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Pharmacology Flashcards

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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

(a P450 isozyme)

*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: > 20mg/dL (20-50)

Type 2: <20

*both can use phototherapy to treat

*type 1 → liver transplant or plasmapherisis

*type 2 → phenobarbital

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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% via induction of UGT-1

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

↑ indirect bilirubin but usually less than 3 mg/dL

(Crigler Najir has higher elevation)

*Hyperbilirubinemia: serum bilirubin levels of ≥ 1.1 mg/dL. In contrast to cholestatic liver disorders, which also has hyperbilirubinemia, Inherited hyperbilirubinemia only has isolated hyperbilirubinemia and does not affect liver enzymes (ALT, AST, AP)

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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
\_ protein binding = ↑ Vd
↓
26
What 2 factors can change Vd and why?
Kidney damage → proteinuria → ↓ protein binding → ↑ Vd Liver damage → ↓ protein (albumin) synthesis → ↑ Vd
27
If ↓Vd where is the drug? why?
In the blood (intravascular) - large/charged molecule - bound to plasma protein like Albumin
28
If ↑Vd where is the drug? why?
In the tissues (even fat) - small lipophilic molecule - bound to tissue proteins
29
The relationship between half life and clearance is a(n) _____ relationship
inverse \*if clearance goes down half life goes up
30
How is Clearance (CL) Calculated?
rate of drug elimination/ Plasma drug concentration (mass/time)/(mass/vol) = CL OR CL= Vd x Ke (elimination constant) Low Yield
31
Volume of distribution is directly proportional to \_\_\_\_\_.
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.
32
In first order kinetics it takes \_\_-\_\_ half-lives to reach steady state
4-5
33
In first order kinetics half life is decreased by what?
half 1 = 50% left 2= 25% left 3= 12.5% left etc.
34
An IV BOLUS of drugs is a loading dose clue In drugs given via IV the Bioavailability (F) is
F= 1
35
How is loading dose calculated?
(Cp x Vd) / F Cp= Target plasma concentration at steady state Vd = Vol of distr F = Bioavailability
36
How is Maintenance dose calculated?
(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
37
Time to steady state is independent of ___ and \_\_\_\_\_
dose dosing frequency (depends on half-life)
38
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 \_\_\_\_\_\_.
parallel slopes same receptor
39
In a dose response curve, the drug with the **greater Affinity** is the slope that is shifted the most to the \_\_\_\_.
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.
40
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)
Left **aka** lower EC50 \*In this case drug A is more potent than drug B.
41
Efficacy is measured on the y-axis of the Dose- Response curve. The higher ______ a drug reaches the more efficacious it is.
% Response **aka** % Maximal effect (ie: the taller the curve is the more efficacious it is)
42
What is the Y axis and X axis of the dose response curve?
Y: % response X: Log dose
43
a ____________ **decreases** drug **potency** and \_\_\_ be overcome by increasing drug concentration.
competitive antagonist CAN
44
A _______ **decreases** drug **efficacy** and \_\_\_\_\_\_ be overcome by increased drug concentration
Non-Competitive Antagonist CANNOT
45
A _______ alone has decreased drug efficacy and acts at ______ site
partial agonist the same site
46
Safer drugs have high ___ values
TI Therapeutic index TI= TD/ED \* middle points of (toxic dose/effective dose)
47
All Beta adrenergic receptors (1,2,3) have what associated G-protein?
Gs
48
Alpha 1 and Alpha 2 beta adrenergic receptors have what associated G-protein?
1 → G**q** 2 → G**i** alpha 1, 2, Beta 1,2,3 → (**qisss**) Kiss
49
MI, M2, and M3 have what associated G-proteins?
M1 → Gq M2 → **Gi** M3 → Gq **M**en an **qiq** (quick)
50
D1 and D2 receptors have what associated G protein class?
D1 → G**s** D2 → G**i** Do you want Dopamine? **Si**!!!
51
H1 and H2 (Histamine) receptors have what associated G-protein class?
H1 → G**q** H2 → G**s** With **Q**ue**s**o I need a lot of anti-Histamine
52
V1 and V2 (Vasopressin) receptors have what associated G-protein class?
V1 → G**q** V2 → G**s** **Q**ue**s**o stresses me out sometimes (Vasopressin raises BP like stress)
53
cAMP has different functions for locations In Skeletal muscle ↑cAMP = Smooth muscle raise ↑cAMP =
(sk) contraction (sm) relaxes
54
Angiotensin II (**AT1**) is coupled to what protein G-class. What does it do to blood vessels?
Gq Vasoconstricts ***Aang on the cover of GQ*** \*RECALL: **Gq** constricts **smooth muscle** via ↑ calcium; **Gs** relaxes **smooth muscle** via ↑ cAMP & ↑PKA ( inhibits MLCK)
55
Recite the Gq mechanism
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
56
Recite the Gs pathway
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**
57
Recite the Gi pathway
Gi inhibits Adenylyl Cyclase thus decreasing cAMP levels thus allowing Myosin Light Chain Kinase to phosphorylate the light chain ⇒ smooth muscle contracts & ↓ Ca2+ in heart (↓ contractility)
58
Beta 1 stimulation causes what 4 things
↑ HR ↑ Contractility ↑ Renin (↑BP) ↑ Lipolysis (energy) *You Bet 1 fat raindeer contracted HR's raise*
59
B2 stimulation causes what 7 things
Bronchodilation (vasodilation) ↑ lipolysis/ Glycogenolysis ↑ Insulin ↑ Aqueous Humor production ↑ K+ uptake by cells ↓ uterine tone (tacolysis) *I bet 2 fat banana lungs have humurous insulation, but let's not TACO 'bout it!*
60
Beta 3 causes what 3 things
↑ Lipolysis ↑ Heat in muscles ↑ bladder relaxation *I bet 3 fatties in the heat don't need to pee*
61
Alpha 1 stimulation causes what 3 things
↑ vasoconstriction Mydriasis (Dialated eyes) ↑ Intestinal/bladder sphincter contraction ↑ Uterine contraction (ß2 effects \> alpha 1) *An alpha leads the attack even as her uterus contracts*
62
alpha 2 causes what 5 things
↑ platelet aggregation ↓ Lipolysis (unlike Betas) ↓ Insulin (unlike Beta2) ↓ aqeous humor production (unlike beta 2) *The second alpha is so skinny her lack of insulation is not humerous. Get her more plates.*
63
M1 stimulation stimulates the _______ nervous system
Enteric
64
M2 stimulation has what 2 effects?
↓ HR ↓ atrial contractility *My 2 HRs lowered their trial contract*
65
M3 stimulation has what 7ish effects?
↑ tears, sweat, salivation ↑ gut motility (diarrhea) ↑ bladder contraction (peeing) ↑ **pupillary sphincter** contraction (Miosis–pinpoint eyes) ↑ **Ciliary** **muscle** contraction (accomodation) ↑ Insulin ↑ endothelin vasodilation *Dial up my 3 fat Dumbells*
66
**Relaxes Renal** Vascular smooth muscle activates **direct** **pathway** in striatum to **initiate movement**
Dopamine on **D1** receptors
67
**_Inhibits_** **indirect pathway** in striatum to **increase** movement
Dopamine on **D2** receptors
68
↑ Pruritis, **Pain**, ↑ naso-broncho **Mucus** production ↑ vascular **_permeability_** **Bronchoconstriction**
Histamine on H1 receptors
69
Increases gastric secretions
Histamine on H2 receptors ## Footnote *His Tummy is 2 gassy*
70
↑ vWF release ↑ Aqua Porin 2 in CD
Vasopressin on V2 receptors
71
\_\_\_ constricts smooth muscle via ↑ calcium; ___ relaxes smooth muscle via ↑ cAMP
Gq Gs
72
\_\_\_\_ in smooth muscle causes dephosphorylation of MLC thus vasodilation
Nitric Oxide
73
Epinephrine activates what receptors
alpha 1, 2 Beta 1, 2
74
Norepinephrine activates what receptors
alpha 1, 2 Beta 1
75
Describe sweat gland and piloerector muscle innervation
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.
76
Describe the Innervation of the Adrenal Medulla Chromaffin cells?
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.
77
The 1st neurotransmitter in ANY pathway is \_\_\_ The first synapse receptor in every pathway is a ______ receptor
Ach nicotinic
78
What type of receptor is found on skeletal muscles
Nicotinic receptors (Nm)
79
Nicotinic receptor are ligand (Ach) gated _____ channels.
Na+/K+ channels
80
NE regulates itself via binding to _____ receptor on the pre-synaptic nerve that released it.
alpha 2 | (Negative feedback)
81
Botulinum toxin cleaves SNARE proteins on the pre-synaptic cell inhibiting the release of ______ from the pre-synpatic cell onto the synaptic cleft
Ach vesicle
82
Describe the effect of **NE** and **Isoproterenol** on MAP, HR, & TPR What happens when administered together?
NE: ↑ MAP ↓ HR (reflex) ↑TPR ISO: ↓ MAP ↑ HR (Reflex) ↓TPR Together they blunt each other's effects
83
What effects does **Epinephrine** have on CO, HR, MAP, and TPR?
All of them increase
84
is used for postoperative or neurogenic ileus or urinary retention. To increase/ stimulate GI & bladder motility.
Bethanechol Cholinomimetic (resistant to AchE)
85
Malathion, Parathion, and Sarin Nerve gas are all:
All organophosphates that irreversibly inhibit **Ach-esterase** \*Malathion, Parathion are pesticides
86
is the antidote to Organophosphates poisoning what else can be given?
**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.
87
Causes respiratory depression, lethargy, seizures, coma
Organophosphates
88
Overstimulation of Muscarinics due to Cholinomimetics causes DUMBBELSS. What does the acronym stand for?
Diarrhea Urination Myosis (pin-point eyes) Bronchoconstriction _Bradycardia_ Emesis Lacrimation Salivation/ Sweat
89
Name 4 **_CHOLinomimetic_** direct agonist
Bethane**CHOL** Carba**CHOL** Meta**CHOL**ine Pilo**CHOL**pine (Pilocarpine, but whatever)
90
Name 7 cholinomimetic indirect agonist (AchE blockers)
Neo**STIGMINE** Physo**STIGMINE** Pyrido**STIGMINE** Riva**STIGMINE** Galanta**STIGMINE** (Galantamine) EdrophonIGMINE (Edrophonium) DonapezIGMINE (Donapezil)
91
How is cocaine used to diagnose Horner's syndrome?
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)
92
How is the lesion in Horner's syndrome localized?
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
93
Atorvastatin is an HMG-CoA reductase inhibitor; worrisome side-effects include ________ and \_\_\_\_\_\_\_\_\* particularly when used in combination with \_\_\_\_\_\_\_\_.
hepatic dysfunction muscle toxicity (rhabdomyolysis) fibrates (lowers TGs) or cyclosporin (immunosuppressant)
94
\_\_\_\_ 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.
Patiromer
95
\_\_\_\_\_ are also used to relieve intraocular pressure in **open-angle** and **closed-angle** glaucoma.
Carbonic anhydrase inhibitors
96
Mucosal hyperplasia (ex: gingivae)is seen in patients treated with
phenytoin
97
Significant ______ can cause muscle weakness, cramps, and possible rhabdomyolysis.
hypokalemia
98
\_\_\_\_\_\_ is used for treating cerebral edema, but causes **_initial_** **intravascular volume expansion** that can worsen pulmonary edema and heart failure.
Mannitol
99
\_\_\_\_\_\_ are the **most potent diuretics** and are used as first-line therapy for rapid relief of symptoms in patients with acute decompensated heart failure.
Loops
100
\_\_\_\_\_\_ promotes **potassium** and **hydrogen** ion **secretion** from the **principal and intercalated cells** of the collecting tubules
Aldosterone \*promotes Na reabsorption via increased ENaC and NaK ATPases
101
HTN w/ DM should be treated with ____ with caution because:
Beta blockers mask hypoglycemia symptoms

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