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ALL TEST 2 DRUGS

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amitriptyline
TCA
imipramine
archetypical TCA
MOA: blocks reuptake of NE and 5HT
tertiary amines - 5HT selective; secondary - NE selective

2-3 weeks to work b/c autoreceptors must downregulate

S/E (1 ergic per ring)
0. Q-like: heart blocks
1. anticholinergic: tachycardia, blurred vision, dry mouth, constipation
2. antihistaminergic: sedation and weight gain
3. antiadrenergic: orthostatic hypotension, dizziness, and drowsiness
4. may ppt a manic phase in bipolar patients
5. acute O/D = very dangerous = resp despression, delerium, hypertension, cardiac arrest!
DESIPRAMINE
TCA
nortriptyline
TCA
tranylcypromine
MAO-A inhibitor (antidepressant)

selective for MAO A, so it inhibits the degredation of all 3 monoamines

S/E:
1. MAOI + TCA = hypertensive crisis
2. MAOI + tyramine = hypertensive crisis
3. MAOI in slow acetylator = hepatotoxiicty
4. cardiovascular side effects
5. acute OD toxicity - agitation, delerium, mania -> sz, hyperthermia. give activated charcoal

selegiline - mao b inhibitor for pd
fluoxetine
SSRI

the first one.
fewer anticholinergic and cardiovascular S/E than TCA

S/E:
1. nausea, diarrhea, constipation
2. insomnia, nervousness
3. sexual dysfunction!!!!
4. MAOI + SSRI => serotonin syndrome =
hyperthermia and muscle rigidity with wild swings in vitals and mental status,
paroxetine
SSRI
CITALOPRAM
SSRI
escitalopram
SSRI

S enantiomer of citalopram, more potent, take less and begins working in 1-2 weeks
SERTRALINE
SSRI
CHLORPROMAZINE
the archetypal first generation antipsychotic

blocks all 4 dopaminergic pathways: mesolimbic, mesocortical, tuberoinfundibular, and nigrostriatal

treats only the positive symptoms

S/E:

D2 dopaminergic
mesocortical: even more negative symptoms
nigrostriatal: extrapyramidal side effects (pseudoparkinsonism, tardive dyskinesia, muscle spasms, motor restlessness)
3. tuberoinfundibular - hyperprolactinemia

antihistaminergic: sedation and weight gain
cholinergic: urinary retention, dry mouth, constipation, blurred vision, impaired cognition/memory
adrenergic - orthostatic hypertension, reflex tachycardia, sexual dysfunction
serotonin - orthostatic hypotension, sedation, and weight gain

Neuroleptic Malignant Syndrome
rigidity and hyperthermia with altered mental status
treat with bromocriptine (DA agonist to reverse neuroleptic action) or dantrolene (RyR blocker)

btw, chlorpromazine also tests pituitary function (prolactin should increase with a dose)
haloperidol
first gen antipsychotic
clozapine
archetypal second gen antipsychotic

fewer S/E than first gen b/c
only mesolimbic is blocked

improve the negative symptoms (cognition, etc) as well as positive symptoms
AGRANULOCYTOSIS is a side effect!
aripiprazole
second gen antipsychotic
cortisone
not quite as potent as cortisol but doesnt agonize mineralocorticoid receptor
hydrocortisone
=cortisol (naturally occuring) short acting
least potent

effects:
1. liver - increases glycogenolysis and gluconeogenesis
2. skel muscle - increases muscle catabolism to make precursors for gluconeogenesis
3. lymphocytes - decreases their proliferation and also blocks the phospholipase A step decreasing PG and LT production
4. skin atrophy and catabolism
5. adipocytes - lipolysis, redistribution to central adiposity
6. brain - CNS arousal - run from that bear!!
8. heart - increased blood pressure

uses:
1. addison's syndrome
2. 11 beta hydroxylase deficiency
given 2/3 in morning and 1/3 at night

has an effect on mineralocorticoid receptor

S/E
1. immune system suppression
2. cushing like body habitus
3. osteporosis (decreases osteoblast activity)
4. peptic ulcers (decreases PG secretion and therefore mucus production)
5. growth suppression in kids
6. motherfucking cataracts
7. behavior problems
don't withdraw cold turkey - iatrogenic adrenocortical insufficiency

also during surgery, either give a ton or wean them off of them.
surgery should trigger a huge cortisol release from pain response. if they can't make enough cortisol, they may become hypotesnive and die!
hydrocortisone sodium phosphate
water soluble glucocorticoid for IV use
prednisone
5x more potent than cortisol
PREDNISOLONE
active form of prednisone
give to people with liver problems who cant metabolize prednisone to its active form (ex alcoholic with chronic liver dz_
triamcinolone hexacetonide
long acting glucocorticoid b/c it has fluorine and an acetonide group

can be used topically or interarticularly b/c it is not freely diffusable
fludrocortisone acetate
mineralocorticoid

1.mineralocorticoid deficiency
2. part of treatment for addison's
AMINOGLUTETHIMIDE
inhibits aromatase and many enzymes in glucocorticoid synth

uses:
1. cushing's syndrome (reduces glucocorticoid prodn!!)
2. breast cancer (no longer used)

chad uses it in his steroid cycles

bad se/e?
BETAMETHASONE
40x more potent than cortisol

can give lower dose and have no effect on mineralocorticoid
solumedrol
water soluble glucocorticoid for IV use
hydrocortisone sodium succinate
water soluble glucocorticoid for IV use
methylprednisolone sodium succinate
water soluble glucocorticoid for IV use
stanozolol
anabolic steroid - inhibits catabolic actions of glucocorticoids

1. burn pt
2. short stature
3. anemia

s/e:cardiotoxic, hepatotoxic, cause rage, androgenize women

work as antiandrogens, feeding back on pituitary and blocking production of gonadotropins and eventually testosterone

cause impotence and decrease secondary sex char

if you take synthetic androgens with them, that's when you get boobies because they are converted to estrogen by aromatase
danazol
steroid which feeds indirectly decreases estrogen production.

it feeds back on the pituitary to decrease FSH and LH production, eventually decreasing estrogen production

use: endometriosis

Dana dreadlock has endometriosis.
ETHINYL ESTRADIOL
modified estrogen which can be given orally...

1. used with norethindrone in the combination pill

2. Aberrant growth. suppresses somatomedins. give progestin too to prevent bleeding

3. Delay of puberty (check to see if there is a gonadotropin deficiency first before using steroids as steroids can prematurely close
epiphyseal plate)

3. Precocious puberty
due to a tumor - use depot progestin (MPA)
to suppress gonadotropin release

4. postmenopausal osteoporosis. give prog to reduce endometrail cancer risk

5. postmenopausal sx such as hot flashes. give progestin too

6. use in huge doses to treat cancer. down reg receptor?

s/e:
1. breast cancer
2. cholestasis
3. feminization, gynecomastia
4. gall stones
5. breast tenderness
medroxyprogesterone
=provera. methyl group added to progesterone increases its activity! acetate increases its t1/2

1. depoprovera for contraception
2. also precocious puberty
NORETHINDRONE
synthetic progestin modified to decrease its metabolism

used alone in minipill and in combination pill and probably in norplant?

similar to levonorgestrel
PROGESTERONE
used in combination with estrogens in contraception

only active in presence of estrogen and primed estroen system

the estrogen system turns on the progestin receptor

2 receptors, PRA and PRB. PRA is antagonist of the other

1. growth delay (if sufficient gonadotropins)
2. precocious puberty
3. excessive growth - large dose of estrogen + progesterone to prevent breakthrough bleeding)
4. dysfunctional uterine bleeding - prog supports endometrium
5. with hirsuitism therapy, use oral contraceptives for normal hormone function
TESTOSTERONE
USE:
1. hypognadism
2. anemia (before epo)
3. anabolic agent (abused)
4. osteoporosis

s/e:
1. edema/ fluid retention
2. increases plasma cholesterol and lowers HDL
3. liver disorders - cholestasis
4. sleep apnea
5. psychol disturb

converted to 5DHT by 5alphaR to have effect in the genitalia and hair follicles

methyltestosterone - orally active but hepatotoxic. also cardiotoxic.
CLOMIPHENE
weak estrogen agonist / antiestrogen

opposes estrogen's inhibition on LH and FSH release.

causes LH and FHS release.

for some reason, LH builds up and is released when you stop giving them clomiphene.

?(mulitiple ova because estrogen receptor is blocked)
flutamide
Flutamide is an oral nonsteroidal antiandrogen used as an antihormonal agent in the treatment of metastatic prostatic carcinoma.


used with gonadotropin agonists (chronic=decrease Gn effect) (Leuprolide) for
1. prostate cancer
2. hirsuitism
3. baldness
(situations of too much androgens)

Mark tidwell plays the skin flute. he is bald and hairy
finasteride
5 alpha reductase inhibitor
1. prevention of prostate cancer
2. also for hair growth
RALOXIFENE
SERM - its large side chain group prevents binding of certain helper proteins in the transcription apparatus

1. agonist in bone
2. antagonist in uterus

use: prevention and treatment of osteoporosis!
high aff for ERalpha and beta
TAMOXIFEN
SERM - anti-estrogen used to prevent and treat breast cancer (estrogen receptor + tumors)

1. anagonist - breast
2. agonist - bone, liver, endometrium (this doesnt matter as much)

mild therapy, effective, doesnt make pt sick

receptor antagonist (antiestrogen) in breast *money*
mifepristone
RU486 - antiprogestin

competitive inhibitor of the progesterone receptor

blocks progesterin support of the endometrium and sensitizes it to prostaglandins.

taken orally with vaginal suppository of progstaglandin E1.

terminates preg in 1st 7 weeks
lorazepam
benzodiazepine

lorazepam can be given IM, but can cause tissue necrosis.
oxazepam
benzodiazepine (very short acting)

good for etoh w/d. use instead of chlordiazepoxide if liver injury is present.
CHLORDIAZEPOXIDE
benzodiazepine
gold standard for for etoh w/d.

if pt has liver failure, use lorazepam or oxazepam
disulfiram
blocks acetaldehyde DH

used to prevent alcoholics from drinking
naltrexone
opioid receptor antagonist (oral)

used to treat opiate intoxication

also used to reduce relapsing and craving in opiate and etoh addiction recovery
NALOXONE
opioid receptor antagonist (IV - not active oral)

USES:
1. opiate intoxication (OD)
2. rehab (opiate and etoh) - reduces relapsing and craving
3. in buperorphine pills to keep addicts from injecting them to get high
chloral hydrate
barbituate like drug
zolpidem
ambien. it's abusable

catch some zzz's motherfucker
gammahydroxybutyrate
good anesthetic, no analgesic properties

1. binds GABA-B receptors and inhibits norepi release
2. inhibit dopamine release at low doses but increase dopamine release at high dose

profound CNS depression with short term amnesia

coma

withdrawal is similar to alcohol but can last 2 wks
unless you put them to sleep they will become psychotic
buprenorphine
opiate partial agonist

can be used to treat opiate withdrawal
opiates
affect mu receptors

suppress cough
slow down the GI tract
decrease urinary flow
respiratory depression
decreases HR and BP
analgesic
METHADONE
opiate agonist (loong acting - long half life)

use:
1. pain
2. opioid withdrawal / rehab

for pain:
long acting
dose q6h
adjust every 6-7 days

excellent for NEUROPATHIC pain
ACETAZOLAMIDE
CA inhibitor

azul - blue sky mountain sickness

Uses:
1. urine alkalinization
a. to increase clearance of acidic drugs
b. to increase solubility of uric acid stones
2. prophylaxis for high altitude pulmonary edema
3. glaucoma (not used anymore)

S/E:
1. hyperchloremic metabolic acidosis
2. calcium phosphate stones
3. K wasting
4. NH3 intoxication (esp in liver failure pt)
FUROSEMIDE
loop diuretic - blocks the Na/K/2Cl transporter in the TAL

Uses:
1. acute volume overload (e.g. pulm edema)
2. hypercalcemia (give saline too because these pts have nephrogenic diabetes insipidus and are not responding to their ADH and are volume contracted)

S/E:
1. K wasting with acidosis
2. ototoxicity (you forget this)
3. hypercalciuria and calcium oxalate stones
HYDROCHLOROTHIAZIDE
works in DCT - blocks Na/Cl transporter

Uses:
1. HTN - hypertension, esp. in pts with poor kidney function
2. CHF - congestive heart failure. they are volume overloaded
3. hypercalciuria and calcium oxalate stones (will increase reabs of calcium. subseq dec in PTH and eventually dec in vitamin D will keep blood Ca from rising). limit salt intake b/c it will blunt effects of thiazide

S/E:
1. K wasting and metabolic alkalosis
2. increase blood lipids, uric acid, and glucose levels

*may work in PCT, too, if used in combination with loop diuretics to unmask PCT action
hydrochlorothiazide + triamterene
thiazide + K sparing diuretic (ENac blocker)

=diazide
mismatch because triamterene is short acting

hydrochlorothiazide + amiloride is a better drug b/c both are long acting
amiloride
ENac blocker (K sparing diuretic)

Uses:
1. Primary and Secondary aldosteronism
primary: conn's syndrome
secondary: liver failure, kidney failure, heart failure

S/E
1. hyperkalemia
2. metabolic acidosis

4. acute kidney injury and kidney stones (rare s/e)
TRIAMTERENE
ENac blocker
(K sparing diuretic)

Uses:
1. Primary and Secondary aldosteronism
primary: conn's syndrome
secondary: liver failure, kidney failure, heart failure

S/E
1. hyperkalemia
2. metabolic acidosis

4. acute kidney injury and kidney stones (rare s/e)
aldoctone
mineralocorticoid blocker(K sparing diuretic)

1. Primary and Secondary aldosteronism
primary: conn's syndrome
secondary: liver failure, kidney failure, heart failure

S/E
1. hyperkalemia
2. metabolic acidosis
3. gynecomastia and BPH with aldoctone and alclarinone
4. acute kidney injury and kidney stones (rare s/e)
alclarinone
mineralocorticoid blocker(K sparing diuretic)

Uses:
1. Primary and Secondary aldosteronism
primary: conn's syndrome
secondary: liver failure, kidney failure, heart failure

S/E
1. hyperkalemia
2. metabolic acidosis
3. gynecomastia and BPH with aldoctone and alclarinone
4. acute kidney injury and kidney stones (rare s/e)
SPIRONOLACTONE
mineralocorticoid blocker(K sparing diuretic)

1. Primary and Secondary aldosteronism
primary: conn's syndrome
secondary: liver failure, kidney failure, heart failure

S/E
1. hyperkalemia
2. metabolic acidosis
3. gynecomastia and BPH with aldoctone and alclarinone
4. acute kidney injury and kidney stones (rare s/e)
CHLORTHALIDONE
thiazide diuretic

works in DCT - blocks Na/Cl transporter

Uses:
1. HTN - hypertension, esp. in pts with poor kidney function
2. CHF - congestive heart failure. they are volume overloaded
3. hypercalciuria and calcium oxalate stones (will increase reabs of calcium. subseq dec in PTH and eventually dec in vitamin D will keep blood Ca from rising). limit salt intake b/c it will blunt effects of thiazide

S/E:
1. K wasting and metabolic alkalosis
2. increase blood lipids, uric acid, and glucose levels

*may work in PCT, too, if used in combination with loop diuretics to unmask PCT action
hydrochlorothiazide + amiloride
hydrochlorothiazide + amiloride

thiazide + K sparing
both are long acting
MANNITOL
osmotic diuretic

1. intracellular volume expansion (cerebral edema)
2. intratubular blockage ( rhabdomyolysis, transfusion reaction -> cast nephropathy)

S/E:
1. hypernatremia
2. volume depletion
3. acute kidney injury due (toxic!)
4. if the kidneys arent working this drug will make things worse!
TOLVAPAN
V2 (ADH receptor) antagonist

tolVapan V V V V V V

use:
1. SIADH (can occur in chronic bronchitis, pulmonary tuberculosis, or lung tumors)
2. heart failure - heart not pumping so body thinks it is volume depleted so ADH is too high

S/E
1. hypernatremia

tolvapan. don't get mixed up with tolcapone (which is a comt inhibitor)
diazepam
benzodiazepine

diazepam can be given IV or rectally (di). according to dr boyce, it is an older agent, not soluble in water and can cause phlebitis

uses:
1. anticonvulsant
2. insomnia
3. anxiety
4. sedation and amnesia for procedures
5. etoh withdrawal and other sedative withdrawal
6. muscle spasm (these are from the brain not modulating the reflex arc)

s/e of bzd
not fatal - therapeutic index of 1000
1. respiratory depression
2. CVS depression

notes:
cross tolerance to ethanol.

synergistic effects with alcohol, opiates, anti-histamines
midazolam
benzodiazepine

can be given IM (Midazolam Muscle)
phenytoin
anticonvulsant (Na blocker)
partial, generalized, and status epilepticus

must monitor serum drug levels!

Notes
1. P450 inducer -> 0 order kinetics, saturates it. additional drug will cause huge increase in conc. -> drug interactions e.g. halothane hepatotoxicity
2. precipitates in D5W, only give with normal saline!
3. can cause tissue necrosis when given peripherally!! (lose a limb! if poor circulation!!) dont give in peripheral IV if at all possible

S/E
1. ataxia, nystagmus, and diplopia
2. Skin exfoliation
3. Stevens-Johnson's syndrome - autoimmune rash, skins sloughs off -> infection. stop taking phenytoin and call your dr. if you get a rash!!!
4. Hirsuitism, Gingival Hyperplasia, Folate depletion
phosphenytoin
anticonvulsant (Na channel blocker)

salt form is better tolerated in the veins with less tissue necrosis
CARBAMEPAZINE
anticonvulsant (Na blocker)

used for partial and generalized seizures

Notes:
1. autoinducer of hepatic enzymes, so must increase dose

S/E
1. diplopia and ataxia
2. leukopenia
3 . bone marrow suppression (rare)
lamotrigine
anticonvulsant (Na blocker)

partial seizures

S/E
rash (lamers have a wash)
somnolence (lamers sleep)

lamer = sleepy person with a rash
topiramate
anticonvulsant (Na blocker and enhances GABA - both classes - unique!)

used for partial and generalized
* used to treat Lenox-Gastaut syndrome (the head banging seizure kids)

mnemonic - so they will stop hitting the top of their heads!!
S/E
slowed speech
kidney stones
paresthesias
glaucoma
ethosuximide
anticonvulsant (Ca blocker)

good for absence sz
S/E
dose dep gastric distress
hyperactivity, dizziness, headache
vigabatrin
anticonvulsant
enhances inhibition by GABA
gabapentin
anticonvulsant
enhances inhibition by GABA
tiagabine
anticonvulsant
enhances inhibition by GABA
ethanol
enhances GABA in VTA
inhibits Glu in VTA
has effects on serotonin and opiate receptors too

CNS depression
phenobarbital
barbituate (increases length of GABA Cl ionophore opening)

good for generalized seizures

prodrug is Primidone

S/E
sedation, depression, hyperactivity, cognitive problems
primidone
prodrug of phenobarbital
barbituate
oxacarbazepine
anticonvulsant (Na blocker)
used for partial and generalized like carbamepazine

1. hyponatremia
VALPROATE ACID
anticonvulsant (Na and Ca blocker)
generalized (common!) and partial

S/E: (Mrs. Val)
1. lethargy
2. tremor
3. alopecia
4. liver failure
5. weight gain
levetiractem
partial sz - unknown MOA
zonisamide
reduces Ca channels
partial sz
trazadone
atypical antidepressant
1. blocks 5HT reuptake
2. blocks postsynatpic 5HT2 receptors (thus increasing 5HT1 activity)
BUPROPION
atypical antidepressant
blocks DA and NE reuptake

used for smoking sessation
lowers seizure threshold - dont give to anorexics or bulemics
venlafaxine
atypical antidepressant
inhibits 5HT and NE reuptake (like TCA...)

causes nausea via 5HT3
receptor
i guess you can throw up while you're fucking
sexual s/e go away
mirtazapine
1. blocks alpha2 autoreceptors
2. blocks postsynaptic 5HT2 receptors

a mirthful blocker
no significant sexual dysfunction
duloxetine
selective 5HT and NE reuptake inhibitor (like a TCA du=2)
lithium carbonate
treats bipolar affective disorder

inhibits phosphatase, blocking regeneration of inositol

S/E - narrow therapeutic index
1. nausea, vomiting, diarrhea, weakness, tremor, polydipsea
2. nephrogenic diabetes insipidus, hypothyroidism, arrhythmia

b/c lithium decreases effect of ADH, it can be used to treat SIADH
olanzepine + fluoxetine
second gen antipsychotic + SSRI

treats bipolar affective disorder
AMANTANDINE
antiviral agent, yet blocks Glutamate Receptors

treats Parkinson's disease
treats dyskinesia caused by levodopa

treats extrapyramidal side effects of first gen antipsychotics (pseudoparkinsonism and tardive dyskinesia)
BENZTROPINE
anticholinergic (a PD drug)

1. treats Parkinson's disease
good for young patients, not for elderly (thinking chemical->dementia)

2. treats extrapyramidal side effects of first gen antipsychotics (pseudoparkinsonism and tardive dyskinesia)
BROMOCRIPTINE
dopamine agonist (ergot alkaloid)

1. Parkinson's Disease
2. acromegaly / gigantism (reduces GH secretion)
3. hyperprolactinemia ass'd with partuition, abortion, and prolactinomas. (decreases prolactin secretion)
4. treat neuroleptic malignant syndrome (caused by first gen antipsychotics)

s/e:fibrosis
s/e: sedation, hallucinations, compulsive behavior (gambling)
dantrolene
ryanodine receptor blocker (a muscle relaxant)

used to treat neuroleptic malignant syndrome
NMS
hyperthermia and rigidity with altered level of consciousness

think carlos dansby = muscle
HYDROMORPHONE
opiate - 3rd tier
CODEINE
antitussive
opiate - second tier - often with acetaminophen
fentanyl
opiate - 3rd tier

fentanyl patch
dont reach Cmax for 24 hours, give them something in the meantime
doesnt go away when patch is off

lasts 24-72 hours
less in skinny pt (fat abs)
less in febrile sweaty pt
meperidine
synthetic opiate. not recommended.

pain reliever.
has its place: normal kidney and liver function and a clear source of pain such as trauma

highly emitogenic (give phenergan with it)

*SEIZURE!! - toxic metabolite normeperidine might build up in patient with renal failure and cause seizure.

contraindication: renal failure or liver failure
oxycodone
opiate - 2nd tier, longer acting oxycodone (like oxycontin) are 3rd tier

OPIATES
conjugated in liver and excreted by kidney

S/E
CONSTIPATION (give a laxative!) - only S/E that wont go away w/o help
nausea/vomitting (use dopamine blocking antiemtics)
urinatry retention
sedation
dry mouth
Resp. Depression is uncommon.
pentazocine
NOT recomended.
mixed agonist. compete with agonists.
ceiling effect
not used much for pain management, but used with anesthesia to reverse opioid effects
PROPOXYPHENE
NOT RECOMENDED opiod
not any better than placebo

3 P's for placebo. the placebo fiend.

toxic metabolite at high doses
dextromethorphan
opiate. antitussive. in cough syrup
immediate acting opiates

Codeine, Hydrocodone, Morphine, Hydromorphone, Oxycodone (plain)
last 3-5 hours given PO or PR
(much shorter when given by IV bolus)
reach max concentration in:
Cmax : 6 / 30 / 60
IV/ SC / PO

give q4h and dose find
mod pain inc 25-50% each day
severe pain inc 50-100% each day
extended release opiates
improve compliance, convenience, no bolus effect (roller coaster), less potential for abuse

if patient goes into renal failure, decrease dosage, switch from routine dosing to prn, change to short acting, and hydrate patient. for the love of god, dont use methadone.

dose tid, bid, or qd

adjust dose every 2-4 days

give 10% as breakthrough dose
selegiline
MAO-B inhibitor

parkinson's drug
may be neuroprotective too if it keeps chemicals like MPTP from being activated

dont eat wine or cheese!
tolcapone
COMT inhibitor

bust a cap in comt!!!!!
it takes a toll on your liver!! black box

decreases LDOPA degredation in the periphery

s/e of LIVER FAILURE! black box warning. must have liver function tests periodically
encaptone
COMT inhibitor
decreases LDOPA degredation in the periphery

safe drug
LEVODOPA
L-DOPA
parkinson's drug
relieves sx but may contribute to progression of the disease. usually reserved for people no longer responsive to dopamine agonists or anticholinergics
carbidopa
Decarboxylase inhibitor
given in sinemit
LDOPA is not converted to dopamine in the periphery by the decarboxylase where it causes nausea
pergolide
dopamine agonist (ergo alkaloid)

use for parkinson's disease


nonselective
s/e: fibrosis
s/e: sedation, hallucinations, compulsive behavior (g
pramipexole
D2 selective agonist (not ergot)

Parkinson's disease drug

good for young patients to delay having to use levodopa
may be neuroprotective

s/e: sedation, hallucinations, compulsive behavior (gambling)

pex = good for young ppl with parkinsons - would have been good for Michael J
ropinrole
D2 selective agonist (not ergot)

Parkinson's disease drug

good for young patients to delay having to use levodopa
may be neuroprotective

s/e: sedation, hallucinations, compulsive behavior (gambling)
BENZOCAINE
commonly used topical anesthetic because it diffuses across membranes easily

benzocaine and procaine are both esters

s/e: methemoglobinemia
bupivicaine
local anesthetic

highly protein bound, so long duration of action
COCAINE
blocks reuptake of catecholamines (potentiates)

amide and ester linkage
used as a local anesthetic long ago (Na channels)
lidocaine
most common local anesthetic

local anesthetic MOA:
1. unprotonated neutral form diffuses into membrane and shifts the Na (and K) channels into unresponsive conformations
2. unprotonated form diffuses through membrane, is protonated, and then goes into the pore, binds to specific domain and blocks the pore

O/D: into central
1. twitching
2. seizure
3. metallic taste
4. tinitis

5. hypotension
6. arrhythmia
EMLA CREAM
Eutectic Mixture of Local Anesthetics (EMLA cream)

mix lidocaine and prilocaine, lowering their melting point and put it in an oily substance. can diffuse across skin and membranes easily. great to use to start IV's in children and superficial laser procedures
PROCAINE
ester anesthetic (most are amides)

used in dentistry (novocaine)
chirocaine
S enantiomer of bupivicaine.

hint: S is SAFE

less cardiotoxic with longer duration than the racemic mixture
local anesthetic toxicity
CNS excitation -> cardiovascular depression

tinnitis, metallic taste, quivering, lethargy, SEIZURE

arrhythmia, hypotension
prilocaine
local anesthetic (topical)

side effect of methemoglobinemia (along with benzocaine)
tetracaine
long lasting local anesthetic used in spinal anesthesia (thru interspinous lig into subarachnoid)
ropivicaine
common local anesthetic. long duration of action, so used in epidurals.

bupivicaine and chirocaine have a long duration of action as well, and they are used in epidurals (epidural = more of a sectional block. bathes spinal nerves in area)
OCTREOTIDE
synthetic somatostatin with a D amino acid

decreases pituitary secretion of the cousins (prolactin, GH, TSH)

Uses:
1. acromegaly (DRUG OF CHOICE, better than bromocriptine)
2. hormone producing GI tumors, carcinoid syndrome, carcinoma
2. hyperprolactinemia?
leuprolide
GnRH analog

1. acute usage: increases LH and FSH release. then increased sex hormone secretion

induce ovulation

2. chronic usage: downregulates GnRH receptors and leads to decreased LH and FSH. then decreased sex hormone secretion.

uses: (acts as antiestrogen)


1. endometriosis
2. prostate cancer
3. breast cancer

1. polycystic ovary syndrome
2. endometriosis
3. precocious puberty
4. prostate cancer
5. breeast cancer
pitocin
synthetic oxytocin (has a D amino acid)

1. milk letdown in lactating women
2. uterine contractions

uses
1. induce labor
2. induce milk letdown with nursing (contract myoepithelial cells)
3. abortifacient
4. stop postpartem bleeding
SOMATROPIN
synthetic GH.
given every night, which is suboptimal (not pulsatile)

uses:
1.growth hormone deficiency

2. sometimes wasting
METHYLERGONOVINE
**
control postpartem bleeding, but NOT for labor induction because it can hurt the baby with too much uterine contraction

stetler
desmopressin
synthetic vasopressin with a D amino acid

V2 receptor agonist (selective for the ones on the kidney)

1. can be used in neurogenic diabetes insipidus to increase water reabsorption
2. nocturnal enuresis
3. obstructive sleep apnea (associated with diabetes insipidus, nocturnal enuresis, and obesity)
IGF1
IGF1

USES:
1. pituitary dwarfism
2. growth problems due to GH resistance (GH receptor prob, bypasses it)
remember that the IGF binding proteins arent there for regulation

may be good for wasting patients, burn patients
prolactin
prolactin stimulates milk production (NOT LETDOWN)

stimulation
1. suckling
2. cold
3. TRH
4. sleep
5. stress
6. pregnancy

inhibition
1. dopamine

MAY CAUSE INFERTILITY!


hypoprolactinemia
1. chlorpromazine
2. haloperidol
(DA blockers)
hyperprolactinemia treated with dopamine agonists
1. bromocriptine (ergo hell yeah)
2. pergolide
3. cabergoline
4. quinagolide
hypoprolactinemia
VASOPRESSIN
triggers:
1. decreased volume
2. increased osmolarity

functions:
V1: vasoconstriction
V2: increased expr of aquaporin 2 at cell membrane, increased water reabsorption

lack of vasopressin causes neurogenic diabetes insipidus

lack of response - nephrogenic diabetes insipidus
combination pill
ethinyl estradiol + norethindrone or levonorgestrel

most effective birth control
suppresses LH and FSH, therefore, ovulation never occurs

days 25-5, hormones are withdrawn and endometrium is shed

S/E:
1. breakthrough bleeding
2. weight gain, breast growth
3. post contraceptive infertility
4. cholestasis. watch out in people with liver disease. could become jaundiced.
5. migraines - indicate risk of stroke!
6. increase glucose tolerance - watch out in diabetics!
7. high doses of estrogen - thromboembolism, myocardial infarction, and stroke (coagulopathY!)
8. high doses - increases breaset cancer risk!
norplant
levonorgestrel in silastic tube slow release
mini-pill
norethindrone only

changes mucus

high failure rate, but
no estrogen s/e

used throughout cycle
androgens
have androgenic and anabolic effects
are estrogen precursors and can lead to increased estrogen production
mestranol
synthetic estrogen which is demethylated for a slow release. avoid bolus effect.
gonadotropins
uses:
1. delayed puberty due to gonadotropin deficiency. allows more physiologic than just giving sex hormones. if gonadotropins are low in a child with delayed puberty, use gonadotropins before sex hormones
DIETHYLSTILBESTROL
stilbene estrogen that is no longer used, thank God

used to be used for birth control until it was realized that it caused uterine cancer and birth defects
SODIUM THIOPENTAL
(same as pentothione / thiopentone)

not same as pentobarbital
barbituate

uses:
1. sedative (not nighttime, bzd is better)
2. detox
3. anticonvulsant
4. good for C sections. wait for fetus to redistribute (3-5 min)

bzds are better sleeping agents

reduce dose in aged, HYPOVOLEMIC, INTOXICATED, anemic, hypothermic, or chf b/c you can kill them

also, do not give with succinylcholine b/c it will precipitate in the IV

S/E: (TI =4)
1. resp. depression.
decreases response to hypoxia
2. hypotension (venodilator)
3. decreases sympathetic output

contraindication:
1. upper respiratory obstruction
2. cardiac tamponade (lower blood pressure in a patient whose heart cant response is a BAD IDEA!)
hypovolemic (pearl harbor)
3. ischemic heart disease congestive heart failure
4. porphyria
KETAMINE
a sedative. similar to PCP. causes dissociative anesthesia, whatever that is

2. only sedative that has analgesic properties. causes analgesia by blocking the ASPARTATE receptor at the spinal cord. blocks wind-up
3. great because of its cardiovascular stability
4. used for pre-emptive analgesia - minimizes requirements for analgesia post op

S/E: excitement, hallucinations, and flashbacks during onset
alprazolam
bzd
FLUMAZENIL
competitive blocker of BZD
blocks the action of benzodiazepines

binds to same site on the GABA Cl ionophore but has no action

USES
1. reverse BZD effects after a procedure
2. BZD overdose
pentobarbital
barbituate
VDSS
apparent volume of distribution in a steady state

after the alpha phase of distribution (drugs goes into tissues),
beta phase should be a straight line when [] is graphed in a log scale because of first order kinetics

if you draw the line back to time 0, you get the imaginary concentration at time 0

divide the weight of the drug by this concentration to get the VDSS
baclofen
for muscle spasm. cuts back on the first half of the reflex arc in the spinal cord. the spinal cord is also in the back btw.

inhibits the release of excitatory transmitters in the spinal cord in the first half of the reflex arc.
etomidate
sedative, neither a barb or a bzd

not smooth on induction, causes clonus which can make a procedure difficult and interfere w/ ecg reading in cardiac procedure

etoh - etomidate
induction isnt smooth. like a shot of cheap whiskey - clonus
sodium amytal
barbituate

used for WADA test

injected into carotid
lateralizes cerebral speech dominance in neurosurgery
buspirone
anxiolytic

used similarly to a bzd

get anxious person out of that downward spiral
GLIPIZIDE
sulfonylurea = secretagogue

MOA: block K channel

Use: Type II DM

S/E:
hypoglycemia
weight gain
GLYBURIDE
sulfonylurea = secretagogue

starts with g and rhymes with wide

MOA: block K channel

Use: Type II DM

S/E:
hypoglycemia
weight gain
REPAGLINIDE
meglinitide = secretagogue

MOA: bind to a different site on the K channel and block it

use: DM Type II

S/E:
hypoglycemia
weight gain

nate and repa
NATEGLINIDE
meglinitide = secretagogue

MOA: bind to a different site on the K channel and block it

use: DM Type II

S/E:
hypoglycemia
weight gain

nate and repa
METFORMIN
biguanide - lowers blood glucose by
1. acting on liver to decrease glucose production
2. increasing glucose uptake (insulin sensitivity!!!)
better than sulfonylureas and meglitinides b/c it is insulin-sparing drug
(does not have their side effects of hypoglycemia or weight gain either)

S/E
1. *lactic acidosis* - board question alert. the liver doesnt do its job of taking up lactate as well **
2. diarrhea
3. abdominal discomfort
PIOGLITAZONE
a thiazolidinedione (increases insulin sensitivity)

*must monitor liver function tests

s/e:
0. LIVER FAILURE!!!!
1. weight gain
2. edema
3. hypoglycemia (esp. if taken with insulin / secretagogues because they work together)
ROSIGLITAZONE
a thiazolidinedione
1. big one - (increases insulin sensitivity)
2. decreases liver release of glucose

(same as biguanides, but reverse importance)
*must monitor liver function tests

s/e:
0. LIVER FAILURE!!!!
1. weight gain
2. edema
3. hypoglycemia (esp. if taken with insulin / secretagogues because they work together)
ACARBOSE
alpha glucosidase inhibitor. delay carbohydrate absorption. this keeps glucose from peaking out so high postprandially (this may be the main cause of damage in DM)

s/E: flatulance and bloating
(do bacteria eat the carbs?)
REGULAR INSULIN
hexameric with zinc
(hexamer favored over monomer)
must take 45 minutes before eating

works for 4-8 hours. too long to optimally control postprandial hyperglycemia but too short for once/ day
LYSPRO INSULIN
rapid acting insulin

AA rearrangement favors monomer over hexamer
insulin detemir
long acting insulin (1/day)
effects for 24 hours

has a fatty acyl group attached to it, so it associates with albumin. it also self associates well.

bound to albumin, it is not filtered by kidney or broken down by proteases as fast

few S/E from binding to albumin b/c there are 100 million albumin binding sites and much less detemir

so the acyl group makes it long lasting
glulisine
rapid acting insulin

AA rearrangement favors monomer over hexamer
ULTRALENTE INSULIN
long acting. similar to NPH (int) but lasts even longer?
insulin aspart
rapid acting insulin

AA rearrangement favors monomer over hexamer
15 in 15
15 g carbs and check in 15 min

used to treat hypoglycemia in conscious patients
glucagon injection
to treat hypoglycemia in an unconscious patient

works for 15 min, long enough to get an IV in
NPH INSULIN
neutral protamine hagedorn
intermediate acting insulin (2/day)

insulin + salmon protamine to bind it and release it slowly

cloudy. when mixing, draw up regular insulin first not to contaminate the regular insulin with the salmon protamine.

twice / day dosage
duration 12-16 hours
GLARGINE
long acting insulin (1/day)

has 2 Arg residues

kept in an acid buffer

98% precipitates in physiologic pH of 7.4 b/c it has an isolectric point (pKa) of around 7.4. normal insulin has a pKa of 5.5. the arginines raise this to 7.4

it releases slowly because of this pH effect

probs:
stings when injected (acid buffer)
CANNOT be MIXED with regular insulin b/c it will precipitate
exubera
inhaled insulin
rapid acting

low bioavailability and $$, but increases compliance

type 1 - should be used in conjunction with a longer acting insulin

type 2 - can be monotherapy or with oral drugs

contraindications:
1. smokers (last 6 mo)
2. lung dz. (asthma, COPD)
3. pregnant women - risk not yet ruled out
treatment for hyperglycemia and hypoglycemia
hyperglycemia
1. IV glucose
2. IV saline
*3* when glucose goes below 300 switch to IV 5% glucose to prevent cerebral edema (happens with rapid change in osmolarity and hypoglycemia (crash)
hypoglycemic / KA
15 in 15 if conscious
if unconscious and seizing
1. glucagon shot
2. start IV
3. IV glucose

anticipate nausea/ vomitting
symlin
synthetic amylin

uses:
1. DM type 1 and 2
2. weight loss??
Amylin - released by the pancreas along with insulin.

3 effects which slow glucose appearance in blood
1. signals brain to stop feeding (satiety center)
2. signals stomach to slow gastric emptying,
3. signals liver to decrease glucose secretion
exenatide
synthetic glp-1

USES:
1. DM Type 1 and 2
2. weight loss!

Glp-1 - 2 effects that decrease glucose appearance
1. increases amylin production
2. tells brain to stop feeding (satiety center)

hint:execute your weight loss
tide yourself over
TUBOCURARINE
the prototypical non-depolarizing neuromuscular blocker (NDNMB)

effect on prejunctional recepors: causes fade (mobilization)

MOA: binds the alpha subunit of the acetylcholine receptor yet has no agonist activity. it blocks the pore.

S/E:
1. hypotension from autonomic ganglionic block
SUCCINYLCHOLINE
the only depolarizing neuromuscular blocker

can act classically (Accom) or nonclassically (Phase II)

1. classical action - causes an accomodation block (phase 1 block), binds the alpha subunit of the acetylcholine receptor. is an agonist, however it stays bound for 5-7 minutes (5-10?) the time dependent gate closes, and the pore is now blocked
used when rapid onset and rapid recovery are desired

2. non classical. prolonged SC (SC drip) can cause a phase II block (desensitization)


effect on prejunctional receptors: causes fasciculation

(curare causes fade)

S/E
MALIGNANT HYPERTHERMIA
1. potassium release**
2. intraocular pressure increase
3. gastric pressure increase
4. muscle pain

All about second does effects

SECOND dose effects, esp in infants-> bradycardia
SC blocks nicotinic and muscarinic. muscarinics recover faster, and in infants, muscarinic system is more mature than their nicotinic system
the second dose will stimulate only muscarinics on the heart, causing bradycardia

infants, denervation patients, spinal chord injury, severe trauma, burns
1. receptors in immature form
2. receptors may be extrajunctinoal due to lack of MEP
they open longer and let more K out. they are not in the junction, and it gets into blood

HYPERKALEMIA!!!--> V tach! in newborns, burn patients, trauma, and denervation
causes immature receptors (gamma rather than epsilon subunits) to stay open longer and release K+, which can cause cardiac arrhythmias). this is especially important in newborns (lots of imm) or denervation, burns, and severe trauma pts (receptors regress back to imm)

contraindicated:
BURNS
NEWBORNS
DENERVATION
SEVERE TRAUMA
CHRONIC RENAL FAILURE (high K already)
atracurium
non-depolarizing neuromuscular blocker (NDNMB)

atra cur - curarine!!!

effect on prejunctional recepors: causes fade (mobilization)

MOA: binds the alpha subunit of the acetylcholine receptor yet has no agonist activity. it blocks the pore.

S/E:
1. hypotension from autonomic ganglionic block

S/E:
atracurium is metabolized by the hoffman reaction. its metabolite, laudanosine crosses the BBB and causes seizures. hoffman means that it will eventually be eliminated even w/o enzymes
botulism toxin
blocks release of Ach (Fusion blocker)
agents which increase NM block and therefore interact with NM blockers
1. inhalation anesthetics which increase NM block.
2. aminoglycoside antibiotics which increase NM block
3. magnesium (preeclamplasia rx) - also increases NM block
aminoglycosides
antibiotics

block AchR, bad for MG patients!
dibucaine
assess plasma cholinesterase activity before giving succinylcholine to make sure it will be broken down. normal is 80% inhibition.

abnormal might be only 20%??
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