular testosterone in males by inhibiting release o LH (via negative feedback), and gonadal atrophy. Premature closure of the epiphyseal plates and increased Ldl and decreased HDL
anti androgens which are they
finasteride, flutamide, ketoconazole, spirolactone
finasteride
five alpha reductase inhibitor and it decreases the conversion of testosterone to DHT, and used for SPH and male-pattern baldness
flutamide
nonsteroidal competitive inhibitor at androgen receptors. Used for prostate cancer
ketoconazole
inhibits steroid synthesis at 17,20 desmolase
spirolactone
inhibits steroid binding and 17 alpha hydroxylase, and 17,20 desmolase
what are the uses of spirolactone and ketoconazole
used for PCOS to reduce androgenic symptoms. Both have side effects of gynecomastia and amenorrhea
tamsulosin
alpha 1 antagonist used to treat BPH by inhibiting smooth muscle contraction, selective for alpha AD receptors (fond o the prostate) and it is not hitting the alpha receptors as much
what are the phosphodiesterase type 5 inhibitors
sildenafil, vardenafil, tadalafil
what is the MOA of sildenafil, vardenafil, tadalafil
inhibit PDE-5 and increased CGMP and prolonged smooth muscle relaxation in response to NO and increases blood flow to the corpus vacernosum of the penis and decreases pulmonary vascular resistance.
what is the clinical use of sildenafil, vardenafilm tadalafil
erectile dysfunction, pulmonary HTN
what is tadafil especially used for
BPH
what is sildenafil, vardenafilm tadalafil adverse effects
headache, flushign, dypepsia, cyanopia blue tinted vision.
what is the associated risk with nitrates and sildenafil, vardenafilm tadalafil
nitrates increase the cGMP and enhance the inhibiton of PDE and this leads to no degraation of PDE and enhanced effects leading to unopposed dilation and hypotension
minoxidil
direct arteriolar vasodilatory and it treats androgenic alopeica and severe refractory hypertension
