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Mechanisms Flashcards

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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

Study These Flashcards
A

Tamsulosin and Doxazosin (alpha adrenoceptor blockers)

23
Q

Give an example of a competitive antagonist

24
Q

Name 2 autacoids

Where do autacoids act on?

What is their effect?

Study These Flashcards
A

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

25
Kidney functions
A WET BED Acid base balance Water balance ELECTROLYTE balance Toxin removal BP regulation Erythropoietin production D Vit D metabolism
26
What is pharmacogenomics?
How your individual GENE may affect your body’s response to the drug
27
Describe the sex steroid synthesis from cholesterol to produce oestradiol
Cholesterol -> Progesterone -> Testosterone -> Estradiol
28
Nam 4 functions of cholesterol
1. Integrity of cell membrane Produce 2. Steroid hormones 3. Bile acid 4. Vitamin D
29
Describe the formation of atherosclerosis
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
How is insulin prescribed? E.g. g,pills
units/mL
31
Name 2 functions that insulin inhibits - regarding blood glucose levels
Inhibits: Gluconeogenesis Glycogenolysis
32
Name 4 factors that increase the production of insulin from beta cells of islet of langerhans?
- High glucose - High incretins (GLP-1) - Low glucagon - Parasympathetic NS via M3-R on pancreatic beta cells
33
Name 3 factors that decrease insulin release from beta cells of islet of langerhans?
- Low glucose - High cortisol - Sympathetic NS via a2-R on pancreatic beta cells
34
What are the 5 stages in a ventricular myocyte AP?
``` 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
What current (give both names) passes through what channel in SAN - which then allows the influx of Na+ via this channel.
Pacemaker potential/*If* funny current passes through HCN channel, thus allowing it to open and allow the influx of Na+ into SAN
36
How do you differentiate between venous thrombosis and arterial thrombosis? Give 3 comparisons
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
What produces prostacyclin? What is the function of prostacyclin?
Endothelial cells Inhibit platelet aggregation
38
In healthy endothelium, how are GPIIb/IIIa made inactive/stable?
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
In platelet activation, name 4 chemical mediators that are released by the platelets that are currently in the subendothelial area? What does this cause?
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
In platelet aggregation, what would be higher: Ca2+ of cAMP? Name 3 effects of the change in Ca2+ levels
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
What is a platelets lifespan?
7-10 days
42
When Aspirin undergoes hepatic hydrolysis, what is formed?
Salicylic acid
43
Giving Aspirin to children under 16 can cause what? 2
Reye’s syndrome - inflammation of brain and liver Premature Ductus Arteriosus closure
44
Prostainds compose of 3 main categories - name them They all directly come from which immediate molecule?
Prostaglandins, Prostacyclins and Thromboxanes. All come from Prostaglandin H2.
45
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?
AA -> (COX-1) -> PGH2 -> Thromboxane A2 -> Platelet aggregation AA -> (COX-2) -> PGH2 -> Prostacyclin -> Inhibition of platelet aggregation
46
What ligands in the vestibular nuclei are involved in the vomiting reflex?
Muscarinic receptor antagonists H1 receptor antagonists
47
What ligands in the visceral afferent of the gut are involved in the vomiting reflex?
5HT3 antagonists D2 receptor antagonists
48
What is antimicrobal stewardship?
The proper use of antimicrobal prescriptions to prevent overuse and antimicrobal resistance in future generations
49
There are 3 known clotting tests. Name them. If they are high what does this SPECIFICALLY mean? What drugs can make them high?
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
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?
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
In Tumour Lysis Syndrome, name 4 contents that are released from the tumour cells into the bloodstream
DNA (pyrimidines and purines) Phosphates (leads to hyperphosphatemia which thus leads to hypocalcaemia) Lactic acid Potassium (leads to hyperkalaemia)
52
In Tumour Lysis Syndrome, what can be a side effect of high purine levels. Describe. How can this effect the kidneys?
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
Give 2 reasons for the presence of arrhythmias in Tumour Lysis Syndrome
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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