Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
200 Cards in this Set
- Front
- Back
|
what are depot formulations?
|
oily based formations delivered IM that slowly leach into circulation- cannot be recalled after delivery
|
|
|
ion trapping?
|
drugs trapped in an E due to pH-PCP
|
|
|
problem with levodopa facilitated diffusion?
|
competition with large neutral amino acids- tryptophan
|
|
|
bioequivalence?
|
same rate of absorption and same availability
|
|
|
what drug has such a sig. first pass effect that no drug is available for the CNS?
|
naloxone
|
|
|
what determines effective duration of action of CNS drug more than half-life?
|
redistribution
|
|
|
what is the therapeutic window?
|
no relationship between blood levels and CNS effects- best indicated by CSF levels
|
|
|
what receptors are in the CTZ?
|
serotonergic and dopaminergic
|
|
|
what prevents diffusion within the CNS?
|
low extracellular space
physical barriers(glia) enzymatic processes and drug reuptake |
|
|
what is selegiline biotransformed to?
|
it is a PD drug transformed to methamphetamine and amphetamine
|
|
|
what CYP's biotransform CNS drugs?
|
CYP2D6
CYP3A4 |
|
|
features of CYP2D6?
|
not induced
genetic polymorphism-ability to transform drugs varies across populations no pharmacokinetic tolerance |
|
|
features of CYP3A4?
|
inducible
no genetic polymorphisms often administered to patients pharmacokinetic tolerance high concentration in GI mucosa INHIBITED by grapefruit juice INDUCED by St. Johns Wart |
|
|
what is pharmacokinetic tolerance?
|
increase in enzyme synthesis due to increased demand
|
|
|
what actively transports drugs out of the brain?
|
arachnoid granulations
|
|
|
do direct or indirect agents usually have more side effects?
|
indirect
|
|
|
what type of receptor is the ACh nicotinic receptor?
|
traditional ionotropic receptor that opens up a ligand-gated Na and K channel
|
|
|
how does a change in receptor number affect drug potency?
|
up regulation increases agonist potency and decreases antagonist
down regulation is the opposite |
|
|
how do autoreceptors work?
|
they reduce NT release and firing rates
so when they are down-regulated it increases release and firing rates(related to anti-depressant efficacy) |
|
|
what drug treats anxiety of morphine withdrawal?
|
clonidine- alpha 2 agonist
|
|
|
what is the withdrawal/abstinence syndrome?
|
upon removal of a drug the system exhibits behavior that is exactly opposite to the originally intended use of the drug
|
|
|
what is physiological tolerance?
|
reduction in the potency of a drug as a result of a compensatory process to chronic exposure involving secondary actions of the drug
|
|
|
pharmacokinetic tolerance?
|
reduction in the potency of a drug following chronic exposure due to alterations in entry of drug body- P450 inductions(phenobarbitol)
|
|
|
difference between phenobarbitol and phenytoin?
|
phenobarbitol induces the P450 that affects itself and other drugs
phenytoin induces enzymes that increase transformation of other drugs only |
|
|
what is cross-tolerance?
|
reduction in potency of drug X as a result of chronic drug Y exposure
|
|
|
what is reverse tolerance?
|
increase in the potency of a drug as a result of chronic exposure- DA agonists
|
|
|
what is disinhibition release?
|
CNS depressants initially cause a state of excitement due to decrease of CNS inhibition
|
|
|
where are the DA bed nuclei found?
|
ventral mesencephalon
|
|
|
what is the DA gating function?
|
regulation of the rate at which neuronal activity passes through the innervated target-more DA, more behavior
|
|
|
DA affect on ACh?
|
inhibition
|
|
|
features of PD?
|
hypokinetic- loss of DA
rigidity loss of postural reflexes REST tremor |
|
|
origin and target of nigrostriatal pathway?
|
O-substantia nigra pars compacta
T- neostriatum(cuadate and putamen) |
|
|
origin and target of mesolimbic pathway?
|
O- ventral tegmental area
T- nucleus accumbens |
|
|
origin and target of mesocortical pathway?
|
O- ventral tegmental area
T- cortical regions |
|
|
origin and target of tubero-infandibular pathway?
|
O- zona incerta, periventricular nucleus
T- pituitary |
|
|
origin and target of the carotid body pathway?
|
O- glomus cells
T- nucleus tractus solitarius |
|
|
origin and target of the SIF cell pathway?
|
O- paravertebral system
T- post-ganglionic sympathetic fibers |
|
|
origin and target of the renal system pathway?
|
O- ?
T- smooth muscle of renal arteries |
|
|
origin and target of the pyloric sphincter pathway?
|
O- ?
T- pyloric sphincter |
|
|
what is MPTP?
|
contaminant from opioid synthesis that is converted to MPP+ by MAO-B- high affinity for DA re-uptake pumps and taken up by mit. and uncouples oxidative phosphorylation at complex one
|
|
|
how is DA degraded?
|
by MAO-B to dihydroxy-phenylacetylaldehyde
by COMT to methoxytyramine |
|
|
what is the most well-known PD genetic abnormality?
|
abnormal alpha-synuclein
most genes associated with proteosomal function leading the belief of protein toxicity |
|
|
what narrows the therapeutic window in PD treatment?
|
as PD progresses there are less DA receptors so more levodopa is given, but at non-target sites the receptor numbers are normal and increased drug leads to psychosis
|
|
|
big side effect of DA agonists?
|
nausea and vomiting- DA receptors in CTZ
|
|
|
how does carbidopa change the side effects of levodopa?
|
without carbidopa the side effects are in the periphery because of AAAD breakdown
with carbidopa the SE's are in the CNS |
|
|
what is an important co-factor of AAAD?
|
pyridoxine
|
|
|
what is the on-off phenomenon?
|
sudden onset of full PD symptoms occurring anytime during dosage of levodopa-due to sensitization of GLU in striatum due to intermittent dosing schedules
|
|
|
pneumonic for anticholinergic tox?
|
hot as a hare
blind as a stone mad as a hatter dry to the bone |
|
|
problem with antimuscarinic tx. of PD in elderly?
|
don't tolerate antimuscarinics well-constipation, dry mouth, can't pee
|
|
|
drug regimen of PD?
|
indirect/direct and antimuscarinics early
MAO-B inhibitor to enhance DA release hold off on levodopa |
|
|
what dominates early PD tx?
|
pramipexole and ropinirole-neuroprotective
|
|
|
what dominates late PD tx?
|
direct DA agonists
|
|
|
comparison of side effects betwen levodopa and direct DA agonists?
|
levodopa causes more dyskinesia
direct agonists cause more psychosis |
|
|
what excitotoxins produce striatal lesions similar to HD?
|
kainic acid and ibotenic acid
|
|
|
what causes the choreiform movements in HD?
|
loss of GABA in striatum
|
|
|
what causes the psychosis of HD?
|
cortical degeneration following loss of striatal trophic support
|
|
|
what is the coprophenomenon?
|
increased cursing and lewd gestures in tourette's
|
|
|
treatment for increased movement in tourette's?
|
resperidone and haloperidol- DA antagonists
|
|
|
what disease runs with tourette's?
|
ADHD
|
|
|
what is the most common neurologic disorder?
|
essential tremor
|
|
|
what are the positive symptoms of schiz?
|
bizarre behavior
inability to think coherently hallucinations or delusions |
|
|
what are the negative symptoms of schiz?
|
withdrawn
poverty of speech blunted affect inappropriate behavior |
|
|
what is paradoxical about the treatment of and presentation of schiz?
|
it is treated with DA antagonists but their brains do not show increased DA or receptor number
|
|
|
what causes the positive symptoms of schiz?
|
disinhibition of the nucleus accumbens by the prefrontal cortex
|
|
|
what causes the negative symptoms of schiz?
|
reduced function of the pre-frontal cortex due to underdeveloped parahippocampal gyrus
|
|
|
what defines the typical anti-psychotics(neuroleptics)?
|
they produce acute extrapyramidal side effects- block of non-target DA receptors that produce parkinsonian side effects, akathisia nd dystonia
|
|
|
time line of typical anti-psychotic side effects
|
dystonia,akathisias and the parkinsonian
mutually exclusive, usually just parkinsonian |
|
|
what drugs are used to combat the extrapyramidal side effects of typical anti-psychotics?
|
trihexyphenidyl and benztropine( antimuscarinics)
effectiveness of DA blockade in nigro-striatal pathway is reduced |
|
|
what defines the atypical anti-psychotic drugs?
|
produce less extrapyramidal side effects
|
|
|
what are the main atypical anti-psychotics?
|
thioridazine and mesoridazine
|
|
|
what are the second-generation atypical anti-psychotics?
|
risperidone
olanzapine clozapine quetiapine ziprasidone aripiprazole |
|
|
side effects of all anti-psychotics?
|
orthostatic hypotension(alpha)
CV problems(antimuscarinic) increased prolactin(galactorrhea or gynecomastia) sedation antiemetic weight gain neuroleptic malignant syndrome(rigidity and hyperthermia) |
|
|
what side effect is associated with chronic anti-psychotic use?
|
tardive dyskinesia- facial movements and other dyskinesias
either from withdrawal or breakthrough(worse) due to DA receptor site up-regulation(permissive) from decreased DA |
|
|
what treats tardive dyskinesia?
|
reserpine and tetrabenzine
increased anti-psychotic(may produce iatrogenic(physician induced) movement disorder) |
|
|
what does efficacy delay of anti-psychotics show?
|
mechanisms other than DA receptor blockade are involved because the DA antagonists reduce DA activity within an hour
|
|
|
which set of anti-psychotics predominantly reduce positive symptoms?
|
first generation
|
|
|
what supports the role of NE in depression?
|
efficacy of NE reuptake inhibitors(desipramine and maprotiline) in treatment
|
|
|
what supports the role of 5HT in depression?
|
increased receptor numbers
decreased 5HT decreased 5HIAA-primary metabolite |
|
|
what causes seasonal affective disorder?
|
increased melatonin due to prolonged darkness
inhibition of 5HT neurons melatonin secretion controlled by NE |
|
|
what breaks down NE?
|
COMT and MAO-A
|
|
|
how is NE involved in sensory processing?
|
NE inhibits inter-columnar fibers which usually decrease sensory attentiveness in the cortex
in depressed patients there is less NE, so less attentiveness |
|
|
major side effect of MAOI's?
|
tyramine effect-accumulation of amines leading to hypertensive crisis
|
|
|
which tests determine the course of depressive treatment?
|
amphetamine provocative- indicates more NE agent
dexamethasone suppression- indicates use of a serotonergic agent(no reduction of cortisol in 5HT decrease) |
|
|
what drugs are used for OCD?
|
SSRI's and heterocyclics(second generation antidepressants)
|
|
|
drugs most used in panic attacks?
|
SSRI's
|
|
|
what other function to TCA's have?
|
treatment of night-time enuresis and geriatric incontinence
|
|
|
what does consciousness require?
|
brain stem
bilateral thalamic unilateral cortical |
|
|
which brain areas facilitate dreaming?
|
locus ceruleus- NE
raphe nuclei- 5HT |
|
|
what happens in sleep atony(glycine clutch)?
|
gigantocellular region of lower brainstem activates Renshaw collateral interneuron which depresses activity in lower alpha motor neuron
|
|
|
what is the pedunculo-pontine cholinergic system?
|
cholinergic fibers project to the thalamus and regulate correspondence between sensory afferent fibers and thalamo-cortical fibers- ACh causes activation of the thalamo-cortical fibers and facilitates sensory traffic to the cortex and arousal
|
|
|
what is adenosine's role in sleep?
|
it builds up during the day and acts on the purinergic heteroreceptors to reduce ACh and arousal
|
|
|
how does caffeine work?
|
an antagonist at purinergic heteroreceptors and prevents adenosine action
|
|
|
when do night-time enuresis and night terrors occur?
|
stage IV sleep
|
|
|
how do depression and REM sleep relate?
|
depression is associated with an early onset of REM
|
|
|
which CNS depressants do not suppress REM sleep?
|
chloral hydrate and zolpidem(ambien)
|
|
|
which CNS depressants do not cause respiratory depression?
|
benzo's
|
|
|
how do benzo's work?
|
increase the affinity of GABA for the A receptor by increasing the FREQUENCY at which the Cl- gate opens
changes tertiary protein structure no interference with GABA binding |
|
|
what is the floor and ceiling effect?
|
as more drug is given, it has less effect due to decreased NT release
|
|
|
how do benzo's effect adenosine?
|
inhibit reuptake
|
|
|
how are the benzo's biotransformed?
|
mostly in liver by N-desalkylation and oxidation followed by conjugation
|
|
|
which benzo's are conjugated outside the liver?
|
OTL
oxazepam temazepam lorazepam |
|
|
signs of benzo toxicity?
|
CNS depression
bitter taste N and V diarrhea epigastric distress |
|
|
what antagonizes benzo toxicity?
|
flumazenil
|
|
|
how do barbs work?
|
bind to Cl- ionophore at site independent of GABA site and increases DURATION of time the gate is open
may open the channel without GABA |
|
|
what herbals contain benzo-like chemicals?
|
kava,valerian,mandrake
|
|
|
what NT's are in the central nucleus of the amygdala?
|
GABA
Glu 5HT NE |
|
|
what drug is used for stage fright?
|
propranolol and other beta antagonists
|
|
|
what kind of waves do seizures create?
|
hypersynchronous low frequency, high amplitude
|
|
|
what is a paroxysmal depolarization shift and what is responsible?
|
occurs in seizure
NMDA receptor activation with displacement of Mg and influx of Ca leading to excitotoxicity and retrograde release of NO |
|
|
what cells are responsible for reducing extracellular K?
|
astrocytes and if they don't it may induce depolarization
|
|
|
how are partial and complex seizures treated differently?
|
partial are treated by reducing excitation and complex by increasing inhibition
|
|
|
side effects of antiepileptics?
|
intention tremor
nystagmus ataxic gait diplopia hyperreflexia seizures at high doses absence seizures |
|
|
what does succinic semialdehyde dehydrogenase do?
|
facilitates GABA entry to the Krebb's cycle, inhibited by valproic acid
|
|
|
what are many of the anti seizure adjunctive agents substrates for?
|
p glycoprotein, epilepsy induces the production of the protein and may confer resistance
|
|
|
what side effects does the induction of the p450 system by anti seizure meds lead to?
|
vitamin K deficiency and decrease in steroid efficacy
|
|
|
what leads to fetal hydantoin syndrome?
|
side effect of phenytoin
usually metabolized to parahydroxyphenytoin by CYP2C8 via arene epoxide intermediate which are detoxified by epoxide hydrolase, during development not all tissues have the hydrolase and the arene attacks DNA leading to transcription errors |
|
|
problem with phenytoin generics?
|
not bioequivalent, causes problems when switching
|
|
|
how is phenytoin transported?
|
mostly bound to albumin, may be displaced by other drugs(aspirin)
|
|
|
when is a seizure considered status epilepticus?
|
after 20 minutes
|
|
|
management of status epilepticus?
|
start with benzo(lorazepam,diazepam)
chase with phenytoin induce barb coma(pentobarbitol) |
|
|
what is the most common migraine?
|
without aura
|
|
|
what is a cluster headache
|
worst pain ever, may be related to circadian rhythm
unilateral and focused around the orbit |
|
|
what is a non-migraine headache and how do you treat it?
|
tension in neck and lower occipital region, bilateral and non-throbbing
treat with stress avoidance, NSAIDs and muscle relaxants(benzos) |
|
|
what is the prostaglandin function in pain?
|
sensitizes pain fibers to the pain signal by altering phosphorylation status of the primary afferent terminal
|
|
|
what is caffeine's effect on drug kinetics?
|
enhances absorption of NSAIDS
|
|
|
what is the prophylactic treatment of choice for migraines?
|
propranolol
|
|
|
what is the vascular hypothesis of Wolff?
|
theory of migraine headache
release of serotonin from platelets causes vasoconstriction and ischemia subsequent loss of serotonin leads to atonic arteries that stretch conn. tissue in response to pulse pressure producing throbbing |
|
|
what is the sterile inflammatory hypothesis?
|
theory of migraines
release of substance P,CGRP and neurokinin from trigeminal nerve, induce vasodilation and histamine release producing inflammation and neural irritation |
|
|
what is the biobehavioral hypothesis?
|
theory of migraine
spreading depression of Leao creates a wave of depolarization across cortex activating the ophthalmic limb of trigeminal nerve stress precipitation and explains menstrual cycle involvement |
|
|
how are anti-migraine meds administered?
|
suppository
|
|
|
what are the side effects of ergot alkaloids?
|
parethesias-tingling
leg cramps confusion |
|
|
what NT is most responsible for migraines?
|
CGRP
|
|
|
problem with newer triptans?
|
enter CNS and associated with serotonin syndrome in patients taking SSRIs
|
|
|
treatment of plan for migraines?
|
NSAIDs
sumatriptan prokinetic with chronic treatment |
|
|
what are the most dangerous drugs in frequent use?
|
anesthetics, very low TI
|
|
|
what is the minimal alveolar concentration?
|
measure of anesthetic potency and describes the gas concentration in blood needed to produce no reflex response to a knife cut in 50% of the population at room temp at sea level
|
|
|
relationship of solubility and anesthetic effect?
|
higher solubility, slower anesthetic induction
|
|
|
how are anesthetics administered?
|
in a closed system and not biotransformed
|
|
|
what is diffusion hypoxia?
|
when NO leaves the blood to enter the lung so quickly it displaces too much partial pressure leaving it insufficient for oxygenation
|
|
|
which anesthetic is biotransformed?
|
halothane
|
|
|
what is the Overton-Meyer hypothesis?
|
suggests anesthetic drugs disrupt membrane fluidity and Na channel function, found to be only at toxic levels
|
|
|
what is the MOA of anesthetics?
|
stereoselective-receptor based
drugs bind at interface between the protein and surrounding lipid to activate GABA-A receptors and depression of ion channels, bind in regions most associated with consciousness(thalamus,cortex,brain stem) |
|
|
effects of anesthetics?
|
respiratory depressant(except NO)
bronchodilators cardiac depressant(except NO) vascular smooth mm relaxer and causes hypoperfusion(NO helps by vasocx.) skeletal mm relaxers at high tensions, malignant hyperthermia-genetic predisposition, abnormal Ca regulation in sarcoplasmic reticulum due to splice variants |
|
|
what is a bad side effect of halothane?
|
halothane hepatitis- invokes immunological response that attacks the liver
biotransformed by CYP2E1 and 2A6 to trifluoroacetyl chloride then trifluoroacetic acid, may bind covalently to hepatocytes or react with 2E1, delayed response to 2E1 |
|
|
what adjuvants are used in anesthesia?
|
diazepam-facilitates drowsiness, anterograde amnesia
atropine reduces bronchial secretions and counteracts cardiac depression muscle relaxants to reduce amount required to paralyze skeletal mm opioids- pain |
|
|
what is the effect of inducing agents in anesthetic treatment?
|
make patient more comfortable
reduce duration of disinhibition release motor excitement NO,thiopental,high dose opioids |
|
|
what is neurolept-anesthesia?
|
droperidol and NO
|
|
|
what is neurolept-analgesia?
|
droperidol and opioid fentanyl
may produce chest wall rigidity |
|
|
what are the IV anesthetic agents?
|
etomidate
propofol thiopental ketamine |
|
|
how do all local anesthetics work?
|
Na channel antagonists, enter channel from inside neuron- prevented during inflammation due to low pH
|
|
|
what are local anesthetics formulated with?
|
Ep or other vasocx. to keep drug local
CO2 to keep solution acidic buffer to overcome effects on pH |
|
|
problems with local anesthetics?
|
cardiovascular toxicity due to Na channel block
CNS depressant which decreases respiration |
|
|
how are local anesthetics broken down?
|
esters converted to PABA which is a common allergen and has risk of delayed type hypersensitivity reaction
amides biotransformed in liver |
|
|
what two systems are involved in pain?
|
sensory and limbic
|
|
|
what system is associated with the suffering aspect of pain?
|
limbic system
|
|
|
what do C fibers transmit?
|
slow pain
|
|
|
where do pain fibers synapse?
|
substantia gelatinosa
|
|
|
what forms the pain gate?
|
serotonin fibers from the raphe nuclei
NE fibers from the locus ceruleus enkephalinergic heteroreceptors |
|
|
what is neuropathic pain?
|
arises from trauma to the CNS or toxic insult
central activation of the pathway by non-chemical or mechanical means |
|
|
what is the treatment for shingles?
|
carbamazepine
gabapentin valproic acid amitriptyline |
|
|
what is a vaccine for shingles?
|
zostavax
|
|
|
what do opioid analgesics mimic?
|
enkephalins and endorphins
|
|
|
where do enkephalins and endorphins work?
|
spinal cord
periaqueductal gray limbic system |
|
|
what are the two enkephalins?
|
met-Enk
leu-Enk |
|
|
how do enkephalins work?
|
reduce substance P release from C fibers in the periphery
effects the PAG |
|
|
how do endorphins work?
|
paracrine effects
mediates ACTH |
|
|
what are the opioid receptors?
|
enkephalin receptors
1 mu- brain and spinal cord, G proteins close Ca channels,decrease NT release and open K channels for hyperpolorization, produce the side effects of euphoria and resp. dep. 2 kappa- spinal cord 3 delta- limbic system, emotional and behavioral effects 4 epsilon-unknown action |
|
|
how do direct acting opioid agonists work?
|
affect pain threshold without affecting consciousness
inhibit substance P release in substantia gelatinosa and activate descending pain suppression pathways from the PAG |
|
|
what is the triad of opioid OD?
|
coma
respiratory depression miosis |
|
|
what drugs are associated with the most severe withdrawal symptoms?
|
barbs-seizures
|
|
|
what type of pain do opioids affect?
|
slow pain, suffering
|
|
|
how do opioids and elderly interact?
|
effects are increased due to decreased blood flow to the liver
|
|
|
what is the deal with loperamide and quinidine?
|
loperamide is an anti-diarrheal agent but only acts peripherally due to P-glycoprotein action which pumps it out of the brain, taken with quinidine which inhibits P-gp it can produce euphoria and respiratory depression
|
|
|
define drug abuse
|
consumption of a drug by self-administration that is outside the societal norm
|
|
|
define recreational drug use
|
self-administration of drugs to experience the euphoriant properties, leads to a pattern of dependence, higher doses that normally prescribed
|
|
|
define drug dependence
|
a pattern of use where the individual perceives the need to continue the use, in chronic pain or abuser
|
|
|
define addiction
|
a pattern of compulsive abuse, extended in time, where the individual is preoccupied with getting the drug
|
|
|
define narcotic
|
all drugs of abuse not including alcohol or tobacco
|
|
|
why are drugs abused?
|
provide incentive salience- an act leading to a reinforcement that further perpetuates incentive to produce that behavior again, not due to tolerance, withdrawal symptoms
|
|
|
common action of all drugs of abuse?
|
increase DA in the nucleus accumbens
|
|
|
what is the effect of continued drug abuse?
|
produces reverse tolerance in the mesolimbic pathway while tolerance in other brain regions-continue to seek out euphoric behavior which has tolerance(frontal cortex) while the reward center has become sensitized
|
|
|
what drugs do not increase DA in the N. accumbens?
|
pot
benzo's inhalants |
|
|
what are the anorexiants?
|
phenteramine
fenfluramine phenylpropanolamine phendimetrazine benzphetamine more NE and 5HT action, no DA action |
|
|
actions of alcohol dehydrogenase?
|
readily saturated
genetic variants not inducible |
|
|
how do alcoholics develop tolerance?
|
greater percentage of alcohol is biotransformed by the p450 system following induction
|
|
|
what enzyme in the alcohol pathway shows genetic variance in the pacific rim?
|
aldehyde dehydrogenase
|
|
|
what is a Mickey Finn?
|
ethanol and chloral hydrate(trichloroethanol),they share alcohol dehydrogenase which favors chloral hydrate and leads to sedation
|
|
|
how do you treat methanol and ethylene glycol toxicity?
|
ethanol followed by dialysis
|
|
|
what is used in alcohol OD?
|
diazepam
|
|
|
what is used to treat phencyclidine OD?
|
diazepam
|
|
|
why are anticholinergics abused?
|
produce delirium with delusions
|
|
|
difference between hallucination and delusion?
|
hallucination is a misperception of reality, a delusion is an image that is not there
|
|
|
what is another name for pseudocholinesterase?
|
butyrylcholinesterase, widely distributed in blood
|
|
|
how do the nootropics inhibit ACh metabolism?
|
1 reversible binding to choline site
2 binding to anionic site 3 act as AChE substrate but are transformed slower |
|
|
what insecticides inhibit AChE?
|
parathione,diazonon and malathione
|
|
|
what are the nootropic toxic effects?
|
Defecation
Urination Miosis Bowl disturbance Emesis Lacrimation Salivation |
|
|
why do people use inhalants?
|
euphoria from oxidative phosphorylation uncoupling
little dependence liability toxicity due to contaminants |
|
|
what is pyramiding?
|
cyclic steroid regimen
starts at low doses and increases for 6-12 weeks and then decreases back to zero |
|
|
what are the toxic effects of steroids?
|
paranoia,agitation,aggressiveness, increased libido,hallucinations,psychomotor retardation or acceleration,fatal liver cysts and cancer,blood clots,hypertension,acne
|
|
|
withdrawal symptoms of steroids?
|
depressed mood, fatigue, restlessness,loss of appetite,insomnia,reduced sex drive,headache and joint pain
|
