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HYMS PPT > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

What immediate therapy would you initiate in a GI bleed?

A

IV fluid - 500mL IV crystalloid

containing up to 130-154mmol/L Na+

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2
Q

What is important to note about the amount of IV fluid administered?

A

Max 2L should be given in 1hr - don’t want to cause K+ overload.

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3
Q

What is the definitive investigation/ intervention for an upper GI bleed?

A

Endoscopy

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4
Q

What is the difference between the Blatchford and Rockall score?

A

Blatchford - Using clinical and lab data, distinguishes between high-risk and low risk-bleeds (can be used to decide who is eligible for endoscopy)

Rockall - predicts mortality for bleed following endoscopy

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5
Q

What agents can be used in a GI bleed?

A

Silver nitrate - cauterises
Adrenaline - causes vasoconstriction of vessels
Banding - blocks off bleed

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6
Q

What is pantoprazole?

A

Acid suppressive therapy with H2 receptor antagonist

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7
Q

Why are oral and IV PPIs used in GI bleeds?

A

Decreases:

  • Length of hospital stay
  • Re-bleed rate
  • Need for transfusion
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8
Q

What would you do with antihypertensives in a patient who has had a GI bleed?

A

Withhold them - they’d promote hypotension which doesn’t help their hypovolemia.

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9
Q

How would you manage long-term prescriptions in an acute situation?

A

Can withhold them for a few days because they won’t have the same long-term effect if the patient isn’t physiologically stable

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10
Q

What are the risk factors in the formation of GI ulcers?

A

H.pylori infection
NSAIDs
Stress
Excess gastric acid

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11
Q

How do aspirin and NSAIDs contribute to the development of peptic ulceration?

A

COX-1 acts as housekeeping for the mucosa in the upper GI tract; inhibiting it encourages mucosal damage

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12
Q

What factors influence development of ulcers by NSAIDs?

A
  • Duration
  • Dose
  • Increasing age
  • Past history of gastroduodenal toxicity from NSAIDs
  • Using steroids, anticoagulants, antiplatelets, bisphosphonates and SSRIs at the same time as NSAIDs
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13
Q

What investigations would you perform if you suspected H.pylori infection?

A

Biopsy urease testing = CLOtest

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14
Q

What is the rationale behind triple eradication therapy?

A

PPI suppressing acid

Dual antibiotic therapy to clear the infection

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15
Q

What interaction would you be wary of before prescribing clarithromycin in a patient with H.pylori infection?

A

Clarithromycin inhibits CYP3AP which would usually metabolise SIMVASTATIN -> accumulation of simvastatin

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16
Q

What advice/ warnings would you give a patient with H.pylori infection during their course of eradication therapy?

A

Avoid alcohol - has a disulfram type reaction with metronidazole

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17
Q

What is an investigative option for patients who cannot tolerate flexi sig?

A

Virtual colonoscopy

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18
Q

What are the drug therapies for ulcerative colitis following IV fluid treatment?

A
  • Budesonide (oral glucocorticoid in severe UC patients)
  • Sulfasalazine (5-ASA)
  • IV steroids in hospital
  • Fulminant disease - broad-spectrum antibiotics
  • VTE prophylaxis
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19
Q

When converting a patient from IV steroid to an oral steroid, which would you use?

A

Prednisolone (when swapping from hydrocortisone; they both exert gluco- /mineralocorticoid effects

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20
Q

What other pharmacological option should you consider if a patient continues with high dose oral steroids?

A

Topical 5-ASAs are first in line for those who are willing to use rectal therapy
Rectal suppositories/ enemas induce remission in 90% of patients with mild-moderate proctitis.

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21
Q

Besides steroids, what oral therapy should you commence in UC patients with the aim of reducing oral steroids?

A

Azathioprine

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22
Q

Why are corticosteroids better weaned off gradually?

A

Addisonian crisis

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23
Q

What is azathioprine’s mechanism of action?

A

Prodrug
Converted to 6-mercaptopurine via nucleophilic attack by sulfahydryl compounds in RBCs
Accumulates in tissues, inhibits purine (and therefore DNA/ RNA) synthesis
Inhibits T and B cells
Immunosuppression

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24
Q

What is infliximab?

A

Chimeric monoclonal antibody

TNFa blocker

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25
Q

What is infliximab’s mechanism of action?

A

Binds to TNFa

Interferes with inflammatory activity

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26
Q

What are the mechanisms of pain in a thoracotomy?

A

Damage to normal anatomical structures -> inflammation -> release of inflammatory & pain mediators -> spinothalamic stimulation -> projection to limbic system -> pain perception
Direct nerve injury

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27
Q

How might an anaesthetic traditionally/ classically reduce pain peri-operatively?

A

Opioids to target central mechanisms involved in pain perception

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28
Q

What are the side-effects of opioids?

A
  • Somnolence
  • Respiratory depression
  • Hypotension
  • Urinary retention
  • Nausea & vomiting (via CTZ)
  • Histamine release can cause prophylactic symptoms
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29
Q

If a patient were to develop opioid toxicity and experience a drop in respiratory rate, what would the treatment be?

A

Naloxone

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30
Q

What is naloxone’s mechanism of action?

A

Opioid competitive antagonist

31
Q

What does the term ‘competitive antagonist’ mean?

A

Drugs bind to receptor in a reversible way without activating the system

32
Q

How might pharmacology help in treating opioid induced constipation in palliative care patients on long term opioids?

A

Methylnaltrexone

It doesn’t cross the BBB so it maintains central analgesic effects without mediating peripheral ones (like constipation)

33
Q

Why do anaesthetics control pain peri-operatively using several agents?

A

Each agent can act at different sites of the pain pathway

Lessens dependence on a single medication and mechanism

34
Q

What is Bupivacaine’s mechanism of action?

A

Local anaesthetic

Disrupts ion channel function within the neurone cell membrane -> prevented transmission of action potential

35
Q

What is the mechanism of action for epidural opiates?

A

Directly binds to opioid receptors
Acts on the presynaptic nerve terminal to inhibit release of neurotransmitter.
Postsynaptic action (usually inhibitory)

36
Q

What is morphine’s mechanism of action?

A

Acts on muscarinic receptors, inhibits noradrenaline, acetylcholine and substance P (neuropeptide)

37
Q

Why are local anaesthetic and opioid administered by IV via epidural catheter for post operative pain?

A

Reduces the required dose

Reduces possible side effects

38
Q

What medication could you add during the operation if you had a concern about break through pain?

A

IV opiate

39
Q

Why do patients develop post operative nausea and vomiting?

A

Drugs & ingested toxins

Efferent impulses from medullary centres influence brainstem nuclei to initiate vomiting reflex

40
Q

What are the drug classes available for prophylaxis or rescue therapy for post operative nausea & vomiting?

A

Serotonin-R antagonists
Corticosteroids
Anticholinergic agents
Neurokinin-R antagonists

41
Q

What is ondansetron’s mechanism of action?

A

Suppresses initiation of nausea and vomiting by blocking 5HT peripherally at vagal afferents and centrally in the chemoreceptor trigger zone.

42
Q

What drug class does ondansetron belong to?

A

Selective serotonin-R (5HT3) antagonist

43
Q

Why is ondansetron most commonly used for post operative nausea and vomiting?

A

IV preparations are available

No sedative side effects

44
Q

Besides ondansetron, what other drugs can be used for post operative nausea and vomiting?

A

Hyoscine - Anti-ACh
Cyclizine - Anti-H1
Dexamethasone - steroid

45
Q

Despite being an antihistamine, why does terfenadine not have anti-emetic properties?

A

It does not cross the blood brain barrier.

46
Q

When is the antipsychotic prochlorperazine indicated as an anti-emetic?

A

Acute nausea and vomiting, e.g. acute gastroenteritis

47
Q

What is metoclopramide’s drug class?

A

Dopamine receptor antagonist

48
Q

Why is metoclopramide contraindicated in Parkinson’s patients?

A

Can cause Parkinsonian like symptoms, would exacerbate symptoms

49
Q

How do you manage a patient’s severe dystonic reaction after taking metoclopramide?

A

Procyclidine = first-line
Diazepam is an alternative treatment
Once metoclopramide has left the system, dystonia should resolve.

50
Q

What agents could you give to counteract opioid accumulation in the CTZ?

A 
Ondansetron
Metoclopramide
Domperidone
Paliperidone
Scopolamine
Aprepitant
51
Q

What is a common cause of hyponatraemia combined with hypokalaemia?

A

Vomiting

52
Q

Which anti-emetics are known to cause constipation?

A

Ondansetron
Prochlorperazine
Dexamethasone

53
Q

How do you add an opiate for breakthrough pain?

A

Rescue dose should be a sixth of the total 24 hour dose; adjusts based on how much was taken in the previous 24 hours

54
Q

What is apparent volume of distribution (Vd)?

A

Theoretical volume necessary to contain total amount of an administered drug at the same concentration as whatever’s in the plasma; reflection of distribution

55
Q

How would you calculate apparent volume of distribution?

A

Amount of drug in body
DIVIDED BY
Plasma concentration of drug

56
Q

What physicochemical properties affect apparent volume of distribution?

A

Solubility
Charge
Size

57
Q

What is a two compartment model?

A

A model which divides the body into a central compartment (1) and peripheral compartment (2).

58
Q

What is the role of the central compartment in the two compartment model?

A

Consists of plasma and tissues; drugs are administered to and distributed from this compartment. Usually linked to all the other compartments.

59
Q

What is the role of the peripheral compartment in the two compartment model?

A

The peripheral compartment consists of tissues and drug distribution is slower.

60
Q

Compared to a two compartment model, how does drug distribution differ in a single compartment model?

A

Drug distribution is considered instantaneous within a single compartment.

61
Q

What is the distribution phase?

A

The decrease in drug plasma corresponding with transfer of drug from the central to the peripheral compartment.

62
Q

What is the elimination phase?

A

Removal of drug from the central compartment

63
Q

In pharmacokinetics, why is the elimination phase longer than the distribution phase?

A

The drug must diffuse back from the peripheral compartment to the central one to be eliminated.

64
Q

If a drug’s volume of distribution approaches that of body water, what does this suggest about the drug’s distribition?

A

The drug must be predominantly distributed in body water

65
Q

How long do drugs typically take to reach steady state?

A

Approx 5 half-lives

66
Q

What action can you take to ensure that lithium (with a very narrow therapeutic index) doesn’t become toxic?

A

Measure blood levels 12 hours after a dose

67
Q

How do standard and modified release formulations affect bioavailability of the drug?

A

Modified release may increase bioavailability, therefore you’d need less of the drug for it do exert its therapeutic (and toxic) effects

68
Q

What is a loading dose?

A

Higher dose of drug is administered when the treatment starts.
Allows the drug to reach steady state concentration faster

69
Q

Why should dosing of digoxin be based on estimated lean body mass?

A

Digoxin has a large volume of distribution and has a high affinity for skeletal and cardiac muscles. Adipose tissue is NOT a reservoir for it.

70
Q

Tubular secretion of digoxin is mediated by p-glycoprotein (p-gp). What drugs are known to inhibit p-gp?

A

Spironolcatone
Quinidine
Verapamil
Amiodarone

71
Q

What factors affect the bioavailability of drugs taken orally?

A
  • Physicochemical drug properties
  • Decomposition of the drug in the gut lumen
  • pH and perfusion of the small intestine
  • Surface and time available for absorption
  • Competing reactions in the gut lumen (e.g. drug vs. food)
  • Hepatic first-pass effect
72
Q

When re-dosing drugs based on bioavailability, what do you do?
[Year 5 calculation]

A
  • Multiply current dose if old drug by the percentage change in bioavailability = dose of old drug with new drug’s bioavailability
  • Result divided by new bioavailability’s dose = concentration of drug to prescribe.
73
Q

How would you manage a patient with a GI bleed?

A

IV fluids - resuscitation
Transfusion of two units of cross-matched packed red cells
Endoscopy once haemo-dynamically stable

74
Q

Give an example of an opioid antagonist that does not cross the blood-brain barrier

A

Methylnaltrexone

HYMS PPT (4 decks)

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