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P32 Flashcards

1
Q

Amlodipine
Felodipine
Lercanidipine
Nifedipine

A

Dihydropyridine (DHP) calcium channel blockers

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2
Q

Ezetimibe

A

Specific cholesterol absorption inhibitors

Oral antilipemic; cholesterol absorption inhibitor indicated to treat hypercholesterolemia.

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3
Q

Bezafibrate

Fenofibrate

A

PPARα agonist

MoA:

  • Lowers cholesterol, LDLs, and triglycerides
  • Increases HDLs
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4
Q

Simvastatin
Atorvastatin
Rosuvastatin

A

Statins

MoA: HMG-CoA reductase inhibitor [rate-limiting enzyme in cholesterol synthesis]

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5
Q

Diltiazem
Verapamil
Fendiline

A

Non-dihydropyridine calcium channel blockers

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6
Q

Hypovolaemic shock stages and blood loss.

A

I - blood loss <750 (15% blood volume)

II - blood loss 750-1500 (15-30%)

III - blood loss 1500-2000 (30-40%)

IV - blood loss >2000 (>40%)

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7
Q

Blatchford score - use?

A

The Glasgow-Blatchford bleeding score (GBS) is a screening tool to assess the likelihood that a patient with an acute upper gastrointestinal bleeding (UGIB) will need to have medical intervention such as a blood transfusion or endoscopic intervention.

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8
Q

Blatchford score - values

A 
Blood Urea (mmol/L):
6.5-8.0	2
8.0-10.0	3
10.0-25	4
>25	6

Haemoglobin (g/dL) for men:
12.0-12.9 1
10.0-11.9 3
<10.0 6

Haemoglobin (g/dL) for women:
10.0-11.9 1
<10.0 6

Systolic blood pressure (mm Hg):
100–109 1
90–99 2
<90 3

Other markers:
Pulse ≥100 (per min)	1
Presentation with melaena	1
Presentation with syncope	2
Hepatic disease	2
Cardiac failure	2

A score of >6 implies need for endoscopic intervention and transfusion.

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9
Q

Rockall score vs Blatchford score?

A

The Blatchford score, unlike the Rockall score, does not take endoscopic data into account and thus can be used when the patient first presents.

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10
Q

Rockall score

A

Rockall risk scoring system attempts to identify patients at risk of adverse outcome following acute upper gastrointestinal bleeding.

Age, shock, comorbidity, diagnosis, evidence of bleeding

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11
Q

Lansoprazole
Omeprazole
Pantoprazole

A

Proton pump inhibitors

MoA: Binds irreversibly to H+/K+ ATPase in gastric parietal cells and inhibits H+ transport
- Activated in acidic pH

Complications:

  • Gastrointestinal disturbance,
  • Headache,
  • Prolonged treatment with PPIs can cause hypomagnesaemia, which if severe can lead to tetany and ventricular arrhythmia.
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12
Q

Ranitidine

Cimetidine

A

H2-receptor antagonist

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13
Q

Upper GI bleed - PPI vs H2 antagonists

A

In the setting of active upper GI bleeding from an ulcer, acid suppressive therapy with H2 receptor antagonists has not been shown to significantly lower the rate of ulcer re-bleeding.

By contrast, high dose anti-secretory therapy with an intravenous infusion of a PPI significantly reduces the rate of rebleeding compared with standard treatment in patients with bleeding ulcers.

Oral and intravenous PPI therapy also decrease the length of hospital stay, rebleeding rate, and need for blood transfusion in patients with high-risk ulcers treated with endoscopic therapy.

PPIs suppress gastric acid secretion by inhibiting the parietal cell H+/K+ ATP pump.

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14
Q

Hypotensive agents and active GI bleed?

A

Withhold all the hypotensive agents – amlodipine and ramipril

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15
Q

H. pylori eradication

Triple eradication therapy!

A

1 PPI
2 Antibiotics
1 Bismuth (extra)

Antibiotic to eradicate H. pylori (Clarithromycin, Amoxicillin + Metronidazole)

PPI to suppress acid and dual antibiotic therapy – occasionally quadruple therapy is indicated and this include a bismuth preparation.

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16
Q

Simvastatin + clarithromycin - problems?

A

Interaction can cause increase simvastatin levels thus increase risk of myositis through CYP3A4.

Clarithromycin is a strong inhibitor of CYP3A4 which is involved with metabolising simvastatin.

Eventually myositis becomes rhabdomyolysis and becomes a burden on kidneys.

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17
Q

UC treatment

A
  • Oral glucocorticoids
  • High dose oral 5-aminosalicylic acid
  • Steroid enema or doam

Patient with fulminant disease should be treated with IV glucocorticoids and broad-spectrum antibiotics (gram negative)

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18
Q

A patient has been receiving hydrocortisone 100 mg IV every 8 hours and you wish to convert him to an oral corticosteroid – which will you use?

A

Oral prednisolone

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19
Q

Mesalazine (aka 5-ASA)

A

Class: Aminosalicylates

MoA: Inhibition of arachidonic acid in the bowel mucosa by cyclooxygenase (COX).

Inhibition of COX diminishes prostaglandins production, thereby reducing colonic inflammation.

Indications:

  • Ulcerative colitis
  • Crohn’s disease
  • Ulcerative proctitis (suppository)
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20
Q

Azathioprine

A

Immunosuppressant

MoA: Azathioprine inhibits purine synthesis. Purines are needed to produce DNA and RNA. By inhibiting purine synthesis, less DNA and RNA are produced for the synthesis of white blood cells, thus causing immunosuppression.

Indications:

  • Crohn’s disease
  • Ulcerative colitis
  • Rheumatoid arthritis
  • Granulomatosis with polyangiitis
  • Kidney transplants to prevent rejection
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21
Q

Consequences of sudden stop of Consequences of long term oral corticosteroids??

A

Addisonian crisis

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22
Q

Consequences of long term oral corticosteroids?

A

Cushing’s syndrome

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23
Q

Infliximab

A

Chimeric monoclonal antibody

Class: Cytokine inhibitor

MoA: Binds to human tumour necrosis factor alpha (TNFa) and interferes with endogenous TNFa activity

Indication:

  • Crohn’s disease
  • Ulcerative colitis
  • Psoriasis
  • Rheumatoid arthritis
  • Ankylosing spondylitis
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24
Q

Pain and temperature sensation?

A

Dorsal horn (spinal cord)

Ascend via spinothalamic tract

Reach reticular activating system + thalamus

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25
Q

Side effects of opioids?

A

Common:

  • Constipation
  • Nausea
  • Sedation
  • Confusion
  • Hallucinations
  • Flushing/sweating
  • Dry mouth
  • Difficulty with micturition
  • Hypotension

Less common:

  • Urinary retention
  • Pruritus/urticaria
  • Delirium
  • Myoclonus/muscle rigidity
  • Hyperalgesia
  • Respiratory depression
  • Sexual dysfunction
  • Biliary/ureteric spasm
  • Visual disturbance
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26
Q

Naloxone

A

Opioid competitive antagonist

Naloxone is a very safe drug, hence given when suspected opiate overdose

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27
Q

Benzodiazepines reversal agent?

A

Flumazenil
Flumazenil is a short-acting agent that reverses benzodiazepine-induced sedation. Re-sedation may occur due to its short duration of action, therefore additional doses may be necessary. Flumazenil is not useful for barbiturate- or opioid-induced sedation.

Flumazenil interacts with a lot of meds so it’s not safe

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28
Q
  • Lorazepam (Ativan)
  • Alprazolam (Xanax)
  • Diazepam (Valium)
A

Benzodiazepines

GABA agonists

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29
Q

Methotrexate reversal agent

A

Leucovorin

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30
Q

Heparin reversal agent

A

Protamine sulphate

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31
Q

Warfarin poisoning antidote

A

Vitamin K

32
Q

Beta blocker poisoning antidote

A

Glucagon

33
Q

Anticholinergic poisoning antidote

A

Physostigmine

34
Q

Aspirin poisoning reversal agent

A

Sodium bicarbonate

35
Q

Paracetamol poisoning antidote

A

N-acetylcysteine

36
Q

Dabigatran poisoning antidote

A

Idarucizumab

37
Q

Carbon monoxide poisoning antidote

A

Oxygen

38
Q

Iron poisoning antidote

A

Deferoxamine

39
Q

Serotonin syndrome antidote

A

Cyproheptadine

40
Q

Organophosphate antidote

A

Atropine

41
Q

Theophylline poisoning

A

Beta blocker

42
Q

Lead, mercury, arsenic poisoning antidote

A

Dimercaptosuccinic acid

43
Q

Full agonists vs partial agonists?

A

Partial agonists are unable to produce a maximal response even at high concentrations

Full agonists can produce maximal responses. They can have different potencies

Both types of agonists are affected by the presence of competitive (reversible) antagonists and non-competitive (irreversible) antagonists.

Unlike competitive antagonists, a non-competitive antagonist reduces the maximal response even at high agonist concentrations, as shown in the curve A2+ IA compared with A2alone.

44
Q

Causes of constipation?

A
  • Bed rest
  • Hypercalcaemia
  • Opiate use
  • Many GI causes
45
Q

Bulk laxative

A

Avoid bulk laxatives in the non-ambulatory patient, the patient who cannot get 8 glasses of water in, because, again, you just make concrete like stool.

46
Q

Constipation treatment

A
  • Large bowel stimulant

- Stool softener

47
Q

Methylnaltrexone

A

Methylnaltrexone is a peripherally-acting μ-opioid antagonists that acts on the gastrointestinal tract to decrease opioid-induced constipation while maintaining central analgesic effects.

Because this opioid antagonist that does not cross the blood-brain barrier, may diminish the peripherally mediated side effects of opioids while maintaining central analgesic effects and does not induce symptoms of opioid withdrawal

Indication: opioid induced constipation (OIC) in patients with chronic pain and inadequate response to traditional laxatives.

It is also a weak CYP2D6 inhibitor.

48
Q

Multimodal analgesia

A

Pain receptor activity directly blocked, e.g. lidocaine.

Anti-inflammatory agents, e.g. NSAIDs, to diminish the local hormonal response to injury, thus indirectly decreasing pain receptor activation.

Some analgesic agents target the activity of neurotransmitters by inhibiting or augmenting their activity, e.g. ketamine, clonidine, paracetamol, gabapentin, pregabalin.

Neurotransmitters are responsible for carrying electrical signals across the gap junctions between neurons. To produce analgesia, the activity of several neurotransmitters can be targeted, including substance P, calcitonin gene-related peptide, aspartate, glutamate, and gamma-aminobutyric acid (GABA).

49
Q

Bupivacaine

A

Local anaesthetic

Desrupts ion channel function within the neuronal cell membrane preventing transmission of the neuronal AP.

50
Q

Paracetamol

A

Action on spinal receptors through the action of its breakdown product NAPQI acting on TPRA1 receptors blocking pain signal transmission.

51
Q

Epidural opiates:

A

Direct action on opioid receptors.

Opioids have actions at two sites, the presynaptic nerve terminal and the postsynaptic neuron.

The postsynaptic actions of opioids are usually inhibitory.

The presynaptic action of opioids is to inhibit neurotransmitter release, and this is considered to be their major effect in the nervous system.

However, the final effect of an opioid in the brain is the result, not only of its action at multiple presynaptic sites on both inhibitory and excitatory neurons, but also of its postsynaptic effects.

52
Q

Isomers of tramadol, ibuprofen and naproxen and biological activity.

A

Tramadol’s 2 isomers act on different levels (dual pain relief)

Ibuprofen and naproxen have one isomer which is biologically active

53
Q

Post operative nausea and vomiting

A

Nausea and vomiting can be induced by many physiological and pathological factors, as well as drugs or ingested toxins.

Nausea and vomiting is primarily controlled by the vomiting centre.

This is an area in the brainstem that integrates responses.

Efferent impulses from these medullary centres influence related brainstem nuclei to initiate the vomiting reflex.

Afferent stimuli arrive from chemoreceptors and pressure receptors in the gut and CNS, as well as peripheral pain receptors. Other sites of input in the CNS include the cerebral cortex (pain, fear and anxiety), vestibular and cerebellar nuclei and the CTZ.

54
Q

Post operative N+V antiemetic drug classes?

A
  • Serotonin-receptor antagonists (most commonly used due to no sedative side effects)
  • Corticosteroids
  • Anticholinergic agents
  • Neurokinin-receptor antagonists
55
Q

Ondansteron

A

Selective serotonin-receptor (5-HT3) antagonist

  • Are most commonly used post-op N+V agents because they do not have sedative side effects

MoA: Suppressive the initiation of nausea + vomiting by blocking serotonin peripherally at vagal afferents and centrally in chemoreceptor trigger zone.

56
Q

Post-operative N+V drug classes and examples

A

Selective serotonin-receptor (5-HT3) antagonist - Ondansetron

Anticholinergics – Hyoscine

Glucocorticoids (prophylaxis) – Dexamethasone

Antihistamines – Cyclizine

57
Q

Dexamethasone (steroid) used for reduction of nausea and vomiting related to chemotherapy?

A

The steroid dexamethasone (150 mcg/kg in children or 8 mg in adults) is used for reduction of nausea and vomiting related to chemotherapy and has been shown to be useful in the treatment of postoperative nausea and vomiting.

The mode of action is unclear; it may be due to decreased release of arachidonic acid, reduced turnover of 5-hydroxytryptamine or decreased permeability of the blood-brain-barrier.

58
Q

Which postoperative antiemetic drug causes QT prolongation?

A

Ondansetron (Serotonin receptor antagonist)

Dose dependent QT prolongatoin

59
Q

Preventative post-op antiemetics

A

Serotonin-receptor antagonist (Ondansteron)

Glucocorticoids (dexamethasone)

Anticholinergic (scopolamine)

Neurokinin-receptor antagonists (aprepitant)

60
Q

Anticholinergic

A

Scopolamine
Hyoscine

Prevents postoperative N+V

Sedating

Contraindicated in narrow-angle glaucoma

61
Q

Aprepitant

A

Neurokinin-receptor antagonist

MoA: blocks neurokinin’s effect (pro-emetic agent) at receptor site

Prevents postoperative N+V

Expensive!

62
Q

Cyclizine

A

Competitive antagonist of histamine H1 receptors

Antiemetic effects may be via blockade of central histamine (H1) ad muscarinic receptors, and by its anticholinergic properties.

Must cross BBB to have antiemetic properties. (terfenadine does not)

63
Q

Metoclopramide or prochlorperazine can also be used to treat nausea and vomiting but usually not as first line for PONV

What is site of action of these drugs and how is it thought that they work?

A

Both are dopamine receptor antagonist.

Prochlorperazine is an antiemetic that often partially alleviates acute nausea and vomiting (eg, acute gastroenteritis).

  • But is associated with risks of hypotension and extrapyramidal side effects.
  • Prochlorperazine should usually be considered in such cases before trying serotonin receptor antagonists or prokinetic drugs.

Metoclopramide is a dopamine receptor antagonist, it has combined antiemetic and prokinetic properties.

  • However, it can be associated with extrapyramidal side effects.
  • It can be given orally or intravenously. When given intravenously, using a slow infusion over 15 minutes is associated with a lower incidence of akathisia compared with bolus dosing, without a decrease in efficacy.
64
Q

If your patient suffered a severe dystonic reaction after treatment with metoclopramide how would you help them?

A

Procyclidine:

  • First line treatment of acute dystonic reactions
  • Response is often dramatic and generally occurs in 5-20mins (short half-life)
  • If symptoms persist after 15-30mins a second dose can be given.
  • If symptoms persist and are not improving after second dose consider the possibility of an alternative diagnosis.
65
Q

Causes of constipation in cancer?

A

Cancer:

  • Intra-abdominal/pelvic cancers
  • Hypercalcaemia
  • Cord compression
  • Autonomic neuropathy

Cancer related:

  • Inanition and asthenia
  • Pain
  • Paralysis
  • Bed rest

Cancer therapy:

  • Bowel surgery
  • Hypokalaemia (vomiting)

Symptom control therapy:

  • Opioids
  • Anticholinergic drugs
  • Tricyclic antidepressants
  • Antihistamines
  • Neuroleptic drugs
  • Antispasmodics
66
Q

Prochlorperazine

A

Dopamine antagonist

Prochlorperazine is an antiemetic that often partially alleviates acute nausea and vomiting (eg, acute gastroenteritis).

  • But is associated with risks of hypotension and extrapyramidal side effects.
  • Prochlorperazine should usually be considered in such cases before trying serotonin receptor antagonists or prokinetic drugs.
67
Q

How often should morphine be given?

A

Should really be given every 4 hours and the dose titrated up to effect.

68
Q

What is the rescue dose of oramorph?

I.e. for breakthrough pain

A

The rescue dose of oramorph (morphine) should be a sixth of the total 24-hour dose

E.g. If total 24 hr dose is 60mg = 10 mg

69
Q

What is the apparent volume of distribution?

A

Volume of distribution (VD, also known as apparent volume of distribution) is the theoretical volume that would be necessary to contain the total amount of an administered drug at the same concentration that it is observed in the blood plasma.

Vd = amount of drug in body / plasma concentration of drug

70
Q

What is a two compartment model?

A

The compartmental modeling of pharmacokinetics consists in describing the fate of a drug in the body, depicted as an entity divided into compartments.

The drug leaves the site of administration (absorption) to enter a central compartment, from which it is both exchanged with peripheral compartments (distribution) and irreversibly eliminated (metabolism and excretion).

Movements of drug from one compartment to another can be characterised by transfer rate constants: in linear kinetics, the rate of transfer is assumed to be directly proportional to the amount of drug available for transfer.

In each compartment, characterised by its own volume, the drug concentrations are proportional to the amount.

Compartments, volumes and constants do not have a direct anatomical or physiological signification. A compartment involves several organs or tissues and is kinetically homogenous.

71
Q

How does the half-life of a drug determine isn’t steady state?

A

Half-life determines the length of the drug effect. It also indicates whether accumulation of the drug will occur under a multiple dosage regimen and it is essential to decide on the appropriate dosing interval.

Circa 5 half lives.

E.g. half life of lithium is 20-24 hours. Steady state is 5-6 days.

72
Q

Lithium has narrow therapeutic index.

Lithium levels much be monitored (blood test) to ensure it is within therapeutic window and not toxic.

A

<0.4 mmol/L: little therapeutic effect


  1. 4–1.0 mmol/L: optimum range for prophylaxis

  2. 8–1.2 mmol/l: optimum range for acute mania

  3. 2–1.5 mmol/L: causes possible renal impairment

  4. 5–3.0 mmol/L: causes renal impairment, ataxia, weakness, drowsiness, thirst, diarrhoea

  5. 0–5.0 mmol/L: causes confusion, spasticity, dehydration, convulsions, coma, death.

(Levels above 3.5 mmol/L are regarded as a medical emergency.)

73
Q

When a drug’s half-life is long and it will take a long time to achieve a steady state what can be done?

A

Give a loading dose.

In some situations, the steady state plasma concentration must be reached more rapidly. A higher dose can then be administered on treatment initiation, to compensate for accumulation.

74
Q

Large volume of distribution means?

A

That the drug is widely distributed outside the water compartment and is also protein bound or distributed by some other tissue type such as fat – in this case tissue binding in certain organs.

75
Q

Bioavailability definition

A

Definition : “Fraction of a dose of drug that is absorbed from its site of administration and reaches, in an unchanged form, the systemic circulation.”

When the drug is administered orally the bioavailability depends on several factors:

  • Physicochemical properties of the drug and its excipients that determine its dissolution in the intestinal lumen and its absorption across the intestinal wall.
  • Decomposition of the drug in the lumen.
  • pH and perfusion of the small intestine.
  • Surface and time available for absorption.
  • Competing reactions in the lumen (for example of the drug with food).
  • Hepatic first-pass effect.
76
Q

Anastrozole

A

Aromatase inhibitor

MoA: reversibly binding to the aromatase enzyme, and through competitive inhibition blocks the conversion of androgens to estrogens in peripheral (extragonadal) tissues.

Indication: Oestrogen receptor positive breast cancers AFTER menopause

Side effects: numbness, tingling of the hands, hot flashes, joint pain, sleep problems, N&V, hair thinning

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