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STEP 1 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Name 4 potassium sparing diuretics and 2 drug classes that are also potassium sparing diuretics

A

Banana (SEAT): Spironolactone Eplerenone Amiloride Triamterene

ACEIs (–pril) and ARBS (–sartan)

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2
Q

List 3 types of potassium wasting diuretics

A

Clorthalidone, Hydroclorothiazide (Thiazides) Furosemide, Torsemide, Bumetanide (Loops) Acetazolamide (CA inhibitor)

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3
Q

_______, a cyp450 inducer, enhances its own toxicity.

A

Acetaminophen

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4
Q

_____ is the antidote to Acetominophen overdose. Which supplies the Glutathione depleted in overdosed patients.

A

N-Acetylcysteine

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5
Q

Codeine is a pro-drug. It’s _____ that converts it to its active form, Morphine.

A

Cyp2D6

*Codeine + P450 Inducer = more side effects?

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6
Q

Codeine + ________ = blocks metabolism stuck as a prodrug thus less effective

A

Cimetidine (P450 inhibitor)

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7
Q

Clopidogrel is a pro-drug that is metabolized to its active form via Cyp-450. _______ blocks that metabolism.

A

Omeprazole (Cyp-P450 inhibitor) *Do NOT give Clopidogrel + Omeprazole together otherwise clopidogrel will not work

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8
Q

Crigler-Nijar (CN) which can be either Type 1 (unconjugated bilirubin greater than ___) or Type 2 (unconjugated bilirubin usually less than ____).

A

Type 1: > 24 Type 2: <24

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9
Q

What drug can be used as a diagnostic tool and the treatment for Crigler-Nijar? Why?

A

Phenobarbital In type 2 it can lower bilirubin levels by about 25% In type 1: it doesn’t change the levels of bilirubin

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10
Q

What’s the difference between CN Type 1 and Type 2?

A

Type 1 = no glucuronosyltransferase enzyme (UGT1a1) Type 2 = deficiency of glucuronosyltransferase enzyme *Phenobarbital induces the metabolism of unconjugated (indirect) bilirubin in Type 2 via being a Cyp-P450 inducer elevating glucuronosyltransferase activity to conjugate the bilirubin

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11
Q

The antibiotic _________ it can give you a side effect in neonates called gray baby syndrome

A

chloramphenicol

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12
Q

Why can’t neonates metabolize chloramphenicol ?

A

Low activity levels of glucuronosyltransferase (UGT1a1) needed for phase 2 glucoronidation of the drug Drug accumulates to toxic levels

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13
Q

Unconjugated (indirect) Bilirubin is cleared by ______-.

A

Glucuronidation The conjugation occurs via glucuronosyltransferase

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14
Q

Mild elevation of Unconjugated (indirect) Bilirubin is seen in what disease?

A

Gilbert Syndrome (Crigler Najir has higher elevation)

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15
Q

Hydralazine is a drug metabolized by _______ via ________, a phase 2 metabolism reaction

A

Acetylation N- acetyltransferase

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16
Q

3 drugs causing Drug Induced SLE

A

Hydralazine (for HTN vasodilates arteriolar smooth muscle) Procainamide ( 1A anti-arrhythmic that binds to fast sodium channels inhibiting recovery after repolarization. It also prolongs the action potential and reduces the speed of impulse conduction) Isoniazid (inhibits mycolic acid/ cell wall synthesis)

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17
Q

Why do some people get Drug Induced Lupus?

A

Slow acetylators because slow N- acetyltransferase (phase 2 activity) *positive test for antihistone antibodies = it was drug-induced lupus. *The other thing that they could do instead of running an is discontinue all drugs and see if the lupus goes away

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18
Q

Phase 2 metabolism reaction called glucoronidation which is just a conjugation reactions. Describe the reaction.

A

In glucoronidation, the enzyme, glucuronosyltransferase, takes a glucose molecule and transfers (attaches) it to the drug being metabolized. This increases the size of the drug consequently making it easier to eliminate *that’s one of the key features of Phase 2 reactions the size of the drug increases.

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19
Q

Macrolides (except ______ ) are CypP–450 ______.

A

Azithromycin inhibitors

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20
Q

_____ dose is going to be unaffected by renal dysfunction because it does not factor in renal function and it doesn’t factor in Clarence.

A

Loading

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21
Q

If renal clearance goes down (renal dysfunction), the half-life of the drug is going to go up and in order to avoid toxicity you’re going to have to lower your _____ dose because of the drug’s increased duration of action.

A

maintenance

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22
Q

How is loading dose and maintenance dose going to differ in someone with renal dysfunction vs someone healthy?

A

Same loading dose Lower maintenance dose

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23
Q

How is Volume of Distribution (Vd) Calculated?

A

amount of drug in the body/plasma drug concentration (Mass mg)/ (mass/vol) = volume

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24
Q

Vd = 1 when?

A

amount of drug is the same inside and outside of blood vessels

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25
Q

_ protein binding = ↑ Vd

A

↓

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26
Q

What 2 factors can change Vd and why?

A

Kidney damage → proteinuria → ↓ protein binding → ↑ Vd

Liver damage → ↓ protein (albumin) synthesis → ↑ Vd

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27
Q

If ↓Vd where is the drug? why?

A

In the blood (intravascular) -large/charged molecule -bound to plasma protein like Albumin

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28
Q

If ↑Vd where is the drug? why?

A

In the tissues (even fat) -small lipophilic molecule -bound to tissue proteins

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29
Q

The relationship between half life and clearance is a(n) _____ relationship

A

inverse *if clearance goes down half life goes up

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30
Q

How is Clearance (CL) Calculated?

A

rate of drug elimination/ Plasma drug concentration (mass/time)/(mass/vol) = CL OR CL= Vd x Ke (elimination constant) Low Yield

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31
Q

Volume of distribution is directly proportional to _____.

A

half-life *If the distribution of the drug goes up that implies that the drug is being sequestered into the tissues which means it’s not being metabolized and excreted.

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32
Q

In first order kinetics it takes __-__ half-lives to reach steady state

A

4-5

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33
Q

In first order kinetics half life is decreased by what?

A

half 1 = 50% left 2= 25% left 3= 12.5% left etc.

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34
Q

An IV BOLUS of drugs is a loading dose clue In drugs given via IV the Bioavailability (F) is

A

F= 1

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35
Q

How is loading dose calculated?

A

(Cp x Vd) / F

Cp= Target plasma concentration at steady state

Vd = Vol of distr

F = Bioavailability

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36
Q

How is Maintenance dose calculated?

A

(Cp x CL x tao) / F Cp= Target plasma concentration at steady state CL= Clearance tao = dosage interval (time between doses if not continuous) F= bioavailability

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37
Q

Time to steady state is independent of ___ and _____

A

dose dosing frequency (depends on half-life)

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38
Q

The only way you can compare 2 drug’s Affinity is if those two drugs have ______ in the graph that indicates those 2 drugs work on the ______.

A

parallel slopes

same receptor

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39
Q

In a dose response curve, the drug with the greater Affinity is the slope that is shifted the most to the ____.

A

Left

*A has a greater affinity for its receptor than B shifted bc it is more to the left, the closer to the y-axis, the greater the affinity.

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40
Q

When you get a question on Potency, it doesn’t matter if they work on the same receptor or not.

All you’re doing when you’re comparing is looking for the curb that is shifted the most to the ____.

Potency is all about the amount of drug that you’re taking. It takes a smaller amount of drug to produce the effect (ie it’s a smaller pill)

A

Left

aka lower EC50

*In this case drug A is more potent than drug B.

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41
Q

Efficacy is measured on the y-axis of the Dose- Response curve.

The higher ______ a drug reaches the more efficacious it is.

A

% Response aka % Maximal effect

(ie: the taller the curve is the more efficacious it is)

42
Q

What is the Y axis and X axis of the dose response curve?

A

Y: % response

X: Log dose

43
Q

a ____________ decreases drug potency

and

___ be overcome by increasing drug concentration.

A

competitive antagonist

CAN

44
Q

A _______ decreases drug efficacy

and

______ be overcome by increased drug concentration

A

Non-Competitive Antagonist

CANNOT

45
Q

A _______ alone has decreased drug efficacy

and

acts at ______ site

A

partial agonist

the same site

46
Q

Safer drugs have high ___ values

A

TI

Therapeutic index

TI= TD/ED

* middle points of (toxic dose/effective dose)

47
Q

All Beta adrenergic receptors (1,2,3) have what associated G-protein?

A

Gs

48
Q

Alpha 1 and Alpha 2 beta adrenergic receptors have what associated G-protein?

A

1 → Gq

2 → Gi

alpha 1, 2, Beta 1,2,3 → (qisss) Kiss

49
Q

MI, M2, and M3 have what associated G-proteins?

A

M1 → Gq

M2 → Gi

M3 → Gq

Men an qiq (quick)

50
Q

D1 and D2 receptors have what associated G protein class?

A

D1 → Gs

D2 → Gi

Do you want Dopamine? Si!!!

51
Q

H1 and H2 (Histamine) receptors have what associated G-protein class?

A

H1 → Gq

H2 → Gs

With Queso I need a lot of anti-Histamine

52
Q

V1 and V2 (Vasopressin) receptors have what associated G-protein class?

A

V1 → Gq

V2 → Gs

Queso stresses me out sometimes

(Vasopressin raises BP like stress)

53
Q
A
54
Q

cAMP has different functions for locations

In Skeletal muscle ↑cAMP =

Smooth muscle raise ↑cAMP =

A

(sk) contraction
(sm) relaxes

55
Q

Angiotensin II (AT1) is coupled to what protein G-class. What does it do to blood vessels?

A

Gq

Vasoconstricts

(RECALL: Gq constricts smooth muscle via ↑ calcium; Gs relaxes smooth muscle via ↑ cAMP)

56
Q

Recite the Gq mechanism

A

Gq activates Phospholipase C (PLC) to cleave PIP2 into DAG and IP3

IP3 then causes release of intracellular calcium form the sarcoplasmic reticulum (SR)

Calcium and DAG activate PKC

57
Q

Recite the Gs pathway

A

Gs activates Adenylyl Cyclase (AD)

which turns AMP to cAMP

cAMP then activates PKA

PKA inhibits myosin light chain Kinase causing dephosphorylation of MLC ⇒ Vasodilation of smooth muscle

PKA causes calcium release ⇒ contraction in myocytes and skeletal muscles

58
Q

Recite the Gi pathway

A

Gi inhibits Adenylyl Cyclase

thus decreasing cAMP levels

thus allowing Myosin Light Chain Kinase to phosphorylate the light chain ⇒ smooth muscle contracts

59
Q

Beta 1 stimulation causes

what 4 things

A

↑ HR

↑ Contractility

↑ Renin (↑BP)

↑ Lipolysis (energy)

60
Q

B2 stimulation causes what 7 things

A

Bronchodilation (vasodilation)

↑ lipolysis/ Glycogenolysis

↑ Renin (↑ BP)

↑ Insulin

↑ Aqueous Humor production

↑ K+ uptake by cells

↓ uterine tone

61
Q

Beta 3 causes what 3 things

A

↑ Lipolysis

↑ Heat in muscles

↑ bladder relaxation

62
Q

Alpha 1 stimulation causes what 3 things

A

↑ vasoconstriction

Mydriasis (Dialated eyes)

↑ Intestinal/bladder sphincter contraction

↑ Uterine contraction (ß2 effects > alpha 1)

63
Q

alpha 2 causes what 5 things

A

↑ platelet aggregation

↓ Lipolysis (unlike Betas)

↓ Insulin (unlike Beta2)

↓ aqeous humor production (unlike beta 2)

64
Q

M1 stimulation stimulates the _______ nervous system

A

Enteric

65
Q

M2 stimulation has what 2 effects?

A

↓ HR

↓ atrial contractility

66
Q

M3 stimulation has what 7ish effects?

A

↑ tears, sweat, salivation

↑ gut motility (diarrhea)

↑ bladder contraction (peeing)

↑ pupillary sphincter contraction (Myosis–pinpoint eyes)

↑ Ciliary muscle contraction (Myosis)

↑ Insulin (Like Beta2)

↑ endothelin vasodilation

67
Q

Relaxes Renal Vascular smooth muscle

activates direct pathway

A

Dopamine on D1 receptors

68
Q

Inhibits indirect pathway in striatum

A

Dopamine on D2 receptors

69
Q

Mediates Pruritis, Pain, Mucus production, ↑ vascular permeability

A

Histamine on H1 receptors

70
Q

Increases gastric secretions

A

Histamine on H2 receptors

71
Q

↑ vWF release

↑ Aqua Porin 2 in CD

A

Vasopressin on V2 receptors

72
Q

___ constricts smooth muscle via ↑ calcium; ___ relaxes smooth muscle via ↑ cAMP

A

Gq

Gs

73
Q

____ in smooth muscle causes dephosphorylation of MLC thus vasodilation

A

Nitric Oxide

74
Q

Epinephrine activates what receptors

A

alpha 1, 2

Beta 1, 2

75
Q

Norepinephrine activates what receptors

A

alpha 1, 2

Beta 1

76
Q

Describe sweat gland and piloerector muscle innervation

A

Sympathetic stimulation

Short Pre-ganglion Cholinergic (Ach) Nerve synapsing onto a Nicotinic receptor

Long Post-Ganglionic Cholinergic (Ach) Nerve synapsing onto a Muscarinic receptor

*This is the exception to the post-ganglionic adreneric (NE) nerve synapsing onto Alpha/ Beta receptors.

77
Q

Describe the Innervation of the Adrenal Medulla Chromaffin cells?

A

SNS stimultion

Short Pre-Ganglionic Cholinergic (Ach) Nerve synapsing onto a Nicotinic receptor.

Epinephrine released by Chromaffin cells travels through the blood activating every alpha/beta receptor in it’s path.

78
Q

The 1st neurotransmitter in ANY pathway is ___

The first synapse receptor in every pathway is a ______ receptor

A

Ach

nicotinic

79
Q

What type of receptor is found on skeletal muscles

A

Nicotinic receptors (Nm)

80
Q

Nicotinic receptor are ligand (Ach) gated _____ channels.

A

Na+/K+ channels

81
Q

NE regulates itself via binding to _____ receptor on the pre-synaptic nerve that released it.

A

alpha 2

(Negative feedback)

82
Q

Botulinum toxin cleaves SNARE proteins on the pre-synaptic cell inhibiting the release of ______ from the pre-synpatic cell onto the synaptic cleft

A

Ach vesicle

83
Q

Describe the effect of NE and Isoproterenol

What happens when administered together?

A

NE: ↑ MAP ↓ HR (reflex) ↑TPR

ISO: ↓ MAP ↑ HR (Reflex) ↓TPR

Together they blunt each other’s effects

84
Q

What effects does Epinephrine have on CO, HR, MAP, and TPR?

A

All of them increase

85
Q

is used for postoperative or neurogenic ileus or urinary retention. To increase/ stimulate GI & bladder motility.

A

Bethanechol

Cholinomimetic (resistant to AchE)

86
Q

Malathion, Parathion, and Sarin Nerve gas are all:

A

All organophosphates that irreversibly inhibit Ach-esterase

*Malathion, Parathion are pesticides

87
Q

is the antidote to Organophosphates poisoning

what else can be given?

A

Atropine ⇒competitive inhibitor that can cross BBB to relieve CNS (not muscular) and muscarinic symptoms

(before this you must wash the pateint’s skin becuase if on the skin it can permeate and still have effects)

Pralidoxime (2PAM) if less than 4 hours which regenerates blocked AchE via dephosphorylation which can relieve nicotinic muscular symptoms.

88
Q

Causes respiratory depression, lethargy, seizures, coma

A

Organophosphates

89
Q

Overstimulation of Muscarinics due to Cholinomimetics causes DUMBBELSS.

What does the acronym stand for?

A

Diarrhea

Urination

Myosis (pin-point eyes)

Bronchoconstriction

Bradycardia

Emesis

Lacrimation

Salivation/ Sweat

90
Q

Name 4 CHOLinomimetic direct agonist

A

BethaneCHOL

CarbaCHOL

MetaCHOLine

PiloCHOLpine (Pilocarpine, but whatever)

91
Q

Name 7 cholinomimetic indirect agonist (AchE blockers)

A

NeoSTIGMINE

PhysoSTIGMINE

PyridoSTIGMINE

RivaSTIGMINE

GalantaSTIGMINE (Galantamine)

EdrophonIGMINE (Edrophonium)

DonapezIGMINE (Donapezil)

92
Q

How is cocaine used to diagnose Horner’s syndrome?

A

Cocaine does not dilate Horner’s eyes

because all three nerves need to be working

*1st and 2nd neurons cholinergic (Ach). 3rd Neuron adrinergic NE)

93
Q

How is the lesion in Horner’s syndrome localized?

A

Eye has 3 neurons

1st 2 are cholinergic (ach)

3rd one to the eye is adrenergic NE (alpha 1)

Hydroxyamphetamine causes the release of NE.

It will go to the 3rd neuron, release NE, and dilate the eye.

If the problem in the eye is 1st or 2nd order neuron the affected eye will be dilated.

but if Hydroxyamphetamine cannot dilate the eye then we can localize the nerve damage to the 3rd order neuron

94
Q

Atorvastatin is an HMG-CoA reductase inhibitor; worrisome side-effects include ________ and ________* particularly when used in combination with ________.

A

hepatic dysfunction

muscle toxicity (rhabdomyolysis)

fibrates (lowers TGs)

or cyclosporin (immunosuppressant)

95
Q

____ is a nonabsorbable cation exchange resin used to treat hyperkalemia.

It binds colonic potassium in exchange for calcium, trapping potassium within the resin where it is then excreted in the feces.

A

Patiromer

96
Q

_____ are also used to relieve intraocular pressure in open-angle and angle-closure glaucoma.

A

Carbonic anhydrase inhibitors

97
Q

Mucosal hyperplasia (ex: gingivae)is seen in patients treated with

A

phenytoin

98
Q

Significant ______ can cause muscle weakness, cramps, and possible rhabdomyolysis.

A

hypokalemia

99
Q

______ is used for treating cerebral edema, but causes initial intravascular volume expansion that can worsen pulmonary edema and heart failure.

A

Mannitol

100
Q

______ are the most potent diuretics and are used as first-line therapy for rapid relief of symptoms in patients with acute decompensated heart failure.

A

Loops

101
Q

______ promotes potassium and hydrogen ion secretion from the principal and intercalated cells of the collecting tubules

A

Aldosterone

*promotes Na reabsorption via increased

ENaC and NaK ATPases

102
Q

HTN w/ DM should be treated with ____ with caution because:

A

Beta blockers

mask hypoglycemia symptoms

STEP 1 (88 decks)

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