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;
206 Cards in this Set
- Front
- Back
|
describe bronchial asthma
|
respiratory syndrome, decreased airflow, inflam of bronchial walls, narrowing airways, increased resistance to airflow; cough, chest tightness, short breath, wheeze
|
|
|
what factors increase airway obstruction
|
bronchoconstriction (contraction of bronchial smooth muscles), mucosal edema (from inflam), bronchiolar secretions (increased due to inflam)
|
|
|
what drugs can precipitate asthma
|
B bockers, aspirin, NSAIDS
|
|
|
two kinds of anti-asthma agents
|
bronchodilators, anti-inflammatory drugs
|
|
|
different kinds of bronchodilators
|
sypathomimetics (B2 adrenoreceptor agonists, A adrenoreceptor agonists), anticholinergics, xanthines
|
|
|
mechanism and advantages of B2 adrenoreceptor agonists
|
increase B2 adrenergic receptors on bronchial smooth muscles to get bronchodilation, decrease mediators release from mast cells; most effective, minimal side effects
|
|
|
names of B2 adrenoreceptor agonists
|
short acting: salbutamol, terbutaline; long acting: salmeterol, formoterol
|
|
|
for B2 adrenoreceptor agonists what is are the indications and route, and maintenance therapy
|
acute attacks - inhalation, IV infusion; maintenance = oral, inhalation
|
|
|
mechanism, indication and route for anticholinergics and one example
|
decrease muscarinic receptors, block cholinergically mediated bronchoconstriction; usually adjunct therapy, acute attacks, maintenance; inhalation; ipratropium bromide
|
|
|
3 kinds of xanthines
|
caffeine, theophylline, theobromide
|
|
|
mechanism of theophylline
|
decrease phosphodiesterases, decrease cAMP hydrolysis, accumulation of cAMP, relaxation of bronchial smooth muscles, bronchodilation
|
|
|
disadvantages, side effects, and routes for theophylline
|
narrow therapeutic range, wide range of side effects; CVS - palpitation, dysrhythmias, CNS - tremors, convulsions, GIT - abdominal pain, nausea; oral, IV
|
|
|
4 anti-inflammatory agents (classes of drugs)
|
glucocorticoids (steroids), mast cell stabilizers, leukotriene receptor antagonists, methotrexate
|
|
|
mechanism and routes of glucocorticoids
|
anti-inflam effect on bronchial mucosa, decrease macrophages, eosinophils, lymphocytes, decrease mucous secretion; inhale, oral, IV
|
|
|
mechanism, indication, route, example of mast cell stabilizers
|
stabilize mast cells, decrease release of chemical mediators that cause bronchoconstriction, decrease incidence of asthma attacks; prophylaxis; inhalation; cromolyn sodium and nedocromil
|
|
|
mechanism, indication, route, example of leukotriene receptor antagonists
|
selective blocking of leukotrienes action on respiratory tract, decrease mucous secretion and bronchoconstriction; adjunct therapy, prophylaxis; oral; montelukast, zafirlukast
|
|
|
indications and side effects of methotrexate
|
mainly for treatment of malignancies and autoimmune diseases, may reduce requirement of corticosteroids; liver toxicity, bone marrow failure
|
|
|
what is hemostasis
|
process that retains blood within the vascular system
|
|
|
what is thrombosis
|
formation of a blood clot (thrombus) within a blood vessel
|
|
|
when does hemostasis occur and what 4 events take place
|
injury of a blood vessel - loss of vascular integrity; vasoconstriction, platelet activation, blood coagulation and clot formation, fibrinolysis
|
|
|
what does vasoconstriction do
|
decrease blood flow to injured vessel, decrease blood loss
|
|
|
what happens during platelet activation
|
platelets adhere to collagen fibrils on injured vessel with help from vWF, platelets aggregate under effect of thrombin and fibrinogen to make a plug, release chemical mediators to activate more platelets
|
|
|
what happens during blood coagulation and clot formation
|
activation of coagulation factors, coagulation pathway, plug becomes more stable blood clot (fibrin network + blood cells)
|
|
|
what is fibrinolysis, describe
|
enzymatic process that dissolves fibrin clot, occurs after coagulation, controls size and spread of clot, carried out by plasmin
|
|
|
what are natural anticoagulants, describe
|
antithrombin - serine protease inhibitor, activated by heparin, inactivates thrombine and factor Xa; protein C - vit K dependent protein, activated by thrombin, inactivates factors V and VIII
|
|
|
what are two kinds of abnormal hemostasis
|
bleeding disorders, thromboembolic disease
|
|
|
3 bleeding disorders, describe
|
vascular defects - vasculaitis, purpura; platelet defects - thrombocytopenia, purpura; coagulation factor defects - hemophilias
|
|
|
describe hemophilias, hint: abc, 3 types (what factor is deficient?)
|
bleeding disorder, congenital or acquired, coagulation factor deficiency, bleeding after trauma or spontaneously; A - factor VIII, B - IX, C - XI
|
|
|
describe thromboembolic disease, examples, tx
|
group of diseases due to hypercoagulable states; DVT, pulmonary embolism, coronary artery disease; antithrombotic agents as tx
|
|
|
3 types of antithrombotic agents
|
antiplatelets, anticoagulants (inhibit coagulation factors), thrombolytic (profibronolytic) agents - break down fibrin, fresh thrombus only - acute events
|
|
|
6 antiplatelet agents
|
cylcooxygenase inhibitors, ADP receptor blockers, phosphodiesterase inhibitors, prostacyclin analogues, adenosine reuptake inhibitors, glycoprotein receptor blockers
|
|
|
mechanism and examples of cyclooxygenase inhibitors
|
decrease cyclooxygenase enzyme, decrease thromboxane A2; acetylsalicylic acid (aspirin), other NSAIDS (ibuprofen)
|
|
|
describe aspirin, dose, side effects
|
most powerful platelet inhibitor, more prolonged effect; 350mg/day for myocardial infarction tx, 75-81mg/day for protection; bleeding, peptic ulcer, bronchial asthma
|
|
|
describe ADP receptor blockers, side effects, examples
|
block ADP receptor, decrease ADP induced platelet aggregation, safe when can't use aspirin; neutropenia, thrombotic thrombocytopenic purpura, bleeding; thienopyridines (ticlopidine, clopidogrel)
|
|
|
describe phosphodiesterase inhibitors, example, indications
|
selective decrease of PDE3, increase cAMP in platelets, increase active PKA, decrease platelet aggregation; cilostazol; intermittent claudication in peripheral vascular disease
|
|
|
describe prostacyclin analogues, examples
|
synthetic analogues of prostacyclin, directly increase cAMP levels in platelets; iloprost, carbacyclin
|
|
|
describe adenosine reuptake inhibitors, example
|
inhibit uptake of adenosine by rbcs, adenosine increases platelet cAMP synthesis, cAMP inhibits platelet aggregation; dipyridamole
|
|
|
describe glycoprotein IIb/IIIa receptor blockers, route, side effects, ex
|
block receptors on platelets, decrease platelet aggregation; IV; thrombocytopenia; abciximab
|
|
|
two kinds of anticoagulants, subtypes
|
heparin - unfractioned heparin, LMWH; oral anticoagulants - warfarin, dicoumarol
|
|
|
mechanism, side effects, routes of unfractioned heparin
|
augments the effects of AT - inhibition of thrombin and factor Xa; bleeding, thrombocytopenia, allergic rx, osteoporosis; IV, SC
|
|
|
difference b/t unfractioned and LMWH, examples
|
lmw, more selective inhibition of Xa w/ relative sparing of thrombin, less side effects, improved pharmacokinetics, no need for coagulation monitoring, SC injection mainly; tinzaparin, enoxaparin
|
|
|
mechanism of warfarin
|
vit K is required to activate factors II, VII, IX, X in liver, reduced first by enzyme, warfarin inhibits enzyme
|
|
|
onset, duration, antidote for heparin and warfarin
|
hep - immediate, short acting (hrs), protamine; warfarin - 2+ days, long (days), vit K
|
|
|
describe thrombolytic agents, examples
|
activate plasminogen, plasmin; tissue plasminogen activator, urokinase, streptokinase
|
|
|
describe tissue plasminogen activator
|
initially isolated from a tumour cell line, promotes conversion of plasminogen to plasmin, selective for fibrin-bound plasminogen, low antigenicity (repeated uses)
|
|
|
describe streptokinase
|
indirect, potential allergic rx, high antigenicity, higher risk of bleeding, cheaper, plasma clearance in 15-25 min
|
|
|
describe the adrenal medulla, actions
|
modified sympathetic ganglion, innervated by preganglionic sympathetic nerve fibers, responds to sns stim in stress conditions; secretes catecholamines - epinephrine, norepinephrine
|
|
|
3 regions of adrenal cortex
|
zona glomerulosa (out) - aldosterone, zona fasciculata - hydrocortisone, zona reticularis (in) - sex hormones
|
|
|
what is the precursor of all adrenalcortical hormones
|
cholesterol
|
|
|
what does aldosterone do (what does it increase/decrease, stimulate)
|
stimulates renal tubules, increase Na and decrease K in blood, increase BV and BP
|
|
|
what factors stimulate aldosterone secretion
|
hyperkalemia, hyponatremia, hypovolemia, hypotension, RAS
|
|
|
how are glucocorticoids regulated
|
corticotropin releasing hormone increases adrenocorticotropic hormone or ACTH, increase glucocorticoids, -ve feedback
|
|
|
what does ACTH do
|
synthesis and secretion of glucocorticoids, growth of the adrenal gland
|
|
|
what is the mechanism of glucocorticoid action
|
cross cell membrane by diffusion, bind to receptors in cytoplasm or nucleus, activate/inactivate genes, alter rate of DNA transcription (change patterns of protein synthesis), affect metabolic activity and structure of target cell
|
|
|
metabolic effect of glucocorticoids
|
increase gluconeogenesis and blood glucose level, decrease glucose uptake and utilization by cells, increase metabolization of protein and amino acids and protein catabolism, increase mobilization of peripheral fat to face and trunk
|
|
|
other effects of glucocorticoids
|
decrease number and activity of wbcs, increase rbcs and neutrophils, decrease lymphocytes and eosinophils, Na and water retention, K excretion, increase BV and BP, mucosal ulceration, increased CNS excitability
|
|
|
therapeutic uses of glucocorticoids
|
adrenal hypofunction, allergic rxns, bronchial asthma, autoimmune diseases (rheumatoid arthritis, SLE), organ transplant, malignancies (acute leukemia), inflammatory conditions (IBD, renal disease)
|
|
|
what ending do glucocorticoids have, routes
|
one; topical, oral, inhale, inject (IM, IV, SC, intralesional)
|
|
|
2 adrenal gland disorders w/ examples
|
adrenocortical insufficiency - addison's disease; adrenocortical hyperfunction - conn's syndrome, cushing's, congenital adrenal hyperplasia
|
|
|
what is addison's, primary and secondary causes
|
hypofx of all zones of adrenal cortex; primary = adrenal gland disorder (autoimmune mediated destruction, tuberculosis, other infections, bilateral adrenolectomy); secondary = pituitary gland disorder - not enough ACTH, sudden withdrawal of long steroid therapy, trauma/tumour of pituitary gland
|
|
|
clinical manifestations and tx of addison's
|
fatigue, muscle weakness, hypotension, anorexia, n/v, abd pain, weight loss, mental depression, shock; hormone replacement (cortisol deficiency - oral hydrocortisone, aldosterone deficiency - oral fludrocortisone)
|
|
|
describe conn's, causes, main features
|
increased aldosterone secretion in absence of activation of RAS; caused by adrenal hyperplasia, adrenal tumours (adenoma, carcinoma); hypertension, hypokalemia, decreased renin level, alkalosis
|
|
|
describe cushings and causes
|
increased glucocorticoid secretion; iatrogenic (excess steroid or ACTH therapy, most common) or spontaneous (adrenal hyperplasia, adrenal tumours, excess pituitary ACTH secretion, ectopic ACTH secretion by some tumours)
|
|
|
clinical manifestations and tx of cushings
|
obesity (moon face, buffalo hump), myopathy, hypertension, hyperglycemia (diabetes mellitus), recurrent infections, thin atrophic skin w/ bruises, osteoporosis, psychosis; treat the cause
|
|
|
describe congenital adrenal hyperplasia, effects, clinical manifestations
|
congenital metabolic disorder - autosomal recessive, due to enzymatic defect; increased adrenal androgens, decreased cortisol and aldosterone; females - masculinization, males - precocious puberty
|
|
|
what are the gonadal hormones and what do they do
|
female: estrogen - develop/maintain sex characteristics, progestins - ovarian cycle, maintain pregnancy; male: androgens - develop/maintain sex characteristics
|
|
|
types of estrogens w/ examples
|
natural - estradiol; semisynthetic - ethinyl estradiol, estradiol valerate; synthetic - mestranol, stilboestrol
|
|
|
describe the pharmacokinetics of estrogens
|
absorbed through GIT, skin, mucous membranes; transported by binding to albumin or sex steroid-binding globulin; metabolized and degraded in liver (synthetic less prone); excreted through kidneys in urine
|
|
|
therapeutic indications of estrogens
|
contraception, replacement therapy (menopausal symptoms, hypogonadism), menstrual disorders, acne, prostatic cancer
|
|
|
what causes female hypogonadism, types, tx
|
impaired ovarian fx; pre-pubertal (primary, delayed puberty), post-pubertal (secondary, secondary amenorrhea and infertility); tx is small doses of estrogen
|
|
|
what are the effects of hyperestrogenemia in males and females
|
male - feminizaton, infertility, breast enlargement; females - endometrial carcinoma, breast cancer
|
|
|
describe 2 antiestrogens
|
tamoxifen - estrogen receptor blocker, tx of breast cancer; clomiphene - inhibits estrogen-mediated negative feedback on hypothalamus, tx of infertility
|
|
|
how does clomiphene work?
|
Hypothalamus makes gnrh – stimulates pituitary to make fsh and lh; these stimulate the ovaries and corpus luteum to make estrogen and progesterone which inhibit fsh and lh; clomiphene blocks this, prevents inhibition of fsh and lh; they increase and stimulate ovulation
|
|
|
types of progestins
|
natural - progesterone (from corpus luteum and placenta); synthetic - 3 generations
|
|
|
therapeutic indications for progestin
|
contraception, hormone replacement therapy, menstrual disorders, dysmenorrhea, endometriosis, endometrial carcinoma
|
|
|
example of antiprogestins, mechanism, indication
|
mifepristone; high affinity for progesterone receptor, competitive decrease of natural progesterone; therapeutic abortion
|
|
|
3 types of hormonal contraception
|
oral contraceptives (OCC), injections/implants, transdermal patch
|
|
|
2 types of OCC
|
combined OCC - estrogen and progestin, most popular, monophasic/fixed dose, bi/triphasic/variable dose; progestin minipill - low dose progestin
|
|
|
mechanism of estrogen-progestin combo
|
suppress ovulation - decrease gnrh from hypothalamus and fsh/lh from pituitary, thicken cervical secretions, inhibit implantation
|
|
|
mechanism of low-dose progestin
|
thicken cervical secretions, inhibit implantation, variable suppression of ovulation by effect on fsh/lh
|
|
|
adverse effects of occ
|
salt/water retention, edema, hypertension, vascular disorders (thromboembolic, coronary artery, cerebrovascular disease), headache/migraine, depression, postpill amenorrhea
|
|
|
contraindications of occ
|
absolute - pregnancy, breast feeding, thromboembolic disease, breast/cervical cancer, undiagnosed vaginal bleeding; relative - hypertension, impaired liver fx, migraine
|
|
|
types of contraceptive injections/implants
|
long-acting progestins; injections - IM inject ever 3m, medroxyprogesterone; implants - SC insertion of small capsules, 3-5 years, levonorgestrel
|
|
|
what can be done in hrt, benefits
|
estrogen in postmenopausal women, low dose estrogen compared to contraceptives, progestin to reduce risk of endometrial carcinoma; prevent changes associated w/ menopause (osteoporosis, flushing, headache, insomnia, genital tract atrophy, cardiovascular disease)
|
|
|
types of androgens
|
natural - testosterone, dihydrotestosterone, dehydroepiandrosterone (DHEA), androstenedione; synthetic - methyltestosterone, ethyloestrenol, stanozolol
|
|
|
actions of androgens
|
regulate gene expression by activating a nuclear receptor, develop male primary/secondary sex characteristics, maturation of sperm, anabolic effect
|
|
|
therapeutic indications of androgens
|
hormone replacement (hypogonadism, hypopituitarism), anemia refractory to tx to stimulate erythropoiesis, breast cancer, compensate for protein loss
|
|
|
types and tx of hypogonadism, routes
|
primary - testicular failure, secondary - hypothalamic-pituitary disease; androgen replacement; oral, transdermal patch, IM injection, subdermal implants
|
|
|
hyperandrogenemia in males and females
|
male - precocious puberty; female - virilization symptoms (hirsutism, acne, amenorrhea, clitoral enlargement, deep voice), masculinization of external genitalia of infants
|
|
|
2 types of anti-androgens, used to treat
|
androgen suppressors - prostatic carcinoma, endometriosis; receptor inhibitors - prostatic carcinoma, hirsutism, virilization, precocious puberty
|
|
|
male oral contraceptive, example, from, action, adverse effects
|
gossypol; from cotton plant, china; inhibits sperm production; irreversibility, hypokalemia
|
|
|
what is valerian
|
sedative and hypnotic; Contains valepotriates-- shown to have CNS depressant activity with less adverse effect than diazepam
|
|
|
what is echinacea
|
antibiotic, immune stimulant; activates T-lymphocytes to fight cold
|
|
|
what is St. John's Wort
|
contains hypericin; high conc inhibits reuptake of serotonin, norepi, dopamine in CNS; antidepressant
|
|
|
what is Kava
|
kava lactones - anti-anxiety
|
|
|
what are the conditions for using OTC drugs
|
condition is mild, not more than 2 wks, if worsening see doc, stop if adverse rxn
|
|
|
problems w/ aspirin
|
toxicity - gastric irritation, tinnitus; reyes syndrom in children w/ fever, allergic rxns
|
|
|
problems/plus side w/ acetaminophen
|
no gi irritation, no reyes, equal to asa; overdose - fatal hepatic necrosis
|
|
|
plus side of ibuprofen
|
equal to asa/tylenol, better anti-inflam
|
|
|
what is naproxen
|
anti-inflam, antipyretic, analgesic - new to market
|
|
|
what do cold preparations contain
|
antihistamines, decongestants, cough suppressant, expectorant, analgesic, antipyretic
|
|
|
what do antitussives do
|
suppress cough (codeine and dextromethorphan), suppress cough center (receptors), contain alcohol
|
|
|
drug of choice for hay fever prep
|
H1 antagonist (no combos)
|
|
|
what two classes of laxatives shouldn't be used
|
stimulant cathartics - castor oil (loss of water and electrolytes), saline cathartics - retain water in fecal mass
|
|
|
examples of bulk forming laxative and emollient laxative
|
methylcellulose (soft stool, drug of choice), dioctyl sodium sulfosuccinate (colace) - water into feces, drug induced constipation
|
|
|
two types of antidiarrheal agents
|
absorbents - attapulgite (clay, adds bulk), loperamide - synthetic opioid, traveler's diarrhea
|
|
|
two kinds of pancreatic glands, purpose
|
exocrine - produce pancreatic digestive enzymes; endocrine - hormones, clusters (islets of langerhans)
|
|
|
purpose of cells in islets of langerhans
|
alpha - glucagon, beta - insulin, delta - somatostatin, PP (F) - pancreatic polypeptide (fx uncertain)
|
|
|
what are the effects of glucagon
|
stimulate gluconeogenesis in liver, glucogenolysis (glycogen to glucose) in skeletal muscles and liver, breakdown of triglycerides in adipose tissue, fatty acid release (lipolysis)
|
|
|
what are the effects of insulin
|
accelerate glucose uptake and utilization, glycogen formation (glycogenesis), triglyceride formation (lipogenesis), amino acid absorption and protein synthesis
|
|
|
what is the normal blood glucose level, fasting and 2hr after meal
|
70-110, under 180
|
|
|
indications for insulin therapy
|
types I and II diabetes, gestational
|
|
|
5 different kinds of insulin preparations
|
ultrashort acting - lispro & aspart, short - regular (crystalline), intermediate - NPH & lente, long - ultralente, mixed types
|
|
|
name 5 oral hypoglycemics (classes)
|
sulfonylureas, biguanides, meglitinides, thiazolidinedones, alpha-glucosidase inhibitors
|
|
|
mechanism of action of sulfonylureas
|
stimulate insulin secretion by beta cell (inhibit K channels on b cell, depolarize, Ca enters, insulin released), only good for type II
|
|
|
pharmacokinetics of sulfonylureas
|
bind to plasma proteins, metabolized in liver, excreted through kidneys, exaggerated in elderly and renal/liver disease, cross placenta
|
|
|
examples of 3 generations of sulfonylureas drugs
|
1 - tolbutamide, chlorpropamide 2 - glipizide, glibenclamide, Ggliclazide 3 - glimepiride
|
|
|
mechanism, indication, advantage, example of biguanides
|
decrease gluconeogenesis, increase glucose uptake by skeletal muscles; obese pts w/ type II; no hypoglycemia b/c they don't alter insulin; metformin
|
|
|
mechanism, indication, side effect, example of meglitinides
|
similar to sulfonylureas; type II; hypoglycemia; repaglinide, nateglinide
|
|
|
mechanism, indication, side effects, example for thiazolidinedion (TZDs)
|
activate transcription regulator (PPARy) - modulate lipogenesis, improve glucose uptake, improve insulin effect; type II; heart failure, myocardial ischemia, liver injury; rosiglitazone
|
|
|
mechanism, side effects, example of alpha-glucosidase inhibitors
|
inhibit a-glucosidase in intestine, reduce absorption of carbs, control glucose levels; GI upset, flatulence; acarbose
|
|
|
tonic colonic (gran mal) seizure drugs
|
Carbamazepine
Valproic acid (valproate) Oxcarbazepine Lamotrigine Phenytoin |
|
|
absence/petit mal seizure drugs
|
Valproic acid (valproate)
Clonazepam Ethosuximide Lamotrigine |
|
|
myoclonic seizure drugs
|
Clonazepam
Valproic acid (valproate) Topiramate |
|
|
status epilepticus drugs
|
Diazepam (i.v.)
Phenytoin (i.v.) |
|
|
partial (focal) seizures, Simple, Complex (Psychomotor epilepsy)
drugs |
Carbamazepine
Valproic acid (valproate) Phenytoin Topiramate Gabapentin |
|
|
what are some strategies for suppressing excitation of glutamate neurons
|
increase inhibition to neuron to suppress firing (increase GABA firing), block electrical activity of nerve to slow nerve impulses, block glutamate receptors so wave of excitation cannot spread
|
|
|
problem w/ phenytoin
|
fetal hydantoin syndrome, similar to fetal alcohol syndrome, avoid in women of child-bearing age
|
|
|
5 components of anesthesia
|
loss of consciousness, loss of memory, response to pain, autonomic response, skeletal muscle relaxation
|
|
|
mechanism of action of general anesthesia
|
global depression of CNS, depression of RAS (reticular activating system), lipid matrix expansion, GABA mediated inhibition at GABAa receptor chloride channel, antagonism of glutamic acid excitation of NMDA channel receptor
|
|
|
3 phases of general anesthetic
|
induction - render pt unconscious; maintenance - maintain unconsciousness, analgesia, muscle relaxation; emergence - elimination/metabolism of drug, antagonsim
|
|
|
what is MAC
|
minimum alveolar concentration - concentration of inhaled anesthetic required to prevent 50% of pts from responding to painful stimulus; Way to compare and measure various volatile agents; high MAC = low potency like nitrous oxide
|
|
|
name/describe volatile anesthetics
|
desflurane, sevoflurane, isoflurane, halothane; liquid at room temp, potent - need vaporizer, decrease bp and resp, bronchial dilation
|
|
|
signs and symptoms/tx of malignant hyperthermia
|
muscle rigidity, tachycardia, acidosis, hypercarbia, hypoxemia, hyperthermia; stop agent, give O2, dantrolene, treat acidosis, cool, support vitals
|
|
|
describe IV anesthetic propofol
|
rapid offset, hypotension, apnea, prevents n/v, ideal ambulatory anesthetic
|
|
|
describe IV anesthetic etomidate
|
block of norepi uptake, no change in bp or hr, apnea, n/v, adrenocrotical suppression; good for hemodynamic compromise
|
|
|
describe IV anesthetic ketamine
|
recreational street drug, hypertension, tachycardia, usually no apnea, provides analgesia, high intracranial pressure, dysphoria, good for hemodynamic compromise
|
|
|
2 kinds of local anesthetics and examples (amino ____)
|
amino esters - procaine, tetrocaine, cocaine; amino amides - lidocaine, bupivacaine, ropivacaine
|
|
|
how do local anesthetics work
|
blockage of voltage gated sodium channels; block nerve transmission and autonomic fx, temp sensation, light touch sensation, proprioception, motor fx
|
|
|
what is the rule about local anesthetics and potency
|
more lipid soluble = more potent
|
|
|
describe the two ways alcohol is metabolized
|
alcohol dehydrogenase - rate limiting (due to coenzyme NAD), hangover; MEOS when alcohol dehydrogenase is saturated
|
|
|
describe the pharmacokinetics of alcohol
|
95% metabolized/biotransformed, primarily in liver, smaller amount in stomach, rest is excreted in breath, urine, sweat; zero-order kinetics - rate of oxidation is independent of time and concentration
|
|
|
why do women have higher peak alcohol concentrations for equal dose
|
lower levels of gastric alcohol dehydrogenase, lower muscle-to-fat ratio, concentrate alcohol in plasma more due to higher fat content
|
|
|
describe the pharmacodynamics of alcohol
|
CNS depressant, inhibits NMDA receptor activity, activates GABA-mediated neuronal transmission leading to inhibition
|
|
|
what is wernickes encephalopathy (inadequate amount of what?)
|
ataxia - lack of coordination, confusion, impairment of short term memory; inadequate intake/absorption of thiamine
|
|
|
what is korsakoffs psychosis
|
anterograde amnesia - no new memories, severe memory loss, confabulation, meager content in conversation, lack of insight/apathy; deficiency of thiamine
|
|
|
3 txs for alcoholism
|
naltrexone - opioid receptor antagonist; acamprosate - weak NMDA-receptor antagonist, GABAa-receptor activator; disulfiram - inhibits acetaldehyde dehydrogenase leading to accumulation of acetaldehyde (hangover)
|
|
|
describe alcohol withdrawal
|
excitability of CNS, convulsions/coma/death, delirium tremens - hallucinations, confusion, psychomotor agitation, disorientation, sleep disorders
|
|
|
3 diagnostic features of FAS
|
growth restriction, craniofacial dysmorphology, CNS dysfunction
|
|
|
5 classes of antimicrobial agents
|
antibacterials, antiviral, antifungal, antiprotozoal, antihelmenthics
|
|
|
3 types of bacteria morphology
|
cocci-circle, bacilli-rod, spiral-spirochete
|
|
|
penicillin G is an example of what kind of antibiotic
|
narrow spectrum gram + cocci
|
|
|
aminoglycosides are an example of what kind of antibiotic
|
narrow spectrum gram - bacilli
|
|
|
tetracyclines are an example of what kind of antibiotic
|
broad spectrum gram +/-
|
|
|
two different effects of antibiotics w/ examples
|
bacteriostatic - inhibit growth/repro, tetracyclines, sulphoamides; bactericidal - kill bacteria, penicillins, cephalosporins
|
|
|
two examples of synergistic effects of antibiotics
|
sulfonamides + trimethoprim; clavulanate + amoxicillin (one drug prevents inactivation of the second)
|
|
|
ex of an antagonistic effect of antibiotics
|
tetracycline inhibits action of penicillin
|
|
|
6 examples of antibiotics (classes)
|
penicillin, cephalosporins, tetracyclines, aminoglycosides, sulphonamides, quinolones
|
|
|
what is the structure of penicillins
|
core of 6-aminopenicillanic acid, B-lactam ring (active), + side (R) group (determines type)
|
|
|
mechanism of action of penicillin (mainly gram + or -?)
|
bactericidal, inhibit formation of peptidoglycan cross-links in bacterial cell wall, mainly gram + bacteria (some exceptions)
|
|
|
describe penicillin resistance
|
destruction by B-lactamase enzyme - synthesized by certain bacteria (staphylococci)
|
|
|
how is penicillin resistance avoided
|
clavulanic acid - potent inhibitor of B-lactamase, combined w/ some penicillins (amoxicillin); B-lactamase resistant penicillin (coloxacillin, dicloxacillin, methicillin)
|
|
|
5 types of penicillin
|
penicillin G, penicillin V, benzathine benzylpenicillin, B-lactamase resistant penicillin, broad spectrum penicillin
|
|
|
what spectrums do the 4 classes of cephalosporins cover
|
first gram +, second gram - w/ some +, third broad spectrum w/ more gram -, fourth broad spectrum w/ more +
|
|
|
mechanism of action of tetracyclines and aminoglycosides
|
Inhibition of protein synthesis through binding to 30S ribosomal subunit
|
|
|
mechanism of action of sulfonamides
|
reversible competitive, prevent making folic acid
|
|
|
mechanism of action of quinolones
|
Inhibit bacterial topoisomerase II (DNA gyrase) enzyme (required for transcription and DNA replication)
|
|
|
indication, example, other facts about quinolones
|
complicated UTI, serious gram - infections, broad spectrum, some are discontinued, saved for serious ones b/c of side effects; ciprofloxacin
|
|
|
what does current theory suggest the cause of depression is
|
reduction in activity of one or more neurotransmitter systems in the CNS regions essential to regulating emotions - norepinephrine, serotonin, dopamine?
|
|
|
4 treatments for depression
|
SSRIs, tricyclic antidepressants (TCAs), monoamine oxidase inhibitors (MAOIs), presynaptic autoreceptor blockade, electroconvulsive therapy (ECT)
|
|
|
examples of drug names of SSRIs
|
Fluvoxamine, Fluoxetine, Paroxetine, Sertraline, Citalopram, Escitalopram
|
|
|
problems w/ SSRIs
|
withdrawal symptoms- discontinuation syndrome; inhibit cytochrome P450 - inhibit drug metabolism, toxicity; serotonin syndrome
|
|
|
common drug names of TCAs
|
Imipramine, Amitriptyline, Desipramine, Nortriptyline, Clomipramine
|
|
|
problems w/ TCAs
|
anticholinergic, antihistaminergic, block a1 adrenergic receptors, block sodium channels
|
|
|
MAOI examples
|
Phenelzine, Tranylcypromine, Moclobemide
|
|
|
problems w/ MAOIs
|
hypo/hypertension, agitation, insomnia, food interactions can be fatal - tyramine leads to hypertensive crisis; serotonin syndrome, hyperpyrexic crisis w/ opiates, hypertensive crisis w/ stimulant meds
|
|
|
two-step process to treat mania
|
antipsychotic to reduce mood to normal range (Haloperidol, Chlorpromazine, New Atypical Antipsychotics), mood stabilizer to keep it there
|
|
|
mood stabilizer drug names examples
|
lithium, valproic acid (valproate, divalproex), carbamazepine, atypical antipsychotics (Olanzapine, Risperidone, Quetiapine, Ziprasidone)
|
|
|
4 major classes of antineoplastics
|
antimetabolites, antimitotics, alkylating agents, topoisomerase inhibitors
|
|
|
mechanism of antimetabolites
|
analogues of purines & pyrimidines - competitive decrease of these metabolites to interfere w/ RNA/DNA synthesis, arrest growth and division of malignant cells during S phase of interphase
|
|
|
3 classes of antimetabolites
|
purine analogues - 6-mercaptopurine; pyrimidine analogues - 5-fluorouracil, cytosine arabinoside; antifolates - methotrexate
|
|
|
mechanism of methotrexate
|
folic acid analogue - decreases DHFR enzyme, decrease THF (essential for purine/pyrimidine bases)
|
|
|
examples of antimitotics
|
vinca alkaloids - vincristine, vinblastine; taxanes - taxol
|
|
|
mechanism of antimitotics
|
bind to tubulin, decrease polymerization, prevent microtubule formation (vinca alkaloids); stabilize microtubules, prevent separation of chromosomes (taxol)
|
|
|
mechanism of alkylating agents
|
attach an alkyl group to DNA, cross-link DNA strands, strands unable to uncoil, abnormal base-pairing, DNA damage and cell death
|
|
|
3 types of alkylating agents
|
nitrogen mustards - cyclophosphamide, chlorambucil; ntirosureas - carmustine; platinum-based drugs - cisplatin
|
|
|
mechanism of topoisomerase inhibitors
|
block DNA ligation, DNA breaks, interrupt protein synthesis and cell division, apoptosis
|
|
|
types of topoisomerase inhibitors
|
topoisomerase I inhibitors - inrinotecan; topoisomerase II inhibitors: antineoplastics -doxorubicin, etoposide antibiotics - quinolones
|
|
|
4 other antineoplastics
|
antitumor antibiotics - interfere w/ RNA/DNA, actinomycin, bleomycin; hormones - selective suppression of tumour cells, tamoxifen; retinoids - vit A analogues, stimulate apoptosis, fenretinide; antiangiogenic agents - interfere with neovascularization
|
|
|
what is a genetic protective factor for alcoholism?
|
single point mutation for aldehyde dehydrogenase; excessive drinking increases acetaldehyde levels causing vasodilation
|
|
|
name 3 isoenzymes of cyclooxygenase enzyme
|
cox-1 (widely distributed, kidney), cox-2 (limited distribution, inflammation), cox-3 (mainly in brain, slightly different)
|
|
|
3 types of antipyretics
|
NSAIDs (ASA, ibuprofen), Acetaminophen, selective cox-2 inhibitors (celecoxib)
|
|
|
mechanism of action of ASA
|
irreversible inhibition of cox-1 and 2, decrease production of prostaglandins and thromboxanes
|
|
|
how does ASA reduce pain, fever, thromboembolic disease
|
inhibition of PG synthesis, prevents sensitization of pain-transmitting nerve fibres to chemical mediators released by tissue injury, inhibits action of transmitters involved in pain pathways; reset temp center in hypothalamus; antiplatelet effect
|
|
|
reyes syndrome associated w/ ASA
|
brain/liver damage can be fatal, children/adolescents who have viral infection and take aspirin
|
|
|
mechanism of action of acetaminophen
|
not fully understood, inhibits cox enzyme
|
|
|
name classes of drugs w/ examples for anxiety/sleep disorders
|
barbiturates (phenobarbital), benzodiazepines (diazepam, pams), Buspirone, Z drugs (zopiclone), serotonin re-uptake inhibitor antidepressants
|
|
|
how is CNS neurotransmission controlled (what controls its excitability?)
|
GABA neurons control CNS excitability by suppressing glutamate nerve firing
|
|
|
mechanism of benzodiazepines
|
promotes GABA - BZ1 (inhibition sleep/wake part of CNS), BZ2 (inhibition of other parts of CNS)
|
|
|
what are the 3 categories of benzodiazepines
|
short (oxazepam, lorazepam), intermediate, long acting (diazepam)
|
|
|
3 ways to increase serotonin to reduce anxiety (what is a precursor for it?)
|
serotonin agonist (buspirone), serotonin reuptake inhibitor antidepressants, dietary tryptophan (precursor amino acid)
|
|
|
2 classifications of analgesics
|
narcotic analgesics (opioids) and non-narcotic analgesics (antipyretics)
|
|
|
4 types of opioids w/ examples
|
endogenous (endorphines), plant alkaloids (morphine, codeine, thebaine), semisynthetic (diamorphine/heroin, hydromorphine), synthetic (pethidine/meperidine, methadone, fentanyl)
|
|
|
two types of opioid antagonists w/ examples
|
antagonists - naloxone, mixed agonists/antagonists - pentazocine
|
|
|
therapeutic use of naloxone
|
tx of opioid drug overdose (antidote), dx and tx of opioid dependence, should be available when opioid drugs are run through IV
|
|
|
how is opioid dependence treated
|
methadone, buprenorphine, naloxone
|
