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IMED3112 > GI Pharmacology > Flashcards

GI Pharmacology Flashcards

1
Q

4 causes of vomiting?

A
  1. Gastrointestinal
  2. Chemical irritation
  3. Vestibular
  4. CNS
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2
Q

4 main sources of afferent input for vomiting?

A
  1. Chemoreceptor trigger zone stimulated from blood or drups as outside BBB (opiods, dopamine, histamine, serotonin
  2. Vestibular system - motion sickness via CN.VIII, muscarinic and histamine receptors
  3. Vagal and spinal nerves from GI tract - 5-HT3 receptor rich
  4. CNS - raised intracranial pressure, anxiety, stress
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3
Q

What is nausea and which motor impulses trigger it?

A

Nausea is conscious recognition of excitation in area close to vomiting center and caused by motor impulses originating from vomit center
Action: CN V, VII, IX, X, XII to upper GI cause mouth to open, tongue out the way then vagal and sympathetic to lower GI and spinal nerves to diaphragm and abdominal muscles

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4
Q

5 drugs targeting CTZ, action, side effects, who should NOT use it?

A
  1. Metoclopramide - enhances response to Ach to enhance motility and gastric emptying and blocks dopamine
    S/E - extrapyramidal (inability to sit still, involuntary muscle movements, tremors, stiff muscles, involuntary facial movements)
    Adverse - Parkinson’s
  2. Prochlorperazine - dopamine and muscarinic receptor antagonism
    S/E - extrapryamidal, increased risk of arrhythmia, irritation if SC
    Adverse - Parkinson’s
  3. Domperidone - peripheral dopamine antagonism blocking dopamine in GI increasing motility
    S/E - well tolerated as doesn’t cross BBB but increases prolactin levels
  4. Aprepitant - highly selective neurokinin receptor antagonism crossing BBB blocking effects at spinal and nerve level
    S/E - fatigue, dizziness, diarrhoea
  5. Cyclizine - histamine antagonist with muscarinic effects
    S/E - tremulousness, hallucinations, drowsiness, dry mouth
    Useful for motion sickness or brain metastasis
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5
Q

Drug targeting vestibular system, action, side effects, who should NOT use it?

A
  1. Hyoscine - anticholinergic at muscarinic receptors with minor histamine and 5HT3 antagonism
    S/E - high incidence of anticholinergic (dry mouth, blurred vision, tachy, confusion, urinary retention)
    Useful for motion sickness
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6
Q

Drug targeting vagal and spinal nerves, action, side effects, who should NOT use it?

A
  1. 5HT3 antagonists - Ondansetron, Palonosetron - peripheral and central actions of blocking serotonin release in upper GI and most useful in gut irritation causes
    S/E - constipation, headache, fatigue
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7
Q

2 drugs targeting CNS, action, side effects, who should NOT use it?

A
  1. Dexamethasone - glucocorticoid steroid reducing peri-tumoural oedema in cases of raised intracranial pressure secondary to tumour
    S/E short - increased blood sugar, hunger, BP, irritability
    S/E long - osteoporosis, steroid induced diabetes, thin skin
  2. Lorazepam - used for anticipatory associated with chemo by binding to benzodiazepine receptors in CNS
    S/E - sedation, dizziness, unsteadiness
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8
Q

Safest drug for children with nausea?

A

Ondansetron (5HT3 antagonist)

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9
Q

Safest drugs for pregnancy (2) and which causes harm?

A

Safe - metoclopramide, pyridoxine
Unsafe - Prochlorperazine

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10
Q

8 complications of obesity?

A
  1. T2D
  2. CVD
  3. HT
  4. Cancer
  5. Fatty liver disease
  6. Osteoarthritis
  7. Sleep apnoea
  8. Gallstones
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11
Q

Hormones that affect body weight (4) and secreted by what?

A
  1. Leptin - satiety hormone decreasing appetite secreted by adipocytes when full
  2. Ghrelin - hunger hormone stimulating appetite secreted by stomach
  3. Insulin - secreted by pancreas
  4. Incretins - satiety hormone decreasing appetite (GLP-1, GIP) secreted by SI
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12
Q

Brown adipose tissue vs white adipose tissue role?

A

BAT - heat producing
WAT - energy storage with excess triglyceride stores. Visceral WAT worse than subcutaneous WAT as its surrounding organs and associated with metabolic disorders

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13
Q

Diagnosis of metabolic syndrome?

A

Any 3 of the 5
1. Visceral obesity
2. High fasting glucose
3. High triglycerides
4. Low HDL cholesterol
5. High BP

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14
Q

4 treatment options for obesity?

A
  1. Lifestyle - diet, exercise, behavioral therapy, counselling to reduce food consumption and increase energy expenditure
  2. Pharmacology - Orlistat which is a pancreatic and gastric lipase inhibitor which decreases nutrient absorption OR incretin based therapies - GLP receptor agonist to increase satiety
  3. Bariatric surgery - physical restriction of food intake and changed in GLP (Vertical sleeve or Roux-en-Y Gastric bypass
  4. Prevention at community level
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15
Q

Explain the negative feedback loop of acid production in the stomach and a bacteria that affects it?

A
  1. G cells produce gastrin which stimulates parietal cells
  2. Parietal cells produce H+ into stomach
  3. Antrum sensor organ senses when enough acid in stomach and stimulated D cells
  4. D cells produce somatostatin which inhibits G cells which inhibits H+ production
    Helicobacter pylori turns off this feedback loop so acid continually produced causing peptic ulcers and ulcerative oesophagitis.
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16
Q

What does bismuth do?

A

Antibacterial agent shown to kill H. pylori and heal ulcers

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17
Q

Where does cancer develop due to H. pylori and why? Treatment?

A

H. pylori can survive on normal surface mucosa but not on intestinal metaplasia in stomach so no cancer in intestinal metaplasia regions. Cancer develops on edge on intestinal islands with local effect of cell that H. pylori is attached to
Treatment - amoxycillin, clathromycin

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18
Q

What are the 3 types of antacids?

A
  1. Gaviscon granules - floats on stomach contents and prevents reflux without damaging mucosa
  2. Antacid tablet - ‘quick eze’ chewed and left in oesophagus for quick relief
  3. Mucosal protective agent - thickens and strengthens mucus to protect from erosion (bismuth)
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19
Q

What is the role of H2 receptor antagonist in acid secretion? Examples? (2)

A

They are competitive inhibitors preventing histamine action on parietal cells therefore reducing acid secretion
1. Cimetidine - also inhibits CYP450 system so metabolism of other drugs affected
2. Ranitidine - hepatic metabolism and renal excretion with occasional CNS symptoms

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20
Q

Role of proton pump inhibitor in acid secretion? Example? (2)

A

In stomach, its absorbed and attracted to low pH where it irreversibly binds -SH groups on ATPase pumps and destroys the pumps. Non-competitive binding allows for total inhibition of acid secretion.
1. Esomeprazole - acts directly on H/K ATPase
2. Potassium competitive acid blocker is a new PPI with longer half life and more protection

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21
Q

Drugs that never cause resistance in H. pylori and drugs that always cause resistance?

A

Never - amoxycillin, bismuth, tetracycline
Always - clarithromycin, metronidazole

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22
Q

What is triple therapy for H. pylori infection?

A

Esomperazole, amoxycillin, clarithromycin

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23
Q

Non-pharmacological considerations for IBD?

A

Stop smoking to reduce crohns, dietary management of diarrhoea, psychological support, manage extra-GIT manifestations, surgery for localized complications?

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24
Q

Role of aminosalicylates, example (2) and side effectsfor IBD?

A

Sulfasalazine and mesalazine which maintain remission in ulcerative colitis
S/E - headaches, nausea, diarrhoea, epigastric pain

25
Q

Role of corticosteroids, examples (3) and side effects for IBD?

A

Hydrocortisone, prednisolone, budesonide which are anti-inflammatory agents used to moderate to severe relapse of UC and CD
S/E short - increase blood sugar, hunger, bp, irritability
S/E long - osteoporosis, steroid induced diabetes, thin skin

26
Q

Role of thiopurines, examples (2) and side effects for IBD?

A

Immunomodulation via induction of T cell apoptosis by modulating cell signaling
1. Azathipurine
2. 6-Mercaptopurine
S/E - antiproliferative action (decrease WCC, platelets) hepatotoxicity, allergin skin rash.
Low TMPT activity leads to increase of 6-TGN and increased risk of myelosuppression

27
Q

Role of anti-TNF-a agents, examples (3) and side effects for IBD?

A

TNFa is a cytokine regulating immune cells so anti-TNFa inhibits this in both UC and CD resulting in immune response suppression
1. Infliximab - engineered antibody against TNFa
2. Adalimumab - fully humanised antibody
3. Biosimilars - which have same AA sequence but are biologically produced by cells having same activity as drug
S/E - immune suppression, increased rate of malignancy, drug induced lupus

28
Q

Role of anti-integrin antibody, example (1) and side effects for IBD?

A

Integrin mediated adhesion allows for leukocytes to attach to capillaries and enter tissue (slow, rolling, binding) so antibody inhibits entry of inflammatory leukocytes into tissues.
1. Vedolizumab - targets a4b7 integrin
S/E - nasopharyngitis, arthralgia, fever, URTI

29
Q

Role of anti IL-12/23 and side effects for IBD?

A

Involved in recruitment of lymphocytes and enhance the cytotoxicity of NK/T cells
1. IL-12 - promotes Th1 response (intracellular killing)
2. IL-23 - promotes Th17 response (produces IL-17, highly inflammatory
3. Also targets p40 subunit on both IL-12/23
S/E - infections, malignancy, hypersensitivity

30
Q

Role of JAK inhibitors, example (1) and side effects for IBD?

A

JAK 1/2/3, Tyk2 are associated with cytokine receptors involved with inflammation signaling
1. Tofacitinib effective for UC not CD
S/E - infection, venous thromboembolism, malignancy

31
Q

4 Causes of constipation?

A
  1. Dietary
  2. Medical condition eg. colon cancer
  3. Drugs
  4. Idiopathic
32
Q

Treatments of constipation? (5)

A
  1. Osmotic laxatives - increasing water content of stool eg. Polyethylene glycol (PEG), magnesium citrate, sodium phosphate, nonabsorbable carbohydrates
  2. Stimulants - encourage bowel motility and speed eg. Senna, docusate sodium, bisacdyl
  3. 5HT3 receptor agonist - stimulates movement eg. puracalopride
  4. Opioid antagonist - for opioid induced constipation especially in pallitive care setting as doesnt cross BBB (doesnt block opioid pain relief) eg. methylnaltrexone
  5. Guanylate cyclase-C receptor agonist - stimulates intestinal fluid secretion/transit eg. linaclotide
33
Q

Routes of admission for constipation medications? (3)

A
  1. Oral
  2. Suppositories
  3. Enemas
34
Q

Acute and chronic causes of diarrhoea?

A

Acute - infective, electrolyte/fluid imbalance
Chronic - malabsorption, chronic constipation, IBD, medication,

35
Q

Treatment for diarrhoea? (5)

A
  1. Bulking agent - plant fiber, guar gum used to increase solidity of stool in patients with IBS
  2. Opioid agonists - reduce gut motility eg. diphenoxylate, loperamide, codeine sulfate
  3. Cholestyramine - bile acid sequestrate where the non-digestible resin binds bile acids leading to increased excretion of bile acids as they cannot be absorbed by body
  4. Probiotics - living organisms eg. lactobacilli reduced duration of acute infective diarrhoea
  5. Diosmectite - absorbent which absorbs toxins, bacteria, viruses to reduce inflammation
36
Q

Causes (2), symptoms (4), secondary complications (2) and treatment (2) of exocrine pancreatic insuficiency?

A

Cause - chronic pancreatitis, CF
Symptom - steatorrhoea, weight loss, fatigue, flatulence
Secondary complications - anaemia, fat soluble vit deficiency
Treatment - creon, panzytrat which replace missing enzymes

37
Q

What is drug clearance dependent on and which drugs have high first pass clearance?

A

Drug clearance dependent on rate of hepatic blood flow which is controlled by symp and parasympathetic (total hepatic flow 1500mL/min)
Drugs with high first pass clearance have low oral bioavailability eg. nitrates, opiates, beta blockers, calcium channel blockers, lignocaine

38
Q

What is enzyme dependent hepatic clearance which which drugs does it affect?

A

Hepatic clearance of less than 300 mL/min have limitations die to hepatic enzyme activity and is changed due to induction or inhibition of CYP450
eg. anti-convulsants, warfarin, benzodiazepines, NSAIDS

39
Q

What role does hypoalbuminaemia play in drug toxicity? Examples? (2)

A

Causes increased Vdist for highly soluble drugs so increases half life and takes longer to clear so prolonged exposure to toxic effects. This is due to liver failure causing decreased albumin so reduced bound drug so increased free drug
eg aminoglycosides, methotrexate

40
Q

How are anticoagulants affected by liver disease?

A

decreased clotting factor synthesis so increased effectiveness of warfarin, heparin, FIX inhibitors therefore increases cleeding risk

41
Q

How are sedatives affected by liver disease?

A

increased sensitivity to sedations especially opiates and benzodiazepines and risk of over sedation and hepatic encephalopathy

42
Q

How are diuretics affected by liver disease? And how is this solved?

A

decreased albumin leads to decreased osmotic pressure so increase in tissue fluid. This leads to decreased renal flow which increases renin angiotensin aldosterone system leading to Na retention and K loss leading to arrhythmias. Fixed by aldosterone antagonist called spironolactone which blocks K excretion in liver failure

43
Q

3 reasons to suppress immune system?

A
  1. Prevention of rejection in organ transplant - suppression of appropriate immune response
  2. Treatment of autoimmune disease - suppression of inappropriate immune reaction to self
  3. Treatment of some resistant inflammatory diseases - suppression of inappropriate response to foreign antigen
44
Q

Process of allograft rejection?

A
  1. APC migration and antigen processing
  2. priming and activation of naive T cells
  3. IL-2 driven T cell clonal expansion and differentiation
  4. Migration of effector cells to graft
45
Q

What is the main target of immunosuppression?

A

IL-2 is the main target of immunosuppressive drugs due to its role in clonal expansion.
IL-2R consists of IL-2Ra (CD 25) IL-2Rb and IL-2Rg and patients lacking IL-2Rg have severe combined immunodeficiencies

46
Q

Outline IL2 transcription, and what blocks it? (2)

A

TCR activation leading to TCR phosphorylation by Lck. PLYg activation leads to increase of Ca which activated calcineurin which dephosphorylates NFAT. NFAT increases IL-2 gene transcription.
Cyclosporin A and tacrolimus are calcineurin inhibitors which decrease allograft rejection by inhibiting activation of IL-2 gene transcription

47
Q

What are the side effects of calcineurin inhibitors?

A

chronic transplant dysfunction eg. immune suppression leading to infection and malignancy, nephrotoxicity, HT, hyperglycaemia, dyslipidaemia, hirsutism and gingival hyperplasia

48
Q

What do anti-proliferatives do (3) and what are their side effects?

A

prevent mitotic response to IL-2 stimulation (IL2 transcription to IL2 to IL2R)
1. Mycophenolate - inhibits IMP which inhibits GMP synthesis (DNA/RNA) which B and T cells need as they lack salvage pathway
S/E - not nephrotic, GIT effects, myelosuppression, infection and malignancies
2. Azathioprine - immunosuppression historically but now replaced by mycophenolate, interferes with DNA replication affecting B and T cells
S/E - anti-proliferative (gut, bone narrow, hair), not nephrotic but hepatotoxic
3. Sirolimus and Everolimus - inhibit mTOR to reduce transaction but don’t inhibit calcineurin so T cell activation still occurs, but protein translation decreases to inhibits IL-2 induced cell cycle progression so no T cell expansion
S/E - not nephrotic, reduced risk of malignancy, myelosuppression

49
Q

What are glucocorticoids used in and examples (2) and what do they target?

A
  1. Induction therapy to treat acute rejection - methylprednisolone
  2. maintanence therapy to treat chronic rejection (prednisolone)
    Targets T and B cells and innate cells to decrease IL-2 production and clonal expansion
50
Q

What do biologics do and 2 examples of monoclonal ones?

A

humanized antibodies and immunodepleting antibodies which are quick and potent immunosuppression.
1. Basiliximab - targets a subunit of IL-2R/CD25 but CD25 only expressed by activated T cells so targeted T cell antibody
2. Rituximab - aCD20 Ab against B cell for antibody mediated rejection

51
Q

What drugs prevent pre and post transplant?

A

Pre - methylprednisolone and basiliximab
Post - tacrolimus, mycophenolate, prednisolone and second dose basiliximab

52
Q

What DDI cause increased CNI response and decreased CNI response?

A

-Increases CNI response causing toxicity (kidney injury and electrolyte imbalance) -
1. P-glycoprotein transporter competitor eg. grapefruit
2. CYP3A4 inhibitors which decrease metabolism so increase levels eg. grape fruit juice, statins, Ca blockers, erythromycin
-Decrease CNI levels meaning reduced drug efficacy
1. Induction of P-Gly transporter to decrease drug availability and decrease levels, eg. St Johns wort
2. CYP3A4 induction which increases metabolism which decreases levels eg. antibiotics and anticonvulsants

53
Q

What vaccines shouldn’t be given of on immunosuppressants?

A

Liv attenuated viruses eg. MMR and varicella

54
Q

6 main drugs affected by renal insufficiency?

A
  1. Anti coagulants - Fxa and prothrombin inhibitors
  2. Diogoxins - arrhythmic
  3. Lithium - fully dependent on renal elimination
  4. Hypoglycaemics - metformin and insulin
  5. Methotrexate - immunosuppressive
  6. aminoglycoside antibiotics
55
Q

What determines creatinine elimination? Example

A

Cr elimination = Cr concentration + Cr clearance
Eg. Digoxin
Cl= 120mL/min normal
Cl total= 70% renal + 30% non-renal
Cl= 60mL/min with renal impairment
therefor Cl= 70%(60/120 renal) + 30%
=35% + 30%
=65% of normal daily dose to be given to renally impaired patient to achieve steady state

56
Q

What 4 factors are used for estimating creatinine clearance and what are the two formulas used?

A
  1. Serum Cr
  2. Age
  3. body weight
  4. gender
    CKD-EPI and Cockcroft-Gault formula used
57
Q

How can you modify regiments if renally imapired?

A
  1. Half dose, same interval
  2. Same dose, double interval
58
Q

Outline how renal insufficiency affects morphine toxicity?

A

Morphine hepatically converted to morphone-6-glucuronide which is toxic. This is renally eliminated so renal impairment causes build up of toxic metabolite which shares toxicity and efficacy with parent morphine

59
Q

What is the consequence of K sparing diuretics in renal impaired patients?

A

Normally, aldosterone reabsorbs Na and excreted K. At end stage renal failure , K elimination suffers so increased K in serum. If a drug that interferes with aldosterone (eg. Spironolactone which is K sparing) is given to patient with renal failure, then potential to excrete K will be paralyzed as no K can be excreted causing retention of K leading to decline in cardiac function and arrhythmias

IMED3112 (17 decks)

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