GI & Surgery Flashcards

1
Q

How do NSAIDS contribute to mucosal injury + peptic ulcer disease

A

normal function is to provide pain relief by inhibition of COX-2 enzymes as in inhibits synthesis of pro-inflammatory markers

as they are non selective they also inhibit COX-1 which normally is responsible for mucus secretion and promotes platelet aggregation which protects the mucosa. this is not done when NSAIDs are taken over a long period of time

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2
Q

what test is done for H.pylori

A

CLO test/ rapid urease test

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3
Q

what is triple therapy for eradication of h.pylori

A

1) lasoprazole

2) clarithromycin/amoxicillin

3) metronidazole

for 7 days

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4
Q

what common antibiotic has an interaction with statins

A

clarithromycin as it inhibits CYP3A4 meaning there are increased levels of statin increasing risk of rhabdomyolysis + myopathy

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5
Q

what drugs fall under class of alginates and antacids

A

Magnesium trisilicate
Aluminium/magnesium mixtures (Maalox)

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6
Q

what are indications for antacids + alginates

A

dyspepsia
GORD

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7
Q

what drugs fall under H2 receptor antagonists

A

ranitidine
famotidine

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8
Q

indications for H2 antagonists

A

dyspepsia, GORD, peptic ulceration, prophylaxis of NSAID associated peptic ulceration

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9
Q

examples of PPIs

A

omeprazole
lansoprazole
pantoprazole

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10
Q

indications for PPIs

A

dyspepsia, GORD, oesophagitis, peptic ulceration, prophylaxis of NSAID associated peptic ulceration, H. pylori eradication

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11
Q

management of GORD

A

PPIs (First-line for moderate to severe GORD): Omeprazole, Esomeprazole
H2 Receptor Antagonists (Mild cases): Ranitidine, Famotidine
Antacids & Alginates: Gaviscon for symptom relief
Prokinetics (Adjunct in refractory cases): Domperidone, Metoclopramide

Non-Pharmacological Approaches:

Weight loss if overweight
Elevate head of bed while sleeping
Avoid lying down after meals (wait at least 3 hours)
Reduce intake of acidic, spicy, fatty foods, caffeine, and alcohol
Smoking cessation

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12
Q

management of PUD

A

Proton Pump Inhibitors (PPIs): Omeprazole, Pantoprazole, Esomeprazole (first-line)
H2 Receptor Antagonists (H2RAs): Ranitidine (less commonly used)
Antacids: Aluminum hydroxide, Magnesium hydroxide (for symptom relief)
Cytoprotective Agents: Sucralfate, Bismuth subsalicylate
H. pylori Eradication (if present): Triple or quadruple therapy (see below)

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13
Q

what meds fall under bulk forming laxatives

A
  • isphagula husk
  • methylcellulose
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14
Q

what are osmotic laxatives

A

lactulose
macrogols
movicol
milk of magnesia/ Mg (OH)2

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15
Q

what are irritant and stimulant laxatives

A

bisacodyl
senna
sodium picosulfate

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16
Q

what are faecal softeners laxatives

A

co-danthrusate
docusate

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17
Q

how do bulk-forming laxatives work

A

absorb water in the intestine increasing th estool bulk and softness promoting peristalsis

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18
Q

what drug is used in hepatic encephalopathy

A

lactulose

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19
Q

what drug is used in bowel prep

A

PEG polyethylene glycol

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20
Q

which laxatives are used for opioid induced constipation

A

stimulants which stimulate the enteric nerves to increase intestinal motility

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21
Q

how to stool softeners work

A

decrease stool surface tension allowing water and fats to mix with stool

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22
Q

which laxatives are safe in pregnancy

A

senna
magnesium salts
lactulose
docusate

  • codanthramer + codranthusate are carcinogenic so dont use
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23
Q

for those with neurological disease affecting bowel motility which laxative should be used

A

faecal softeners

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24
Q

which anti-diarrhoeal drugs are used

A

codeine phosphate

loperamide

diphenoxylate

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25
what other drugs can be used in treatment of IBS
mebeverine hyoscine butylbromide (buscopan) peppermint oil
26
what drugs are used in UC
Aminosalicylates – mesalazine, olsalazine, sulfasalazine Corticosteroids – hydrocortisone, prednisolone, budesonide Cytokine Modulators – adalimumab, infliximab (Anti-TNFα antibodies) Antimetabolites – azathioprine, methotrexate Antibiotics – metronidazole
27
what are significant SE of steroids
systemic infections gastritis diabetes HF osteoporosis growth suppression in children
28
management of UC flare: proctitis or left sided disease
mesalazine suppository mesalazine enema budesonide enema oral 5ASA max dose
29
management of pancolitis/extensive disease
max oral 5 ASA + topical therapy + oral steroids Pred
30
what two drugs react seriously with azathioprine
allopurinol febuxostat slow elimination of 6MP
31
MOA of infliximab
Infliximab is a chimeric monoclonal which has a high specificity for and affinity to tumor necrosis factor (TNF)-alpha. Infliximab neutralizes the biologic activity of TNF-alpha by inhibiting binding to its receptors. Infliximab can also stimulate apoptosis of activated lymphocytes in the gut mucosa
32
MOA of adalimumab
Adalimumab is a recombinant fully human monoclonal antibody that binds to TNF-alpha, thereby interfering with binding to TNF-alpha receptor sites and subsequent cytokine-driven inflammatory processes.
33
drawbacks of using empiric antibiotic therapy for acute infective diarrhoea in developed countries
SE bacterial resistance eradication of normal flora (ABA colitis and increased risk of C.diff) cost-effectiveness
34
what drugs are used for C diff diarrhoea
oral vancomycin fidoxamin IV metronidazole
35
what are the side effects of chemotherapy
GI = diarrhoea, N+V BM = myelosupression, --> anaemia, neutropenia and thrombocytopenia Alopecia infertility tumour lysis syndrome = Rapid breakdown of malignant cells can cause hyperuricaemia, hyperkalaemia, hyperphosphatemia, hypocalcaemia (due to the former) with consequent renal damage / arrhythmias.
36
MOA of capecitabine
- anti-metabolites is a pro-drug of fluorouracil interferes with DNA synthesis stops cells from making + repairing DNA (pyrimidine antagonist)
37
how is capecitabine taken
oral twice a day for 14 days
38
Oxaliplatin class and MOA
platinum based chemo drug MOA - causes DNA crosslinking which inhibits replication and transcription --> inhibition of DNA synthesis --> apoptosis (binds to guanine) induces both interstrand and intrastrand cross links unlike cisplatin often used in CRC cancer alongside fluorouracil and leucovorin gastroesophageal pancreatic
39
common SE of oxaliplatin
N+V, nephrotoxic, ototoxic, peripheral neuropathy and myelosuppression Neuropathy (Peripheral Neuropathy) – cold-induced paresthesia, chronic sensory neuropathy Nausea and vomiting Myelosuppression – neutropenia, thrombocytopenia, anemia Diarrhea Fatigue Hypersensitivity reactions – can cause anaphylaxis in some cases Hepatotoxicity – sinusoidal obstruction syndrome Acute laryngopharyngeal dysesthesia – sensation of throat tightness when exposed to cold
40
other plantinum compounds and uses
oxiplatinin cisplatin carboplatin used for solid malignancy cisplatin and carboplatin for ovarian and lung tumours SCLC + NSCLC
41
class of anastrozole + MOA
class = aromatase inhibitor inhibits aromatase enzyme which converts androgens into oestrogens. so decreased oestrogen deprives tumour of it however due to lower levels of oestrogen the SE are like menopause and osteoporosis
42
what is stevens johnson syndrome
Severe skin reaction, mucous membranes frequently involved Blisters, fever, flu-like symptoms If left untreated can progress to sepsis, multi-organ failure and death
43
what is tamoxifen and MOA
selective estrogen receptor modulator (SERM) Acts as an estrogen receptor antagonist in breast tissue, blocking estrogen's ability to promote cancer growth. Acts as an estrogen receptor agonist in other tissues, such as the bone, uterus, and liver, which contributes to some of its side effects. regimen = 20mg once a day for 5 years side effects = menopausal, VTE and stroke (so contraindicated in Fhx of vte or genetic predisposition)
44
tamoxifen drug interactions
SSRIs thought to reduce action of tamoxifen warfarin: tamoxifen inhibits CYP3A4 so increases risk of bleeding
45
stages of chemotherapy
Induction (of remission) – intensive IV treatment including intrathecal treatment, aimed at destroying as many leukaemia cells as possible and achieving remission (no leukaemia cells on bone marrow biopsy). Lasts 4-6 weeks, 3-4 agents (see next slide). Consolidation (of remission) – 3-4 months- aimed at remission and preventing spread. Often involves intrathecal injections (methotrexate) and then tablets. Maintenance (of remission) – lasts 1-3 years. Involves regular tablets and possible injections. Often 6-MP and weekly PO methotrexate
46
hyper CVAD regime
cyclophosphamide vincristine doxorubicin dexamethasone
47
why are several combinations of drugs used in chemo
Combinations of chemotherapy drugs are often used as this exploits multiple mechanisms of action and efficacy at different stages of the cell cycle. Combination treatments can result in enhanced response and reduced development of drug resistance.
48
cyclophosphamide
- alkylating agent used in breast cancer, lymphomas, leukemias, and sarcomas. Alkylates DNA, forming covalent bonds with DNA bases, leading to DNA cross-linking. --> inhibits rep and trasncription --> apoptosis
49
SE of cyclophosphamide
Bone marrow suppression and neutropenia Can develop other malignancies e.g.: Acute Myeloid leukaemia, Bladder cancer (risk reduced by giving Mesna (mercaptoethane sulphonic acid) prior to treatment) Haemorrhagic cystitis Impaired fertility lifelong Hair loss, GI upset (pre-medication with anti-emetic)
50
vincristine MOA
Member of the Vinca Alkaloids Miotic inhibitors Binds to tubulin molecules and prevent the formation of microtubules, preventing chromosome separation Leads to cell death Sensory and motor neuropathies are common and cumulative.
51
doxorubicin
- is a cytotoxic antibiotic (anthracycline) Inhibits topoisomerase II, an enzyme that unwinds DNA during replication. This results in the accumulation of DNA breaks.
52
SE of doxorubicin
dilated cardiomyopathy myelosuppression NV alopecia red urine
53
methotrexate
Folic acid antagonist Antimetabolite DMARD used in rheumatoid arthritis, psoriasis etc Other uses include molar or ectopic pregnancy Renal excretion Hepatotoxic/cirrhosis, pneumonitis, photosensitivity and ulceration (plus usual myelosuppression, GI toxicity of other chemotherapies)
54
Define hyperalgesia and allodynia in the context of pain management.
Hyperalgesia is an increased sensitivity to painful stimuli, while allodynia is the perception of pain from non-noxious stimuli, often resulting from tissue trauma and the release of inflammatory mediators.
55
Describe the pathway of pain impulses in the spinal cord.
Pain impulses are transmitted to the dorsal horn of the spinal cord, where they contact second-order neurons that cross to the opposite side and ascend via the spinothalamic tract to the reticular activating system (RAS) and thalamus.
56
Do pain pathways involve modulation, and if so, how?
The transmission of nociceptive impulses is modulated by dorsal horn circuitry that receives input from peripheral touch and nociceptors, as well as from descending pathways involving the limbic cortical systems and other brain regions.
57
Define common side effects of opioids.
constipation, urinary retention, nausea, pruritis/urticaria, sedation, and respiratory depression.
58
List less common side effects of opioids.
Less common side effects of opioids include delirium, confusion, myoclonus/muscle rigidity, hallucinations, hyperalgesia, flushing/sweating, dry mouth, sexual dysfunction, hypotension, biliary/ureteric spasm, difficulty with micturition, and visual disturbance.
59
What treatment is indicated for significant opioid toxicity with reduced respiratory rate?
Naloxone
60
Explain the term 'competitive antagonist' in relation to naloxone.
A competitive antagonist, like naloxone, reduces the potency of an agonist by competing for the same binding site, but high concentrations of the agonist can still produce a maximal response.
61
Does naloxone have a short half life and if yes what does this mean in clinical practice
A shorter half-life means that naloxone may need to be administered multiple times or monitored closely, as its effects may wear off before the effects of the opioid have fully dissipated.
62
Explain how the limbic system is involved in pain perception.
The limbic system, including structures like the orbital frontal cortex and amygdala, provides emotional context to pain perception and can modulate the experience of pain.
63
Describe the concept of multimodal analgesia in pain management.
Multimodal analgesia is an approach to pain management that utilizes a combination of different medications and techniques to control pain effectively, targeting various pain pathways to enhance analgesic effects and reduce the need for opioids.
64
best med for breakthrough pain
strong short acting opioid - buccal fentanyl?
65
How can postoperative nausea and vomiting (PONV) be treated according to the content?
ondansetron is a 5HT3 receptor antagonist at both peripheral and chemoreceptor trigger zone
66
what other classes of drugs can be used for PONV
1) dexamethasone as preventative 2) anticholinergics like scopolamine as a preventative patch 3) neurokinin receptor antagonists like aprepitant as preventative. * is expensive 4) metoclopramide D2 antagonist
67
adverse effects of metoclopramide
1) extrapyramidal effects like acute dystonia (oculogyric crisis) 2) diarrhoea 3) hyperprolactinemia 4) tardive dyskinesia 5) parkinsonism
68
what drug is used in acute dystonia
procyclidine
69
To be able to formulate a basic management plan and identify drugs (and nonpharmacological approaches) indicated for the management of an adult patient with drug- induced (especially opiate) vomiting.
- ondansetron = gold standard - Anti-histamines like promethazine - anti-cholinergics like scopolamine if N persistent - D2 antagonists like metoclopramide Non-Pharmacological Approaches Dose adjustment or switching opioids (e.g., morphine to fentanyl) to reduce nausea. Hydration and electrolyte balance – IV fluids if vomiting is severe. Ginger or acupressure – complementary therapy.
70
First lines for motion sickness
1) hyoscine butylbromide 2) anti-histamines like cinnarazine and cyclizine more sedating = promethazine Avoid reading and focus on the horizon. Sit in the front seat of a car or near the wings of a plane. Fresh air and hydration. Acupressure wristbands (P6 stimulation).
71
PONV TREATMENTS
1) ondansetron 2) metoclopramide 3) dexamethasone 4) scopolamine 5) aprepitant
72
cytotoxic N+V treatment
in acute phase use ondansetron after or dexa/aprepitant before chemo in delayed phase also use aprepitant and dexa Non-Pharmacological Approaches Dietary modification – small, bland meals. Psychological techniques – guided imagery, relaxation therapy. Ginger, acupuncture – adjunct therapies.
73
pregnancy related N+V treatment
non pharm: - rest, oral hydration and dietary changes - ginger - chlorpromazine - cyclizine -doxylamine with pyridoxine - metoclopramide - ondansetron
74
Explain the types of IV fluids that are isotonic.
0.9% sodium chloride and compound sodium lactate (Hartmann’s solution). 5% glucose (initially isotonic but becomes hypotonic)
75
Define hypertonic glucose solutions and provide examples.
Hypertonic glucose solutions are those with higher concentrations of glucose, such as 10% glucose, 20% glucose, and 50% glucose.
76
How does the NICE guideline recommend managing IV fluid therapy?
The NICE guideline recommends using 0.9% sodium chloride, compound sodium lactate (Hartmann’s), and 5% glucose, with or without KCl.
77
Fluid regime for maintenance
Balanced crystalloid (first-line): Plasma-Lyte 148 or Hartmann’s solution (Ringer’s lactate) Alternatives (if no balanced crystalloids available): 0.18% NaCl + 4% glucose + 27 mmol/L KCl at 25–30 mL/kg/day 5% dextrose with KCl if sodium levels are normal Typically 1,000 mL over 8–12 hours, adjusted based on patient condition.
78
fluid regime for resus
in hypovolemia/shock First-line fluid: Balanced crystalloid (Hartmann’s or Plasma-Lyte 148) at 500 mL IV over 15 minutes. Repeat up to 2 L if needed (reassess after each bolus). 0.9% Normal Saline (NS) if no balanced crystalloids are available.
79
fluid regime in hypokalemia
Step 1: Identify & Correct the Cause Common causes: Diuretics (loop/thiazides), diarrhea, vomiting, alkalosis, insulin therapy, magnesium deficiency. Step 2: Choose the Correct IV Potassium Replacement Mild (K⁺ 3.0–3.5 mmol/L, asymptomatic): Oral KCl 40–80 mmol/day (preferred if patient can tolerate oral intake). Moderate (K⁺ 2.5–3.0 mmol/L, symptoms present): IV KCl 20–40 mmol in 1,000 mL of 0.9% NaCl over 4–6 hours. Severe (K⁺ <2.5 mmol/L, ECG changes, severe symptoms): IV KCl 20 mmol in 100 mL 0.9% NaCl over 1 hour (via central line if rapid correction is needed). Maximum rate: Peripheral IV: 10 mmol/hr. Central line: 20 mmol/hr (requires cardiac monitoring). Check Mg²⁺ levels – replace if low (Mg²⁺ is necessary for K⁺ retention).