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Therapeutics P2 > exam 2 lecture 5 > Flashcards

exam 2 lecture 5 Flashcards

1
Q

what are ion channels

A

Proteins that form pores on plasma membrane

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2
Q

Three ways ion channels are categorized

A

gating (opening and closing mechanism)
ion selectivity
Pharmacology

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3
Q

which ion channel is most selective

A

K channels

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4
Q

two tyoes of ion chnnnales that are categorized by gating

A

Ligand gated
voltage gated

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5
Q

are ion channels active or passive

A

Passive

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6
Q

Difference between ion channels and trasnporter

A

ion channels are pores that respond to stimulus (voltage, Ach) to open them. The ions will pass through the channel and flow down their electrochemical gradient. NO ENERGY REQUIRED

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7
Q

What determines direction of flow for ions

A

Concentration gradient
Electrical gradient

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8
Q

membrane potential

A

98 mv

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9
Q

excitable cells have what kind of potential across the membrane? why is that?

A

Excitable cells have a negative inward potential across the membrane

This is due to selective permeability of resting membrane to K

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10
Q

Levels of K inside and outside of cell

A

High inside cell (155mm)
low outside (4mm)

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11
Q

Levels of Na inside and outside of the cell

A

Low inside the cell (12)
high outside

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12
Q

how is gradient Na and K gradient maintained

A

By active trasnport of Na out and K into cell.

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13
Q

Levels of free Ca2+ inside vs outside of the cell

A

Free Ca2+ is very low inside cell (100nm)
High outside of cell (1.5mm)
15,000 fold difference

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14
Q

what is the role calcium channels play in myscle contraction

A

When Na rushes into the cell and depolarizes it, Ca channels open. And they stay open, FOR A LONG TIME(broad action potential). This is where contraction occurs (broad part of calcium channels opening)

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15
Q

why is K channel so selective?

A

because of its selectivity filter. potassium ion makes contact with carbonyls that strip the water of ion as it passes through filter. (it is called a long pore due to long narrow passage)

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16
Q

Open vs closed shape of K channel

A

V is closed
/\ is open

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17
Q

most important target for calcium channel blockers

A

Ca v 1.2

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18
Q

what will happen if we block Ca influx through Ca v 1.2

A

It will inhibit contraction of cardiac and vascular muscle

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19
Q

what is the use of calcium channel blockers

A

Used to block Ca V 1.2 channels in vasculature and create VASODILATION to relax smooth muscle.

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20
Q

effect of calcium channel blockers on BP and Angina

A

Lower BP and relieve angina

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21
Q

Use of blocking of channels in cardiac muscle and SA/AV node

A

It is ANTIARRHYTHMIC

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22
Q

what is CICR

A

calcium inducedd calcium release

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23
Q

Explain CICR mechanism

A

Ca2+ influx via Ca v 1.2 induces release of Ca from intracellular stores via RYR2 in SR

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24
Q

what does RYR2 do

A

indices release of calcium stores in SR

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25
Q

Use of Ca release in SR

A

Drives contraction of muscle

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26
Q

how does epinephrine affect Ca V 1.2

A

Epinephrine binds to B receptor in heart andgenerates phosphorylation of Ca V 1.2 and increases Ca influx.

Leads to
1. greater contraction force
2. increased AV nodal action potential (Increased HR)

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27
Q

difference in vascular smooth muscle contraction and cardiac muscle and skeletal muscle for Ca required

A

extracellular Ca is required for vascular smooth muscle and cardiac muscle. Not for Skeletal muscle

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28
Q

how does volatage gated calcium channel lead to vascular smooth muscle contraction

A

-Calcium comes in
-releases calcium from stores by activating RYR2, increasing intracellular Ca concentration
-Ca binds calmodulin and activates Myosin LC kinase
-myosin LC kinase phosphorylates myosin LC
- Phosphorylated Myosin lc combines with actin and initiates contraction

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29
Q

how does volatage gated calcium channel lead to cardiac muscle contraction

A

-Calcium comes in
-releases calcium from stores by activating RYR2, increasing intracellular Ca concentration (these two steps similar in vascular muscle)
-In cardiac muscle (and skeletal muscle) Ca ions are released from SR and bind Troponin C
- Ca binding by troponin C causes displacement of tropomyosin, allowing actin to bind to myosin. leading to contraction

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30
Q

how does volatage gated calcium channel lead to skeletal muscle contraction

A

Extracellular Ca not required. Ca V 1.1 and RYR 1 used instead of 1.2 and RYR 2
-Ca ions are released from SR and bind TroponinC
- Ca binding by troponin C causes displacement of tropomyosin, allowing actin to bind to myosin. leading to contraction

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31
Q

similarity and difference of vascular, cardiac and skeletal contraction

A

vascular and cardiac have similar 1st 2 steps
–Calcium comes in
-releases calcium from stores by activating RYR2, increasing intracellular Ca concentration

Cardiac and skeletal have similar last 2 steps
-Ca ions released from SR and bind troponin C
- Ca binding of troponin c causes displacement of troponin C allowing myosin and actin to bind

Skeletal muscle extracellular Ca not required, but is required for cardiac and vascular muscle.

skeletal uses CaV 1.1 and RYR 1,
Cardiac and vascular use CAV 1.2 and RYR 2

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32
Q

Name the 3 calcium channel blockers

A

Dihydropyridines
Phenyalkylamines
Benzothiazepines

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33
Q

Indication and use of CCB (Calcium channel blockers)

A

HTN, arrythmia, angina

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34
Q

Name DHP drugs (how to recognize the name)

A

-dipine
Amlodipine
Nimodipine
Clevidipine
Nifedipine

35
Q

KNOW STRUCTUREE FOR DHP (dihydropyridine)

A

Has

36
Q

KNOW STRUCTURE FOR AMLODIPINE AND NIMODIPINE

A
37
Q

Why is amlodipine special

A

Ether group side chain and primary amine

38
Q

Use of ether group side chain in amlodipine

A

Give it characteristics of very slow onset and very long duration of action

39
Q

Why is Nimodipine special

A

It has an ether group and is EXTREMELY hydrophobic

40
Q

What is the use of extreme hydrophobia of Nimodipine

A

Nimodipine can be used to relax the vascular muscle within an area of hemorrhage (bleeding) to try and restore blood flow due to its hydrophobia.

41
Q

Why is clevidipine special

A

half life is short and is given IV

42
Q

why is clevidipine half life short? What is contraindicated

A

Breaks down rapidly due to esterase

Not given in patients with soybean or egg sensitivity

43
Q

Tissue selectivity of DHP (vascular or smooth)
What do DHPs work well in

A

High degree of selectivity for relaxing vascular smooth muscle. not a strong effect on cardiac muscle.

Work well in coronary arterty

44
Q

what is the reason for the vascular smooth muscle selectivity viewed in DHP

A

difference in membrane potential property. vascular smooth muscle tends to have a more depolarized resting membrane potential than cardiac muscle

45
Q

Is DHP voltage dependent? Why?

A

Prefers the more depolarized vascular smooth muscle over the cardiac smooth muscle

46
Q

DHP binding site

A

They do not bind in the pore, they bind on an allosteric site outside of pore

47
Q

do DHP have tonic or frequency dependent block

A

Tonic

48
Q

How does DHP work

A

Bind to closed channels and prevent opening

49
Q

DHP effect on peripheral resistance

A

Reduction of peripheral resistance

50
Q

Effect of DHP on venules and arterioles

A

Dilation of arterioles
Little effect on venules

51
Q

Which DHPs are vasoselective

A

Amlodipine, nifedipine, felodipine, nislodipine, isradipine

52
Q

effect of DHP on afterload and on HR or force of contraction

A

Decreased afterload and little effect on HR and force of contraction.

53
Q

reflex tachycardia is caused by all DHPs except for

A

Amlodipine

54
Q

Nimodipine exhibits selectivity for_________. What is it used in?

A

nimodiine exhibits selectivity for cerebral arteries.

Used to prevent neuropathy

55
Q

how do DHPs show efficacy in angina

A

reduce O2 demand in heart

56
Q

T/F all DHPs undergo first pass effect
T/F DHPs are highly bound to protiens

A

True for both

57
Q

which DHP could depress cardiac function? what happens when this DHP is promptly released?

A

Nifedipine.

Prompt release nifedipine solutions may increase risk of subsequent heart attack

58
Q

What is the only phenylalkylamine drug

A

Verapamil

59
Q

What does phenylalkylamine do?

A

Causes vasodilation.

60
Q

Which one causes more vasodilation (more potent) DHP or verapamil (phenylalkylamine)

A

DHP more potent

61
Q

What can Verapamil (phenylalkylamine) do that DHP can not

A

Increase HR and force of contraction

62
Q

is there reflex tachycardia in phenylalkylamine (verapamil)

A

It is blunted

63
Q

is verapamil (phenylalkylamine) tonic block or frequency dependent

A

Frequency dependent block

64
Q

What is the use of verapamil being frequency dependent

A

It is useful in arhythmias

65
Q

Where does verapamil bind

A

Binds the pore (entry) not allosteric site.
In order to bind, the drug has to get inside pore to bind.

66
Q

Name benzothiazepine drug

A

DIltiazem

67
Q

is diltiazem (benzothiazepine) frequency dependent or tonic block

A

Exhibits both a little bit

68
Q

Which one inhibits the heart rate more? DHP, Verapamil or diltiazem

A

Verapamil the most, diltiazem next, last is DHP

69
Q

Which one causes the most vasodilation?
DHP, verapamil or diltiazem

A

DHP (second is diltiazem)

70
Q

Which one causes tachycardia DHP, Verapamil or diltiazem

A

Non-amlodipine DHPs cause most tachycardia.
Second is Diltiazem

71
Q

Which ones slow conduction through SA and AV node? DHP, Verapamil or Diltiazem

A

Verapamil (most ) and diltiazem (second)

72
Q

which ones treat super ventricular arrythmias? DHP, Verapamil or Diltiazem?

A

Verapamil and Diltiazem

73
Q

Why do verapamil and diltiazem treat ventricular arrythmias

A

Because they are frequency dependent

74
Q

Which CCB (calcium channel blocker) suppress HR? why?

A

Diltiazem and Verapamil

75
Q

How does DHP affect HR

A

increases it through reflex tachycardia

76
Q

Why do diltiazem and verapamil lower HR

A

Due to frequency dependent kinase

77
Q

DHP effect summary on HR, AV conduction, myocardial contraction and arterial vasodilation

A

HR- increase (only one to increase hr)
No effect on AV conduction
No effect on myocardial contraction
Best at DILATING arterial vasodilation

78
Q

Verapamil summary on effect on HR, Av conduction, Myocardial contraction, Aretrial vasodilation

A

HR- Lowers HR (the most)
Lowers AV conduction
Lowers Myocardial contraction
Raises arterial vasodilation

79
Q

Diltiazem Summary on HR, Av conduction, Myocardial contraction, aretrial vasodilation

A

Lowers HR
Lowwers AV conduction
Lowers Myocardial contraction
Raises Arterial vasodilation

80
Q

which CCB has no effect on Myocardial contraction and AV conduction

A

DHP

81
Q

which CCB is the best as arterial vasodilation

A

DHP

82
Q

DHP side effets

A

Facial flushing, tachycardia, ankle edema (ankle edema is on all CCBs)

83
Q

Verapamil side effects

A

Constipation and ankle edema

84
Q

Diltiazem side effects

A

Ankle edema

Therapeutics P2 (41 decks)

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