Pharm

Front 1

Lispro, aspart

Soluble or regular insulin

NPH

Ultralente

Glargine

Back 1

Ultra Rapid

Rapid Acting

Intermediate acting

Slow

Ultraslow peakless

Front 2

Sulfonylureas
1st gen – Tolbutamide, Chlopropamide
2nd gen – Glyburide, Glipizide

Back 2

 Stimulate insulin release from the pancreas
 Requires β cell for action
 Binds to ATP-sensitive K+ channel ↓ its conductance → mimic normal insulin secretion from pancreas
 Effectively absorbed through the GI tract
 T2DM therapy Risk of inducing hypoglycemia → can progress to coma & death
 Very long half life
 Stimulates appetite → contribute to obesity problem

Front 3

Glitinides
 Repaglinide
 Nateglinide

Back 3

 Similar action to sulfonylureas
 Very rapid-acting & short duration
 Take orally @ mealtimes
 ↓ post prandial peak in blood glucose
 Flexible dosing

Front 4

Biguanides
 Metformin (Glucophage)

Back 4

 Lowers blood glucose levels
 Does not stimulate insulin release

2 main actions:
 ↓ gluconeogenesis - ↓ glucose output from liver
 ↓ insulin resistance - enhanced insulin action on peripheral tissues
 T2DM
 NO risk of hypoglycemia
 Associated anorexia may lead to weight loss
 May be used in combo w/ sulfonylureas
 GI disturbances: Lactic acidosis:
o Potential fatal lowering of blood pH

Front 5

Thiazolidinediones (TZDs) or Glitazones
 Rosiglitazone (Avandia)
 Pioglitazone (Actos)
 Troglitazone

Back 5

 Potentiates insulin action on peripheral tissue
 ↓ insulin resistance
 Does not stimulate insulin release
 Agonistic binding of peroxisomal proliferator activator receptor (PPARγ) found in white adipocytes
 T2DM
 NO risk of hypoglycemia
 Useful following failure of sulfonylureas and/or metformin or in combo
 Edema; CI in pts w/ CVD
 Potential hepatoxicity

Front 6

Incretins

Back 6

 Oral glucose induces release of gut hormone GLP-1 → acts on β cell to amplify insulin release

Front 7

Exenatide (Byetta)

Back 7

 Newly approved GLP-1 analog from reptilian salivary glands
 Longer half life than endogenous form
 Resistant to DPP-4 protease turnover
 Induces insulin release
 Depress glucagon releases
 Blunt post-prandial glucose surge
 Delays gastric emptying T2DM
 SubQ injection
 Significant weight losses through blunting of appetite
 Nausea
 ↑ risk of hypoglycemia when used in combo w/ sufonylureas

Front 8

DDP-4 Inhibitors
 Sitagliptin

Back 8

 Newly approved
 ↑ half life & action of endogenous GLP-1
 T2DM
 PO drug
 No associated GI disturbances No effect on weight loss
 Possible toxicities

Front 9

α-Glucosidase inhibitors
 Acarbose
 Miglitol

Back 9

 ↓ intestinal absorption of glucose
 Slows intestinal degradation of starches & sucrose
 Blunt post prandial spiking of blood glucose levels
 T2DM
 Not effective as 1o therapy
 May be used w/ other drugs
 Flatulence
 diarrhea

Front 10

Levothyroxine

Back 10

T4

Front 11

LiothyronineNA

Back 11

T3

Front 12

Thioureylenes
-Methimazole
propulthiouracil

Back 12

Inhibit tyrosyl iodination vs competitive inhibition on thyroid perox.
takes several weeks to months due to large store and slow turnover of t3/t4

Front 13

High dose Iodide

Back 13

Lowers hyperthyroid only intially used presurgically reduces size and vascularity

Front 14

Proponolol for hyperthyroidism

Back 14

Sx relief (tachy card, arryth, tremor)
Used during lag period whcih follows thioureylene therapy.

Front 15

Prednisone

Back 15

Liver to act --> prednisolone
SE: Cusingoid appearance/ lethal infections.
Think skin,moon face, cataracts, atheroscler, Osteoporosis (osteoblast inh lower ca uptake and inc. excretion)

Front 16

Immunophinin binding agents (IL-2 inhib)
Calcinuerin inhibitors

Back 16

Cyclosporin (binds cyclophins can block mitogen induced act of synovial monnuc cells)
Tacrolimus(binds FKBPs lower IgE mediated resp)

Immunosup effects come from binding and inhibiting calcinuerin phosphatase inhibiting action of NF-AT.
1) T-helper
2) variable bioavailability (monitor)
3)p450/ needs bils salt for abs

Front 17

Non calcinuerin inhibiting agent: sirolimus

Back 17

Binds immunophillins, interferes w/ signal transduction via TOR.
Limits growth factor induced prolif
SE: dyslipidemia, thrombocytopenia, antifibroblast action p450 same as tacro/cyclosporin

Front 18

Azathioprine

Back 18

Abs. by liver X.O.
-->6-MP lowers purine synth -->IL-2
Maintain organ tx.
SE: mylosupression, anemia, alopecia, lethal w/ Allopurinol(blcoks XO)

Front 19

Methotrexate (PS/RA)

Back 19

Structural analog folic acid irrev.
effects DHFR--> effects purine/pyrimidine synth
SE- Allopecia, CNS fatigue, GI

Front 20

Cyclophosphamide (SLE, Wegeners, RA)

Back 20

Metab in liver -> 4OHphosphamide+aldophosphamide(active)
bind to enz od DNA- interfere
Drug interactions
1) w/ sux up NM blockade due to lowering of psudeoCHE
2)alter hepatic microsomal enz act will alter cyclophosphamide levels
3)TC antidepressents may decrease bladder emptying and lead to prolonged bladder exposure to acrolein (hemmorhagic cystitis)
Se: alopecia, anorexia, diarrhea.

Front 21

Mycophenolate Mofetil

Back 21

Lympo specific due to inhib of de novo purine pathway. Inhibits IMPD lowering guanosine monophosphate adn increase adenosine (inhibits the PRPP).

Front 22

Leflunomide

Back 22

Inhibit pyrimidine synth.
Inhibit dihyroorate dehydrogenase
Effective w/ Myco. Mofetil.
SE: liver, kidney, tetragenic

Front 23

 3 factors that contribute to airway narrowing in asthma:

Back 23

o smooth muscle contraction
o ↑ mucous secretion
o mucosal inflamm & swelling

Front 24

Early onset/Extrinsic Asthma

Back 24

 occur mostly in children and young adults
 family hx common
 (+) skin hypersensitivity test

Pathogenesis:
 abnormal immune response associated with allergy
 IgE, mast cell and Ca2+ mediated factor release (histamine, 5HT, Leuk)
 Leuk can recruit more inflamm cells to airway
 Therapeutic target is Ca2+ & cAMP mediated degranualtion

Front 25

Late onset/Intrinsic Asthma

Back 25

 Can occur at any age but most are adult pts
 provoked by cold air, perfume, paint, tobacco smoke
 Emotional stress, infection, severe exertion
 no family hx
 (-) skin hypersensitivity test

Pathogenesis:
 ↓ β-adrenergic responses
o β2 receptor esponse normally relaxes bronchial muscle & ↓ gland secretion
 ↑ cholinergic responses
o Muscarinic receptor response normally contracts bronchial muscle & stimulates gland secretion

Front 26

Bronchodilators

Back 26

 inhibit smooth muscle contraction and ↓ release of mediators
 can rapidly reverse bronchospasm
 β2 agonist binding → Gs protein activation → activation of AC → ↑ cAMP
o ↓ active form of MLCK = less smooth muscle contraction = bronchodilation
o ↑ cAMP affects cAMP:cGMP ratio = ↓exocytosis of chemical mediators = ↓ bronchial gland secretion
 α receptor activation → IP3 stimulated Ca2+ release from ER → constrict bronchial mucosal vessel & ↓ blood flow → ↓ congestion & edema

Front 27

Albuterol
(salbutamol

Back 27

 short-acting
 racemic mixture
B2 agonist selective

Front 28

Levalbuterol

Back 28

 short-acting (R-isomer)

FDA approved for:
 prevention and txmt of bronchospasms in pt at least 12yo
 useful in pt refractory to racemic mixture of albuterol
Selective β2 agonists

Front 29

Pirbuterol

Back 29

 short-acting
Selective β2 agonists

Front 30

Formoterol

Back 30

 long-acting

FDA approved for:
 maintance txmt
 prevention of exercise-induced bronchospasm
Selective β2 agonists

Front 31

Xanthines-Theopylline

Back 31

 Stage I (mild asthma w/ little obstruction )
 PO: Stage II (moderate obstruction)
 IV: Stage III (severe obstruction) & Stage IV (marked hypoxemia)
 ↑ cAMP by diff route than β2 agonist
 inhibits the actions of phosphodiestease
 can be used as synergistic therapy
SE: Narrow therapeutic window → must monitor carefully
 plasma conc > 25 ug/ml
o high probability of seizure
o arrhythmia, hypotension, cardiac arrest
 Adverse effect: N/V

Drug interaction/Toxic effect:
 Babituates → speed rate of elimination & interfere with blood level
 Caffeine → competes w/ common metabolic enzyme & CNS/ CV effects

Front 32

Inhaled corticosteroids
 Budesonide
 Fluticasone

 Beclomethasone
 Triamcinolone
 Propionate
 Mometasone furoate
 Flunisolide

Back 32

Fluticasone & Budesonide:
 preferred agents bc their long duration of action & high local potency w/ less systemic effects indirectly act on to relieve or prevent airflow obstruction

***have NO effect on IgE-dependent secretion of mediators

 suppress hypothalamic-pituitary-adrenal fxn
o cushion’s syndrome
o growth retardation
 if ↓ suddenly → danger of no recovery of adrenal fxn and poor response to stress
 SEs more prevalaent w/ systemic administration than inhalants

Front 33

 Prednisone
 Prednisolone

Back 33

Oral Corticosteroids
 PO or IV
 dramatic relief in severe asthma – stage III and IV
 not effective in inhibiting IgE mediated release
 thought to stabilize biomembrane
 inhibit inflammatory rxt
 enhance response of B receptor to adrenergic transmission

Front 34

Cromolyn Sodium

Back 34

Oral Corticosteroid
 used extensively for prophylactic tx of mild to moderate asthma  stabizes membrane of mast cell to prevent release of mediators
 probably block Ca channel
 inhibit Ca influx across mast cell membrane  does not relax smooth muscle
 NOT to be used for acute bronchospasm
 Few SEs → sore throat, dry mouth, skin rash, head ache, dizziness

Front 35

Alprostadil (PGE1)

Back 35

 Still in experimental stages, not yet in clinical use  activate AC → ↑ cAMP
 have effects on airway smooth muscle relaxation

Front 36

Anticholinergenic Asthma agents

Back 36

Anticholinergic agents
 Historically Atropine was used to treat bronchial asthma but have severe cholinergic SEs
 w/ the availability of β agonists these anticholinergic agents are no longer used to treat bronchial asthma ***KNOW THIS***
 inhalational analogs may used for chronic bronchitis & COPD
 Ipratropium bromide
o Short acting bronchodilator for patients with chronic bronchitis and COPD
 Tiotropium bromide
o Long acting anti-cholinergic drug approved by FDA for once-daily txmt of bronchospasm associated with COPD

Front 37

Zileuton

Back 37

affect the allergic reactions upstream of inflammatory cascade
 Not used anymore
 Freq doses req for effectiveness  Leukotriene synthesis inhibitor 

Front 38

Zafirleukast

Back 38

affect the allergic reactions upstream of inflammatory cascade
 Not used anymore  Leukotriene synthesis inhibitor  Interacts w/ food in the stomach

Front 39

Montelukast (Singular)

Back 39

affect the allergic reactions upstream of inflammatory cascade
 PO drug
 Used for asthma, seasonal allergic rhinitis and perennial allergic rhinitis in adults & children  Cysteinyl Leukotriene D4 receptor antagonist

Front 40

Omalizumab (Xolair)

Back 40

affect the allergic reactions upstream of inflammatory cascade
 SQ
 Used for pts at least 12yrs old
 Moderate to sever asthma  Inhibits IgE

Front 41

Xanthines

Back 41

Theopylline

Front 42

Theopylline

Back 42

Stage I (mild asthma w/ little obstruction )
PO: Stage II (moderate obstruction)
IV: Stage III (severe obstruction) & Stage IV (marked hypoxemia)
↑ cAMP by diff route than β2 agonist
inhibits the actions of phosphodiestease
can be used as synergistic therapy
NarrowSE: therapeutic window → must monitor carefully
plasma conc > 25 ug/ml
o high probability of seizure
o arrhythmia, hypotension, cardiac arrest
 Adverse effect: N/V

Drug interaction/Toxic effect:
Babituates → speed rate of elimination & interfere with blood level
Caffeine → competes w/ common metabolic enzyme & CNS/ CV effects

Front 43

Methimazole

Back 43

Thiourelene
Inhibit tyrosyl iodination vs competitive inhibition on thyroid perox.
takes several weeks to months due to large store and slow turnover of t3/t4

Front 44

Glipizide

Back 44

2nd gen Sulfonylureas
Stimulate insulin release from the pancreas
Requires β cell for action
Binds to ATP-sensitive K+ channel ↓ its conductance → mimic normal insulin secretion from pancreas
Effectively absorbed through the GI tract
Risk of inducing hypoglycemia → can progress to coma T2DM therapy & death
Very long half life
Stimulates appetite → contribute to obesity problem

Front 45

Glyburide

Back 45

2nd gen sulfonylureas
Stimulate insulin release from the pancreas
Requires β cell for action
Binds to ATP-sensitive K+ channel ↓ its conductance → mimic normal insulin secretion from pancreas
Effectively absorbed through the GI tract
Risk of inducing hypoglycemia → can progress to coma T2DM therapy & death
Very long half life
Stimulates appetite → contribute to obesity problem

Front 46

Tolbutamide

Back 46

1st gen Sulfonyurea
Stimulate insulin release from the pancreas
Requires β cell for action
Binds to ATP-sensitive K+ channel ↓ its conductance → mimic normal insulin secretion from pancreas
Effectively absorbed through the GI tract
Risk of inducing hypoglycemia → can progress to coma T2DM therapy & death
Very long half life
Stimulates appetite → contribute to obesity problem

Front 47

Chlopropamide

Back 47

1st gen Sulfonyurea

Stimulate insulin release from the pancreas
Requires β cell for action
Binds to ATP-sensitive K+ channel ↓ its conductance → mimic normal insulin secretion from pancreas
Effectively absorbed through the GI tract
Risk of inducing hypoglycemia → can progress to coma T2DM therapy & death
Very long half life
Stimulates appetite → contribute to obesity problem

Front 48

Norepinephrine (levarterenol

Back 48

ADRENERGIC AGONISTS
Direct Acting

mostly α agonist, some β1 vasoconstrict = ↑systolic and diastolic BP, reflex ↓HR. Maybe tx for shock; NEVER used for asthma

Front 49

▫Isoproterenol

Back 49

ADRENERGIC AGONISTS
Direct Acting

β1& β2 agonist, synthetic ↑↑HR, contraction = ↑CO = tx. AV block or cardiac arrest; dilates dilates sk. musc. aa = ↓BP
Up Sys down Dias can lower CO if pooling of blood too much

Front 50

Dobutamine

Back 50

ADRENERGIC AGONISTS
Direct Acting

β1> β2 agonist used to ↑CO in congestive heart failure w/o affecting HR or myocardial O2 demands ↑atrial conduction, so beware if pt. has atrial fibrillation

Front 51

Phenylephrine

Back 51

ADRENERGIC AGONISTS
Direct Acting

α1>α2 agonist, synthetic ↑syst & diast BP w/o effect on heart, but causes reflex bradycardia; also nasal decongestant, mydriatic, shock not catechol derivative, so not substrate for COMT

Front 52

Methoxamine

Back 52

ADRENERGIC AGONISTS
Direct Acting

α1>α2 agonist vasoconstricts →↑peripheral resistance; has good effect on vagus = tx for supraventricular tachycardia or to overcome hypotension induced by halothane in surgery

Front 53

▫Clonidine(catapress)

Back 53

ADRENERGIC AGONISTS
Direct Acting

α2 agonist tx. HTN, or to minimize withdrawal from opitates/benzodiazos sudden withdrawal = HTN crisis; drymouth is very common side effect

Front 54

▫Methyldopa(aldomet)

Back 54

ADRENERGIC AGONISTS
Direct Acting

α2> α1> β met. by DD, then DBH to α-methyl NE, which has ↓affinity for , but for ; stored and released with NE; controls CNS and JG of kidney to ↓renin = ↓BP penetrates BBB

Front 55

▫Terbutaline, ▫Albuterol, ▫Ritodrine

Back 55

ADRENERGIC AGONISTS
Direct Acting

β2 agonist bronchodilator, or ↓ uterine contractions in premature labor

also ▫Orciprenaline

Front 56

Dopamine

Back 56

ADRENERGIC AGONISTS
Direct Acting

activates β1 in heart = ↑CO, at high dose, activates α = vasoconstriction; dilates renal and splanchnic BVs via D receptors = independent of adrenergic action = tx. shock much better than NE b/c NE blocks blood to kidney and may lead to kidney shutdown

Front 57

Cocaine

Back 57

Indirect Acting
reversibly binds NET = potentiates NE and Epi = CNS stimulation; has local anesthetic action @ high doses

Front 58

▫Amphetamine

Back 58

Indirect Acting
branched chain = high affinity for MAO, but poor substrate accum. in nerve release of NE non-exo = tx for narcolepsy & ADD; but OD=psycho, BP, angina, arrhythmia; lasts 3 hrs crosses BBB, CNS arousal, tolerance dev. to amphets “tachyphylaxis”

Front 59

Tyramine

Back 59

Indirect Acting
decarboxylation of tyrosine, found in wine/cheese, given IV accum. by NET in neuronrelease of NE, causes dose-dep HR, BP, resembles NE; lasts 3 minutes NO BBB, Ca independent, substrate for MAO = don’t give w/ MAOIs, delays oxidation of NE

Front 60

tricyclic antidepressants

Back 60

Indirect Acting
(imipramine, desipramine, amitryptyline) very potently block NET, also block 5HT, and at high conc, block receptors for muscarinic, histamine and 1 cause tremor, insomnia, blurry vision, orthostatic HTN

Front 61

Ephedrine

Back 61

Direct and Indirect Acting (Mixed)
similar to amphet, but has adrenergic effects too. 3hrs tx. asthma; mydriatic; decongestant OD=confusion, anxiety, BP, angina, arrhythmia, ↓appetite, ↓sleep

Front 62

Metaraminol

Back 62

Direct and Indirect Acting (Mixed)
has actions similar to NE; tx. shock or HTN

Front 63

Phenoxybenzamine

Back 63

ADRENERGIC ANTAGONISTS
Alpha Blockers
irrev. & noncomp. blocks all alphas, ACh,5HT,histamine prevents vasoconstriction, reverses alpha effects of EPI; tx. pheochromocytoma, Raynaud’s disease adverse = postural hypotension, nausea, vomiting, may HR, impotence

Front 64

Phentolamine

Back 64

ADRENERGIC ANTAGONISTS
Alpha Blockers irrev. & noncomp. blocks all alphas same as phenoxybenzamine, may be used to dx pheochromocytoma, or to tx. HTN crisis after eating tyramine

Front 65

Prazosin

Back 65

ADRENERGIC ANTAGONISTS
Alpha Blockers comp. block α1 ↓peripheral resistance, ↓BP w/o affecting heart or kidney = good HTN tx.; tx. benign prostatic hypertrophy by  urine flow; ↓preload and afterload = tx. congestive heart failure prazosin often leads to edema = give with a diuretic; Doxazosin (Cardura) = newer analog w/ longer t1/2

Front 66

▫Tamsulosin (flomax)

Back 66

ADRENERGIC ANTAGONISTS
Alpha Blockers selective for α1a blocks a1a, which is all over prostate = tx. ben. pros. hypertrophy

Front 67

Yohimbine

Back 67

ADRENERGIC ANTAGONISTS
Alpha Blockers
blocks a2 only tx. for impotency (actual effectiveness is questionable.)

Front 68

▫Propanolol
▫Carteolol, ▫Nadolol ▫Levobunolol, ▫Pindolol, ▫Timolol
▫Penbutolol

Back 68

Beta Blockers
blocks b1 & b2 ↓HR, ↓force=↓CO; ↓conduction; blocks renin release = tx. HTN, angina and arrhythmias; also tx. coronary artery disease b/c blocks stress-induced demands for 02 by heart; useful to tx. heart probs in hyperthyroidism; tx. migraines, anxiety, glaucoma via ↓ prod of aq. humor. not for pts. w/ COPD or asthma; must withdraw gradually; NEVER use w/ verapamil or diltiazam = AV block
note: Pindolol doesn’t block renin, but is still good tx. for HTN

Front 69

Acebutolol
▫Betaxolol, ▫Esmolol
▫Atenolol, ▫Metoprolol

Back 69

Beta Blockers
blocks only b1 = cardiac selective remember A BEAM of b1 blockers

Front 70

Labetelol

Back 70

Alpha AND Beta Blockers
competitively blocks b1,b2,a1 (but not a2) tx. HTN w/ angina, pheochromocytoma; not as potent as individual  or  blockers; mem. stabilizer = local anesthetic action; also can block neuron uptake of NE = cocaine-like action

Front 71

Guanethidine
(ismalin)

Back 71

Synthetic, oral ↓BP, ↓HR, ↓renin; taken up by NET, blocks exocytosis independent of Ca: 1. enters neuron, blocks transmission (acute); 2. blocks NET (acute); 3. ↓NE stores (chronic)

Front 72

Reserpine(serpasil)

Back 72

alkaloid, oral, irreversible binding; no effects on cholinergics=parasymp tone progressive loss of NE tissue stores =↓↓↓autonomics; blocks NE transport; MAO oxidizes the NE; also blocks DA trans=↓ DA in brain; also ↓5HT from nerves, ↓histamine from platelets lasts 1 wk; also miosis, salivation, gastric sec., ↓HR, ↓BP, depression, diarrhea, peristalsis, tremor, suicide

Front 73

alpha-methyl-tyrosine (metyrosine)

Back 73

TH inhibitor, competes w/ tyrosine, blocks formation of DOPA = depletes NE stores. Former tx. for pheochromocytoma no longer used. Crystallizes out in urine = renal damage

Front 74

Colchicine, Vinblastine & Vincristine (Vinca Alkaloids)

Back 74

depolymerize cell cytoskeleton, block fast axonal transport = blocks NE from cell body going to synapse

Front 75

Acetylcholine

Back 75

AGONISTS
direct intracoronary injection to dx. vasospastic angina pectoris

Front 76

▫Pilocarpine

Back 76

AGONISTS
natural, tertiary, M -topical miotic for glaucoma
-tx. drymouth in cancer or Sjogren’s synd. (autoimmune salivary dysfxn)

Front 77

▫Cevimeline (Exovac)

Back 77

AGONISTS
M tx. for drymouth met. by CYP2D6 and 3A3/4= maybe toxic w/ ketoconazole etc

Front 78

Methacholine

Back 78

AGONISTS
synthetic, quaternary, M in heart -old tx for tachycardias
-aerosol to dx. bronchial hyperreactivity not met. by cholinesterases = longer duration than ACh

Front 79

▫Carbamylcholine (Carbachol)

Back 79

AGONISTS
synthetic, quaternary, M & N topical miotic agent not met. by AChE

Front 80

▫Bethanechol (Urecholine)

Back 80

AGONISTS

synthetic, quaternary, M in GI & UT -tx. stasis conditions of bladder or GI, esp. post-partum and after general anesthesia -not. met by cholinesterases
-don’t give if GI obstruction (P)

Front 81

Nicotine

Back 81

AGONISTS
natural, lipid soluble tertiary, N -leads to conversion from activation to depolarizing blockade
-tx. for nicotine withdrawal sx.
-maybe good for cognition in Alzheimer’s, ↓Parkinson’s
BEWARE acute poisoning = ANS stim, CNS excitation, convulsions, depression, sk. m. paralysis -crosses placenta, sec. in milk
-widely dist. in CNS
-highly addictive

Front 82

▫Physostigmine (Antilirium)

Back 82

REVERSIBLE CHOLINESTERASE INHIBITORS
natural, tertiary, M & N topical miotic for glaucoma met. by plasma ester hydrolysis
-can cause seizures

Front 83

▫Neostigmine (Prostigmin)

Back 83

REVERSIBLE CHOLINESTERASE INHIBITORS
synthetic, quaternary, N -Anticholinesterase AND agonist action = tx myasthenia gravis
-motility of GI or UT
-reverses sk. m. blockade by competitive antagonist (d-tubocurarine) -oral abs. 15X less than parenteral
met. by plasma ester hydrolysis

Front 84

Pyridostigmine

Back 84

REVERSIBLE CHOLINESTERASE INHIBITORS
same as neo, but longer duration = most common oral tx for myasthenia

Front 85

Edrophonium

Back 85

REVERSIBLE CHOLINESTERASE INHIBITORS
synthetic, quaternary -Anticholinesterase AND agonist action at motor endplate = systemic action is almost totally on sk. m. = diagnostic for myasthenia only lasts 5 min

Front 86

Tacrine

Back 86

REVERSIBLE CHOLINESTERASE INHIBITORS

not used much anymore -tx. cognitive sx. of Alzheimer’s (but not dementia) -crosses BBB, hepatotoxic

Front 87

Donepezil

Back 87

REVERSIBLE CHOLINESTERASE INHIBITORS
piperidine-based -tx. cognitive sx. of Alzheimer’s w/ long duration = once daily dose
milder side effects, no hepatotoxicity met. by CYP2D6 and 3A3/4

Front 88

▫Rivastigmine (Exelon)

Back 88

REVERSIBLE CHOLINESTERASE INHIBITORS
carbamate structure Alzheimer’s tx that is met. slower, also inhibits pseudoChE good if poor response to donepezil

Front 89

▫Galantamine (Reminyl)

Back 89

REVERSIBLE CHOLINESTERASE INHIBITORS

tertiary alkaloid Alzheimer’s Tx

Front 90

Echothiophate

Back 90

IRREVERSIBLE CHOLINESTERASE INHIBITORS (ORGANOPHOSPHATES)
very polar, exc. in urine, lipid soluble, so can be abs. thru skin
topical miotic agent for eye (effects last 3 days)

Front 91

malathion

Back 91

IRREVERSIBLE CHOLINESTERASE INHIBITORS (ORGANOPHOSPHATES)
very polar, exc. in urine, lipid soluble, so can be abs. thru skin
common home and garden insecticide, controls lice topically can be met. by mammals

Front 92

Parathion

Back 92

IRREVERSIBLE CHOLINESTERASE INHIBITORS (ORGANOPHOSPHATES)
very polar, exc. in urine, lipid soluble, so can be abs. thru skin
must first be conv. in liver to active form, paraoxon; only for pros is NOT met. by mammals

Front 93

Sarin

Back 93

IRREVERSIBLE CHOLINESTERASE INHIBITORS (ORGANOPHOSPHATES)
very polar, exc. in urine, lipid soluble, so can be abs. thru skin
“nerve gas” for war, terrorism

Front 94

Atropine

Back 94

MUSCARINIC ANTAGONISTS
natural alkaloid tx for motor symptoms of Parkinson’s
-can block vagal afferents to heart = tachycardia = tx. for sinus bradycardia after MI
-↓motility in GI, threshold volume for sensory micturation reflex
-sustained cyclopegia and mydriasis topically on eye “atropine flush” @ toxic levels
-mainly met. in liver, some exc. unchanged in urine
"Dry as a bone, red as a beet, blind as a bat, mad as a hatter"

Front 95

Scopolamine

Back 95

MUSCARINIC ANTAGONISTS
100X more potent than atropine in ascending reticular core =produces somnolence and hypnosis with amnesia
may produce delerium and hallucinations
-anti motion sickness (abs. thru skin well enough to give as patch)

Front 96

Tolterodine

Back 96

MUSCARINIC ANTAGONISTS
tertiary tx. for urinary urgency met. by liver

Front 97

Oxybutinin

Back 97

MUSCARINIC ANTAGONISTS
tertiary tx. for post-operative bladder spasm, also tx for urinary urgency met. by liver, available as patch

Front 98

Tropicamide

Back 98

MUSCARINIC ANTAGONISTS
tertiary short-duration mydriatic/cycloplegic topical on eye

Front 99

Ipratropium

Back 99

MUSCARINIC ANTAGONISTS
quaternary tx. as aerosol for COPD, asthma, etc…

Front 100

Propantheline

Back 100

MUSCARINIC ANTAGONISTS
quaternary spasmolytic for GI tract, tx. for GI hypermotility

Front 101

▫Benztropine (Cogentin)

Back 101

MUSCARINIC ANTAGONISTS
tertiary -tx parkinson’s motor sx.

Front 102

Pirenzepine

Back 102

MUSCARINIC ANTAGONISTS
tertiary, M1 under investigation for peptic ulcer. No heart side effects

Front 103

▫d-tubocurarine

Back 103

NICOTINIC COMPETITIVE ANTAGONISTS
natural alkaloid -↓BP initially due to: 1. ANS ganglia block, 2. Histamine from Masts t0.5=3.8hr, ½ met., ½ exc kidney

Front 104

vecuronium

Back 104

NICOTINIC COMPETITIVE ANTAGONISTS

synthetic, steroid-based slight ganglionic blockade can reduce GI tract motility, very popular
no histamine release biliary excretion

Front 105

atracurium

Back 105

NICOTINIC COMPETITIVE ANTAGONISTS
synthetic only a little Histamine release, intermediate duration of action
landanoside, a breakdown. product, may excite the CNS inactivated by spont. breakdown. since unstable at plasma pH = safe for renal and hepatic failure

Front 106

doxacurium

Back 106

NICOTINIC COMPETITIVE ANTAGONISTS
specific for neuromuscular jxn = few side effects, no Hist., long action exc. by kidney

Front 107

mivacurium

Back 107

NICOTINIC COMPETITIVE ANTAGONISTS
shortest duration, slow onset, only a little Histamine release met. by pseudoChE’s in plasma

Front 108

Succinylcholine

Back 108

DEPOLARIZING BLOCKERS
synthetic rapid onset, 5 min duration; significant hyperkalemia
best for relaxing laryngeal mm. to insert an airway pseudoChE met. to succinic acid and choline
some hist release

Front 109

▫Trimethaphan (Arfonad)

Back 109

GANGLIONIC BLOCKADE AGENTS
blocks early EPSP and thus ganglionic transmission
tx. HTN emergencies, or create hypotension for brain surgery

Front 110

Hexamethonium

Back 110

GANGLIONIC BLOCKADE AGENTS
quaternary amine possible HTN drug

Front 111

Mecamylamine

Back 111

GANGLIONIC BLOCKADE AGENTS
secondary amine possible use for nicotine-sensitive CNS disorders like Tourette’s

Front 112

▫Botulinum Toxin A (Botox)

Back 112

ACh RELEASE BLOCKERS
local injection to tx strabismus, torticollis, wrinkles, possibly migranes

Front 113

Dantrolene

Back 113

blocks Ca from sarcoplasmic reticulum. Used only for spasticity tx. in pts w/ upper motor neuron lesions, malignant hyperthermia

Front 114

Cromolyn Sodium

Back 114

Block Ca influx and release of hitamine.

Front 115

Compound 48/80
Polymixin B

Back 115

Ionophores result in influx of Ca release of hist

Front 116

Morphine and Turbocurarine

Back 116

Also stimulate histamine release
Dissoc histamine from heparin-chondotrin complex inside granules

Front 117

H1 receptors

Back 117

Smooth muscle of gut and bronchi, endothelium, and in brain PLC pathway

Front 118

H2 receptors

Back 118

Gastic mucosa and cardiac muscle cells, brain cAMP pathway

Front 119

First Generation Antihistamines

Back 119

Diphenhydramine
Dimenhydrinate
Chlorpheniramine
Hydoxazine
Meclizine
Promethazine

Front 120

Second Generatin AntiHist

Back 120

Fexfenadine
loratadine
cetirizine

Front 121

Serotonin Clinc signficiance

Back 121

Migraine and cluster headaches

Front 122

Effects of Aluminum

Back 122

Constipation

Front 123

effects of Magnesium

Back 123

Diarrhea

Front 124

Antihistamines: (to reduce gastric acidity)

Back 124

H2 Antagonists effective in healing of gastric and duodenal ulcers.
Dine w/ FRANC
Famotidine, Ranitidine, Nizatidine, Cimetidine

Front 125

Famotidine

Back 125

H2 Antagonists effective in healing of gastric and duodenal ulcers.

Front 126

Ranitidine

Back 126

H2 Antagonists effective in healing of gastric and duodenal ulcers.

Front 127

Nizatidine

Back 127

H2 Antagonists effective in healing of gastric and duodenal ulcers.

Front 128

Cimetidine

Back 128

H2 Antagonists effective in healing of gastric and duodenal ulcers.

Front 129

Proton Pump Inhibitors

Back 129

-prazole; activated in acid enviroment of secreteory canaliculus of parietal cell. Useful in gastric and duodenal ulcers, severe gastroesophogeal disease, and Zollinger-Ellisons

Front 130

Somatostatin Analog

Back 130

Octreotide
Somatostatin suppresses the release of gastrointestinal hormones
Gastrin
Cholecystokinin (CCK)
Secretin
Motilin
Vasoactive intestinal peptide (VIP)
Gastric inhibitory polypeptide (GIP)
Enteroglucagon

Front 131

Sucralfate

Back 131

Directly inhibits pepsin and bile action w/ out changing pH of stomach.Not an antacid. Coats ulcerbed

Front 132

Bismuth Subsalicylate

Back 132

Ulcer, coating, and protection from acid and pepsin.

Front 133

Prostaglandins In GI

Back 133

May prevent Gastric acid secretion by blocking histamine stim cAMP. Misoprostol is crug of choice esp when ulcers from NSAID.

Front 134

Metoclopramide

Back 134

Choinomimetic, increase resting ton eof lower esophageal sphinc. and stomach that makes the compoud useful in reflex esoph. accelerates gastric emptying and shortens bowel transit time. Dopamine antagonist so strong antiemetic properties.

Front 135

Treatment H.pylori

Back 135

2 ab w/ a proton pump inhbitor
= Amox, Clarithro+ propumpI
oor bismuth, metronidazole, h2 blocker, tetracycline

Front 136

Apomorphine

Back 136

Emetic Agent
potent DA agonist binds CTZ on 4th vent->Reticular Medulla

Front 137

Vommiting Physiology

Back 137

Sensor->CTZ (DA rec 4th vent)->reticular core medulla-> vomit
Inc pulse, salivation,dilation of pupils, pallor. contract of pylorus and relax of gi smooth muscle, tensing of abdominal and intercostal m, reverse paristalis in lower esophogus. After: reflex bradycardia, fall in bp, faintness.

Front 138

Ipecac syrup

Back 138

Stomach irritant and some direct CTZ action

Front 139

Antiemetics

Back 139

Most are Da Antagonists at CTZ
Chlorpromazine
prochlorperazine
trimethobenzmide
metochlopramide
ondansetron

Front 140

Chlorpromazine

Back 140

Antiemetics

Front 141

prochlorperazine

Back 141

Antiemetics

Front 142

trimethobenzmide

Back 142

Antiemetics

Front 143

metochlopramide

Back 143

Antiemetics

Front 144

Dimenhydrinate

Back 144

Anti motion sickness agent Block H1 receptor
anti histaminic and acts by blocking synaptic relay along 8th cranial nerve.

Front 145

Castor Oil

Back 145

TAG of ricinoleic acid from castor beans. Acid stimulates GI tract motility by irritant action from the small intest on. Premotes evac of small and large intest. Used prior to surgery should not be used during pregnancy may induce premature labor

Front 146

Dipheylmethanes-phenolphthalein

Back 146

motility stimulant

Front 147

Emodin alkaloids

Back 147

aloes cascara, senna stimulate peristalsis metabolized by bacteria.

Front 148

Mineral Oil

Back 148

Stool softener-promote laxation by coating and lubricating fecal matter, prevent norm absorption water.

Front 149

Glyercerin

Back 149

Administered as rectal supposityro, lubricate and produces local irriation of the rectum that helps initate defecation reflex

Front 150

Opiates in Gi

Back 150

Anti diarrheal-sustained contract of intesting and interrup normal seq of peristaltic contractions.

Front 151

Diphenoxylate and atropine

Back 151

Antidiarhetic

Front 152

Loperamide

Back 152

Inhib ach from presynaptic opiod recep. in ENS Antidiarrhetic motility agent

Front 153

Absoben powders

Back 153

absorb water and toxins to provide protective coating to inflamed intestine-kaolin,pectin,bismuth subsalicate

Front 154

Aspirin(acetyl sialicylic acid)

Back 154

Irreversible
Absorbed/accumulate in stomach lining
Metab by liver, 0 order @ pharm doses, excreted kidney
Inhibits cox 1> cox 2 irrevsibly acetylates enz.
Limitations- gastric irritation- inhibits cox 1 PG imp in mucin secretion
Percipitates gouty attacks, reyes syndrome, renal tox, allergy
OD: tinnitis, vertigo, hypervent ->resp alkalosis->metabolic acidosis tx to alk urine.

Front 155

Acetameniphen (not nsaid)

Back 155

Nonspecific cox inhibitor
Analgesic, antipyretic, not anti inflam.
can cause irrev hepatotoix/renal tox prompt treat w/ acetylcystine

Front 156

Nonselective cox inhibitors- Antiinflam,analgesic,antipyretic

Back 156

Ibuprofen, Naproxen, indomethacin

Front 157

Ibuprofen, Naproxen (longer 1/2 life than ibu)

Back 157

Milder GI effects than other cox inhibitors. rare hematological,renal comp.

Front 158

Indomethacin

Back 158

Powerful NSAID
SE: GI, ANemia,Coronary artery, Hyperkalemia
Used in gout short term, not in children unless ductus arteriosus

Front 159

Celecoxib

Back 159

Cox 2 inhibitor- reversible
Lower GI irritability
Increase Prothrombin time
High incidense of MI/sudden cardiac death

Front 160

Misoprostol

Back 160

Synthetic Prostoglandin, prevent ulcers when used w/ NSAID/ sever diarrhea +miscarrige

Front 161

NSAID renal effect and DDI

Back 161

lowers renal PH synth-> lowers BF->fluid retention
lowers effictivness of b-blockers, diuretics, ACE inhibitors, increases tosix effects of many drugs

Front 162

Methotrexate

Back 162

Standard for RA
Lymphocytes ( lowers cytokine prolife) PMN's (lower chemo, free rda)
Inhibit DHFR-> thymidine def
SE:GI, HEmatological,Hepatic, teratogenic

Front 163

Hydroxychloroquinone

Back 163

Malaria/Ameoba's (also RA)
Reduce chemotaxis,phagocyt,superox in PMN's
3-6 months
no mylosupression
not for G6PD def. monitor vision

Front 164

Sulfasalazine

Back 164

Inflam bowel disease/RA
split in GI-> Aminosialic acid+sulfapyridin (active)
SE:rashes, GI,photosen
NOT for G6PD

Front 165

Leflunomide

Back 165

Hepatic Metab to act p450 (used in RA)
Inhibit Dihydrorotate dehydrogenase
Pyrimidine def
Diarrhea, hair loss, Hepatic damage

Front 166

Azathioprine

Back 166

Converted to 6-MP
Inhibit purine synth

Front 167

TNF-a Inhibitors

Back 167

T(adal) N(et) F(lix)
Adalimumab- human Ig
Etanercept- TNF rec/ IgG Fc
Imfliximab- chimera human mouse anti tnf
SE: MS, Heart failure,SLE

Front 168

Anakinra

Back 168

IL-1 rec competitive antagonist

Front 169

Abatacept

Back 169

T lymp asoc Ag 4 +Fc
RA-inhibit T cell
Dont give w/ TNF inhitors-Infection
COPD pulm effects

Front 170

Rituximab

Back 170

RA-Chimeric Ab B cell cd20->apop
used w/ methotrexate when resist to TNF-a
SE: infusion reactions, act hep B, Viral infections

Front 171

Gout

Back 171

Xanthine->Hypoxanthine->uric acid(recurrent inflam)
Ibuprofin, Indomethacin Tx

Front 172

Allopurinol

Back 172

Inhibit XO, prevent attacks no relief. SE: skin rxn.Gi, marrow sup

Front 173

Probenecid

Back 173

Inhibit urate prox reabsorption
(asprin inhbits urate exretion raises gouty attacks)
SE: aplastic anemia, dermititis