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Year 2 > Drugs - Enzyme and transporters > Flashcards

Drugs - Enzyme and transporters Flashcards

1
Q

What is an enzyme inhibitor

A

A molecule that binds to an enzyme decreasing its activity

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2
Q

What are irreversible inhibitors

A

React with enzyme to change it chemically

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3
Q

What are reversible inhibitors

A

Bind non-covalently

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4
Q

What is the top most prescribed drug

A

Statin

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5
Q

How do statins work

A

Block rate limiting step in cholesterol pathway reducing bad cholesterol:

3-hydroxy-3-methylglutaryl-CoA to Mevalonic Acid

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6
Q

When are ACE inhibitors used

A

For BP

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7
Q

How does the RASS system work

A

Liver - > angiotensinogen -> angiotensin I -> angiotensin II in lung by ACE

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8
Q

What is the role of angiotensin II

A 
Tubular reabsorption of Na and CL
K excretion
H2o retention 
Arteriolar vasoconstriction 
Increased BP
ADH secretion 
Aldosterone secretion
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9
Q

Where is ACE found

A

Surface of pulmonary and renal endothelium

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10
Q

What is the consequence of inhibiting ACE

A

Reduces Angiotensin II levels

Causes reduction in BP

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11
Q

How is Parkinson’s disease treated

A

Many enzyme inhibitors that work in the nigrostriatal pathway to prevent dopaminergic degeneration

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12
Q

How is L-DOPA produced

A

From L-Tyrosine

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13
Q

Process of L-DOPA function

A
  1. L-DOPA crosses BBB from peripheral to CNS
  2. Converted to Dopa Decarboxyl
  3. Dopamine
  4. D1 and D2 receptors
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14
Q

How does carbidopa work

A

Prevents L-DOPA -> Dopamine in periphery to reduce levels

Acts on DDC

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15
Q

How do Tolcapone and Entacapone function

A

Prevent L-DOPA -> 3-methyl DOPA by inhibiting COMT

less dopamine

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16
Q

How do central COMT inhibitors work

A

Work directly in CNS (Tolcapone) by preventing Dopamine -> 3MT

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17
Q

What inhibitors act on MAO-B

A

Selegiline and Rasagiline act on MAO-B in CNS to stop Dopamine -> DOPAC

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18
Q

What dopamine receptor AGONISTS work on D1 and D2 receptors

A 
Pramipexole
Ropinirole
Rotigotine
Pergolide
Bromocryptine
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19
Q

Define transport

A

When molecules move across a cell membrane

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20
Q

What are uriporters

A

Use energy from ATP to pull molecule in

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21
Q

What are symporters

A

Use movement of one molecule to pull another molecule against a conc. gradient (co-transporter)

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22
Q

What are antiporters

A

One substance moves against conc. gradient using energy from a second substance moving DOWN its gradient (co-transporter)

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23
Q

Give an example of a symporter

A

NKCC

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24
Q

How do NKCCs work

A

Move ions n the same direction

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25
Q

Why is furosemide a diuretic

A

Inhibits luminal NKCC in thick ascending loop of hence so Na, Cl and K lost in urine

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26
Q

When is Furosemide given

A

For hypertension and edema

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27
Q

What are ENaC channels inhibited by (Epithelial Na Channels)

A

Amiloride with Thiazide

Thiazide targets Na/Cl cotransporters

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28
Q

When is amiloride and Thiazide used

A

Anti-hypertensives

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29
Q

What inhibits voltage-gated calcium ion channels

A

Amlodipine

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30
Q

Whats special about amlodipine

A

Its angioselective that stops movement of Ca into vascular smooth muscle and cardiac cells preventing Ca ion influx

Results in vasodilation and peripheral vascular resistance decrease lowering BP + prevents excessive constriction in coronary arteries

31
Q

What drug blocks transmission of action potential by voltage gated Na Channels

32
Q

When is Lidocaine given

A

To reduce arrhythmia by blocking signalling in the heart

33
Q

What three states can voltage-gated K+ channels be found in

A

Closed
Open
Inactivated

34
Q

Where can voltage gated potassium channels be found

A

In Beta cells of the islets of langerhans

35
Q

Describe the release of insulin from the pancreas

A
  1. Glucose enters beta cells by GLUT2
  2. Glucose phosphorylated to glucose-6-phosphate by glucokinase
  3. Glucose used in glycolysis increasing ATP:ADP ratio in cell
  4. High ATP:ADP closes ATP-sensitive K+ channel
  5. K+ ions accumulate in cell
  6. Depolarisation
  7. Voltage-gates calcium channels open
  8. Causes vesicles containing insulin t one released
36
Q

How many phases are involved in the release on insulin

A

Two:
First -phase: Rapid release
Second - phase: Slow release of newly formed vesicles

37
Q

What hormone strongly inhibits the release of insulin

A

Noradrenaline

38
Q

What three drugs block voltage-gated potassium channels involved in insulin secretion

A

Repaglinide
Nateglinide
Sulfonylureal

39
Q

When is repaglinide, nateglinide and sulfonylureal prescribed

A

Type II diabetes

40
Q

What are ligand-gated ion channels also known as

A

Ionotropic receptors

41
Q

What is the role of GABA in the CNS

A

Major inhibitor

42
Q

Where are GABA A receptors found

A

Post-synaptically

43
Q

What happens when ligand binds to GABA A receptor

A

Cl- channel opens - hyper polarisation

44
Q

In what way can drugs effect GABA A receptors

A

Enhance their activation (efficacy)

45
Q

Role of barbiturates

A

Increase permeability of channel to Cl-

46
Q

When is barbiturate given

A

Depressant

47
Q

How do Benzodiazepine effect GABA-A receptors

A

Acts as an agonist (depressant)

48
Q

What two other drugs can effect GABA-A receptors and why do they bring out different outcomes

A

Steroids (anaesthetics)
Picrotoxins (convulsants)

They bind to different sites within the child ride channel

49
Q

How do Na/K ATPase work

A

Pumps 3Na out and 2K into cells

50
Q

What type of transporter is Na/K ATPase

A

antiporter

51
Q

What drug inhibits the Na/K ATPase and in which part of the body

A

Digoxin in the myocardium

52
Q

When is digoxin used

A

Atrial fibrillation, atrial flutter and heart failure

53
Q

What is the consequence of digoxin

A

Increased intracellular Na and Ca as activity of Na/Ca exchanger decreases

Leads to a decrease in heart rate by lengthening cardiac action potential

54
Q

Where are K/H ATPase found

55
Q

What type of protein are H/K ATPase

A

Heterodimeric

56
Q

Define heterodimeric

A

Product of 2 genes

57
Q

How do K/H ATPase function

A

Move H+ ions out into stomach lumen and K+ into cell

58
Q

Role of Omeprazole

A

Inhibits acid secretion by inhibiting H/K ATPase irreversibly

59
Q

Half-life of Omeprazole

60
Q

How long does Omeprazole work for

61
Q

Under what conditions is Omeprazole metabolised (activated)

A

Acid pH which alters its own bioavailability

62
Q

What cell releases PGE2 (Prostaglandin E2)

A

Chromaffin cells

63
Q

What do PGE2 bind to

A

EP3 receptors on parietal cells

64
Q

What is the consequence of PGE2 binding

A

Decreased activity of H/K ATPase - inhibits parietal cells

65
Q

What is the antagonist to PGE2

66
Q

What two irreversible inhibitors of ACh esterase

A
  1. Insecticides (Siazinon)

2. Nerve gas (Sarin)

67
Q

Symptoms of muscarinic receptor irreversible inhibition

A

Salivation, Defecation, Urination, Bradycardia, Hypotension

68
Q

Symptoms of nicotinic receptor irreversible inhibition

A

Twitching, severe weakness paralysis, diaphragm

69
Q

Symptoms of irreversible inhibition to the CNS

A

Confusion
Loss of reflexes
Convulsion
Coma

70
Q

Define Pharmacokinetics

A

Study of drug metabolism

71
Q

Define xenobiotics

A

Compounds foreign to an organism’s normal biochemistry such as a drug

72
Q

What are the principals of pharmacokinetics

A

MADE

M-etabolism
A-bsorption (how will it get in?)
D - Distribution (where will it go?)
E - xcretion (how does it leave)

73
Q

Where are CYPs found

A

Inner membrane of mitochondria or ER

74
Q

role of CYPs

A

Deactivation of drugs (75% of all metabolisms)

or bioactivation of drugs

Year 2 (155 decks)

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