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Drugs & Their Actions > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Which ion contributes most to resting potential?

A

Potassium.

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2
Q

Which ions are most concentrated inside the cell? ECM?

A

Potassium. Sodium, Chloride, and Calcium.

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3
Q

Which mechanisms maintain resting membrane potential?

A

Sodium Potassium ATPase pumps, leak channels, and potassium inward rectifying channels.

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4
Q

How does the Na/K ATPase pump keep the membrane negative?

A

By pumping out 3 sodiums and pumping in 2 potassiums.

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5
Q

How do leak channels keep the membrane negative?

A

There is much more potassium leak channels so positive charge is leaking out of the cell more than it’s leaking in.

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6
Q

What do inward rectifying channels do?

A

Open in response to the membrane becoming too negative. This allows potassium to leak in.

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7
Q

What is the difference between a closed and inactive conformation of a voltage-gated ion channel?

A

When it is closed, it’s able to open. When inactive, it cannot open due to the refractory period.

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8
Q

What ends the depolarization phase of a myocyte action potential?

A

Inactivation of Sodium channels.

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9
Q

Why do myocytes action potential have a plateau phase?

A

Slow calcium influx and most potassium channels closed.

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10
Q

What causes repolarization for myocyte action potentials?

A

Inactivation of calcium ion channels and opening of inward rectifying potassium channels.

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11
Q

Why do the atria and ventricle contract at different times?

A

Conduction pause between SA and AV node.

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12
Q

What is considered the pacemaker of the heart? Why? What else influences heart rate?

A

SA node because it generates the fastest action potential. ANS also affects HR.

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13
Q

What is the pacemaker potential? What does this mean about these cells resting membrane potential?

A

Slow depolarization from opening of funny/leak sodium channels and closing of potassium channels.

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14
Q

What signifies the start of depolarization for pacemaker cells? What does it involve?

A

When threshold is reached. Involves opening of calcium ion channels.

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15
Q

What does repolarization of pacemaker cells entail?

A

Inactivation of calcium ion channels and opening of inward rectifying potassium channels.

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16
Q

How does the ANS generally work?

A

Preganglionic neuron from CNS releases AcH at ganglion (synapse). AcH binds to nicotinic receptor on postganglionic neuron.

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17
Q

For the parasympathetic system, what does the postganglionic neuron release upon activation? What effects does this have?

A

Releases AcH that binds to muscarinic (M-2) receptors. This slows heart rate.

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18
Q

For the sympathetic system, what does the postganglionic neuron release upon activation? What effects does this have?

A

Releases norepinephrine that binds to adrenergic (beta-1) receptors. This increases cAMP and PKA production which promotes the opening of calcium and sodium ion channels. This increases cardiac output.

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19
Q

Which G-protein do muscinic receptors couple with? What about adrenergic receptors?

A

Gi. Gs.

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20
Q

What is mean arterial pressure (MAP) a product of? What is equivalent to MAP?

A

Cardiac output (CO) and systemic vascular resistance (SVR). Equivalent to blood pressure.

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21
Q

What is cardiac output a product of?

A

Heart rate (bpm) and stroke volume (blood volume per beat).

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22
Q

What is ionotropy?

A

Force of contractions (SV).

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23
Q

What is chronotropy?

A

Rate of contractions (HR).

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24
Q

What is dromotropy?

A

Electrical conductance (related to SVR).

25
Q

What are the 3 extrinsic controls which cause vasoconstriction? How do they work?

A

Angiotensin II, norepinephrine, and L-type calcium channels. All increase calcium ion concentrations which causes contraction.

26
Q

What is angiotensin II’s receptor? What about norepinephrine?

A

At-1. Adrenergic alpha-1.

27
Q

What are the 4 factors that increase MAP? What is each factor a function of?

A

Increased heart rate, contractility, SVR, and fluid volume. The first three are a function of the sympathetic nervous sytem. SVR and fluid volume are also a function of angiotensin II. Fluid volume also a function of aldosterone.

28
Q

What are the 3 general mechanisms of treatment for hypertension? What are the agents of each mechanism?

A
  1. Reduction of fluid volume. (diuretics)
  2. Negative ionotropic/chronotropic agents. (2 calcium channels and beta blockers)
  3. Vasodilation. (1 calcium channel, ACE-inhibitors, AT-1 blockers, and alpha blockers)
29
Q

What is sympatholytics?

A

Blocking of the sympathetic nervous sytem.

30
Q

What does the sympathetic system release? What are the receptors and effects of these neurotransmitters?

A

Norepinephrine and epinephrine (from adrenal glands). Increase rate and force of contraction (beta-1 receptors) and also cause vasoconstriction (alpha-1 receptors).

31
Q

What is the function of the beta-1 receptor?

A

Couples with Gs protein to increase heart rate, force of contraction, and conduction.

32
Q

What is the function of the beta-2 receptor?

A

Couples with Gs protein for smooth muscle relaxation in the lungs, etc. Also glucose breakdown in liver.

33
Q

What is the function of the alpha-1 receptor?

A

Couples with Gq protein to cause vasoconstriction.

34
Q

What is the function of the alpha-2 receptor?

A

Couples with Gi protein to inhibit neurotransmitter release and insulin release.

35
Q

What are the modifications of the R3 group? What do they indicate?

A
  1. Presence of 4’-OH indicates beta agonist.
  2. A lone 3’-OH indicates alpha agonist.
  3. Substitute at 4’-OH indicates an antagonist.
36
Q

What are the modifications of the R1 group? What do they increase?

A
  1. 2-3 methyl groups increases beta selectivity.

2. Nitrogenous rings increases alpha selectivity.

37
Q

What is the modification of the R2 group? What does it indicate?

A

Large alkyl and ring substitutions decrease beta receptor activity.

38
Q

What is the modification of the beta position? What does it indicate?

A

Insertion of OCH2 favors beta antagonist.

39
Q

What is SLUDGEM? Which system and receptor is it associated with?

A

Salivation, lacrimation (tears), urination, defacation, GI cramping, emisis (vomiting), muscle spasms and/or pinpoint pupils. Caused by parasympathetic - M-2 receptors.

40
Q

What is the function of non-selective beta blockers? What are some of the common side effects? Give examples.

A

Block both beta receptors. Side effects include shortness of breath and exercise fatigue, major dose limiting factors. (ex: propranolol)

41
Q

What is the function of selective beta blockers? Why are these advantageous? Give examples.

A

Higher affinity for beta-1 receptors. Reduces the side effects associated with beta-2 receptors. (ex: atenolol and metoprolol).

42
Q

What is the function of selective beta blockers with intrinsic sympathomimetic activity (ISA)? What patients are these usually given to? Give examples.

A

Partial agonists that reduce the effects of beta receptors. Used for patients who become hypotensive easily or have severe bradycardia. (ex: acebutolol and pindolol).

43
Q

What is the function of alpha-1 selective antagonists? What do they treat and what are their side effects? Give examples.

A

Relaxes smooth muscle to induce vasodilation (decrease SVR). Used as an add-on therapy or to treat difficult urination due to enlarged prostate.

Side effects: orthostatic hypertension from first dose effect & reflex tachycardia (increased heart rate).

Examples: terazosin, prazosin, doxazosin, lamsulosin

44
Q

What is the function of mixed alpha/beta blockers? What are they used for and what are the side effects?

A

Vasodilation and increased stroke volume. Drug of choice for congestive heart failure. Less reflex tachycardia but not beta-1 selective so bad for patients with lung problems.

45
Q

How does intracellular calcium increase MAP?

A

Cardiac nodal cells increased HR by reducing time till threshold. Cardiomyocytes increase SV by increasing myosin-actin coupling during systole. Smooth muscle contraction increases SVR and vasoconstriction.

46
Q

What are dihydropyradines (DHP) selective for? (Hint: they are calcium channel blockers)

A

Vascular smooth muscle.

47
Q

What are calcium channel blocker phenylalkamines selective for?

A

Heart.

48
Q

What are calcium channel blocker benzothiazepines selective for?

A

Smooth muscle and heart.

49
Q

Be able to draw the different calcium channel blocker’s structures.

A

Okay.

50
Q

What are the binding sites of the different calcium channel blockers?

A

DHP: extracellular part of conductance pore.
Phenylalkamine: intracellular part of channel pore/gate.

51
Q

What is the function of calcium channel blockers, dihydropyradines (DHP)? What do they treat and what are their side effects?

A

Vasodilation that reduces SVR. Used to treat angina (chest pain caused from low oxygen). Useless for arrhythmia. Side effects include dizziness/headache, increased HR, ankle edema (fluid buildup), & constipation.

52
Q

What is the function of calcium channel blockers, phenylalkamines? What do they treat and what are their side effects?

A

Decreases SV and HR (shortens plateau phase). Used to treat arrhythmia. Side effects include dizziness/headache, fatigue, nausea, and constipation.

53
Q

What is the function of calcium channel blockers, benzothiazepines? What do they treat and what are their side effects?

A

Decreases SV and SVR. Used to treat arrhythmia and angina. Side effects include dizziness/headache, bradycardia/hypotension, & potential drug-drug interactions.

54
Q

What is the function of Renin? Where is it produced from?

A

Converts angiotensinogen into angiotensin I. Produced from the kidneys.

55
Q

What is the function of ACE? Where is it produced from?

A

Converts angiotensin I into angiotensin II. Produced from the lungs.

56
Q

How does angiotensin II increase MAP?

A
  1. Direct constriction of vascular smooth muscles from M-2 receptors. This causes vasoconstriction.
  2. Causes adrenal glands to release aldosterone which promotes sodium and water retention. This increases blood volume.
57
Q

How do ACE inhibitors work? What are some general side effects

A

Replace c-terminal and don’t have a peptide bond at the corresponding cleavage site. This inhibits ACE from cleaving angiotensin I into the active form.

58
Q

Why are ACE inhibitors considered prodrugs?

A

Because they are not active due to their ester group until they enter the bloodstream.

59
Q

What are some general side effects of ACE inhibitors?

A

Dizziness, hypotension, syncope (fainting), dry cough, hyperkalimia (high potassium), and angiodema (rapid throat swelling). Also not given to pregnant women.

Drugs & Their Actions (2 decks)

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