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97 Cards in this Set

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PG's that are biologically active (4)
1)PGE
2)PGF
3)PGI
4)ThromboxaneA
PG's that are metabolic intermediates (2)
1)PGG
2)PGH
PG receptors
a)5 types
b)type of receptors they are
c)____ have been ID'd for each
a)EP, FP, IP, DP, TP
b)coupled to G-protein
c)selective inhibitors
Major source of PG
cell membrane phospholipid esters
2 other MINOR sources of PG
1)triglyceride esters
2)cholesterol esters
All sources of PG provide what?
ARACHIDONIC ACID
Arachidonic acid can produce what and how? (2)
1)prostaglandin via COX
2)leukotrienes via lipooxygenase
What make up "slow-reacting substance of anaphylaxis" (2)
leukotrienes:
LTC4
LTD4
2 classes of inhibitors of PG biosynthesis
1)NSAIDS
2)corticosteroids
NSAIDS inhibit...
COX1, COX2, COX3
NSAID related side effects due to PG inhibition (3)
1)GI bleeding due to lack of PG cytoprotective effect
2)prolongation of bleeding time due to inhibition of thromboxane synthesis
3)increased LK synthesis b/c PG biosynthesis is inhibited
Corticosteroids mechanism of inhibition of PG (3)
1)corticosteroid gets into cell and interacts w/ a receptor in the cytoplasm
2)this activates Lipomodulin which inhibits Phospholipase A2
3)Inhibiting PLA2 inhibits PG, LK, TX synthesis by preventing release of free arachidonic acid
Resistance to steroids is seen where? (2)
1)cells w/ lotsa free arachidonic acid
2)cells w/ no protein synthesis (they can't synthesize lipomodulin)
Cardiovascular effects of PG (4)
1)decrease BP via vasodilation
2)reflex incr in CO and HR
3)short duration/rapid action
Ductus arteriosus effects of PG
maintain patency(openness) of this during pregnancy
Blood platelets effects of PG (2)
1)PG is potent inhibitor of platelet aggregation
2)TX potent inducer of platelet aggregation and synthesized by platelets
Smooth muscles effected by PG (3)
1)Broncheal SM
2)Uterine SM
3)Intestinal SM
Broncheal SM effects of PG (2)
1)PG relax bronchioles
2)LK constrict bronchioles
Uterine SM effect of PG (2)
1)PGF contract, PGE relax NONpregnant uterus
2)All PG contract pregnant uterus
Intestinal SM effect of PG
contract intestine which is the MAJOR obstacle to therapeutic use of PG
Gastric Secretions effect of PG (4)
1)inhibit gastric acid secretion
2)decr pepsin
3)mucus secretion is incr
4)produce a cytoprotective effect
Peripheral Nerves/Pain effect of PG (2)
1)cause pain and irritation
2)sensitize nerve endings
Inflammatory/Immune Response effect of PG (2)
1)involved in inflammation
2)potentiate the pain producing effects of other autocoids
Reproduction effects of PG (3)
1)[]ed in male and female reproductive tract
2)amniotic fluid PG elevated during labor
3)treatment w/ NSAIDS may prolong pregnancy/labor
Therapeutic applications of PG (9)
1)therapeutic abortion
2)labor induction
3)treat dysmenorrhea
4)ED
5)prevent platelet aggregation
6)HTN
7)treat GI ulcers
8)open angle glaucoma
9)keep ductus arteriosus open in infants
Dinoprostone
a)type of PG
b)effect
c)brand name
a)therapeutic abortion
b)PGE2
c)Cervidil
____ is used to treat dysmenorrhea
NSAIDS
Alprostadil
a)PG type
b)effect (4)
c)brand name
a)PGE1
b)placed in urethra for ED, keep open ductus arteriosus in infants, prevent platelet aggregation, harvest platelets
c)Caverject
81mg Aspirin
a)fxn
inhibit thromboxanes to prevent platelet aggregation
Epoprostenol
a)PG type
b)effect
c)brand name
a)prostacyclin
b)in IV to treat HTN
c)flolan
Misoprostol
a)PG type
b)fxn
c)brand name
a)synthetic analog of PGE1
b)cytoprotective agent for ppl on long term NSAID therapy
c)Cytotec
Latanoprost
a)PG type
b)fxn
c)Brand name
d)warnings
a)PGF2
b)open angle glaucoma
c)Xalatan
d)don't use w/ contact's, may change eye color to brown
T/F
a)COX is the enzyme reqd for LK biosynthesis
b)PGG is considered a metabolic intermediate in PG biosynthesis
c)Aspirin is the most potent inhibitor of PG biosynthesis
d)No specific receptors for the PG have been ID'd
a)F
b)T
c)F (steroids)
d)F
T/F
a)Steroids inhibit both PG and LK biosynthesis
b)PGE1 and prostacyclin are responsible for SRS-A
c)Xalatan is used to prevent GI irritation caused by NSAIDS
d)Aloprostadil is a PGE1 derivative used to harvest blood platelets
a)T
b)F
c)F
d)T
3 classes of adrenal steroids
1)glucocorticoids
2)mineralocorticoids
3)gonadal steroids
Physiological axns of glucocorticoids (8)
1)carb/protein metabolism
2)calcium metabolism
3)lipid metabolism
4)action on RBCs
5)antiinflammatory
6)immunosuppressive
7)CNS fxn
8)suppress ACTH
Mineralocorticoids physiological axns
electrolyte metabolism
Cellular mechanism of adrenal steroids (4)
1)Carrier brings steroid to cell and releases it so S can get into cell
2)S binds a receptor that has hsp's bound to it, hsp release receptor
3)a steroid-receptor dimer is formed (this is active form)
4)dimer binds to DNA and acts as transcription factor
Carb/Protein metabolism axns of Glucocorticoids (2)
1)induce gluconeogenesis (leading to catabolic effect and osteoporosis/wasting)
2)decr peripheral utilization of glucose (leads to incr glucose blood levels)
Calcium metabolism axns of Glucocorticoids (2)
1)decr Ca absorption from GI
2)incr Ca excretion in urine
Lipid metabolism axns of glucocorticoids (4)
1)fat redistribution
2)"moon face", "buffalo humps"
3)loss of fat from arms/legs
4)can result in Cushing's Syndrome when in excess of glucocorticoids
Action on RBCs of Glucocorticoids (3)
1)decr in circulating immune cells (decr immunity)
2)decr fxn of lymphocytes and macrophages
3)atrophy of lymphoid tissue
Anti-inflammatory and Immunosuppressive Axns of Glucocorticoids (3)
1)related to decr in lymphocytes
2)inhibition of PLA2
3) 2) results in decr synthesis of PG, LK, TX
CNS effects of Glucocorticoids (2)
1)hyper/hypo secretion of GCs cause depression, irritability, psychosis
2)altered EEG
Suppression of ACTH effects of Glucocorticoids (2)
1)decr ACTH leads to adrenal atrophy
2)so dont do long term steroid therapy w/o proper precautions
Electrolyte metabolism effects of Mineralocorticoids (3)
1)Na and water retention
2)K loss, H+ loss
3)act on distal tubules and collecting ducts of kidney
Steroids w/ ONLY glucocorticoid activity (3)
1)triamcinolone
2)dexamethasone
3)betamethasone
Steroid w/ ONLY mineralocorticoid activity
DOC
Steroids considered mineralocorticoids b/c they have more MC activity than GC (3)
1)fludocortisone
2)DOC
3)aldosterone
Steroids considered GCs b/c they have more GC activity than MC (4)
1)cortisone
2)prednisone
3)prednisolone
4)methylprednisolone
What would be a proper steroid to use w/ CHF?
Triamcinolone, Dexamethasone, Betamethasone (have no mineralocorticoid activity so no edema)
ACh synthesis
AcoA + choline via choline acetyl transferase
ACh is degraded by ____ to ___
AChEsterase

choline and acetate
What causes exocytosis of ACh into synapse
Ca++ influx
Types of cholinergic receptors
Nicotinic (Nm(muscle), Nn(ganglionic))

Muscarinic (M1-M5)
Types of adrenergic receptors
Alpha1, alpha2

Beta1, Beta2, Beta3
Nicotinic receptors
a)2 agonists
b)receptors are...
a)ACh, nicotine
b)ion channels which have subunits that allow ions to flow thru
Muscarinic receptors
a)2 agonists
b)receptors are...
a)ACh, muscarine
b)G protein-coupled receptors
Drugs Affecting Cholinergic Receptors (5)
1)cholinergic agonists (ganglionic and muscarinic)
2)muscarinic/nicotinic antagonists
3)Neuromuscular blocking agents (nicotinic antagonists)
4)cholinomimetics (act @ receptors)
5)cholinesterase inhibitors (do NOT act at receptor just at enzyme)
Cholinomimetics (that are choline esters)
ACh (endogenous)
Cholinomimetics (synthetic ACh analogs) (4)
1)methacoline
2)carbachol
3)bethanechol
4)dexpanthenol
Choline chemical properties
primary alcohol

quaternary nitrogen
Carbamylcholine fxn
cholinomimetics w/ high NICOTINIC activity
Methacholine fxn (2)
more stable than ACh b/c of methyl providing steric hindrance to AChE

little nicotinic activity
Bethanechol fxn (2)
1)NO nicotinic activity, only muscarinic activity
2)more stable than ACh and methacholine via using carbamate
ACh chemical properties
ester w/ quaternary nitrogen
Cholinomimetic Alkaloids (5 and what makes them alkaloids?)
1)nicotine
2)muscarine
3)pilocarpine
4)Arecholine (M1)
5)Oxotremorine (M1)
Special property of Muscarine?
Is the only cholinomimetic alkaloid w/ a quaternary nitrogen, so it does NOT cross the BBB
Reversible Cholinesterase inhibitors desc
act as substrate and a stable/reversible ES complex
Irreversible Cholinesterase inhibitors desc (2)
act as substrate and a permanent ES complex

organophosphates
Cholinesterase Reactivator?
antidote for organophosphate poisoning or an irreversible agent
Do most enzymes have a reactivator?
NO
Anticholinesterase agent (reversible) that are NOT quaternary nitrogens (5)
1)physostigime
2)rivastigmine
3)edrophonium
4)donepezil
5)tacrine
Anticholinesterase agent (reversible) that are quaternary nitrogens (3)
1)neostigmine
2)pyridostigmine
3)ambenonium
Irreversible anticholinesterase agents categories (3) (are also known as...)
1)drugs
2)insecticidal agents
3)chemical warfare agents

organophosphorous inhibitors
Irreversible anticholinesterase agents (that are drugs (2))
1)echothiophate
2)isoflurophate
Irreversible anticholinesterase agents (that are insectides (2))
1)malathion
2)parathion
Irreversible anticholinesterase agents (that are chemical warfare agents (2))
1)sarin
2)soman
How do Anticholinesterase Irreversible agents work?
Will have phosphorous ester to form P-O bond which is irreversible
Cholinesterase Reactivator
2-PAM
How does 2-PAM work? and why won't it work sometimes?
breaks P-O bond

won't work if irreversible inhibitor has "aged" onto the AChE
Classical muscarinic antagonists (4 of many)
1)atropine
2)scopolamine
3)ipatropium
4)benztropine
M1 selective antagonists
1)Pirenzipine (m1)
2)telenzepine (m1)
M2 selective antagonists
3)methoctramine (m2)
4)gallamine (m2)
Nicotinic Antagonists categories
1)neuromuscular blocking agents
2)specific depolarizing agents
3)specific nondepolarizing agents
4)Steroid based agents
5)tetrahydroisoquinoline based agents
Specific depolarizing agents (2)
1)decamethonium
2)succinylcholine
Specific nondepolarizing agents (nicotinic antagonists)(2)
1)curare
2)metocurine
Steroid based agents (nicotinic antagonists) (4) (and primary feature)
1)Pancuronium
2)Vacuronium
3)Pipecuronium
4)end in -onium

MUST HAVE Quaternary Nitrogen
Tetrahydroisoquinoline-based Agents (4) (and primary feature)
1)Atracurium
2)Doxacurium
3)Mivacurium
4)end in -urium

Must have quaternary nitrogen
Gold standard of nicotinic antagonists
curare
Primary feature of Neuromuscular blocking agents
2 quaternary nitrogens separated by 10C's, rest of structure dicatates physiochemical properties
Therapeutic classes of drugs affecting the cholinergic system (4)
1)cholinomimetic agents
2)AChE inhibitors
3)muscarinic antagonists
4)NM blockers (nicotinic antagonists)
Adrenal Cortical Secretory Regulation (4)
1)STRESS
2)hypothalamus releases CRF
3)this stimulates anterior pituitary to release ACTH
4)Glomerulosa releases aldosterone and fasciculate reticutaris releases cortisol
What happens to Adrenal Cortical Secretory Regulation when:
a)High blood cortisol
b)low blood cortisol
a)decr CRF which leads to decr ACTH which leads to decr cortisol
b)incr CRF which leads to incr ACTH which leads to incr cortisol
Aldosterone pathway (3)
1)aldosterone acts at kidney
2)results in incr Na, H2O
3)results in decr K+,H+
ACE pathway (5)
1)decr BP, blood volume, Na, or INCR K+ stimulates juxtaglomerular cells
2)JX cells release renin
3)Renin converts angiotensinogen from liver to angiotensinI
4)angiotensinI to angiotensinII via ACE
5)angiotensinII stimulates glomerulosa to secrete aldosterone
Glomerulosa and ACTH
ACTH does NOT stimulate Glomerulosa but the glomerulosa needs it to work