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Step 1 pharmacology > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

zero order elimination. What is it, and what are examples

A

PEA, phenytoin, ethanol, aspirin. zero order means that rate of elimination is constant regardless of Cp.

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2
Q

first order elimination. What is it

A

rate of elimination is proportional to Cp

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3
Q

Weak acid drugs: Examples, where are they trapped, how to treat overdose

A

phenobarbitol, methotrexate, apririn. they are trapped in basic environments. treat overdose with bicarbonate.

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4
Q

Weak base drugs: Example, where they are trapped, how to treat an overdose

A

Amphetamines. they are trapped in acidic environments. Treat overdose with ammonium chloride

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5
Q

What is phase 1 drug metabolism

A

redox, hydrolysis. via Cyp450 system. Yields slightly polar metabolites that are often still active. Geriatric patients lose phase 1 first!

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6
Q

What is phase 2 drug metabolism

A

Geriatric patients still have this, still have GAS, glucoronidation, acetylation, and sulfation. usually yields very polar, inactive metabolites that are renally extracted.

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7
Q

What is efficacy.

A

refers to the maximum effect that a drug can produce. Examples of high efficacy drugs include analgesics, antibiotics, antihistamines, decongestants. a partial agonist is less efficacious than a full agonist.

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8
Q

potency

A

the amount of drug needed for a given effect. if there is increase potency, there is increased affinity for the receptor. examples of highly potent drugs include: chemodrugs, antihypertensives, lipid lowering drugs.

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9
Q

competitive antagonist

A

decrease potency, no change in efficacy. can be overcome by increasing agonist. Flumezanil is a competitive antagonist on GABA receptors

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10
Q

noncompetitive antagonist

A

decreases efficacy. Is not overcome by increasing agonist concentration. Ketamine is a noncompetitive antagonist on NMDA receptors.

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11
Q

irreversable competitive antagonist

A

decreases efficacy. is not overcome by increasing agonist concentration. phenoxybenzamine is an irreversible competitive antagonist on alpha receptors

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12
Q

flumazenil

A

competitive antagonist on GABA receptors

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13
Q

Ketamine

A

noncompetitive antagonist on NMDA receptors

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14
Q

phenoxybenzamine

A

irreversible competitive antagonist on alpha receptors

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15
Q

partial agonist

A

acts at same site as full agonist but lower efficacy, independent of potency. buprenorphine is a partial agonist of mu opioid receptors when compared to morphine.

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16
Q

bupronorphine

A

partial agonist of mu opioid receptors

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17
Q

Therapeutic index. what does it represent, how to calculate it, and examples of drugs with low TI values.

A

TITE. Therapeutic index is TD50/ED50. Higher is better. Low TI drugs include digoxin, lithium, theophylline, and warfarin.

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18
Q

parasympathetic uses which NTs?

A

ACh on muscarinic receptors.

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19
Q

sympathetic uses which NTs?

A

ACh at the preganglionic neuron. For Sweat glands, ACh at postgang. Usually Norepi at postgang. Dopamine for renal vasculature and smooth muscle. ACh straight from spinal cord for the adrenal medulla (which then releases NE and E).

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20
Q

Nicotinic ACh receptors are found where?

A

they are ligand gated Na/K channels. they are found in autonomic ganglia (Nn), and neuromuscular junction (Nm).

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21
Q

Muscarinic ACh receptors are found where?

A

G protein coupled receptors that usually act through 2nd messengers. there are 5 subtypes M1-M5.

22
Q

Alpha 1 GPCRs. What G protein class and major functions

A

G protein class q
Major functions:
1. increase VSMC contraction
2. Pupil dilatory muscle contraction. Mydriasis
3. intestinal and bladder sphincter muscle contraction

23
Q

Alpha 2 GPCRs. What G protein class and major functions

A 
G protein class i
Major functions:
1. decreases sympathetic outflow
2. deceases insulin release
3. decreases lipolysis
4. decreases platelet aggregation
24
Q

Beta 1 GPCRs. What G protein class and major functions

A 
G protein class s
Major functions:
1. increase heart rate,
2. increase contractility
3. increase renin release
4. increase lipolysis
25
Q

Parasympathetic M1. What G protein class and major functions

A

G protein class q.
Major Functions:
1. CNS, enteric system

26
Q

Parasympathetic M2. What G protein class and major functions

A

G protein class i.
Major functions:
1. decease heart rate
2. decrease atrial contractility

27
Q

Parasympathetic M3. What G protein class and major functions

A

G protein class q
Major Functions:
1. Increase endocrine gland secretions (lacrimal, salivary, gastric)
2. increase gut peristalsis
3. increase bladder contraction
4. bronchoconstriction
5. increase pupillary sphincter muscle contraction (miosis)
6. ciliary muscle contraction (accomodation)

28
Q

Dopamine D1. What G protein class and major functions

A 
G protein class s
Major functions:
1. relaxes renal vascular smooth muscle
29
Q

Dopamine D2. What G protein class and major functions

A

G protein class i
Major Functions:
1. Modulates NT release, especially in the brain

30
Q

Histamine H1 What G protein class and major functions

A 
G protein class q. 
Major Functions:
1. increase nasal and bronchial mucus production
2. increase vascular permeability
3. contraction of bronchioles
4. pruritis
5. pain
31
Q

Histamine H2. What G protein class and major functions

A 
G protein class s.
Major functions:
1. increase gastric secretions
32
Q

Vasopressin V1. What G protein class and major functions

A 
G protein class q.
Major functions:
1. increase vascular smooth muscle contraction
33
Q

Vasopressin V2. What G protein class and major functions

A 
G protein class s.
Major functions
1. increase H2O permeability and reabsorption in the collecting tubules of the kidney
34
Q

What do Gq receptors do?

A

activate phospholipase C -> cleave PIP2 to IP3 and DAG. to activate Protein Kinase C and increase intracellular calcium

35
Q

What do Gs receptors do?

A

stimulate adenylyl cyclase to make cAMP and protein kinase A to increase Ca intracellularly in the heart, and block myosin light chain kinase in smooth muscle.

36
Q

What do Gi receptors do?

A

inhibit adenylyl cyclase to stop making cAMP and protein kinase A to decrease Ca intracellularly in the heart, and allow myosin light chain kinase in smooth muscle.

37
Q

action of hemicholinium in the ANS

A

blocks choline transport into axon terminals. (that choline is then used to acetylcholine). this drug is typically not used clinically

38
Q

action of vesamicol in the ANS

A

blocks acetylcholine entering into vesicles in the axon terminal. this drug is typically not used clinically.

39
Q

action of boutlinum in the ANS

A

blocks release of acetylcholine filled vesicle release from axon terminals

40
Q

action of metyrosine in the ANS

A

blocks tyrosine’s conversion to DOPA on the way to forming dopamine and NE. not typically used in clinic

41
Q

action of reserpine in the ANS

A

blocks transport of dopamine into the vesicles in the axon terminals.

42
Q

action of amphetamines in the ANS

A

increases release of NT laden vesicles (dopamine or NE) into synapse, and deceases reuptake

43
Q

action of bretylium in the ANS

A

decreases release of NT laden vesicles (dopamine or NE) into synapse

44
Q

action of cocaine, TCAs,

A

decreases reuptake of NTs like dopamine and NE

45
Q

action of guanethidine in the ANS

A

blocks release of NT laden vesicles (dopamine and NE). not usually used in clinic

46
Q

action of angiotensin II in the ANS

A

increase release of NE from nerve endings

47
Q

action of Alpha 2 receptors in the ANS

A

blocks release of NE from nerve endings.

48
Q

bethanechol. action and clinical application

A

Used for postop ileus, neurogenic ileus, and urinary retention. actives bowel and bladder smooth muscle. it is resistant to AChE

49
Q

carbachol. action and clinical application.

A

used for glaucoma, pupillary constriction, relief of intraocular pressure. is a carbon copy of acetylcholine

50
Q

pilocarpine. action and clinical application

A

potent stimulator of seat, tears, saliva. used for both open angle and closed angle glaucoma. 1. causes contraction of cilliary muscle (open angle glaucoma).
2. contracts pupillary sphincter (closed angle glaucoma)
it is resistant to AChE,

you drool, cry and sweat on your PILOw

Step 1 pharmacology (1 decks)

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