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223 Cards in this Set
- Front
- Back
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3 parasympphatolytic drugs
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1. atropine
2. scopolmine 3. ipratropium |
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sympathoplegics
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1.CNS agents:
(alpha 2) clonidine, methyldopa (prodrug) 2. gag.-r-blockers: hexamethonium, trimethaphan 3. postganglionic symp. nerve terminal blockes: reserpine, guanethidine 4. adrenorecepteo blockers- prazosin (alpha1), prpranolol(beta)) |
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name the types of sumpathomimetics
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1. direct agoinsts
(alpha agonists, beta agonists) 2. indirect acting (releasers, uptake inhibitors) |
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direct acting sympathomimetics:
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EPI
NE ISOPROTERENOL (synthetic) DOBUTAMINE (alpha,beta D1, D2) |
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beta sympatomimetics:
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dobutamine- beta1 (=CHF)
metaproterenol- beta 2(=asthma) terbutaline- beta2 (=reduce premature labour) albutelol- beta2 (=relive bronchospasm) |
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alpha symphatomimetics:
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phenyleprine- alpha1>alpha2 (VC thus activate baro reflex-bradycarida) raise BP reduces SVT
methoxamine- alpha1 (") PSVT clonidine- alpha2 (reduce HT) |
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indirect sympathomimetics:
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1. displacement of stored catecholamines from nerve endings:
A.amphetamine (block MAO)-(treat depression,hyperactivity, apetite control) B. tyramine- 2. reuptake inhibitors: A. cocaine- block reuptke B. tricyclic anti depressent- IMIPRAMINE |
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3 ACE inhibitors:(not prodrugs)
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captopril
enalaprilat lisinopril |
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3 ACE inhivitors (prodrugs)
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benazepepril
fosinopril ramipril |
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side affect of ACE inhibitors:
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cough and angioedema (due to high bradykinin)
contraindicated in pregancy-cause fetal HT,anuria, renal failure |
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AT receptor blockers:
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losartan
valsartan ibesantan |
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alpha blockers:
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1.phentolamine
2.phenoxybenzamine 3. prazosin, terazosin, doxazosin |
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phentolamine:
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competitive antagonits of both alpha 1&2
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side effects of phentolamine:
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tachcardia
arrhythmia MI ( contraindicated in low coronary BF) diarrhia' incresed gastric acid secretion |
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phenoxybezamine
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irriversible blocker with low alpha 1 selectivity
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phenoxybenzamine side effects:
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1. decrease in TPR (postural hypotension) thus tachycardia
2. inhibition of ejaculation 3. fatigue sedation nausea |
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prazosin. teazosin, doxazosin
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selective competitive blockers of alpha 1
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half life of prazosin. teazosin, doxazosin
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prazosin 3 H- bioavailability 50%- should be given with diuretic due to NA & wate retention
terzosin- 9-12H for BPH doxazosin- 22 H |
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use pf alpha antagonits
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1. pheochromocytoma
2. TH emergencies 3. chronic HT 4. urinary obstruvtion due to BPH 5. male sexual dysfunction |
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alpha 1
alpha 2 |
alpha 1 = Gq
alpha 2 = Gi |
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beta 1,2,3
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Gs
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M1
M3 M5 |
Gq`
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M2
M4 |
Gi
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major groups of anti hypertensive drugs
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1. diuretics
2. sympatoplegics 3. vasodilators 4.AT aantagonists |
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main diuretics used in hypertension
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hydrocholorothiazide
furosemide |
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main symphatoplegic used in hyper tension
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1. clonidine
2. methyldopa 3. ganaloion blockers 4. reserpine 5.alpha 1 blockers 6. beta blockers |
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main vasodilators used in hypertension
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1. hydralazine
2. minoxidol 3. nifedipine 4. nitroprusside |
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angiotensin antagonists used in hypertension
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ACE inhibitors
angiotensin receptor blockers |
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major groups of anti hypertensive drugs
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1. diuretics
2. sympatoplegics 3. vasodilators 4.AT aantagonists |
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main diuretics used in hypertension
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hydrocholorothiazide
furosemide |
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main symphatoplegic used in hyper tension
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1. clonidine
2. methyldopa 3. ganaloion blockers (hexamethonium, trimethaphan) 4.post ganglionic nerve terminal blockers (reserpine, guanethisine, MAO inhibitors) 5.alpha 1 blockers (prazosin) 6. beta blockers (propranolol) |
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main vasodilators used in hypertension
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1. hydralazine
2. minoxidol 3. CCB (nifedipine, verapamil, diltiazem) 4. nitroprusside, diazoxin, fenoldopan |
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angiotensin antagonists used in hypertension
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ACE inhibitors (captopril)
angiotensin receptor blockers (losartan) ((aliskiren- blocks renin)) |
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mechanism of nitroprusside, hydralazine
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releease of NO from endothelium or drug
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mechanism of minoxidil sulfate, diazoxide
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hyperpolarization of endothelium by openning of K channels
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mechanism of verapamil, diltiazem, nifedipin r
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eduction of Ca influx
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mechanism of fenoldopam
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activation of dopamin receptors
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E=? (effect)
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E= Emax X Concentration/ concentration + EC 50
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B=? (the relationship between the drug and the receptor)
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B= Bmax X C/
C + Kd Bmax= total num of receptor sites Kd= dissociation constant (the smaller the Kd the higher the affinty) |
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efficacy
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the maximal response that can be achieved by the drug (Emax)
1, determined by the dru's mode of interaction with the receptor 2. characteristics of the receptor effector system |
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potency
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the conc. EC50 or dose ED50 of a drug required to produce 50 % of the drugs max. effect
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list the direct acting cholinomimetic drugs:
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1. acethylcoline
2. bethanechol 3. carbachol 4. pilocarpine 5. nicotine |
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list the indirect acting cholinomimetic drugs:
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1. edrophonium
2. neostigmine 3. physiostigmine 4. pyridostugmine 5. echothiophate 6, parathione |
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all of the cholinomimetic drugs work on both N&M receptors, what are the exeptions?...
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M- betanechol (due to the methylated choline), pilocarpine
N- nicotine |
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the shortest nd longest acting direct cholinomimetics
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shortest- acethycholine 5-30 S
longest- nicotine 1-6 H |
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the shortest nd longest acting indirect cholinomimetics
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edrophonium- 5-15 min
parathion 7-30 days |
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give a clinical use of a direct cholinomimetic drug:
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glucoma (carbachol)
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give a clinical use of a indirect cholinomimetic drug:
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myastenia gravis (neostigmine)
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cholinomimetic toxicity:
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DUMBBELESS
Diarrhea Urination Miosis Bronchoconstriction Bradycardia Excitation of skeletal muscle &CNS Lacrimation Salivation Sweating |
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Ca channel blockers:
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Dihydropyridines: amlodipine
nifedipine (nisodipine, felodipine) Nondihydropyridines: verapamil diltiazem |
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half life of CCB
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3-6 h
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indication for CCB
|
prophylatic for both effort and vasospastic angina
HT SVT migraine, preterm labour, stroke raynond phenomenom hemorrhagic stroke |
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CCB effects
|
BV relaxation (also uterus, gut brochi)
reduced HR & contractability AV nodal arrythmia prevention |
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CCB toxicity
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constipation, pretibial edema, mausea, flushing. dizziness
HF, AV bloc, SA depression |
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muscarinic blockers:
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1. atropine
2. scopolamine 3. ipratropium ... |
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effects of antimuscarinic blockers:
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CNS- sedations, amnesia, delirium, antimotion sickness, antiparkinson action
EYE- (M3)cyckoplegia, mydriasis Bronchi-(M3) bronchodilation GI-(M1,3) relaxation GU-(M3) urinary retention Heart-(M2) brady...than tacycardia BV- block of VD Glands-(M1,3) reduction of salivation sweating, less gastric secretion |
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clinical use of antimuscarinic agents:
|
CNS- reduce parkinsonism and motion sickness (scoloamine)
EYE- reduce mydriasis and cycloplegia Brochi- dilation GI- reduce motility GU- reduce urgency all- antidote to organo phosphate poisioning |
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toxicity of antimuscarinic agents:
|
"dry as bone, red as bit; mad as a hatter"
atropine fever contraindicated to babies- hyperthermia, glucome patients, PBH |
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|
nicotinic antagonists
|
1. ganalione receptor blockers-
Hexamethonium, Mecamylamine Trimethaphan 2.neuromuscular blockers- tubocrurarine |
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effects of ganglion receptor blockers:
|
CNS- improvment of tourette syndrome
and reduction of nicotine starving Eye- mydriasis cycloplegia GI- contipation GU- reduced contractability Vessels- orthostatic hypotension Glands- reduction of salivation |
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toxicitis of ganglion blockers:
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dry mounth, blurred vision, constipation, sexual ompairment
thus rarly used |
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effects of neuromuscular blocking drugs
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1. Nondepolarizing- tubocrurarine
flaccid paralysis for 30-60 min 2. Depolarizing group- (N agonist), succinylcholine- also flaccid paralysis |
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choline esterase regenerator
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Pralodoxime- a chemical antagonists that contain an oxime group with an high affinty to the phosphate of the organophosphate, my displace the enzyme before aging
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D1=
D2= |
D1= Gs
D2= Gi |
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alpha 1 (4 actions)
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VC
mydriasis hair erction glycogenolysis |
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alhpa 2
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inhibits tranmitter release
stimulate platlet aggreagtion VC lipolysis inhibition of insulin release |
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beta 1
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heart- stimulate reate and force
stimulate renin release |
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beta 2
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airway& uterine relaxation,VD
glycogenolysis unsuline release tremor |
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beta 3
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lipolysis
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D1
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VD of renal and splanchnic arteries
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D2
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inhibits adenylyl cyclase at the nerve terminals
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a direct symphatomimetic
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epinephrine
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an indirect sympathomimetics (releases)
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amphetamine
epedrine tyramine |
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an indierct sympathomimetics (uptake inhibitors)
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cocaine
tricyclic antidepressants |
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selective alpha 1
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phenylephrine
midodrine |
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selective alpha 2
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clonidine
oxymetazoline |
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beta agonist
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isoproterenol
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beta 1 selective
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dobutamine
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beta 2 selective
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albuterol
metaproterenol terbutaline |
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dopamine agonist
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dopamine
bromocriptine |
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clinical uses of catecholamines
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treatment of anaphylaxis, asthma, glucoma, shock. HF
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clinical uses of symphathomimetics
amphetamine epherine phenylephrine cocaine |
amphetamine- hyperkninetic disorder, obesity
epherine- utrinary incontinance, neurogenic hypotension phenylephrine- mysriasis, VC cocaine- local anasthsia with VC |
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catechoamine toxicity:
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excessive VC ,arrthmias, MI, hemorrhagic stroke, pulmonary edema or hemmorhage
(low CNS penetrtion) |
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symharomimetics toxicity:
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phenylisoprrophylamine- from nervousness anorexia and insomnia to anxiety, agressiveness, paranoidism and convulsions, HT; tachycardia, tremor,
cocaine- arrythmias, MI, sonvulsions |
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3 types of angiotensin antagonists
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1, ACE inhibitors
2. angiotensin receptor blockers 3. renin inhibitor |
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ACE inhibitors
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captopril
enalapril fosinopril |
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angiotensin receptor blockers
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losartan
valsartan |
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renin inhibitor
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aliskiren
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ACE inhibitors toxicity:
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cough renal damage (although protect diabetic kidney)
contraindicated at preganancy |
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angiotensin receptor blockers toxicities:
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less cough
also contraindicated at preganancy |
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renin inhibitor toxicities:
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headache
diarrhea hyperkaelmia |
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alpha 1 selective blocking drugs:
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Prazosine
doxazosin terazosin tamsulosin |
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alpha 2 slective blocking drugs:
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yohimbine
rauwolscine |
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irreversible non selective long acting alpha blocking drugs:
and duration of action |
phenoxybenzamine
(slightly alpha 1 selective) 48 H |
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revesible non selective shorter avting alpha clocking drugs:
and duration of action |
phentlamine
20-40- min |
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effect of nonselective alpha blockers
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arterial and veinous VD with a compensatory tachcardia
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what is an epinephrine reversal
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a predictable effects of drugs with alpha blockers action
is a reversal in blood pressure effect of epinephrine from a pressure (alpha) to a depressor (beta 2) |
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effect of alpha 1 blockers
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no blockage of alpha 2 on the heart fibers thus less reflex tachycardia
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clinical uses of non selective alpha blockers
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presurgica ltreatment of pheochromocytoma in preveting HT
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clinical uses of selective alpha 1 blockers
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prevention of urinary histancy and retention in BPH
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toxcity of alpha blockers
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orthostatic hypotension
(relex techcardia in a case of nonselective) nausea and vomiting |
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antiarrthythmic drugs classification
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1. Na channel blockers
2. Beta blockers 3. K channel blockers 4. Ca channel blockers * miscellaneous (adenosine, K, Mg) |
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class 1 subdivision of antiarrhytthmic drugs
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IA- AP prolongation-(procainaminde)
IB- AP shortennig in some cardiac tissues (lidocaine) IC-no effect on AP-(flecainnide) |
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1.class IA antiarrhythmic
2.uses 3. side effects 4. interactions |
1. procainamide
Quinidine ((amiodarone)) 2. all types of arrhythmias (mostly those in acute MI) 3. hypotension reversible lupus quinidine- cinchonism, cardiac depression, GI upset, AI reactions torsads de point 4, Digoxin- clearance may be imparied by quinidine hyperkalemia- may exacerbate the toxicity |
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1.class IB antiarrhythmic
2.uses 3. side effects 4. interactions |
1. Lidocaine
Mexiletine Phenytoin 2. acute ischemic VENTRICULAR arrhythmias following MI 3. lidocaine always IV or IM not orally (due to high 1st pass &cardiotoxic metabolits) CV depression anesthtsic toxicity 4. hyperkalemia increases cardiac toxicity |
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1.class IC antiarrhythmic
2.uses 3. side effects 4. interactions |
1. Flecainide
Ecainide Propafenone 2. flecainide- atrial and ventricular arrhythmias, refractory ventriculat tachyarrythmia, 3. local anesthetic like CNS toxicity 4. hyperkalemia increases cardiac toxicity |
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class 2 antiarrhtyhmic drugs
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Propanolol
Esmolol ((sotalol, amiodarone)) *reduction od cAMP, Na, Ca of abnormal pacemakers |
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class 2 antiarrhtyhmic drugs
1. uses 2. toxicity |
1. esmolol- short acting for actue arrhythmias
propanolo, metoprolol and timolol- prophylactic for post MI 2. cardiac depresion |
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classa 3 ant arrhythmic drugs
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1. sotalol
2. ibutilide 3. dofetilide 4. amiodarone (also prolongs AP) * prolongation of AP duration |
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class 3 antiarrhtyhmic drugs
1. uses 2. toxicity |
1. sotalol- for torsade de points ans sinus arrythmias or asthma for excessive use of beta blockers
ibutilide, dofetilie- atrial flatter and fibrillation 2. induction of torsade de points * AMIODARONE- all types of arrhythmias block Na K CA & beta used only for the resistant arrhythmias 2. microcrystaline deposits in the skin cornea thyroid. parasthesia tremor pulmonary fibrosis (DRONEDARONE less toxic) |
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class 4 anti arrhythmic drugs
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1. verapamil
2. diltiazem *Ca blockers |
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class 4 anti arrhythmic drugs
1. uses 2. toxicity |
1. AV nodal reentry (sinus tacycardia) convertion to sinus
2. significant reduction of the BP' heart contractability, AV cinduction. |
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miscellaneous antiarrhythmic drugs:
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1. adenodine
2. K ion 3. Mg ion |
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miscellaneous antiarrhythmic drugs:
1.uses 2. side effects 3. toxicity |
adenosine:
1.in AV nodal arrythmias 2. flashing and hupotension trasient chest pain, dyspnea. 3. AV block K ion: 1. depress ectopic pace makers especially from digitalis toxicity 3. reentry arrythmias Mg ion: 1. similar to k teatment of torade de points |
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anti arrhythmic drug with the shortest half life?
longest ? |
shostest - adenosine 3 s
longest - amiodarone -1-10 weeks |
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mention the beta 1 blockers
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1. metoprolol
2. atenolol 3. esmolol 4. acebotolol (all the rest are non selective) |
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mention those beta blockers with a partial agonist activity
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1, acebolotol
2. labetolol (also parial on beta 2) 3. pindolol |
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mention the beta blocker with the higheset lipid solubility
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propranolol
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metion the beta blocker with longest half life and the one with the shortest half life
|
nadolol- 14-24 H
esmolol- 10 min |
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clinical use of beta blockers
|
1. HT (reduction in CO & renin secretion)
2. angina pectoris (reduced CR &force) 3. post MI arrhythmia ( reduced automaticity) 4. SVT 5. HF (unknown) 6. hyperrophic cardiomyopathy 7. migrain prophylaxis 8. thyrotoxicosis (reduced conversion of t4 to t3) 9. glucoma (reduction of aquaous humor) |
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toxicity of beta blockers
|
bradycardia, AV block, HF
brinchoconstriction, reduced unsulin secretion, sedation fatigue sleep disturbances |
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drug for glucoma
|
beta blockers (timolol)
PG cholinomimetic (physiostigmine) alpha agonists alpha 2 selctive (praclonidine) diuretics (acetazolamide) |
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drugs used in angina pectoris
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VD- nitrates
cardiac depressents- CCB beta blockers metaolism modifires and rate inhibitors |
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types of nitrates
|
very short acting- inhald amyl nitrate- 3-5 min
short- sublingual nitroglycerin or isosorbide dinitrate- 10-30 min intermediate- oral/ sustained release nitroglycerin or isosorbid di/mono nitrate- 4-5 h long- transdermal nitroglycerin- 8-10 h * tolerace develope after 8-10 h |
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toxicity of nitrates
interaction |
1.tachycardia (from baro reflex)
2.orthostatic hypotension 3.headache from meningeal artery VD 1. sildenafil- PDE 5 inhibitor maycause together hypotension& hypoperfusion to vital organ 2. nitrIte- prevent cyanide poisioninig |
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mention 5 lipid lowering drugs
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1. HMG-CoA reductase inhibitors (statins)
2. Rezins 3. Ezetimibe 4. Niacin 5. Fibrates (Gemfibrizil) |
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HMG-CoA reductase inhibitors
|
1. lovastatin
2. simvastatin 3. atorvastatin 4, pravastatin 5. fluvastatin 6. rosuvastatin |
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HMG-CoA reductase inhibitor
1. mechanism of action 2. clinical use |
1. statin is a straxtural analogue of HMG-CoA, lead to increase in the LDL-R which clear LDL and VLDL.
2. reduction of LDL, rosuvastatin,atorvastatin and simvastatin also reduce TG anf elevate HDL |
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HMG-CoA reductase inhibitor toxicity
and contraindications |
elevation of liver aminotransferase,
muscle CK , rhabdomyolusis. contraindicated with c-450 inhibitors such as grapefruit juice also should not be used during pregnancy. |
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what types of Resins so u know?
|
1. cholestyramine
2. colestipol 3. cholesevelam |
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Resins
1. mechanism of action 2. clinical use |
1, bile acid binding resins are large polymers that bind bile and similar steroids and inhibit their absorption.
thus liver synthsizes more LDL-reduction of cholesterol pool 2. used in patients with hypercholesterolemia, also used to reduce pruritus in a case of cholestasis. |
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side effects of resins
|
bloating, constipation, inpleasent gritty taste
impaired absorption of vitamins-(K, folate) and drugs- digitalis, thiazide, wafarin, pravaststin, fluvastatin |
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Ezetimabe
1. mechanism 2. clinical use |
a prodrug coverted to the active glucoronide form in the liver whice block the absotption of cholesterol and phytosterols thus excreted into the feces, reduction in the hepatic pool
and elevated LDL-R used in hypercholesterolemia and phytosterolemia |
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ezetimabe toxicity
|
when combined with statins some hephatic toxicity
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Niacin
1. mechanism 2. clinical use |
1. in the liver reduces VLDL synthesis whice in turn reduced LDL levels
in adipose activate hormone sensitive lipase thus reduces FA and TG 2. reduction of LDL and TG, elevtion of HDL thus is used to treat hypercholesterolemia, hypertrigliceridemia and low HDL levels. |
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niacin toxicity
|
cutaneous flushing, nausea, abdominal discomfort, pruritus.
hepatotoxicity, hyperuricemia impaired carbohydrate tolerance |
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Fibric acids
|
1. gemfibrozil
2. fenofibrate |
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|
Fibric acids
1. mechanism 2. clinial use |
1. act as a ligand for PPAR-alpha, peroxisome proliferator activatorreceptor alpha which results in an induction of LPL by asipose tissue, clear TG form the blood,
in the liver FA stimulate FA oxidationwhich limits the TG supply and decreases the VLDL, elvated the HDL usually there is no effect on LDL or slight elevation 2. used in hyper trigliceridemia, due to there interaction with the LDL are given together with another VLDL and LDL lowering drugs |
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fibric acid toxicity
|
nausea
skin rashes decrease inthe WBC or hematocrit anticoagulent potentiation increased cholesterol gallstone formation |
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agents in insuline resistance
|
1. solfunylurea
2. metformine 3 .thiazolidinediones 4. alpha glucosidase inhibitors |
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3 types of sulfonylureas
|
1. tolbutamine
2. glyburide 3. glipizide |
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sulfonylureas
1. mechanism of action 2. contraindications |
1.*. stimulate insuline release
*. inhibit glucagon release *. increase insuline binding to target tissues and receptors 2. hepatic or renal insufficiency (decreased excretion may lead to hypoglycemia) preganancy- deplete from the fetal pancrease. side effects: rash,allergic reactions weight gain |
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metformin (Biguanide)
1. mechanism 2. side effects 3. contraindications |
an euglucemic agent (not hypoglycemic)
1.*.decrese hepatic glucogneogenesis *. increased peripherial insulin sensitivity *. slowing of glucose absorption from the GI *. reduction of plasma glucagon 2.nausea, vomiting,diarrhea decreased absorption of B12 3. hepatic or renal insufficiency, since they may lead to lactic acidosis. |
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Thiazolidinediones -2 types:
|
1. troglitazone- causes liver cirrosis
2. rosiglitazone- more effective |
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Thiazolidinediones:
mechanism of action and side effects |
1. acute post receptor insuline mimetic activity
2.induce PPAR gamma- whicw blocks resistin synthesis and increases insuline resistance 3. decreases PAI-1 levels in the plasma 4. decrease TG and elevate HDL 5. decrease LDL peroxidation processes 6. direct vascular antithrombogenic effect side effects: fluid retention, anemia edema, elevate the HF risk |
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alpha glucosidase inhibitors
mechanism and side efects |
block it in the intestinal brush border thus decreases starch and dissacharide absorption
do not cause hypoglycemia! side effects: flatulence, diarrhea, abdominal pain |
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digitalis
1.action 2. clinical uses 3.heart responses |
1. inhibition of Na/K ATPase
2. CHF- reduces the synptomes but does not prolong life atrial fibrilation/flatter- reduced conduction velocity 3. early response- shortened OT interval, T inversion. ST depression late response- increased automaticity-extrasystole, tachycardia, fibrillartion |
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digitalis
1. interactions 2. toxicity |
1, Quinidine- reduce digoxin clearance
lowered EC K/ Mg- inhibited elevated EC Ca- facilitated 2. arryhthmia, vomiting, diarrhea confusion, hallocinations (severe intoxication inhibit all pacemaker activity) treatment: 1. correction of K &Mg deficiency 2. antiarrhythmic drugs- lidocain, phenytoin 3. Digoxin antibodies- Digibind |
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ACUTE CHF treatment:
|
A. diuretics
1. furosemide- reduction of pulmonary edema 2. hydrochlorothiazide 3. spironolactone/epelrenone-chronic B. beta 2 agonists (acute) 1. dobutamine 2. dopamine C. PDE inhibitors (acute) 1. amrinone 2. milrinone D. vasodilators (acute) 1. nitroprusside 2. nitroglycerine 3. nestritide (natriuretic+VD) |
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CHRONIC CHF treatment:
|
A. diuretics
1. furosemide- reduction of pulmonary edema 2. hydrochlorothiazide 3. spironolactone/epelrenone- B. angiotensin antagonists- (chronic) 1. losartan 2. captopril C. beta blockers (chronic) carvediol, labetelol, metoprolol F. vasodilators (hydralyzine & isosorbid dinitrate for chronic) |
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posotive ionotropic drugs
|
1.digoxin
2.beta agoinist-dobutamine, dopamine 3. PDE inhibitors- amirnone, milrinone |
|
|
1st order drug elimination:
O order drug elimination |
Rate of elimination=clearane X conc.
Rate of elimination= Vmax X conc./ Km + conc. |
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half life
|
T1/2= 0.7 X Vd / clearance
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clearane
extraction ratio |
clearance=rate of elimination/conc.
OR clearance= BF X extraction extraction ratio= conc. IN -conc. OUT / conc. IN |
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K loosing diuretics
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1. acetazoleamide
2. furosemide, ethacrynic acid 3.hydrochlorothiaide * always apply volume replacement to diuretics in order to prevent hamoconcentration |
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Acetazolamide (carbonic anhydrase unhibitors)
1. effect 2. clinical uses 3. side effects |
1. bicarbonate anf K depletion-hypokalemic metacolic acidosis
2. glucoma, mountain sickness, edemas only in a case of metabolic alkalosis 3. drowsiness and parastesia, cross allergy,renal Ca stones, contraindicated at liver impairment- to prevernt hepatic encephalopathy due to increased NH4 reabsorption |
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loop diuretics (furosemide, ethacrynic acid)
1.effect 2. clinical use 3. side effects |
1. increased Ca excretion
hypolaemic metabolic alkalosis pulmonary VD effect 2. edematous state, especiallt pulmonary edema treatment of hyperlycemia 3. may cause hypovolemia ototoxicity, allergy |
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hydrochlorothiazide
1. effect 2. clinical uses 3. side effects |
1. hpokalemic metabolic alkalosis, reduction in the urine Ca content,dilutional hyponatremia
2. HT, chornic therapy for edema, control of renal stone formation 3. hypnatremia, K wasting in the long term. hyperglycemia in diabetics, elevation of uric acid and lipid levels allergy |
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accumulation factor
loding dose dosing rate maintainance dose |
accumulation factor= 1/ fraction lost in 1 dosing interval
loading dose= target con. X Vd dosing rate= rate of elimination= clearance X target conc. maintainance dose= dosing rate X dosing intervals |
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K sparing diuretics:
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1. spironolactone
2. epelrenone 3. amiloride 4. triamterene |
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K sparing diuretics:
1. mechanism 2. clinical use 3. side effects |
1. spironolactone & epelrenine- reduce expression of genes related to n channels and Na/K ATPase
amiloride & triamtrene- blockng Na channels * both cause hyperkalemic metabolic acidosis 2. in aldosteronism (HF,chirrosis) 3. hyperkalemia, spironolactone- gynecomasti, antiandrogenic effect also epelrenine but less. |
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osmotic diuretics- mannitol
1. mechanism 2. clinical use 3. side effects |
1. water reabsorption, lead to increased Na excretion
2, reduction of intraocular pressure in acute glucoma, and intracranial pressure 3. hyponatremia, pulmonary edema hypernatremia, following water excretion, also headache nausea vomiting |
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1.ADH agonists-
2. emechanism 3. clinical use 4. side effects |
1. ADH, desmopressin
2. placement of AQP-2 3.in pituitary diabetes insipidus (should be used together with salt restriction thiazide and loop diuretics) 4. hyponatremia |
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1. ADH antagonists
2. emechanism 3. clinical use 4. side effects |
1. demeclocycline, conivaptam, lithium
2. conivaptam-V1 &V2 antagonist demeclocycline,lithium- inhibit water channel insertion. 3.SIADH 4. demeclocycline- bone and teeth defects, Li cause diabetes insipidus. |
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1. iron supplements
2. toxicity |
1. Oral-ferrous sulfate,ferrous gluconate, ferrous fumarate
Parenteral- iron dextran * contraindicated at hemolytic anemia due to elevated iron stors 2. acute- necrotizing gastroenteritis, shock, metabolic acidosis, coma, death treated with- deferoxamine,an iron chelator chronic- hemochromatosis, defereoxmine |
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B12 supplements
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1. cyanocobalamine, hydroxycobalamine
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hematopoetic growth factors
1.red cell colony stimulating factor 2.myeloid growth factors 3. megakryocytes growth factor |
1. erythtopoetin, darbepoetin alpha (glycosylated with longer half life)
2. filgrastin (G-CSF)- stimulate neutrophils sargramostim (GM-CSF)- neutrophils,myeloid & megakaryocytes are used for neutropenias, stem cell mobilization Tx- G-CSF- minimal,cone pain GM-CSF- fever, arthralgia, capilary damage,edema. 3. oprelvekin (IL-11)- in thrombocytopenia Tx- fatigue, headeche, dizziness, fluid retention. |
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list 3 types of anticoagulants
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1. heprain
2. direct thrombin inhibitors 3. warfarin |
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heparin
1. types 2. mechanism 3. clinical uses 4. side effects |
1.unfractionated heparin
LMH- enoxaparin, dalteparin (longer duration and bioavailability) Fondaparinux-LMH +HMH 2. UMH -bind AT3 and inactivates F10 and thrombin (aPTT) LMH& fonfaparinux- bind AT3 and F10 only. 3.rapid effect- DVT, PE,acute MI 4. excessivr bleeding, hemorhagic stroke, (protamine can partially reversve LMH, HIT (usually UNH) |
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direct thrombin inhibitors
1. types 2. mechanism 3. clinical uses 4. side effects |
1. lepirudin, bivalirudin, desirudin,argatroban
2. argatroban bind thrombin active site, all the rest bind also to the thrombin substrate, bivalirudin also inhibits platlet activation. 3. used when HIT occurs (aPTT) 4. bleeding, prolong use of bivalirudin may induce Ab that prolongs its action. |
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Wafarin & Cumarin
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1. both interfere with the post translational modification od vit K factors, action is seen only after the previous factors eliminated, can be reveresed by vit K.
2. for chronic use, like heparin 3. bleeding, though initially hyper coagulability may occur together with dermal vascular necrosis. (due to protein C deficiency),bone defect and fetal hemorrhage 4. p450 inducers- (barbaiturtes,rifampine) reduce effect,while inhibitors amiodarone and cimentidine reduce. |
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types of thrombolytics agents:
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1.tPA- alteplase, reteplase,tenecteplase
2. streptokinase |
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list 3 types of anticoagulants
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1. heprain
2. direct thrombin inhibitors 3. warfarin |
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heparin
1. types 2. mechanism 3. clinical uses 4. side effects |
1.unfractionated heparin
LMH- enoxaparin, dalteparin (longer duration and bioavailability) Fondaparinux-LMH +HMH 2. UMH -bind AT3 and inactivates F10 and thrombin (aPTT) LMH& fonfaparinux- bind AT3 and F10 only. 3.rapid effect- DVT, PE,acute MI 4. excessivr bleeding, hemorhagic stroke, (protamine can partially reversve LMH, HIT (usually UNH) |
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direct thrombin inhibitors
1. types 2. mechanism 3. clinical uses 4. side effects |
1. lepirudin, bivalirudin, desirudin,argatroban
2. argatroban bind thrombin active site, all the rest bind also to the thrombin substrate, bivalirudin also inhibits platlet activation. 3. used when HIT occurs (aPTT) 4. bleeding, prolong use of bivalirudin may induce Ab that prolongs its action. |
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Wafarin & Cumarin
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1. both interfere with the post translational modification od vit K factors, action is seen only after the previous factors eliminated, can be reveresed by vit K.
2. for chronic use, like heparin 3. bleeding, though initially hyper coagulability may occur together with dermal vascular necrosis. (due to protein C deficiency),bone defect and fetal hemorrhage 4. p450 inducers- (barbaiturtes,rifampine) reduce effect,while inhibitors amiodarone and cimentidine reduce. |
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types of thrombolytics agents:
1. types 2. mechanism 3. clinical uses 4. side effects |
1.tPA-(alteplase,> reteplase, >tenecteplase)
streptokinase 2. tPA- act on plaminogen bound plamin, streptokinase not an enzyme just help to cinversion 3. PCI, stroke, PE 4. bleeding, cerebral hemorrhage, previous Ab for streptococcus |
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mention 4 antiplatlet drugs
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1. aspirin
2. glycoprotein IIB/IIIA inhibitors (abciximab, epitibatide, tirofiban) 3. ADP inhibitors (clopidogrel, ticlopidine) 4. PDE/ adenosine inhibitors (dupyridamole, cilostazol) |
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mention 4 antiplatlet drugs
1. mechanism 2. clinical uses 3. side effects |
1.aspirin- cox inhibitor
abciximab- Ab that inhibits glycoprotein IIB/IIIA receptor binding to fibrin clopidogrel- ADP receptor inhibition dipyridamole/cilostazol- elevating IC cAMP in platlets by inhibiting PDE 3 and inhiibit adenosine uptake by endothel thus it bind platlets and prevent their aggregation. 2. aspirin- prevent TIA ischemic stroke. glycoprotein IIB/IIIA inhibitors- prevent restenosi after angioplasty clopidogrel- in a case of aspirine allergy, prevet thrombus after stent pacement dipyridamole- intermitent claudication of peripherial arterial disease. 3. aspirin-GI&CNS effects glycoprotein IIB/IIIA inhibitors- thrombocytopenia, ticlopidine- bleeding neuthropenia TTP dupyridamole- headache palpitations |
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drugs used in bleeding disorders
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1. vitamin K- deficiency mostly in new borns and elderl, Phytonadione (vit K1)
also given in warfarin excess 2. F8 & F9 for hemophilia vasopressin V2 receptor agonist- Desmopressin acetate- increases VWF& F8 (in hemophilia A and VWD) 3. antiplasmin agent- Aminocaroic acid & Tranexamic acid- inhibit fibrynolysis by inhibiting plasmin activation Aprotinin- serine protease inhibitor that inhibit fibrinolysis by plasmin and plasmin streptokinase complex |
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agents used in asthma
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1. beta agonists
2. methylxanthine 3. muscarinic antagonists 4. release inhibitors 5. glucocorticoids 7. leukotriene antagonists 8. anti Ig-E antibody |
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beta agonists in asthma
1. types 2. effect 3. clinical 4.side effects |
1.beta 2 selective agonists:
albuterlol, terbutaline, metaproterenol salmeterol, formoterol- long acting 2. elevates cAMP-BD 3. albuterol, metaproterenol, terbutaline-short acting for acute attacks salmetrol, formoterol-prophylaxis and not for acute attacks COPD may also benefit 4, skeletal muscle tremor,tachycardia,arrhythmias, tachyphylaxis of the short acting. |
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methyxanthines
1. types 2. effect 3. clinical 4.side effects |
1.theophylline type is used to treat asthma
2. block PDE, BD, increased diaphragm contraction strenght, also block adenosine-unknown effect 3. slow release for the use of noctural asthma 4. GI stress, tremor, insomnia, nusea, vomiting, hypotension, cardiac arrhythmias, convulsions, beta blockers may reverse the CV effects of the theophyline |
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muscarin agonists in asthma
1. types 2. effect 3. clinical 4.side effects |
1. ipratopium, tiotropium (long acting)
2. prevent BC by vagal discharge 3. mostly effective in the acute brochospasm episodes among the COPD paitents. 4. minor atropine like effects |
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release inhibitors in asthma
1. types 2. effect 3. clinical 4.side effects |
1. cromolyn, nedocromolyn
2. unknown, but limit the realase of mediators (leukotriens&histamine) from mst cells- only prevent BC. prevent some allergy, has local efect 3. asthma,hay fever, food allergy 4. cough and airway irritation |
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steroids in asthma
1. types 2. effect 3. clinical 4.side effects |
1. beclomethazone, prednisone
2.reduce arachnidoic acid synthesis and COX-2 inhibition, elevate responsiveness to beta agonists, decrease luekotriense 3. used for astham that is not fully responsive for beta agonists 4. adrenal suppression, candidiasis, mild growth retardation in children |
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leukotriene antagonists
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1. leukotriene receptor blockers- zafirlukast, montelukast
effective in preventing excersice,antigen and aspirin induced BS. not for acute attacks, low toxiciy.churg strauss, allergic granulomatous angiitis 2. zileuton- 5-lipooxygenase inhibitor, prevent leukotrien production from arachinidonic acid. prevent excersice and antigrn induced BC, effective against "aspirin allergy", elevates liver enzymes |
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anti ig-E anntibody
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omalizumab
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Drugs for acid peptic disease
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1. antiacids
2. H2 blockers 3. proton pump inhibitors 4. mucosal rotetctive agents 5. antibiotics |
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antiacids
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1. non sustemically active:
A. MgOH2- protetctive salt layer on the mucosa, S.E. diarrhea B.AlOH3- elevates pH, inhibit pepsin S.E. constipation, hypophosphatemmia(reduces Ca stones), Al produces Alzheimer disease 2. systemically active antiacids NaHCO3- elevate pH to 7, later releases CO2 and strexhes the wall and release gastrin in the long run. S.E. bletching, metabolic alkalosis |
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H2 blockers
1. types 2. mechanism 3. clinical 4. side effects |
1. cimentidine, ranitidine, famotidine, nizatidine.
2.reduces secretion og acid, promot healing 3. zollinger ellison, gastric hypersecretory states 4. cimentidine slows metabolism of warfarin, theophilin, phynytoin, diazepem |
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proton pump inhibitors
1. types 2. mechanism 3. clinical 4. side effects |
1. omeprazole, iansoprazole, pantoprazole, rabeprazole
2. block the H/K/ATPase from the external side 3. ulcers, gastroesophageal reflex, NASID induced ulcers, zolinger ellison, systemoc mastocytosis, combunation therphy for H.pylori 4. headace, dizziness, insomnia, diarrhea,impotence and gynecomastia, intestinal cacinoma by nitrosamine colonizing bacteria. |
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mucosal protective agents
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1. bismute salts
bind the ulcer, protect itfrom acid and pepsin, absorb pepsin, stimulate PG synthesis, anf mucus production, antimicrobial activity against H.pylori. 2. sucralfate- the negative charged Al bind the posotive glycoproteins on the ulcer, also directly absorbs bile, stimulate PG synthesis S.E. constipation, nusea, vomiting, dry mouth, interacts with digoxin 3. misoprostol- analogue of PG used in NSAID induced ulcer, inhibits gastric secretion S.E. diarrhea, contraindicated in pregnany-induce uterine contractions. * octreotide- synthetic somatostatin decrese HCL used in zolinger ellison, S.E HS reactions |
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antibiotics used to prevent acid peptic disease
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combination therapy against H. pylori
1. omeprazole +tetracycline+metronidazole+ bismute salt 2. omeprazole +amoxicilin+ clanitromicin |
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drug spromoting GI motility
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1. cholinomimetic agents- betanechole
2. erythromycin- acts as a motilin agoinst. effective in diabetic gastropathy and intestinal pseudo obstruction 3. domperidone- D2 antagonist increases the lower esophageal spincter for treating reflux S.E. hyperprolactinemia 4. metoclopramide (D2 antagonists) & cisapride (5HT-4 agonist)- prokineric activities without secretions. increase esophageal clearance, increases spincter activity and prevent reflux, increase gastric emptying since only meoclopramide enter the CNS central enti emetic effect used against chemotherapy S.E. cisapride- fatal ventricular arrhythmias(thus only as a last option) metoclopramide- nervosness parkingsonism, prolactin elevation |
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antiemetic drugs
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1. H1 antihistamines- hydroxyzine, diphenhydramine, have antimuscarinic and sedative effects though are ineffective for substancces that work on the chemoreceptor trigger zone.
2, anticholinergic agents- scopolamine,ineffective for substancces that work on the chemoreceptor trigger zone. 3. phenothiazines- prochlorperazine & promethazine, block D2 receptor on the chemoreceptor trigger zone S.E.- extrapyramidal sign, hypotension,sedation 4. metoclopramide- dopaminergic antagonist 5. 5HT-3: ondansteron, granisteron, dolasteron block all serotonin receptor (except viscera) 6. corticosteroinds- dexametazone 7. dronabinol (marikuana derivatives) |
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laxatives: name 3 major groups
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1. irritant or stimulant laxatives
2. bulking laxatives 3. stool softeners |
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irritanat or stimulant laxatives
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1. castor oil- increases gut peristalsis
2. senna- the released emodine stimulate the colonic activity 3. phenolpthalien- colon stimulant |
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bulking lazatives
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1. bulk laxatives- methyl cellulose, agar, bran, hydrophilic colloides.
2. osmoric laxatives- non absorbable salts: saline cathartics- NaSO4, MgOH2 lactulose- galactose+fructose not absorbed retain water, bacteria convert it to lactic and acetic acids which evoke peristalsis and kill nitrosamine producing bacteria-decrease cancer risk 3. sorbitol |
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stool softeners
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mineral oil, glycerin- emulsified the feces
also detergents such as docusate |
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antidiarrheal agents
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1. synthetic morphine analouges (opoid derivatives)
LOPERAMIDE- no BBB crossing DIPHYNOXYLATE-crosses BBB may cause sedation both activate presynapthic opoid receptors in the ENS and inhibit the Ach release thus reduces preistalsis. S.E. abdominal cramps, toxic megacolon 2. adsorbants: KAOLOIN. PECTIN, absorbes intestinal toxins & microorganisms 3. agents that modify fluid and electrolyte transport NSAIDs (reduced PG priduction) BISMUTE SUBSALICYCATES- decreases secretions 4. antispasmodic agents PROPANTHELINE- M-receptor antagonist DICYCLOMINE- M-receptor antagonist with direct action on SM. MEBEVERINE- reserpine derivative with direct relaxant action on SM |
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treatment of Chronic inlammatory bowel diseases
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1. NSAID-salicyclic acid derivatives
SULFASALAZINE- 5 aminosalicyclic acid bound to sulfonamide by azo bond which is degraded at the terminal illium by the flora, used for both diseses but not in the case of terminal illium damage. S.E. serum sickness, BM depression OLSALAZINE- two 5 aminosalicyclic acid molecules linked via diazo bond- no toxicity BALSALAZIDE- links 5 aminosalicyclic acid to an inert carrier via diazo bond UC-sulfasalazine, olsalazine crohn- mesalazine 2. immunosuppressives CORTICOSTEROIDS CYTOTOXIC AGENTS- (AZATHIOPRINE & MERCAPTOPURIN) S.E. pancreatitis INFLIXIMAB- anti TNF alpha |
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2 types of pancreatic replacements:
diet alteration |
1. pancreatin- alcoholic excatrat of hog pancrese.
2. pacrelipase- lipase enriched hog pacrease preparation. *since it is sensetive to pH below 4 it should be therefore taken with meals for protection or with cimentidine daily stool fat should be monitored and the dose increased till thearapuatic dose S.E. high purine and lactose content in the preparation, contraindicated among lactose intolerances uric acid and renal stones may be formed diet alteration: if no pain- protein poor diet stimulate CCK which induce regenerative changes if there is pain protein rich diet of several meals. |
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exogenous insulin treatment
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human insuline by genetically altered E coli, or form pork and beef
the human is faster and has shorter durations S.E. hypoglycemia, lipodystrophy, allergic reactions rapid action insulin- soluble crystalline zinc insulin intermediate- 1. semilente insulin suspention, 2. isophane insulin suspention(insulin+protamin)(IV) 3. lente insulin (IV) |
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infectious liver hepatits:
hepatitis A hepatitis B hepatits C |
hepatits A- RIBAVIRIN-a guanosine anlogue, inhibits mRNA synthesis.
hepatitis B- HBIG within 2 days after infection, for newborns passive/active LAMIVUDIN- inhibits the RT IFN ALPHA- degradation of viral mRNA. S.E. flu like symptome, psychosis, myelosuppression, hepatic injurry. hepatitis C- IFN ALPHA RIBAVARIN |
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alcoholic liver hepatits
|
hepatic protectant drug:
1. SILYMARINE- decrease the formtion of free radicals 2. glutathion elevators- N-ACETHYLCYSTEIN, S- ADENOSINE METHIONINE 3. LIPOIC ACID *also, stop alcohol consumption, gastric lavage, laxative to prevent the enterohepatic circulation,hemoperfusion, in acute: glucose, B1, AA infusion protein rich diet |
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drug induced hepatits:
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1. direct hepatotoxic compunds- dose dependent damage (CCl4)(Tx- like alcoholic)
2. indierect hepatotoxic compunds (cytotoxic agents, drugs that cause cholestasis- contraceptives, imipramine, tulbotamide) 3. idiosyncranic reaction- drug or its metabolite act as an hapten paracetamol, amoxicilin, phenytoin, isoniazide. |
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1. treatment of fulminant hepatitis
2. treatment of encephalopathy |
1. glucose, folic acid, B1, vit K, FFP, thrombocyte suspension, albumin (to prevent edema, can also be reduced by mannitol)
2. reduce protein intake, lactulose (degraded to acetic and lactic acids-pH elevations,ammonia is converted to ammonium- no absorption) NEOMYCIN- kill the ammoniu,a producing bacteria increase ammonia incorparation into the cycle by arginine and zinc that catalize the entering stage. liver inducers: alcohol.rifampin and barbiturates |
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treatment of hypokinetic gallbladder
oddi spincter dyskinesis hypotonic hypertonic gallstones |
1. cholinergic drugs, CCK, erythromycin (act as motilin)
2. hypotonic dyskinesis- CHOLESTYRAMINE & LOPERAMIDE- decrease bile irritation caused by bile overflow. hypertonic dyskinesis- low fat diet, NO, THEOPHYLLIN, SALBUTAMOL (prevent spasm and thus reduce pain), ATROPIN (antispsmodic) gallstone solubilization: 1. UCDA- ursodeocolic acid 2. CDCA- chenodeoxycolic acid S.E. diarrhea acute- DIMETHYSULFUXIDE chronic- URSOFALT |
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sympathplegic drugs:
|
reduce the sympathetic nerve flow as a result reduces the HR, CO, contractile force, venous tone.
1. CNS active agents- CLONIDINE, METHYLDOPA 2. ganglion blocking drugs- HEXAMETHONIUM, TRIMETHAPHAN 3.psot ganglionic sympathetic nerve terminal blockers (RESERPINE, GUANETHIDINE) 4. adrenoreceptor blockers |
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centrally acting sympathplegic drugs:
CLONIDINE. |
CLONIDINE- enters the BBB
interacts with alpha 1-partial agonists (lowers the BP through the medulla) imidazoline receptors- in the nucleus tractus solitarius and in the rostral ventrolateral medulla- reduction of the vasomotor activity- decrease in BP S.E. dry mouth, sedation, hould not be givan to patirnts who are in depression risk. tricyclic antidepreddants block their avtion (GUANABENZ & GUAFACINE- derivativs of clonidine) |
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centrally acting sympathplegic drugs:
METHYLDOPA: |
an L-DOPA analogue form alpha methyldopamine & alpha methylnorepinephrine which is the one that repalces the epinephrine at the nerve ending storage.
S.E. sedation, impaired mental concentrarion, nightmares depression extrapiramydal signs vertigo posotive coobs test, hemolysis. fever. hepatitis lowers the HT by TPR CO HR, |
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ECHINACEA
1. mechanism 2. clinical 3. side effects |
1.flavonoids, polyacetylenes, caffeoyl conjugates from echinacea species.
cytokines activation (increased IL & TNF) and anti inflammatorey properties. 2. reduces cold symptomes 3. unplesent taste, GI effects, dizzines, headache |
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EPHEDRA (MA HUANG)
1. mechanism 2. clinical 3. side effects |
1. contains epedrine and pseudoepedrine, indirect sympathomimetics that release NE from nerve endings
2. respiratory dysfunction, bronchitis asthma, mild CNS stimulant, weight loss 3. dizziness, anorexia insomniaflushing palpitations tachcardia, urinary retention in high doses BP elevations, arrhythmias, toxic psychosis contraindicated at anxiety states, bulimia, cardiac arrhythmias, DM. HF, hypertension, glucoma, hyperthyroidism. pregnancy |
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GARLIC
1. mechanism 2. clinical 3. side effects |
1, contain thiosulfate in the form of allicin, which inhibits HMG -CoA reductase, ACE, platlet aggregation, NO release, fibrinolytic, antimicrobial activity, anticarcinogenic
2. used for CV diseases 3. nusea hypotension and allergy |
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GINKGO
1. mechanism 2. clinical 3. side effects |
1. form leaves of ginkgo biloba, containg flavone glycosides and terpenoinds.
antioxidants,radical scaveging effect and NO elevation 2. treatment of intermittent claudication, cerebral insufficiency and dimentia 3. GI effects, anxiety, insomnia, headache may be epileptogenic |
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HINSENG
1. mechanism 2. clinical 3. side effects |
1, panax genus that cintain triterpenoids and saponin glycosides.
2.mental and ohysical performance 3. estrogenic effects- mastalgia, vaginal bleeding, insomnia nervousness, HT |
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MILK THISTLE
1. mechanism 2. clinical 3. side effects |
1. from silybum marianum which contain flavonoliganans
lipid peroxydation reduction, scavenges free radical, enhaces super oxide dismutase, inhibits formation of leukotriens, increases hepatocytes RNA polymerase activity 2. protects against liver injury caused by alcohol, acetaminophen and amanita mushrooms! 3. loose stool |
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ST. JOHN'S WORT
1. mechanism 2. clinical 3. side effects |
1. from hyperricin perforatum
hyperforin- decreased activity serotonergic reuptake systems. hyperricin-antiviral and anticancer effect 2. treatment for mild to moderate depression 3.GI disturbances, contraindicated to MAO inhibitors or bipolrity, induce p450, decreases efficiency of contraceptives, cyclospotins, digoxin warfarin HIV drugs |
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SAW PAMETTO
1. mechanism 2. clinical 3. side effects |
1. serenoa repens or sabal serrulata, containing phytosterols, aliphatic alcohols, polyprens and flavonoids
2. 5 alpha reductase inhibitors and androgen antagoniis, improves the symptoms og BPH 3. absominal pain GI distress, decresed libido headaches HT |
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COENZYME Q-10
1. mechanism 2. clinical 3. side effects |
1. ubiquinol serves as an antioxidant (reduced from the benzoubiquinone the Q10)
2. for reducing SP, DP, CAD, chronic stable angina slow parkingson progression and reduce migraine freaquency. 3. GI disturbancess, rash thrombocythopenia, irritability, dizziness headache |
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GLUCOSAMINE
1. mechanism 2. clinical 3. side effects |
1. a precursor of nitrogen containing sugars
2. for pain associated with osteoarthrithis 3. diahreaa, nausea, cross allergy to shellfish |
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MELATONIN
1. mechanism 2. clinical 3. side effects |
1. serotonin derivative from the pineal gland
2. for jet lag, mood fatigue, improves sleep duration onset quality 3. sedation headache suppers LH thus should not be used in pregnancy or trying to concieve reduces sperm quality |
