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Boards Review by Topic > Pharmacology First Aid Review > Flashcards

Pharmacology First Aid Review Flashcards

1
Q

In enzyme kinetics, how do Vmax and Km change with competitive and non-competitive inhibitors?

A

Competitive: acts as if to decrease the affinity of the receptor for the substrate to Km will increase but Vmax will remain the same

Non-competitive: acts as if to remove some of the enzyme from the equation so affinity (Km) remains the same but Vmax is diminished

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2
Q

Define volume of distribution

A

Amount of drug in body divided by plasma concentration

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3
Q

For low, med, high volume of distribution, what are the compartments and drug types?

A

Low: Blood compartment, large or charged molecules; plasma protein bound

Med: ECF, small hydrophilic molecules

High: All tissues including fat, small lipophilic molecules, especially if bound to tissue protein

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4
Q

Equation for half life

A

T1/2=0.7*Vd/CL

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5
Q

How does time to steady state change with dose and dosing frequency?

A

It doesn’t

Time to steady state generally is only affected by t1/2

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6
Q

Equation for loading dose

A

Target Concentration* Vd/bioavailability

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7
Q

Equation for maintenance dose

A

(Cp) x (CL) x tau / (F)

Cp= target plasma concentration
CL=clearance rate
tau=dosage interval
F=bioavailability

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8
Q

What is a tachyphylactic drug response?

A

Acute decrease in response to drug after initial/repeated administration

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9
Q

3 drugs with zero order elimination

A

Phenytoin, Ethanol, Aspirin

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10
Q

How is pH of urine changed to increase clearance of drugs?

A

Remember that ionized particles are trapped in the urine and excreted.
Bicarbonate makes the urine more basic which ionizes acids
Ammonium chloride make urine more acidic ionizing bases

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11
Q

What are the phases of drug metabolism?

A

Phase I: reduction, oxidation, hydrolysis by p450; lost first in geriatric patients

Phase II: Conjugation–Methylation, Glucuronidation, Acetylation, Sulfation; ultimately inactivates drug; Geriatric patients still have this phase

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12
Q

Efficacy vs potency

A 
Efficacy = Effect
Potency = how much drug needed for effect
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13
Q

What is EC50?

A

Amount of drug needed to achieve 1/2 maximal effect

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14
Q

How does potency and efficacy of a drug change with administration of a competitive antagonist vs noncompetitive or partial agonist given alone?

A

Competitive antagonist: decreased potency but unchanged efficacy because can be overcome by increased concentration

Noncompetitive: removes some receptors from the equation so efficacy is lost but potency is unchanged

Partial agonist given alone: efficacy is lost and potency is completely independent from original drug

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15
Q

Therapeutic index vs window

A

Index = TD50/ED50; it is the ratio of dose that is toxic to 50% of patients over dose effective in 50%

Window is the dosage range that can safely and effectively treat the disease

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16
Q

In all of the first synaptic terminals in the ANS and Somatic NS, what is the NT and receptor?

A

Acetylcholine and Nicotinic

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17
Q

What two structures or functions in the body are unique in that they are Sympathetically innervated but NT is ACh? What receptor?

A

Sweat glands: ACH on muscarinic

Adrenal medulla: ACH on Nicotinic

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18
Q

How do Nicotinic and Muscarinic receptors exert their effects?

A

Nicotinic: ligand gated Na/K channels
Muscarinic: G-protein coupled

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19
Q

In order to remember the G-protein associated with each receptor, what is the order to list the receptors?

A 
Alpha 1,2
Beta 1,2,3
M 1,2,3
D 1,2
H 1,2
V 1,2

QISSS QIQ SIQ SQS

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20
Q

What are the effects of alpha-2 receptor?

A

Decreases: sympathetic outflow, insulin release, lipolysis, aqueous humor production
Increases: platelet aggregation

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21
Q

Beta-1 receptor effects

A

Increases: HR, contractility, renin release, lipolysis

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22
Q

Beta-2 receptor effects

A

Vasodilation, bronchodilation
Increased: lipolysis, insulin release, aqueous humor production
Decrease: uterine tone, ciliary muscle tension

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23
Q

Beta-3 receptor effects

A

Increase: lipolysis, thermogenesis in skeletal muscle

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24
Q

M1 receptor effects

A

CNS and enteric nervous system

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25
Q

M2 receptor effects

A

Decrease HR and contractility

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26
Q

M3 receptor effects

A

Increase: exocrine gland secretions (lacrimal, sweat, salivary, gastric), gut peristalsis, bladder contraction, bronchoconstriction, pupillary sphincter, ciliary muscle

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27
Q

D1 receptor effects

A

Relaxes vascular smooth muscle

28
Q

D2 receptor effects

A

Modulates transmitter release in brain especially

29
Q

H1 receptor effects

A

Increase: nasal and bronchial mucous production, vascular permeability, contraction of bronchioles, pruritis, pain

30
Q

H2 receptor effects

A

Increase gastric acid

31
Q

V1 receptor effects

A

Vascular smooth muscle contraction

32
Q

V2 receptor effects

A

Increase H2O permeability and reabsorption in the collecting tubules of the kidneys

33
Q

Describe the Gq pathway

A

Gq activates Phospholipase C that turns PIP2 into DAG and IP3
DAG stays at the membrane while IP3 releases Ca
Ca signals DAG to activate Protein Kinase C and also signals the contraction of smooth muscle

34
Q

How do Amphetamines work?

A

Use NE Transporter (NET) to enter presynaptic terminal and then use VMAT to enter vesicles and displace NE
Once NE reaches high level in presynaptic terminal, NET action is reversed and NE spills into synapse and re-uptake is inhibited

35
Q

What happens when a patient on MAOI’s eats something with Tyramine?

A

Tyramine normal in food and processed by MAO in the gut
Increased Tyramine enters noradrenergic nerves and produces increased NE and leads to increased sympathetic stimulation and often an HTN crisis

36
Q

With all cholinomimetic agents, including AChE inhibitors, what should be watched out for?

A

Exacerbation of COPD, asthma, and PUD

37
Q

What is the antidote for Cholinesterase inhibitor poisoning?

A

Atropine and Pralidoxime

38
Q

Effects of Atropine overdose

A

No sweating —> Dry as a bone —> increased body temp (Hot as a hare) and skin flushing (Red as a beet)
Cycloplegia (Blind as a bat)
Disorientation (Mad as a hatter)

39
Q

What Dopamine agonist might you give for HTN crisis?

A

Fenoldopam: D1 agonist

Vasodilator–coronary, peripheral, renal, splanchnic

40
Q

What is the action of Phenylephrine?

A

agonist at alpha-1 > alpha-2

41
Q

Epinephrine receptor action?

A

Beta over Alpha
Alpha predominates at high dose
Significantly stronger Beta-2 than NE

42
Q

Dopamine receptor actions

A

D1=D2 > beta > alpha
Used for unstable bradycardia, HF, and shock
Heart effects at lower doses (beta) and vasoconstrictive effects at higher doses (alpha)

43
Q

What should never be given if cocaine intoxication is suspected and why?

A

Never give a Beta blocker because would result in unopposed alpha activation leading to HTN crisis

44
Q

MOA of Ephedrine

A

Releases stored catecholamines from presynaptic terminal similar to Amphetamine

45
Q

NE receptor activation

A

Alpha’s over Beta’s and no Beta-2

46
Q

NE, Epi, Isoproterenol compared activation of beta vs alpha

A

NE: alpha over beta
Epi: alpha = beta
Iso: beta over alpha

47
Q

Of NE, Epi, and Isoproteronol, which will cause the greatest increase in MAP? Which causes an increase in diastolic pressure?

A

NE and Epi both increase MAP, but NE is greater

NE is only one to increase diastolic pressure

48
Q

What sympatholytic agent is given for HTN in pregnancy?

A

alpha-methyldopa

49
Q

What drug can be given to patients on MAOI’s who eat tyramine containing foods?

A

They will have a HTN crisis

Treat with Phentolamine to block alpha receptors and bring down BP

50
Q

Mirtazapine

A

Alpha 2 selective blocker

Depression treatment

51
Q

How do reversals by Phentolamine differ between Epi and Phenylephrine?

A

Because Epi has alpha and beta action, administration of Phentolamine will reverse the overall effects of Epi by blocking the pressor effects and leaving the beta effects unopposed
Phenylephrine’s effects will be diminished, but not reversed because it only has alpha effects

52
Q

General rules for the selectivity of Beta blockers

A

Beta-1 selective blockers tend to go from A to M in the alphabet
Nonselective blockers tend to go from N to Z
Nonselective beta and alpha blockers tend to have modified suffixes other than -olol

53
Q

How is Nebivolol unique?

A

Combines cardiac-selective beta-1blockade with stimulation of beta-3 which activates NO synthase in vasculature

54
Q

What is Methemoglobin?

A

A form of hemoglobin that has a heme group in the ferric (3+) state instead of the ferrous (2+) that makes it so it cannot bind O2
Has a bluish, chocolate brown color
An NADH dependent enzyme–methemoglobin reductase–is responsible for reducing it back to hemoglobin

55
Q

What drugs can cause coronary vasospasm?

A

Cocaine, Sumatriptan, ergot alkaloids

56
Q

What drugs can cause cutaneous flushing?

A 
Think VANCE
Vanco
Adenosine
Niacin
Ca channel blockers
Echinicandins
57
Q

What drugs can lead to dilated cardiomyopathy?

A

Anthracyclines (doxorubicin, daunorubicin)

Prevent with dexrazoxane

58
Q

What drugs can cause Torsades?

A 
Think ABCDE
AntiArrhythmics (class IA, III)
AntiBiotics (like macrolides)
Anti"C"ychotics (like Haloperidol)
AntiDepressants (like TCA's)
AntiEmetics (like ondansetron)
59
Q

What drugs can cause gingival hyperplasia?

A

Phenytoin, Ca channel blockers, Cyclosporine

60
Q

What drugs can cause hyperuricemia?

A

Pyrazinaminde, Thiazides, Furosemide, Niacin, Cyclosporine

61
Q

What drugs can cause pulmonary fibrosis?

A

Methotrexate, Nitrofurantoin, Carmustine, Bleomycin, Busulfan, Amiodarone

62
Q

What are the P-450 inducers?

A 
Think: Chronic Alcoholics Steal Phen-Phen and Never Refuse Greasy Carbs
Chronic alcohol use
St. Johns Wart
 Phenytoin
Phenobarbital
Nevirapine
Rifampin
Griseofulvin
Carbamazepine
63
Q

What are the P-450 inhibitors?

A 
Think: AAA RACKS IN GQ Magazine
Acute Alcohol Abuse
Ritonavir
Amiodarone
Cimetidine/Ciprofloxacin
Ketoconazole
Sulfonamides
Isoniazid (INH)
Grapefruit Juice
Quinidine
Macrolides (except azithromycin)
64
Q

MOA of the antivirals ending in -ivir

A

Neuraminidase inhibitors

65
Q

MOA of antivirals ending in -navir

A

Protease inhibitor

66
Q

MOA of antivirals ending in -ovir

A

DNA polymerase inhibitor

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