Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Nick's MD1 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Define partial agonist

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Define potency

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Define pharmacokinetics

A

What the body does to the drug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What type of receptor is the nicotinic cholinergic receptor?

A

Ligand-gated ion channel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Define efficacy

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Define pharmacodynamics

A

What the drug does to the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Define affinity and how it is measured

A
  • 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Define each of ADME

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the 6 steps in pharmacokinetics?

A

Administration, absorption, distribution, elimination, metabolism, excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe the 3 steps in ACh synthesis

A

1 Choline taken up into cell by choline carrier

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

3 ACh put into vesicle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is a clinical use for nicotinic receptor antagonists?

A

Pre-surgical muscle relaxant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Name 3 clinical uses of ACh esterase inhibitors

A

Dx of myasthenia gravis

Rx of myasthenia gravis

Rx of Alzheimer’s disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is a clinical use for nicotinic receptor agonists?

A

Smoking cessation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

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

A

Muscarinic antagonist.

Bronchodilation and decrease respiratory mucous in anaesthesia

To increase heart rate.

Pupil dilation for eye examination.

AChE-inhibitor poisoning (organophosphates)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the mechanism of action of botulimin toxin

Name 3 conditions it may be used for

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

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

A

Used to treat peptic ulcers.

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

H1 antagonists:

What class of drugs are these?

Name 5 things they are used to treat.

Name 2 new generation drugs

A

Antihistamines

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe the 4 steps in NA synthesis

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are 7 clinical consequences of adrenaline administration?

A

Vasoconstriction

GI muscle relaxation

Salivation

Hepatic glycogenolysis

Increased heart rate

Increased cardiac contractility

Bronchodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the mode of action of aminoglycosides?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How do beta lactams exert antimicrobial effects?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

List 3 enzymes that beta lactams may inhibit

A

Transpeptidase
Transglycosylase
Carboxypeptidase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the mechanism of action of loop diuretics?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

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

A

Block Na transporter in collecting tubules and ducts

Plus or minus:

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the mechanism of action of thiazide diuretics?

A

Inhibit Na/Cl transporter in distal tubule

27
Q

What are 7 clinical consequences of adrenaline administration?

A

Vasoconstriction

GI muscle relaxation

Salivation

Hepatic glycogenolysis

Increased heart rate

Increased cardiac contractility

Bronchodilation

28
Q

How does penicillin exert its antimicrobial effect?

A

Penicillin stops formation of pentapeptide bridge by blocking transpeptidase

29
Q

List 3 enzymes that beta lactams may inhibit

A

Transpeptidase
Transglycosylase
Carboxypeptidase

30
Q

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

A

Dry eyes

Dry mouth

Urinary retention

Constipation

Tachycardia

Confusion

31
Q

What type of receptor is the muscarinic cholinergic receptor?

A

G-protein coupled receptor

32
Q

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

A

IL-1,4,5,8

GM-CSF

TNFalpha

33
Q

What are 6 effects of histamine on H1 receptors?

A

Pain and itch

Bronchospasm

Mucus secretion

Vasodilation

Increased vascular leak

Increased wakefullness

34
Q

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

A

Beta 2 adrenoceptor –> bronchodilation

Annexin-1 –> inhibits PLA2

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

35
Q

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

A

PLA2

COX-2

iNOS

36
Q

Describe 6 steps in GCS transactivation

A

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
Q

What are the effects of histamine acting on H2 receptors?

A

Positive inotropic effects on heart

Positive chronotropic effects on the heart

Gastric acid secretion

38
Q

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

A

ICAM

E-selectin

39
Q

Name 3 classes of molecule that GCS inactivates through transrepression

A

Cytokines

Adhesion molecules

Inflammatory enzymes

40
Q

In which organelles are P450s located?

A

Endoplasmic reticulum and mitochondria

41
Q

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

42
Q

Name two D2 antagonists used to treat nausea

A

Metoclopramide (maxolon)

Prochlorperazine (stemetil)

43
Q

CYP 2A6

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

A

Family. Subfamily. Form

44
Q

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

45
Q

When is the P450 cycle of reactions initiated?

A

When a substrate binds to the P450

46
Q

When is P450 found in microsomes?

A

In vitro only

47
Q

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

A

<!--StartFragment-->

Chronic drug/toxin exposure will result in higher levels of that P450 being expressed <!--EndFragment-->

48
Q

What is the point of CYP450 enzymes?

A

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

49
Q

What is anakinra?

A

IL-1 antagonist

50
Q

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

A

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

51
Q

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

52
Q

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

A

7 half lives

53
Q

Which cytokines do glucocorticosteroids suppress the synthesis of?

A

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

54
Q

How do glucocorticoids suppress prostaglandin synthesis?

A

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

55
Q

Which cytochrome P450 metabolises steroids?

56
Q

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

A

Cytokines. Inflammatory enzymes. Adhesion molecules

57
Q

What are the 3 actions/indications of NSAIDs?

A

Anti-inflammatory, analgesic, antipyretic

58
Q

Which NSAID is generally best as an antipyretic?

A

Paracetamol

59
Q

How do NSAIDs cause analgesia?

A

NSAIDs decrease production of PGs. PGs sensitise sensory nerve endings

60
Q

What are the 4 main adverse effects of NSAIDs?

A

Gastric ulcers. Increased bleeding time. Renal impairment. Bronchoconstriction

61
Q

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

A

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

62
Q

What is the main target of NSAIDs?

63
Q

How do NSAIDs cause gastric ulcers?

A

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

64
Q

Describe the 4 steps in NA synthesis

A

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)

Nick's MD1 (28 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions