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PPT Flashcards

1
Q

Example of Bulk forming laxative

A

Ispaghula Husk

Sterculia

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2
Q

Example of osmotic laxative

A

Lactulose
Macrogolis
Polyethylene Glycolis

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3
Q

Example of irritant and stimulant laxatives (act on enteric nerves):

A

Bisacodyl
Docusate Sodium
Senna

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4
Q

Example of faecal softeners

A

Co-danthrusate

Docusate Sodium

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5
Q

What laxatives are safe to use in pregnancy?

A

Senna
Magnesium salts
Docusate Sodium

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6
Q

What laxatives are good to use for the elderly or for terminally ill with opioid induced constipation?

A

Bisacodyl
Co-danthramer
Co-danthrusate

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7
Q

What drug can be used for opioid induced constipation when other laxatives are ineffective?

A

Methylnaltrexone - peripheral opioid receptor antagonist

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8
Q

What drug is specifically used to treat constipation in hepatic encephalopathy?

A

Lactulose

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9
Q

What drugs should be used in patients where constipation is due to neurological disease affecting motility?

A

Faecal softeners

Regular enemas or rectal washouts

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10
Q

What drugs can be used to treat IBS in general?

A

Antimuscarinic drugs:

  • Dicycloverine
  • Propantheline

Antispasmodic agents:

  • Mebeverine
  • Peppermint oil
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11
Q

What are the subtypes of IBS?

A

IBS-C - with constipation
IBS-D - with diarrhoea
IBS-M - when there’s both hard and loose stool over a short period of time
IBS-U - where bowel habits fluctuate problematically over a longer period of time

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12
Q

What drugs can be given to treat IBS-D

A

Loperamide
5-HT antagonists (Aloestron)
Bile acid sequestrants (cholestyramine)

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13
Q

What is the drug therapy for UC?

A
  • Aminosalicylates (Mesalazine, olsalazine, sulfasalazine)
  • Corticosteroids (hydrocortisone, prednisolone, budenoside)
  • Cytokine modulators (Adalimumab, infliximab)
  • Immunosuppressants (azathioprine, methotrexate)
  • Antibiotics (Metronidazole)
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14
Q

Examples if Anti-TNFa antibodies used in treating UC

A

Adalimumab, infliximab

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15
Q

Why are corticosteroids used in IBD, examples, what needs to be monitored for and side effects?

A

Used to induce remission, not for long-term therapy.

Examples: Prednisolone, dexamethasone, budesonide, IV hydrocortisone

Monitor for osteoporosis, Cushiingnoid features, hyperglycaemia, cataracts and glaucoma

SE: Infections, gastritis, diabetes, psychiatric effects, sleep disturbance, osteoporosis, growth suppression in children

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16
Q

Why are Aminosalicylates (5-ASAs) used in IBD, examples, what needs to be monitored for and side effects?

A

Not usually used as monotherapy for Crohn’s

Examples: Mesalazine, Sulfasalazine

Monitor mesalazine annually and sulfasalazine: FBC and LFT’s every 3 months

SE: Headache, can occasionally worsen UC

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17
Q

Examples of Immunosuppressants used in IBD treatment, things to monitor and side effects:

A

Examples: Azathioprine, mercaptopurine. methotrexate

Monitor FBC and LFTs every 3 months, U&Es every 6 month or 3 month for methotrexate

SE: Increased susceptibility to infections, sunburn, cervical abnormalities and lymphoma

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18
Q

Examples of Biological agents used in IBD treatment, things to monitor and side effects:

A

Infliximab, Adalimumab, Golimumab, Vedolizumab, Ustekinumab

Monitoring not done in 1* care but check for FBC, CRP, U&E, LFT every 3-6 months. Lipid profile and Hep B also checked periodically

SE: Injection site skin reaction, Increased susceptibility to infections including TB

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19
Q

What is the treatment for a UC flare in primary care when it is a left-sided disease or procititis?

A

Proctitis: Mesalazine suppository 1g nocte, Pentasa 1d suppository nocte

Left sided disease: Mesalazine foam enema 1-2g nocte, Pentasa liquid enema 1g nocte or Salofolk liquid enema 2g

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20
Q

What is the treatment for a UC flare in primary care when it is a Pancolitis or extensive disease?

A

Maximise oral 5-ASA (mesalazine)

Still symptomatic consider adding topical therapy:
Mesalazine foam enema 2g nocte, Pentasa liquid enema 1g
Or add Clipper 5mg (beclomethasone) OD for 28 days

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21
Q

IF UC flare hasn’t gotten better despite initial treatments what can be given in primary care?

A

Oral prednisolone 40mg OD for 7 days then 35mg OD for 7 days.

Reduce by 5 mg each week over 8 weeks

Remember GI and bone protection. Inform IBD team when steroids are given. Should not have more than 1 course a year without steroid sparing agents

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22
Q

How does Azathioprine work?

A

Prodrug that is quickly converted to 6-mercaptopurine via a nonenzymatic nucelophilic attack by sulfhydryl-containing compounds e.g. glutathione (present in RBC and tissues)

6-MP is then metabolised in the liver and gut by one of 3 enzymes.

2 serious drug interactions are ALLOPURINOL and FEBUXOSTAT which slow elimination of 6-MP by inhibiting xanthine oxidase

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23
Q

How does Infliximab and Adalimumab work?

A

Infliximab is a chimeric antibody

  • 75% human and 25% murine sequences
  • High specificity for TNF-a
  • Neutralises biological activity of TNF-a by inhibiting binding to its receptors and can also stimulate apoptosis of activated lymphocytes in gut mucosa

Adalimumab:

  • recombinant fully human monoclonal antibody
  • binds to TNF-a and interferes with subsequent cytokine-driven inflammatory processes
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24
Q

When can elevated TNF-a levels be found and what is its role?

A

In patients with Rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis, plaque psoriasis, Crohn disease and UC.

Activities of TNF-a include:
~ Induction of pro-inflammatory cytokines (interleukins)
~ Enhancement of leukocyte migration
~activation of neutrophils and eosinophils
~induction of acute phase reactants and tissue degrading enzymes
~can cause polyarthritis

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25
Q

In what patients would a more empiric antibiotic treatment be required?

A
  • Severe disease (fever, more than six stools per day, volume depletion warranting hospitalization).
  • Features suggestive of invasive bacterial infection, such as bloody or mucoid stools (except in cases of non-severe disease when fever is low or absent).
  • Host factors that increase the risk for complications, including age >70 years old and comorbidities such as cardiac disease and immunocompromised patients.
26
Q

What is Fidaxomicin?

A

Fidaxomicinis a relatively new drug which was originally discovered in actinomycetes. It inhibits bacterial RNA polymerase. It is not used to treat systemic infections as it is poorly absorbed from the gut, but has a role in treatingC. difficileinfections.

27
Q

What is Vancomycin?

A

Vancomycinis a glycopeptide antibiotic similar to teicoplanin – also used to treat MRSA.

28
Q

Describe the pain pathway:

A

Tissue injury -> release of inflammatory mediators -> nociceptor stimulation.

Pain impulses are then transmitted to the dorsal horn of the spinal cord -> make contact with second-order neurons that cross to the opposite side of the cord and ascend via the spinothalamic tract to the reticular activating system (RAS) and thalamus.

The localization and meaning of pain occurs at the level of the somatosensory cortex.

29
Q

What is the classical model for central pain sensation in surgical trauma?

A

The transmission of incoming nociceptive impulses is modulated by dorsal horn circuitry that receives input from peripheral touch receptors and from descending pathways that involve the limbic cortical systems (orbital frontal cortex, amygdala, and hypothalamus), periaqueductal endogenous analgesic center in the midbrain, pontine noradrenergic neurons, and the nucleus raphe magnus (NRM) in the medulla.

30
Q

How might the anaesthetist traditionally reduce pain peri-operatively?

A

Traditionally, management has relied solely on opioids. Morphine is the prototype opioid.

Better approach is a multinodal analgesia (acts at different sites of pain pathway).

  • Pain receptor activity directly blocked e.g. lidocaine
  • Anti-inflammatory agents e.g. NSAIDS
  • Inhibit neurotransmitters like Substance P, glutamate, asparate, GABA and calcitonin gene-related peptide e.g. ketamine, clonidine, gabapentin, paracetamol, pregabalin
31
Q

What are the acute side-effects of opioids?

A

~Somnolence (drowsiness)
~Depression of brainstem control of respiratory drive
~Hypotension (more common in hypovolaemic pts follow rapid injection)
~Urinary retention
~Confusion, hallucinations
~Difficulty urinating and dry mouth
~N & V due to direct stimulation of chemoreceptor trigger zone

Histamine release often follows morphine admin and may cause flushing, tachycardia. hypotension, pruritus and bronchspasm

GI transit slows with prolonged admin resulting in constipation

32
Q

If the patient developed significant opioid toxicity and experience a marked drop in respiratory rate what would your treatment be?

A

Naloxone

Competitive antagonist of opioids and has a shorter half life than most opioids

33
Q

What is the difference between competitive and non-competitive antagonists?

A

Competitive antagonists are drugs that bind to the receptor in a reversible way without activating the effector system for that receptor.
The log dose-response curve is shifted to higher doses (ie, horizontally to the right on the dose axis) but the same maximal effect is reached.

Irreversible antagonist causes a downward shift of the maximum, with no shift of the curve on the dose axis unless spare receptors are present (Figure 2-5B). The effects of competitive antagonists can be overcome by adding more agonist. Irreversible antagonists cannot be overcome by adding more agonist.

Competitive antagonists increase the ED50; irreversible antagonists do not (unless spare receptors are present).

34
Q

How does local anaesthesia work?

A

Local anaesthetics disrupt ion channel function within the neurone cell membrane preventing the transmission of the neuronal action potential. This is thought to occur via specific binding of the local anaesthetic molecules (in their ionised form) to sodium channels, holding them in an inactive state so that no further depolarisation can occur.

Examples: Bupivacaine

35
Q

How do epidural opiates work?

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. For example, presynaptic inhibition of neurotransmitter release may result in excitatory effects in a target neuron if the neurotransmitter normally produces an inhibitory effect. However, if the opioid also has a postsynaptic inhibitory effect on the target neuron, the excitatory effects may not occur. Thus, the location and density of opioid receptors on a neuron determines the overall effect of opioids on the neuron.

A combination of a local anesthetic and opioid is commonly administered by infusion via an epidural catheter for postoperative pain, especially for abdominal and thoracic surgical procedures. This combination reduces the dose required and the frequency of side effects.

Goal is to establish the appropriate analgesic level at least 30 minutes before the end of surgery.

36
Q

How does morphine work epidurally?

A

Morphine, by an action on m receptors, inhibits release of noradrenaline, acetylcholine and the neuropeptide, substance P. The opioid drugs produce analgesia by actions at several levels of the nervous system, in particular, inhibition of neurotransmitter release from the primary afferent terminals in the spinal cord and activation of descending inhibitory controls in the midbrain.

37
Q

What is Acetaminophen?

A

Paracetamol

38
Q

Examples of multi-nodal analgesia that can act on brain, descending modulation, transmission at dorsal horn, transmission at peripheral nerves and transduction at nociceptors?

A

Brain: Opioids, Alpha-2 agonists, SSRIs, SNRIs, TCAs

Descending modulation: TCAs, SSRIs, SNRIs

Dorsal root transmission: LAs. alpha-2 agonists

Peripheral nerve transmission: LAs, opioids

Nociceptors: LAs. Anticonvulsants, NSAIDS, ASA, nitrate, capsaicin, paracetamol

39
Q

Physiology behind nausea and vomiting:

A

Primarily controlled by the vomiting centre (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.

40
Q

What drug classes can be given as prophylaxis for post-operative nausea and vomiting?

A

Serotonin-receptor antagonists, corticosteroids, anticholinergic agents, and neurokinin-receptor antagonists.

41
Q

What is Ondansetron and why is it used for PONV?

A

Selective serotonin-receptor (5-HT3) antagonists

Used for PONV because they do not have sedative side effects and intravenous preparations are available. They can be used prophylactically (4mg IV) or for rescue treatment (1mg IV) of PONV.

They suppress the initiation of nausea and vomiting by blocking serotonin peripherally at vagal afferents and centrally in the chemoreceptor trigger zone

Can get dose dependent QT prolongation.

42
Q

Example of a glucocorticoid, anticholinergic and neurokinin-receptor antagonist that can be used for PONV and their doses:

A

GC: Dexamethasone

  • Preventative (IV 4 mg)
  • No QT prolongation
  • no increase in periop hyperglycaemia or wound infections

AC: Scopolamine

  • Preventative (1.5 mg patch)
  • Sedating
  • Don’t use in patients with narrow angle glaucoma

NRA: Aprepitant

  • Blocks neurokinin’s effect at receptor site
  • Preventative (40mg PO 3 hours pre-surgery)
  • Expensive
43
Q

What is the treatment for acute dystonia?

A

Procyclidine Hydrochloride
- Parenterally given and is first line treatment in AD
- Response is often dramatic and occurs in 5-20 mins
- second dose given if symptoms persist after 30 mins
- Adults: 5-10 mg slow IV injection or IM
Child 1 month -1 year: 0.5-2mg
Child 2-9 years: 2-5 mg
Child 10-17 years: 5-10mg
Usually effective in 5-10 mins but may need 30 mins for relief

44
Q

What % of glucose containing IV fluid therapy is isotonic?

A

5% glucose

45
Q

What anti-emetic would be useful in giving to patients that also need an opioid but have bowel obstruction

A

Dopamine antagonist, such as prochlorperazine or metoclopramide – but metoclopramide a pro-kinetic could worsen colic when there is bowel obstruction

Haloperidol 1.5 mg at night could be used and carefully titrated up and is effective in opiate induced vomiting.

A serotonin receptor antagonist e.g. ondansetron but - Chronic use of the serotonin receptor antagonists causes constipation, which in itself can be a cause of nausea.

46
Q

How often should oromorph be given for breakthrough pain?

A

Given every 4 hours and the dose titrated up to effect

47
Q

How is the rescue dose of oromorph calculated?

A

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

48
Q

What is pharmacodynamics?

A

Concentration of drug at the site of action and the biochemical and physiological effec

49
Q

What is apparent volume of distribution?

How is it calculated?

A

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

𝑉𝑑=(𝐴𝑚𝑜𝑢𝑛𝑡 𝑜𝑓 𝑑𝑟𝑢𝑔 𝑖𝑛 𝑏𝑜𝑑𝑦)/(𝑃𝑙𝑎𝑠𝑚𝑎 𝑐𝑜𝑛𝑐𝑒𝑛𝑡𝑟𝑎𝑡𝑖𝑜𝑛 𝑜𝑓 𝑑𝑟𝑢𝑔)

50
Q

What is the compartment model?

A

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

51
Q

In the compartment model, what is meant by the distribution and elimination phase?

A

The transfer from the central compartment to the peripheral compartment can be quite fast, and the corresponding rapid decrease in the drug plasma concentration is called the distribution phase.

The second phase is the elimination phase, which is longer, because the drug must first diffuse back from the peripheral compartment to the central compartment in order to be eliminated.

52
Q

What does a small Vd suggest?

A

Predominantly distributed in body water

53
Q

Drugs to treat oral and oesophageal candidiasis

A

Nystatin

Fluconazole

54
Q

Drugs for Protozoal and C.Diff infections

A

Vancomycin

Metronidazole

55
Q

Drugs for treating GI Helminthic infections

A

Ivermectin

Albendazole

56
Q

Which anti-diarrhoeal won’t cause BBB?

A

Loperamide

Acts as an opioid without all its effects

57
Q

Whats our first definitive investigation choice in a patient with general abdo tenderness, blood and slime in poo, 8 week history of diarrhoea and no illness.

A

Flexible sigmoidoscopy

If there was inflammation a colonoscopy could perforate it

58
Q

What are patients tested for before being given Azathioprine?

A

TPMT tested for in every patient given azathioprine as some people are genetic polymorphisms which mean some peopel can have lower amounts of it and will not metabolise 6-MP well. This will cause toxicity in the patients

59
Q

What can prolonged treatment with PPIs cause?

A

Hypomagnesaemia

This can lead to ventricular arrhythmia

60
Q

What are the adverse effects of PPI’s

A

Hyponatraemia, hypomagnesaemia
Osteoporosis
Microscopic colitis
Increased risk of C diff infections

GI (10 decks)

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