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Pharmacology > Mechanisms > Flashcards

Mechanisms Flashcards

1
Q

Name 2 drugs that bind to GABAa receptor found in the brain

Briefly state what each drug can be used for

A

Barbiturates (anxiolytic drug) and Benzodiazepines (epilepsy)

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2
Q

What type of enzyme is CYP1A (an isoenzyme of Cytochrome P450)

What induces it, and what does this mean?

A

A Phase 1 Enzyme

Induced by smoking so the enzyme is up-regulated, so drugs that are metabolised by this enzyme get metabolised at a quicker rate than normal as there is a greater number of the CYP1A enzymes present

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3
Q

What isoenzyme metabolises alcohol?

A

CYP2E

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4
Q

What is bioavailability (F)?

A

The measure of drug being absorbed that reaches the systemic circulation

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5
Q

Where does first pass metabolism occur?

A

Gut (lumen, wall) and liver

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6
Q

Describe the graph seen in a graph used to calculate bioavailability

x: time y: concentration of drug in plasma

A

Initially: steep - absorption
Decreases: distribution (tissue, protein bound, receptors)
Further decrease: elimination

ADE

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7
Q

Where would you find a low (1) and high (2) volume of distribution Vd?

A

Low: plasma (drug free)
High: ECF (bound to albumin) then tissue (lipophilic drugs bound to fat in cells)

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8
Q

What demographic have an overactive CYP2D6 enzyme and name 2 drugs that this would effect.

Would their metabolism be faster or slower?

CYP2D METABOLISES MOST DRUGS!!!

A

East Africans.

SSRIs and B-blockers

Faster metabolism

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9
Q

What Phase 1 enzyme does Grapefruit inhibit and what does this mean?

Name 1 drug type that would be effected by this and what effect would be present

A

Grapefruit inhibits CYP3A4 enzymes - leading to high plasma statin levels as their metabolism rate is drastically reduced

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10
Q

What is the definition of drug clearance?

A

Rate of elimination + [drug plasma]

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11
Q

Where does drug metabolism (a part of elimination) take place?

What is formed?

A

Liver -> bile

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12
Q

Where does drug excretion (a part of elimination) take place?

A

Kidneys

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13
Q

What is the Enterohepatic circulation?

Name 2 drugs involved in this circulation

A

Conjugated substances (so bilirubin and some drugs (e.g. Warfarin and Morphine)) leave the liver as bile (some of the material is conjugated in the liver, other conjugated substances enter the liver from the general circulation), enter the SI, then colon/rectum, here BACTERIAL HYDROLYSIS occurs, and the conjugated substance returns to the liver then GENERAL CIRCULATION

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14
Q

List 3 reasons for giving a modified release preparation

A
  1. Improve compliance
  2. Have fewer doses to take
  3. Reduce fluctuations in [plasma drug]
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15
Q

Alcohol is a zero order drug.

What does this mean about its half life?

Name 2 other drugs that are zero order drugs

A

Half life is not constant (drug can easily pass its therapeutic window and enter its toxic window, its [plasma] is unpredictable

Warfarin
Alcohol, Aspirin/Salicylic acid
Theophylline
Phenytoin

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16
Q

How do you keep a steady state plasma drug concentration Css?

Maintenance dose

A

Rate of administration = Rate of elimination

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17
Q

Give 2 reasons why you would give a loading dose?

A

Drug has a long t1/2

Drug has a large Vd (↑ bound drug - in ECF and tissue)

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18
Q

What is an inverse agonist

A

A drug that binds to the same receptors as agonists but induces a response opposite to the agonist

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19
Q

Give an example of a full agonist

A

Adrenaline, Codeine, Morphine

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20
Q

Give an example of an inverse agonist

A

Propranolol (a beta blocker)

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21
Q

Give an example of a partial agonist

A

Formoterol (a LABA)

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22
Q

Give two examples of non-competitive antagonists

A

Tamsulosin and Doxazosin (alpha adrenoceptor blockers)

23
Q

Give an example of a competitive antagonist

A

Naloxone

24
Q

Name 2 autacoids

Where do autacoids act on?

What is their effect?

A

Bradykinin and nitric oxide both act on endothelium and vascular smooth muscle to aid their vasodilation

25
Q

Kidney functions

A

A WET BED

Acid base balance

Water balance
ELECTROLYTE balance
Toxin removal

BP regulation
Erythropoietin production
D Vit D metabolism

26
Q

What is pharmacogenomics?

A

How your individual GENE may affect your body’s response to the drug

27
Q

Describe the sex steroid synthesis from cholesterol to produce oestradiol

A

Cholesterol -> Progesterone -> Testosterone -> Estradiol

28
Q

Nam 4 functions of cholesterol

A
  1. Integrity of cell membrane

Produce

  1. Steroid hormones
  2. Bile acid
  3. Vitamin D
29
Q

Describe the formation of atherosclerosis

A

LDL’s are OXIDISED AT damaged endothelium (so tunica interna) due to:

Necrotic tissue and ROS

LDL’s bind to scavenger receptor on macrophage in the vessel lumen -> foam cells

Foam cells build up in the intima and lead to the proliferation of SM cells in the tunica media

Fatty streaks develop

30
Q

How is insulin prescribed?

E.g. g,pills

A

units/mL

31
Q

Name 2 functions that insulin inhibits - regarding blood glucose levels

A

Inhibits:

Gluconeogenesis
Glycogenolysis

32
Q

Name 4 factors that increase the production of insulin from beta cells of islet of langerhans?

A
  • High glucose
  • High incretins (GLP-1)
  • Low glucagon
  • Parasympathetic NS via M3-R on pancreatic beta cells
33
Q

Name 3 factors that decrease insulin release from beta cells of islet of langerhans?

A
  • Low glucose
  • High cortisol
  • Sympathetic NS via a2-R on pancreatic beta cells
34
Q

What are the 5 stages in a ventricular myocyte AP?

A 
Phase 0 - Na+ influx (passive)
Phase 1 - K+ efflux (ligand gated)
Phase 2 - Ca2+ influx (L type VGCC)
Phase 3 - K+ efflux (ligand gated)
Phase 4 - resting potential
35
Q

What current (give both names) passes through what channel in SAN - which then allows the influx of Na+ via this channel.

A

Pacemaker potential/If funny current passes through HCN channel, thus allowing it to open and allow the influx of Na+ into SAN

36
Q

How do you differentiate between venous thrombosis and arterial thrombosis?

Give 3 comparisons

A

VT caused by stasis of blood so there is NO endothelial damage present, whereas AT caused by rupture of atherosclerotic plaque so there is endothelial damage present

VT has high fibrin, whilst AT have low fibrin

VT have low platelet, whilst AT has high platelet (PA)

37
Q

What produces prostacyclin?

What is the function of prostacyclin?

A

Endothelial cells

Inhibit platelet aggregation

38
Q

In healthy endothelium, how are GPIIb/IIIa made inactive/stable?

A
  1. Prostacyclin released from endothelial cells
  2. PGI2 (Prostacyclin) + Platelet-R -> increase cAMP
  3. High cAMP leads to reduced Ca2+
  4. So get less platelet aggregation as GPIIb/IIIa-R is made stable
39
Q

In platelet activation, name 4 chemical mediators that are released by the platelets that are currently in the subendothelial area?

What does this cause?

A

Thrombaxone A2, ADP, Serotonin and PAF are released, this recruits more platelets and increases internal platelet Ca2+levels - in platelet aggregation a platelet plug is formed

40
Q

In platelet aggregation, what would be higher: Ca2+ of cAMP?

Name 3 effects of the change in Ca2+ levels

A

Ca2+

  1. Activate Thromboxane A2 synthesis in the platelet
  2. Activate GPIIb/IIIa receptors on platelet surface (binds to fibrinogen)
  3. Release platelet granules/chemical mediators
41
Q

What is a platelets lifespan?

A

7-10 days

42
Q

When Aspirin undergoes hepatic hydrolysis, what is formed?

A

Salicylic acid

43
Q

Giving Aspirin to children under 16 can cause what?

2

A

Reye’s syndrome - inflammation of brain and liver

Premature Ductus Arteriosus closure

44
Q

Prostainds compose of 3 main categories - name them

They all directly come from which immediate molecule?

A

Prostaglandins, Prostacyclins and Thromboxanes.

All come from Prostaglandin H2.

45
Q

Regarding the activation and inhibition of platelet aggregation, when Arachnoid acid is being converted to Prostaglandin H2 by COX-1 and COX-2 enzymes, what prostanoids would be formed and how would this effect platelet aggregation?

A

AA -> (COX-1) -> PGH2 -> Thromboxane A2 -> Platelet aggregation

AA -> (COX-2) -> PGH2 -> Prostacyclin -> Inhibition of platelet aggregation

46
Q

What ligands in the vestibular nuclei are involved in the vomiting reflex?

A

Muscarinic receptor antagonists

H1 receptor antagonists

47
Q

What ligands in the visceral afferent of the gut are involved in the vomiting reflex?

A

5HT3 antagonists

D2 receptor antagonists

48
Q

What is antimicrobal stewardship?

A

The proper use of antimicrobal prescriptions to prevent overuse and antimicrobal resistance in future generations

49
Q

There are 3 known clotting tests.

Name them.

If they are high what does this SPECIFICALLY mean?

What drugs can make them high?

A
  1. High PT/INR, due Warfarin, means that it’ll take you longer for your blood to clot via the extrinsic pathway due to the extrinsic pathway being blocked
  2. Fondaparinux (a synthetic pentasaccharide) inhibits Xa - which is involved in both pathways so PT, INR and PTT will all increase and it’ll take longer for your blood to clot via both pathways
  3. High PTT, due to Heparin (an un-fractionated Heparin), can lead to increased clotting due an inhibition of the intrinsic pathway
50
Q

Vitamin K’s function in the clotting cascade:

  • Name the 4 coagulants that it aids to produce.
  • Name the 2 anti-coagulants that it aids to produce.

What organ does this production take place in?

A

Aids the hepatic synthesis of:

Coagulants:

  • II
  • VII
  • IX
  • X

Anti-coagulants:
- protein C
- protein S
(Antithrombin III’s production is INDEPENDENT of Vitamin K)

51
Q

In Tumour Lysis Syndrome, name 4 contents that are released from the tumour cells into the bloodstream

A

DNA (pyrimidines and purines)

Phosphates (leads to hyperphosphatemia which thus leads to hypocalcaemia)

Lactic acid

Potassium (leads to hyperkalaemia)

52
Q

In Tumour Lysis Syndrome, what can be a side effect of high purine levels.

Describe.

How can this effect the kidneys?

A

Purines are broken down into xanthines via xanthine oxidase. Product produced is uric acid so you get hyperuricaemia.

Uric acid can crystallise in the kidney, leading to AKI

53
Q

Give 2 reasons for the presence of arrhythmias in Tumour Lysis Syndrome

A

Hypocalcaemia (as a result of hyperphosphataemia - so phosphate acts as a chelating agent and binds to the calcium so calcium is ‘inactive’)

Hyperkalaemia

Pharmacology (4 decks)

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