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Flashcards in Pharmacology Deck (64):
1

Define partial agonist

A drug that  fails to produce maximal effects even when all receptors are bound by the drug

2

Define potency

Potency is the amount of drug required to produce 50% of the maximal response the drug is capable of inducing

3

Define pharmacokinetics

What the body does to the drug

4

What type of receptor is the nicotinic cholinergic receptor?

Ligand-gated ion channel

 

5

Define efficacy

• Efficacy is the probability of a drug activating a receptor once bound
• Aka the degree to which a drug is able to produce maximal effects

6

Define pharmacodynamics

What the drug does to the body

7

Define affinity and how it is measured

• Affinity is the probability or strength of a drug binding to its receptors
• Measured with equilibrium dissociation constant

KA =  drug concentration required for 50% occupancy of receptors

8

Describe the journey a PO medication must take to reach systemic circulation

 GIT -> liver -> R) heart -> lung -> L) heart -> systemic circulation

9

Define each of ADME 

Absorption - how drug gets into circulation
Distribution - how drug spreads through body
Metabolism - chemical changes to the drug
Excretion - physical expulsion of the drug

10

What are the 6 steps in pharmacokinetics?

Administration, absorption, distribution, elimination, metabolism, excretion

11

Describe the 3 steps in ACh synthesis

1 Choline taken up into cell by choline carrier

2 Choline + acetyl-CoA → acetylcholine + CoA via choline acetyltransferase

3 ACh put into vesicle

12

What is a clinical use for nicotinic receptor antagonists?

Pre-surgical muscle relaxant

13

Name 3 clinical uses of ACh esterase inhibitors

 

Dx of myasthenia gravis

Rx of myasthenia gravis

Rx of Alzheimer's disease

 

14

What is a clinical use for nicotinic receptor agonists?

Smoking cessation

15

What is the mechanism of action of atropine?
What are 4 clinical uses of atropine?

 

 

Muscarinic antagonist.

Bronchodilation and decrease respiratory mucous in anaesthesia

To increase heart rate.

Pupil dilation for eye examination.

AChE-inhibitor poisoning (organophosphates)

 

16

What is the mechanism of action of botulimin toxin

Name 3 conditions it may be used for

Botulimin toxin inhibits presynaptic ACh release by inhibiting vesicular exocytosis by acting as a protease on SNARE proteins.

Used to treat dystonia, migraine or underarm sweating

17

What are H2 antagonists used to treat and what is their mechanism of action?

Used to treat peptic ulcers.

Inhibit acid secretion by parietal cells in stomach by disrupting proton pump.

 

18

H1 antagonists:

What class of drugs are these?

Name 5 things they are used to treat.

Name 2 new generation drugs

 

Antihistamines

Used to treat hayfever, itchiness, motion sickness, anaphylaxis, bites/stings
New generation = cetirizine, loratidine

 

19

Describe the 4 steps in NA synthesis

1 Tyrosine taken up into cell
2 Tyrosine → L-Dopa (catalysed by tyrosin hydroxylase)
3 L-DOPA → Dopamine (catalysed by dopa decarboxylase)
4 Dopamine taken up into vesicle and converted into NA (catalysed by dopamine beta hydroxylase)

20

What are 7 clinical consequences of adrenaline administration?

Vasoconstriction

GI muscle relaxation

Salivation

Hepatic glycogenolysis

Increased heart rate

Increased cardiac contractility

Bronchodilation

21

What is the mode of action of aminoglycosides?

Aminoglycosides bind to specific proteins in 30s ribosome subunit and inhibit binding of formylmethionyl-tRNA (fmet-tRNA) to ribosome, thus inhibit protein synthesis,

Also cause misreading of mRNA codons

22

How do beta lactams exert antimicrobial effects?

Beta lactams inhibit synthesis of cell wall by binding to PBPs (penicillin-binding proteins)

23

List 3 enzymes that beta lactams may inhibit

Transpeptidase
Transglycosylase
Carboxypeptidase

24

What is the mechanism of action of loop diuretics?

Inhibit Na/K/2Cl carrier in ascending loop of Henle

25

What is the mechanism of action of potassium-sparing diuretics?

Block Na transporter in collecting tubules and ducts

Plus or minus:

Inhibit synthesis of Na/K cotransporter in collecting tubules and ducts

26

What is the mechanism of action of thiazide diuretics?

Inhibit Na/Cl transporter in distal tubule

27

What are 7 clinical consequences of adrenaline administration?

Vasoconstriction

GI muscle relaxation

Salivation

Hepatic glycogenolysis

Increased heart rate

Increased cardiac contractility

Bronchodilation

28

How does penicillin exert its antimicrobial effect?

 Penicillin stops formation of pentapeptide bridge by blocking transpeptidase

29

List 3 enzymes that beta lactams may inhibit

Transpeptidase
Transglycosylase
Carboxypeptidase

30

What are 6 clinical effects of muscarinic antagonists (aka anticholinergics)?

Dry eyes

Dry mouth

Urinary retention

Constipation

Tachycardia

Confusion

31

What type of receptor is the muscarinic cholinergic receptor?

 

G-protein coupled receptor

 

32

The transcription of which cytokines is inhibited through transrepression by GCSs?

IL-1,4,5,8

GM-CSF

TNFalpha

33

What are 6 effects of histamine on H1 receptors?

Pain and itch

Bronchospasm

Mucus secretion

Vasodilation

Increased vascular leak

Increased wakefullness

34

The transcription of which genes is activated through transactivation by GCSs?  And what are their effects?

Beta 2 adrenoceptor --> bronchodilation

Annexin-1 --> inhibits PLA2

SERPINA3 --> codes for alpha 1 antichymotrypsin --> inhibits neutrophil elastase

35

The transcription of which inflammatory enzymes are inhibited through transrepression by GCSs?

PLA2

COX-2

iNOS

36

Describe 6 steps in GCS transactivation

GCS cross plasma membrane and enters cell

--> binds to cytosolic glucocorticoid receptor

--> dimerises

--> enters nucleus

--> binds to glucocorticoid response element (GRE) in the promoter region of the target genes

--> gene transcription

37

What are the effects of histamine acting on H2 receptors?

Positive inotropic effects on heart

Positive chronotropic effects on the heart

Gastric acid secretion

38

The transcription of which adhesion molecules is inhibited through transrepression by GCSs?

ICAM

E-selectin

39

Name 3 classes of molecule that GCS inactivates through transrepression 

Cytokines

Adhesion molecules

Inflammatory enzymes

40

In which organelles are P450s located?

Endoplasmic reticulum and mitochondria

41

Which cytochrome P450 is involved in the metabolism of 25% of all prescription drugs?

CYP2D6

42

Name two D2 antagonists used to treat nausea

Metoclopramide (maxolon)

Prochlorperazine (stemetil)

43

CYP 2A6

What does the 2 refer to? What does the A refer to? What does the 6 refer to?

Family.  Subfamily.  Form

44

The cytochrome P450 oxidises all foreign chemical with a molecular weight greater than what?

5,000

45

When is the P450 cycle of reactions initiated?

When a substrate binds to the P450

46

When is P450 found in microsomes?

In vitro only

47

What does it mean to say that a specific cytochrome P450 is inducible?

Chronic drug/toxin exposure will result in higher levels of that P450 being expressed 

48

What is the point of CYP450 enzymes?

Add -OH and sugar group onto small hydrophobic molecules to make them water soluble so they may be excreted by the kidneys

49

What is anakinra?

IL-1 antagonist

50

According to first order kinetics, what determines rate of clearance of a drug?

Drug concentration in the body (and a constant for the drug)

51

If a drug is given regularly every half life, what will the trough concentration be relative to peak concentration?

Half

52

How long will it take for an IV infused drug to reach 99% of its steady state concentration?

7 half lives

53

Which cytokines do glucocorticosteroids suppress the synthesis of?

IL-1,4,5,8, TNF alpha and GM-CSF

54

How do glucocorticoids suppress prostaglandin synthesis?

Transactivate annexin 1, which inhibits PLA-2, thus preventing formation of prostaglandins

55

Which cytochrome P450 metabolises steroids?

CYP3A4

56

Which three classes of proteins do glucocorticosteroids suppress the synthesis of?

Cytokines. Inflammatory enzymes. Adhesion molecules

57

What are the 3 actions/indications of NSAIDs?

Anti-inflammatory, analgesic, antipyretic

58

Which NSAID is generally best as an antipyretic?

Paracetamol

59

How do NSAIDs cause analgesia?

NSAIDs decrease production of PGs. PGs sensitise sensory nerve endings

60

What are the 4 main adverse effects of NSAIDs?

Gastric ulcers. Increased bleeding time. Renal impairment. Bronchoconstriction

61

Name 2 enzymes that glucocorticoids increase the transcription of? How do these decrease inflammation?

SERPIN A3 => codes for anti-chymotrypsin, which inhibits neutrophil proteases ANNEXIN 1 => inhibits PLA2

62

What is the main target of NSAIDs?

COX-2

63

How do NSAIDs cause gastric ulcers?

NSAIDs inhibit mucosal synthesis of PGE2. PGE2 normally protects mucosa by increasing mucous secretion, reducing acid secretion, promoting blood flow and promoting angiogenesis

64

Describe the 4 steps in NA synthesis

1 Tyrosine taken up into cell
2 Tyrosine → L-Dopa (catalysed by tyrosin hydroxylase)
3 L-DOPA → Dopamine (catalysed by dopa decarboxylase)
4 Dopamine taken up into vesicle and converted into NA (catalysed by dopamine beta hydroxylase)