echinocandins

have no activity against cryptococcus

caspofungin

micofungin

anidulafungin

which antifungal prevents ergosterol synthesis by inhibiting squalene epoxidase

what is the example

allylamines

terbinafine

which antifungal drug is very insoluble, and binds to keratin, making it ideal for growth/infections found in rapid skin growth areas hair, or nails

because it binds to keratin, this drug is good for what type of infections

but what drug(s) is/are more effective than this drug for these same infection locations

griseofulvin

dermatophytes

itraconazole and terbinafine are much more effective

amphotericin B

all azoles

caspofungin

micofungin

anidulafungin

amphotericin B

voriconazole

posaconazole

caspofungin

amphotericin B

itraconazole

ketoconazole

fluconazole

amphotericin B

itraconazole

ketoconazole

amphotericin B + flucytosine

intraconazole or fluocnazole

acyclovir

famciclovir

valacyclovir

ganciclovir

foscarnet

adefovir

cidofovir

lamivudine (inhibits DNA polymerase)

or

telbivudine (more potent than lamivudine; inhibits DNA polymerase)

or

adefovir, tenofovir, entecavir, ribavirin

slow progression of HIV

increase circulating CD4 T cells

decrease number of infections (prophy)

prolong survival of pts with HIV

used in pregnancy and delivery

reverse transcriptase inhibitors

protease inhibitors

fusion inhibitors

integrase inhibitors

entry inhibitors

nuceloside reverse transcriptase inhibitors

they competitively inhibit reverse transcriptase by inhibiting the incorporation of native nucleotides and by terminating the elongation of pro-viral DNA because they lack the 3'-hydroxyl group

zidovudine (AZT)

stavudine (D4T)

didanosine (DDI)

lamivudine (3TC)

emtricitabine (FTC)

abacavir (ABC)

tenofovir

tenofovir

(popular in ART combo)

non-nucleoside reverse transcriptase inhibitors (NNRTIs)

they are also eliminated by the liver (CYP3A4)

nevirapine (NVP)

delavirdine (DLV)

efavirenz (EFV)

list the protease inhibitors

which one is recommended to "boost" the activity of another PI

saquinavir

ritonavir - mostly used to decrease the metabolism of other PI drugs, because it is a potent CYP3A4 inhibitor

atazanavir

darunavir

enfuvirtide

maraviron

which group of anti-retrovirals blocks the integration of viral DNA into cellular DNA, and is typically effectivde against both HIV 1 and 2

what is the main one in this group

integrase inhibitors (they bind to the integrase enzyme)

raltegravir

no tolerance, physical or psychological dependence

individual variability in response

inhibition of cyclooxygenase (COX1 and 2)

(need to give the max recommened dose for atleast one to two weeks and then if they are still complaining of pain, you can stop that NSAID and try another)

what are the two major disadvatages to giving a large dose of NSAIDS

and what are the advantages of giving an NSAID with an opioid

a larger dose of NSAIDS: doestn' give them any further relief, and they are at a greater risk of toxicity

combining the two: delays the response of the opioid, and not having to give as large a dose of the opioid, and they have different MOAs, therefore, not adding to one another's side effects

what is the MOA of NSAIDS

and tNSAIDS specifically

they block the cyclooxygenase enzyme, inhibiting the production of prostaglandins, forcing all of the arachodonic acid to go down the leukotrienes pathways

tNSAIDS 

COX1 is constitutive everywhere

COX2 is constitutive in the kidneys, but inducible in other locations via pain, fever, and inflammation

analgesia - the prevention of prostaglandin production decreases the amount of nociception sensitization

anti-inflammatory - prostaglandins are mediators of inflammation because they cause erythema and edema and pain

anti-platelet - PGI2 predominates after ASA administration compared to TXA2 and TXA2 is a potent vasoconstrictor and platelet aggregator, while PGI2 is a potent vasodilator and platelet DEaggregator

primary dysmenorrhea - normally there is an increase in endometrial synthesis of PGE2 and PGF2 during menstruation causing the pain, cramps and HA

ductus arteriosus - PGs keep it opening while in the womb, but if it needs to be closed after birth, need to inhibit production of the PGs

GI complications

cardiovascular complications

platelet function disturbances

allergic rxns

prolongation of gestation or delay in spontaneous labor, increases postpartum bleeding

hepatic issues

hematologic issues (very rare)

NSAIDs inhibit PGI2 and PGE2 which causes an increase in acid secretion, a decrease in mucus prodcution (the main protective mechanism of the stomach against the acidity) and bicarb

the increased risk of bleeding is also caused by the antiplatelet effect of the drug

>60 years

high dose of NSAIDs

previous Hx

concurrent use of glucocorticoids

anticoags and antiplatelets

choice of NSAID

increased levels of PGs in the kidneys cause an increase in renal blood flow (because of their vasodilative effect) which increases the GFR, causing an increase in the excretion of water and Na out of the kidney - aka increase diuresis and natriuresis

highest risk: ASA - causes an increased bleeding time for several days

lower risk: non-acetylated salicylates (sodium, salicyl, methyl, and choline salicylates), acetaminophen

list the nonacetylated salicylates

Diflunisal

Salicylsalicylate

Methylsalicylate

Sodium salicylate

Magnesium choline salicylate

propionic acids (ex - ibuprofen)

oxicams

acetic acid derivatives (ex - ketorolac)

naproxen (longest half life)

ibuprofen

ketoproen

all three are nonsalicylate NSAIDs (under the nonselective COX inhibitors)

indomethacin (Indocin)

a nonsalicylate acetic acid derivative (a type of nonselective COX NSAID

selective COX2 inhibitor (celecoxib - Celebrex) does NOT have anti-platelet effects (and can be prescribed to pts on anticoag therapy)

also: pts allergic to ASA/NSAIDs may also show allergy to this drug, and it is NOT recommended for use in children, want to use minimal effective dose for the shortest possible time

at high enough doses, you can still inhibit COX1, hence adverse GI symptoms (diarrhea, nausea, dyspepsia, ABD pain, lower extremity edema (most common)

renal toxicity (similar to non selective NSAIDs)

prothrombosis - coxib increases the levels of TXA2 (posten vasoconstrictor and platelet aggregator) while decreasing the levels of PGI2 (potent vasodilator and platelet deaggregator)

sulfa allergic rxn

tNSAIDs decrease the therapeutic efficacy of all anti-HTN drugs except CCB (because most anti-HTN drugs go through the pathway of PGs to work)

NSAIDs may increases the toxicity of lithium and methotrexate

celecoxib is contraindicated in pts allergice to sulfa drugs

abatacept

anakinra

these drugs are administered intermittently by injection and appear to benefit many pts with RA, but all carry the risk of increased infections

gold salts

glucocorticoids

leflunomide

hydroxychloroquine

sulfasalazine

penicillamine

uricosuric drugs (probenacid, and sulfinpyraszone)

allopurinol

reduce/alter the course of RA

retard the progress of arthritic tissue destruction

common to combine with a tNSAID

the biological DMARDs:

adalimubab

infliximab

etanercept

TNF antagonists:

infliximab

etanercept

adalimimab

obesity

weight gain

alcohol intake

high blood pressure

abnormal kidney function

certain drugs

antiinflammatory therapy - prompt, attempt to reverse the symptoms of an acute attack

antiinflammatory prophy - reverse/minimize the recurrence of the gout

antihyperuricemic therapy - prevent and reverse the consequences of the deposition of the uric crystals in the joints, kidneys, and tissues

tNSAIDs (naproxen, ibuprofen, indomethacin)

colchicine

corticosteroid (intraarticularly or parenterally)

pain and inflammation improve significantly within 24-36 hours

GI disturbance becomes intolerable - go to a corticosteroid

total dose teached 6 - 8 mg

when gout pts have frequent acute attacks (>3/year)

t has an attack during initial months of antihyperuricemic theray

before and after elective surgery

colchicine

then tNSAIDs

uricosurics

xanthine oxidase inhibitors

probenecid

sulfinpyrazone

they increase urate excretion

allopurinol

febuxostate

acute attack of gout during the initial days of tx; to minimize:

start antiinflamm prophy drug (colchicine) at same time

after an acute attack, delay the start in the antihyperuricemic

start with a lower therapeutic dose and gradually increase to max dose over weeks to moths

urate stone formation in the kidneys; to prevent:

excessive fluid intake (2-4 L/day)

sulfinpyrazone

can be used to probenecid to have an additive effect

xanthine oxidase inhibitors

allopurinol

febuxostat

azathioprine

ampicillin

cyclophosphamide (will induce bone marrow suppression)

pain impulses are sent by primary afferent neurons to the spinal cord where ascending connections from the what project to the limbic structures and the cortex

(aka - what spinal tract is involved in sending pain info to the brain)

which opioid agonists (the "strong) act on the mu receptor

which ones are used in the treatment of severe or moderate pain

and which one is normally used in the treatment of opioid addiction

morphine, fentanyl, meperidine, and methadone

to treat severe to moderate pain: morphine, fentanyl, mepereidine

to treat addiction: methadone

why are the "moderate" opioid agonists typically combined with a nonopioid analgesic

list these opioids

because the moderate opioid agonists produce maximally analgesia at doses that cannot be tolerated

codeine, hydrocodone, propoxyphene (they are used to treat moderate or mild pain)

the mixed opioid agonist-antagonists: buprenorhine, butorphanol, nalbuphine, pentazocine

they produce less respiratory depression and are associated with a lower risk of drug dependence than full opioid agonists

presynaptically, activation of mu receptors blocks the opening or closing of voltage sensitive Ca channels;

postsynaptically, mu receptor activation enhances or inhibits the opening of K+ channels

activation of mu receptors presynaptically blocks the opening of voltage sensitive Ca channels

mu receptor activation postsynaptically enhances the opening of K+ channels

other meds (sedatives), alcohol,

sleep (normally respirations decrease during sleep)

age (newborns and elderly are more sensitive to resp depression)

diseases (COPD, renal disease)

signs and symptoms that are opposite to the acute opioid effects:

ABD cramps, muscle aches, insomnia, hyperventilation, sweating, chills, fever, anorexia, muscle and join tpain, diarrhea, tachycardia

increase BP and hyperexcitability

clonidine: autonomic symptoms

muscle relaxants: spasms and twitching

NSAIDs: aches

antiemetics: N/V

antidiarrheal bismuth subsalicylate: diarrhea

trazodone: insomnia

methadone HCL

(levomethadyl acetate - an analog of methadone, is also used for heroin detox, but has an even longer halflife than methadone)

anticonvulsants (valproate)

antidepressants(amitriptyline)

NSAIDs (naproxen)

beta antagonists (propanolol)

CCBs (verapamil)

5HT receptor antagonists (methysergide)

what are some groups of drugs used for aborting migraines

and generally, how do these work

ergot alkaloids (ergotamine)

triptan drugs (sumatriptan)

these drugs stimulate 5HT receptors, this stimulation causes cerebral vasoconstriction, inhibits the release of peptides and other mediators of inflammation and vasodilation from trigeminal neurons, and inhibits activation of trigeminal nucleus in brain stem

other drugs include:

NSAIDs, opioid analgesics and isometheptene (sympathomimemtic)

what are some common side effects of ergots

what are some common sid effects of triptans

ergots: N/V, and muscle cramps

triptans: chest tightness and drowsiness

which drugs are effective against preventing cluster headaches

and which drugs are effective against aborting them

prevention:

lithium

methysergide

verapamil

aborting:

ergot alkaloids

sumatriptan

inhaled O2

intranasal lidocaine

glucocorticoids

nonselective COX inhibitors include:

and which one doesn't cause gastric irritation and bleeding and it's use doesn't cause peptic ulcer

acetaminophen, ASA, ibuprofen, indomethacin, ketoprofen, ketorolac, and naproxen

except for acetaminophen, all of these agents can cause gastric irritation and bleeding and their long term use can lead to peptic ulcers

which drug causes tinnitus at high therapeutic doses, and hyperventilation and respiratory alkalosis, followed my metabolic acidosis at toxic doses

what drug then counteracts the acidosis, increasing urinary excretion of salicylic acid

ASA

sodium bicarb

drug tolerance

withdrawal syndrome

the treatment of drug dependence and withdrawal can include some type of substitution therapy, such as:

(for alcohol, opioids, and cigarettes)

a benzodiazepine substituted for alcohol

methadone for an opioid

and nicotine chewing gum or skin patches for cigarettes

alcohol and opioid dependent pts can be treated with naltrexone (opioid antagonist that blocks opioid receptor link in dopamine reinforcement pathway) transdermal patches as well