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Pharm > High Yield General Questions > Flashcards

High Yield General Questions Flashcards

1
Q

What G-protein class and major functions are associated with the alpha 1 receptor?

A

Gq. Vascular smooth muscle contraction (incr BP). Pupillary dilator muscle contraction (mydriasis). Increase intestinal and bladder sphincter tone.

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2
Q

What G-protein class and major functions are associated with the alpha 2 receptor?

A

Gi. Alpha 2 is the auto receptor -> decrease sympathetic outflow (decr BP). Decr lipolysis and insulin release. Incr platelet aggregation.

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3
Q

What G-protein class and major functions are associated with the beta 1 receptor?

A

Gs. Incr HR, contractility, lipolysis and renin release.

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4
Q

What G-protein class and major functions are associated with the beta 2 receptor?

A

Gs. Vasodilation and bronchodilation. Incr HR and contractility (compensatory effects of the dilation). Incr lipolysis and insulin release. Tocolysis (dec uterine tone). Ciliary muscle relaxation and increased aqueous humor production.

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5
Q

What G-protein class and major functions are associated with the M1 receptor?

A

Gq. CNS and enteric nervous system.

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6
Q

What G-protein class and major functions are associated with the M2 receptor?

A

Gi. Decrease heart rate and contractility of atria (via vagus n).

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7
Q

What G-protein class and major functions are associated with the M3 receptor?

A

Gq. Incr exocrine gland secretions (ie lacrimal, gastric acid), incr gut peristalsis, incr bladder contraction, bronchoconstriction, incr pupillary sphincter muscle contraction (miosis), incr ciliary muscle contraction (accomodation)

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8
Q

What G-protein class and major functions are associated with the D1 receptor?

A

Gs. Relaxes renal vascular smooth muscle (incr renal perfusion)

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9
Q

What G-protein class and major functions are associated with the D2 receptor?

A

Gi. Modulates transmitter release (esp in the brain)

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10
Q

What G-protein class and major functions are associated with the H1 receptor?

A

Gq. Incr nasal and bronchial mucous production, contraction of bronchioles, pruritus, and pain.

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11
Q

What G-protein class and major functions are associated with the H2 receptor?

A

Gs. Incr gastric acid secretion.

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12
Q

What G-protein class and major functions are associated with the V1 receptor? V1 = vasopressin 1.

A

Gq. incr vascular sm. muscle contraction

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13
Q

What G-protein class and major functions are associated with the V2 receptor V2 = vasopressin 2.

A

Gs. vasopressin = ADH. Increase H2O permeability and reabsorption by increasing aquaporins in the collecting tubules of the kidney (V2 is in 2 kidneys)

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14
Q

G-protein pneumonic

A

Qiss (kiss) and qiq (kick) until you’re siq (sick) of sqs (super kinky sex)

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15
Q

Mechanism of Gq receptors?

A

Gq: PIP2 —PLC—-> DAG and IP3.
DAG -> PKC
IP3 -> incr intracellular calcium -> sm. muscle contraction

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16
Q

Mechanism of Gs receptors?

A

Gs: STIMULATE Adenylyl cyclase. ATP —AC—-> cAMP.

cAMP -> PKA -> 1. Incr intracellular calcium in heart 2. Inhibit MLK in sm. muscle

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17
Q

Mechanism of Gi receptors?

A

Gi: INHIBIT Adenylyl cyclase. ATP —AC—-> cAMP.

cAMP -> PKA -> 1. Incr intracellular calcium in heart 2. Inhibit MLK in sm. muscle (these two things are decreased)

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18
Q

Subtypes and mechanism of Nicotinic ACh receptors

A

Nn (found in autonomic ganglia-> both sympathetic and parasympathetic). Nm (found in neuromuscular junctions). These receptors are ligand gated Na+/K+ channels.

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19
Q

What two sympathetic nervous system structures are innervated by cholinergic fibers (ACh)?

A

Sweat glands and adrenal medulla.

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20
Q

How does choline enter a cholinergic neuron and what substance inhibits its entry?

A

It is co-transported with sodium using sodium’s gradient. Hemicholinium.

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21
Q

What reaction makes acetylcholine? Facilitated by what enzyme?

A

Acetyl CoA + choline –> acetylcholine. Choline acetyltransferase (ChAT). ChAT also packages ACh into vesicles.

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22
Q

What substance is needed for vesicular fusion with plasma membrane and release of ACh and NE?

A

Ca++

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23
Q

How is ACh removed from the synapse?

A
  1. Broken down by AChE 2. Diffusion away from synapse. Note: No reuptake mechanism present
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24
Q

How is NE removed from the synapse?

A
  1. Broken down by COMT or MAO. 2. Reuptake
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25
Q

What substance inhibits vesicular ACh release?

A

Botulinum toxin -> causes FLACCID paralysis

26
Q

What substance increases vesicular ACh release?

A

Black widow spider toxin

27
Q

What substance inhibits enzyme choline acetyltransferase (ChAT)?

A

Vesamicol

28
Q

What is the precursor to tyrosine?

A

Phenylalanine

29
Q

How does tyrosine enter noradrenergic neurons?

A

Co-transported with sodium down its gradient.

30
Q

What is the rate limiting enzyme in NE synthesis? What is the reaction?

A

Tyrosine hydroxylase. Tyrosine -> L-dopa.

31
Q

What enzyme converts L-dopa into dopamine?

A

L-AAAD (L-aromatic amino acid decarboxylase)

32
Q

What enzyme converts Dopamine into NE ?

A

DBH (dopamine beta hydroxylase)

33
Q

What is the mechanism of action of reserpine?

A

Inhibits VMAT (the transporter that fills vesicles with monoamines -> DA, 5-HT, NE)

34
Q

Non-selective MAO inhibition puts a patient at risk for what?

A

Tyramine induced HTN crisis. MAO in the gut normally inhibits amount of tyrosine entry into body. Tyramine promotes release of stored NE.

35
Q

What substances increase vesicular NE release?

A

Amphetamine, Ephedrine, Tyramine

36
Q

What substances decrease vesicular NE release?

A

Guanethidine, Bretylium

37
Q

What drugs inhibit NE reuptake?

A

Cocaine, Amphetamine, TCAs

38
Q

What receptor does NE bind to on the presynaptic nerve terminal? What other two receptors on the presynaptic nerve terminal modulate NE release?

A

NE binds the alpha 2 autoreceptor and decreases NE release. AII (angiotensin 2 receptor) increases NE release while M2 (muscarinic 2 receptor) inhibits NE release.

39
Q

What are the breakdown products of NE by COMT and MAO?

A

VMA, metanephrines, normetanephrines

40
Q

What is the equation for therapeutic index? Is it better to have a high or low TI?

A

TI=LD50/ED50. High.

41
Q

How does a partial agonist’s efficacy and potency compare to a full agonist?

A

Efficacy- always decreased

Potency- can be increased or decreased

42
Q

What is the effect of a competitive inhibitor (antagonist)?

A

Increase the Km (decrease affinity of enzyme for substrate-> decreased potency) but no change in efficacy (same maximal effect as the same Vmax can be achieved, albeit at a higher substrate concentration).

43
Q

What is the effect of an non-competitive (irreversible) inhibitor?

A

Decrease Vmax/ efficacy with no change in Km/ potency.

44
Q

Zero order elimination: constant ____1____ of drug eliminated per unit time. Does the plasma concentration of the drug change the rate of elimination? Plasma concentration decreases ____2_____ (think graphically) with time.

A
  1. Amount. No. 2. Linearly

Remember: zero order is enzyme saturation kinetics.

45
Q

First order elimination: constant ____1____ of drug eliminated per unit time. Does the plasma concentration of the drug change the rate of elimination? Plasma concentration decreases ____2_____ (think graphically) with time.

A
  1. proportion. Yes, they are directly proportional. 2. Exponentially
46
Q

What drugs are metabolized at zero order kinetics?

A

PEA -> a pea is shaped like a zero. Phenytoin, Ethanol, Aspirin.

47
Q

Phase 1 drug metabolism: what reactions? describe products.

A

cytocRHOme p450 -> reduction, hydrolysis, oxidation reactions. Slightly polar, water soluble metabolites.

48
Q

Phase 2 drug metabolism: what reactions? describe metabolites.

A

Conjugation reactions -> GAS (glucuronidation, acetylation, sulfation). Very polar, inactive metabolites (more easily renal excretion)

49
Q

Do elderly patients lose phase I or phase II drug metabolism first?

A

They lose phase I and still have GAS (phase II)

50
Q

What forms of drugs are trapped in urine vs reabsorbed in urine?

A

Ionic (charged) drugs get trapped and neutral drugs get reabsorbed.

51
Q

In what form are weak acids charged? So, would we want to make the pH higher or lower than the pKa to trap and excrete weakly acidic drugs in the urine?

A

Weak acids are charged in their non-protonated form (A- + H+). If the pH is below (more acidic) the pKa the protonated form (AH) is favored because there are extra protons around in the acidic environment. Therefore, we want to raise the pH (more basic) above the pKa so that the non protonated, charged form (A-) of the acid is favored. This will cause trapping in the urine and excretion the weak acid drug.

52
Q

What drugs are weak acids? What would we administer in an overdose?

A

Phenobarbital, Aspirin (salicylates), Methotrexate. Alkalinize the urine with NaHCO3.

53
Q

In what form are weak bases charged? So, would we want to make the pH higher or lower than the pKa to trap and excrete weakly basic drugs in the urine?

A

Weak bases are charged in their protonated form (BH+). If the pH is above (more basic) the pKa the non-protonated form (B + H+) is favored because there are not many extra protons around in the basic environment. Therefore, we want to lower the pH (more acidic) below the pKa so that the protonated, charged form (BH+) of the base is favored. This will cause trapping in the urine and excretion the weak base drug.

54
Q

What drug is a weak base? What would we administer in an overdose?

A

Amphetamines. Acidify the urine with NH4Cl

55
Q

What is the equation for volume of distribution (Vd)?

A

Vd = amount of drug in body/ plasma drug concentration

56
Q

What is the equation for T1/2?

A

T1/2 = (0.7 x Vd) / CL

57
Q

What is the equation for CL?

A

CL = (0.7 x Vd) / T1/2

58
Q

What factors can change the loading dose and the maintenance dose. What is the equation for each?

A

Loading dose is influenced by Vd. Ld = Css x Vd
Maintenance dose is influenced by CL. Md = Css x CL
Css= plasma concentration steady state (what the desired plasma concentration is).

59
Q

What is the slope in a Lineweaver-Burk plot?

A

Km / Vmax

60
Q

What is the Y-intercept in a Lineweaver-Burk plot? Increasing your Y-intercept, but not changing your X-intercept is done by what? How does it affect values?

A

1/ Vmax. Non-competitive (irreversible) inhibitor. Increasing Y-intercept decreases Vmax (since Y= 1/ Vmax). No change in X intercept means no change in Km.

61
Q

What is the X-intercept in a Lineweaver-Burk plot? Making the X intercept less negative (moving it to the right) and not changing Y-intercept is done by what? How does it affect values?

A

1/ -Km. Competitive inhibitor. The X-intercept on a Lineweaver-Burk plot will always be negative so this cancels out the negative in 1/ -Km. Since the numbers get smaller as we move to the right (since we are on the negative X-axis) this would increase Km since they inversely related (therefore raising Km -> decreased affinity and potency). There is also no change in the Y-intercept and therefore no change in Vmax just as we would expect with a competitive inhibitor.

62
Q

What is the Km?

A

The substrate concentration at which 1/2 Vmax (50% maximum enzyme reaction velocity) is reached.

Pharm (4 decks)

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