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GI Flashcards

1
Q

What is GERD?

A

Gastro-esophageal reflux disease;
is a condition in which acid reflux, the back flow of stomach contents into the esophagus (the tube connecting the throat to the stomach), causes distress and/or complications. ​

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2
Q

What are the 3 classifications of GERD and its characteristics?

A

1) Non erosive reflux disease (NERD):
- most benign
- may be associated with belching, discomfort

2) Tissue-injury based GERD:
- esophagitis, more typically distal esophagus
- Barrett’s esophagus: lining of esophagus is changed to resemble that of the colon, typically greater association with cancer of esophagus

3) Extra-oesophageal reflux syndromes:
- Asthma
- Chronic cough etc.

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3
Q

What are some of the risk factors for GERD?

A
  • Family history
  • Smoking
  • Alcohol consumption
  • Certain Medications and foods
  • Respiratory diseases
  • Reflux chest pain syndrome
  • Obesity
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4
Q

List foods that may worsen GERD symptoms by reducing lower esophageal sphincter pressure

A
  • Fatty meal
  • Mint: peppermint, spearmint
  • Chocolate
  • Coffee, cola, tea
  • Garlic
  • Onions
  • Chili peppers
  • Alcohol
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5
Q

List foods that are direct irritants to the esophageal mucosa (SCOTT)

A
  • Spicy foods
  • Orange juice
  • Tomato juice
  • Coffee
  • Tobacco
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6
Q

Give examples of medications that may worsen GERD symptoms by reducing lower esophageal sphincter pressure

A
  • Anticholinergics
  • Barbiturates
  • Caffeine
  • Dihydropyridine Calcium channel blockers e.g. nifedipine, amlodipine
  • Dopamine
  • Estrogen
  • Nicotine
  • Progesterone
  • Nitrates
  • Tetracycline
  • Theophylline
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7
Q

Give examples of medications that are direct irritants to the esophageal muscosa

A
  • Aspirin
  • Bisphosphonates
  • NSAIDs
  • Iron
  • Quinidine
  • Potassium chloride
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8
Q

What is the pathophysiology of GERD?

A

Relaxation of lower esophagus, torn lower esophageal sphincter, increase in pressure of stomach, delayed gastric emptying could be involved in the pathophysiology.

Food that reduces lower esophageal pressure/ medicines can worsen GERD

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9
Q

What are the typical clinical presentation of symptom-based GERD?

A

Symptoms may be aggravated by activities that worsen the gastroesophageal reflux such as lying position, bending over, or eating a meal high in fat:
- Heartburn (hallmark symptom; substernal sensation of warming or burning rising up from the abdomen that may radiate to the neck; may be waxing and waning in character)
- Regurgitation/ belching
- Reflux chest pain (may be mistaken with MI; MI generally associated with pain down the left side of the body)

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10
Q

What are some of the alarm symptoms which may indicate complications of GERD? e.g. Barrett’s esophagus, esophageal strictures, esophageal adenocarcinoma

A
  • Dysphagia (common); difficulty in swallowing
  • Odynophagia; pain in swallowing
  • Bleeding; may be assoc/w cancer
  • Weight loss
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11
Q

What are the clinical presentations of tissue injury-based GERD syndrome?

A
  • Esophagitis
  • Strictures (closing of esophagus due to inflammation)
  • Barrett’s esophagus
  • Esophageal adenocarcinoma

Note: symptoms may present with alarm symptoms such as dysphagia, odynophagia, or unexplained weight loss

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12
Q

What are some of the clinical presentations of extraesophageal GERD syndromes?

A
  • Chronic cough
  • Asthma (~50% with asthma have GERD)
  • Laryngitis
  • Wheezing

Note: these symptoms have an assoc/w GERD, but causality should only be considered if a concomitant esophageal GERD syndrome is also present

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13
Q

List the non-pharmacological treatments of GERD

A
  • Elevate the head end of the bed
  • Weight reduction (esp. obese)
  • Avoid food that may reduce LES pressure or increase transient LES relaxation
  • Include protein-rich meals in diet (augments LES pressure)
  • Avoid food that have direct irritant effect on esophageal mucosa
  • Eat small meals and avoid sleeping immediately after meals (sleep after 3h if possible)
  • Stop smoking (decreases spontaneous esophageal sphincter relaxation)
  • Avoid alcohol (increases peristaltic waves, frequency of contraction)
  • Avoid tight-fitting clothes
  • Always take medications in the sitting upright or standing position and with plenty of fluid, especially for those with direct irritant effects
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14
Q

Therapies to be considered for mild, infrequent, episodic heartburns (can be self-treated); describe the steps to be taken next based on response to therapy

A
  • Lifestyle/dietary modifications
  • Antacid or
  • Alginic acid/ antacid or
  • OTC low dose H2RA or
  • OTC H2RA/ antacid

Responds to treatment: continue non-pharm, may repeat treatment up to 2 weeks if symptoms recur

If do not respond to treatment, consider different agent or tx with OTC omeprazole or medical management

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15
Q

Therapies to be considered for moderate, infrequent, episodic heartburns (can be self-treated); describe the steps to be taken next based on response to therapy

A
  • Lifestyle/dietary modifications
  • Antacid or
  • Alginic acid/ antacid or
  • OTC higher dose H2RA

Responds to treatment: continue non-pharm, may repeat treatment up to 2 weeks if symptoms recur

If do not respond to treatment, consider different agent or tx with OTC omeprazole or medical management

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16
Q

Therapies to be considered for frequent heartburns 2 or more days per week (can be self-treated); describe the steps to be taken next based on response to therapy

A
  • Lifestyle/dietary modifications and
  • OTC omeprazole 20mg/day x 14 days

Heartburn resolves after 2 weeks: stop omeprazole, may repeat regimen every 4 months if needed

Heartburn does not resolve after 2 weeks: medical management

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17
Q

When does GERD needs to be referred to the doctor?

A

1) Duration/ frequency:
- Symptoms persist for more than 2 weeks despite self treatment
- Frequent heartburn for over 3 months
- Take more than one course of PPI treatment every four months

2) Symptoms:
- Heartburn while taking recommended dosages of nonprescription H2RA or PPI
- Heartburn and dyspepsia that occur when taking prescription H2RA or PPI
- Severe heartburn & dyspepsia
- Nocturnal heartburn
- Difficulty/ pain on swallowing solid foods
- Vomiting up blood or black material or black tarry stools
- Chronic hoarseness, wheezing, coughing, or choking
- Unexplained weight loss
- Continuous n/v/d
- Chest pain accompanied by sweating, pain radiating to shoulder, arm, neck, or jaw, and SOB

3) Patient demographic:
- Pregnant
- Nursing mothers
- Children younger than 12 years (for antacids, H2RA) or younger than 18 years (for omeprazole)
- Are over 40 y/o and experiencing GERD symptoms for the first time

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18
Q

What is the typical recommended 1st-choice for pregnant women?

A

Alginic acid (gaviscon); forms a raft on top of the stomach, prevent reflux of contents. Has no systemic absorption

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19
Q

Which type(s) of antacids causes constiptation?

A

Aluminum and calcium

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20
Q

Which type of antacid causes diarrhea?

A

Magnesium

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21
Q

What is the minimum age for antacids?

A

> 12 years; children < 12 with GERD is a cause for concern

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22
Q

Which type(s) of antacids has drug interactions? List some examples of the agents that it has interactions with

A

Calcium, magnesium, aluminum

Agents: Tetracyclines, fluoroquinolones, imidazoles, phenytoin, bisphosphonates, penicillamine

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23
Q

Which antacid(s) require caution to be taken care of in patients with heart disease?

A

Sodium and alginates
* sodium load in preparations contributes to BP

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24
Q

Can antacids be given in pregnancy and breastfeeding?

A

Yes

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25
Q

When should antacids be taken

A

After food

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26
Q

What is the minimum age for PPIs?

A

18 years

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27
Q

Which H2RA has a higher association with drug interactions?

A

Cimetidine- inhibits CYP450 (2D6, 1A2), incr. plasma conc of anti-depressants, warfarin, theophylline, paracetamol, caffeine

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28
Q

What are the long-term adverse effects of PPIs?

A
  • Osteoporosis/bone fractures: common with high dose and long term use for 1 year and longer
  • Vitamin B12 deficiency: PPIs may inhibit secretion of intrinsic factor, not common, usually assoc/w use for 3 years and longer
  • Hypomagnesemia: observed as soon as 3 months after starting therapy; more likely in those on PPIs for 1 year or greater
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29
Q

PPIs may cause an increased risk of _?

A

community acquired pneumonia; particularly within first 30 days of therapy

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30
Q

What are some adjunctive agents that may be given in GERD?

A

Promotility agents e.g. metoclopramide, domperidone
- increases peristaltic activity
- effective in combination, especially with bloating etc.
- on their own, not hugely effective

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31
Q

How do antacids work?

A

Neutralize gastric acid

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32
Q

MOA of H2RA

A

Competitively, reversibly blocks histamine stimulation of gastric acid secretion by reducing cAMP, reducing protein kinase stimulation on proton pump (H+K+ ATPase), hence reducing gastric acid (H+) secretion into the lumen

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33
Q

When should H2RA be taken?

A

At night- can achieve 90% inhibition as it is highly effective in inhibiting fasting and nocturnal secretion (histamine dependent)

Less effective for meal-stimulated acid secretion as this process is gastrin + ACh + Hist dependent. (60-80% inhibition)

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34
Q

What are some SE of H2RA?

A

Constipation or diarrhea, headaches, fatigue, dizziness, somnolence

Rare: agitation

Cimetidine:
- headaches, mental confusion in elderly, bowel movement disturbances
- Rare: impotence, gynecomastia, blood dyscrasias

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35
Q

What is the MOA of PPIs?

A

Protonated drug undergoes molecular conversion to active thiophilic sulfonamide cation in acidic canaliculi of parietal cell

Blocks proton pump (H+ K+ ATPase), which is the final step in gastric acid secretion- antagonizes all stimulants of gastric secretion

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36
Q

PPIs are what type of inhibitors?

A

Irreversible inhibits proton pumps;
effect persists even after drug is eliminated effective for 18-24h;
It takes 3-4 days before full inhibition of all proton pumps. Takes 4-5 days after drug withdrawal to return to pre-treatment acid level due to time required to synthesize new proton pump

37
Q

When should PPIs be taken and why?

A

Taken 1h before meals for better bioavailability- food affect rate of absorption;
this allows concentration of PP at parietal cell canaliculi to be high after meals where the proton pumps are at their most active state for PPIs to exert its efect

38
Q

What are some SE of PPIs esp. Omeprazole?

A

Nausea, abdominal pain, diarrhea, constipation, somnolence, dizziness, headache, rashes;

Reduced gastric acid barrier- bacterial overgrowth -> enteric infection, increased risk of pneumonia;

Transient increase in hepatic aminotransferase occasionally;

Inhibition of CYP450 (2C19)- incr diazepam conc.

39
Q

What are some possible causes of constipation?

A

1) GI conditions: Irritable bowel syndrome, hemorrhoids, upper GIT diseases

2) Cardiac conditions: Heart failure

3) Pregnancy

4) Metabolic & endocrine disorders: hypothyroidism, hypercalcemia

5) Lifestyle factors: Dietary changes, inadequate fluid intake, low dietary fibre, decreased physical activity

6) Neurogenic: CNS diseases, parkinson’s CNS tumours

7) Psychogenic causes: ignoring/postponing urge to defecate

40
Q

What are some medications that can cause constipation?

A
  • Opiates
  • Anticholinergics: antihistamines, antiparkinsonian agents (benztropine, trihexyphenidyl), TCAs
  • Antacids (calcium carbonate/ aluminum hydroxide)
  • Diuretics (non-potassium sparing)
  • Iron preparations
  • NSAIDs (both constipation and diarrhea)
41
Q

What are the clinical presentations of constipation?

A
  • Infrequent bowel movements (<3 per week)
  • Stools that are hard, small or dry
  • Straining
  • Feeling of incomplete evacuation
42
Q

What are some red flags that requires referral?

A
  • Hematochezia (fresh blood in stools)
  • Melena
  • FHx of colon cancer
  • FHx of IBD
  • Anemia
  • Weight loss
  • N/V
  • Severe, persistent constipation that is refractory to treatment
  • New onset or worsening constipation in elderly without evidence of primary cause
43
Q

Give examples of non-pharmacological interventions for constipation

A
  • Increase daily fiber intake to 20-30g, through dietary change (e.g. vegetables, fruits, cereals, wholegrain breads) or fiber supplement products
  • Increase intake of fluids
  • Exercise regularly
  • ## Empty your bowels whenever you feel the urge
44
Q

What are the general first-line recommendations?

A

Dietary modification to increase fiber +/- supplementation with bulk-forming agents

45
Q

List down different recommended agents for different classifications of constipation if first-line management is insufficient

A

1) Acute (<3-6 months): add osmotic laxative if no relief; trial 2-4 weeks
2) Chronic (>6 months): trial intestinal secretagogue e.g. lubiprostone
3) Opioid induced (>4 weeks): osmotic or stimulant laxative, lubiprostone or opioid receptor antagonists

46
Q

Explain bulk-forming agents

A
  • Increases water content of stool to increase stool bulk and weight
  • Relieves symptoms of constipation within 3 days of initiating therapy
  • Advice patients to increase water intake to increase efficacy
  • Examples: methylcellulose, psyllium hydrophilic colloids
47
Q

Explain emollient laxatives (stool softeners)

A
  • Facilitate mixing of aqueous and fatty materials within the intestinal tract
  • Softening of stool occurs within 1-3 days of therapy
  • Examples: docusate sodium (surfactant)
  • Used as prevention rather than treatment of constipation
  • Useful in situation where straining of stool should be avoided (e.g. after rectal surgery)
48
Q

Describe hyperosmolar agents

A
  • Lactulose: non absorbable disaccharide that is metabolized by colonic bacteria to low molecular weight acids, increases peristalsis within 2-3 days of use
  • PEG3350: not absorbed systemically and not metabolized by colonic bacteria, daily use in low dose (17g) may be safe and effective up to 3 months even in children, PEG solution can also be used for bowel cleansing regimens
  • Magnesium salts: should not be used on routine basis; used for bowel preparations, saline cathartics
  • Glycerin: can be administered as a suppository, can be used on an intermittent basis for constipation or fecal impaction in children
49
Q

Describe stimulant laxatives

A
  • Stimulate the mucosal nerve plexus of the colon and may also affect intestinal fluid secretions
  • Examples: Senna, bisacodyl
  • May cause severe abdominal cramping & electrolyte imbalance with chronic use
  • Reserved for intermittent use for patients or in patients who fail to respond adequately to bulking and osmotic laxatives
50
Q

Describe intestinal secretagogues E.g. lubiprostone

A
  • Open calcium chloride channels on GI luminal epithelium, increase intraluminal fluid secretion, helps to soften stool and accelerate GI transit time
  • For chronic idiopathic constipation & opioid-induced constipation
  • Bowel movement occurs within 24-48h of administration
  • Recommended dose 24mcg capsules daily
  • Reserved for patients who fail first-line agents e.g. fiber, osmotic laxatives
51
Q

Describe opioid receptor antagonist- methylnaltrexone

A
  • Peripherally acting mu-receptor antagonist for treatment of opioid induced constipation
  • Administered by s/c injection, weight-based dose
  • Patients with reduced CrCl or moderate-severe hepatic impairment should receive a reduced dosage
52
Q

What is diarrhea?

A

Diarrhea is the passage of loose, watery stools and an increase in frequency of passage of stools to 3 or more per day

53
Q

What are the different classifications of diarrhea?

A
  • Acute diarrhea: < 7 days
  • Prolonged diarrhea: 7-13 days
  • Persistent diarrhea: > 14 days
  • Chronic diarrhea: > 30 days
54
Q

What are some causes of chronic diarrhea?

A
  • IBD
  • Malabsorption syndrome
  • Medications
  • Intestinal Infection
55
Q

List some drugs that can cause diarrhea

A
  • Laxatives
  • Antacids containing magnesium
  • Antibiotics
  • NSAIDs
  • Cholinergics
  • PPI
  • H2RA
  • Antineoplastics e.g. cisplastin
  • Anti hypertensives
56
Q

What is gastroenteritis?

A

Inflammation of stomach and intestines.
- Can be caused by infection with bacteria, parasites or viruses
- viruses include norovirus (most common), rotavirus, sapovirus, astrovirus
- Infection by virus is called viral gastroenteritis, or also known as stomach flu

57
Q

What are some common organisms responsible for causing food poisoning in SG?

A
  • Bacillus cereus
  • Staphylococcus aureus
  • Campylobacter spp.
  • Enterotoxigenic E. coli
  • Salmonella spp.
58
Q

What are symptoms of traveler’s diarrhea?

A
  • Malaise
  • Anorexia
  • Abdominal cramps
  • Sudden onset of diarrhea
59
Q

What causes traveler’s diarrhea?

A

Contaminated food or water

60
Q

What are the different classifications of traveler’s diarrhea?

A

Mild: 1-3 loose stools/day & < 14 days
Moderate: 4 loose stools assoc/w dehydration
Severe: presence of blood in stools or a fever

61
Q

What are the four main pathophysiological causes of diarrhea?

A
  • Secretory
  • Osmotic
  • Exudative
  • Altered intestinal motility
62
Q

When does acute diarrhea needs to be referred?

A

Presence of fever or systemic symptoms

63
Q

Explain how symptomatic treatment is given for acute diarrhea (self-treated)

A
  • Fluid/electrolyte replacement
  • Loperamide/diphenoxylate/ absorbent
  • Diet
64
Q

Explain the MOA of opioid derivatives e.g. loperamide for diarrhea

A

Binds to mu-opioid receptor on the gut wall, inhibits ACh & prostaglandin release, thus reducing peristaltic activity by a direct effect on circular and longitudinal muscles of intestine -> slows GI motility -> reduces abdominal cramps (increase intestinal transit time)
- Affects water and electrolyte movements through bowel

65
Q

What are some SE of opioid derivatives? e.g. loperamide

A
  • Constipation
  • Dizziness, drowsiness
  • Nausea
  • Stomach cramps
66
Q

Can loperamide be given in children <2 years old?

A

No

67
Q

What is the dosage of loperamide?

A

Adults: 4mg orally, followed by 2mg after each loose stool, up to 16mg/day

68
Q

Is loperamide generally associated with dependence? Why or why not?

A

No, because loperamide only acts peripherally and not centrally as it does not penetrate the brain due to P-glycoprotein

69
Q

Can opiate derivatives be used in infectious diarrhea?

A

No, it can worsen diarrhea in selected infectious diarrhea instead

70
Q

Why does diphenoxylate have abuse potential?

A

Because it can cross the blood brain barrier and act centrally

71
Q

What measures are taken to prevent abuse of diphenoxylate?

A

Combined with atropine, causes side effects, discourage abuse

72
Q

What is the dosage of diphenoxylate?

A

Adults: 2.5-5mg TDS-QDS, MAX: 20mg/day

73
Q

What is the MOA of adsorbents?

A

Adsorb nutrients, toxins, drugs and digestive juices

74
Q

How can traveler’s diarrhea be prevented and treated?

A
  • Fluid & electrolyte replacement initiated at the onset of diarrhea replacement
  • Loperamide 4mg stat, followed by 2mg after each loose bowel movement up to 16mg/day
  • A single does of antibiotic and up to 3 days of treatment will improve the condition within 24 hours
  • Fluoroquinolone recommended, when FQ-resistant, use azithromycin
  • 3 day course of rifaximin for non-invasive traveler’s diarrhea
75
Q

What are some non-pharmacological measures to help with diarrhea?

A

Fluid and electrolyte replacement
Drink lots of water and clear fluids such as barley water, clear soup
Avoid milk, cream and dairy products
Avoid caffeine and alcohol

76
Q

What are some red flags for diarrhea?

A

Bloody/mucus in stools, fever, signs of dehydration (headaches, rapid heart rate, dark urine, confusion)

77
Q

What are the 4 pharmacological classes of antiemetics used for prevention, treatment and management of nausea & vomiting?

A

1) Anti-histamines
2) 5HT3- receptors antagonist
3) Dopamine-2 receptor antagonist
4) Muscarinic receptor antagonist

78
Q

What receptors are found in the vomiting center?

A

Muscarinic receptors;
when stimulated, triggers vomiting reflex

79
Q

What receptors are found in the chemoreceptor trigger zone?

A

1) Dopamine-2 receptors
2) 5HT receptors (serotonin receptors);
when stimulated, it stimulates muscarinic receptors of the vomiting center, cause vomiting reflex

80
Q

Where is the chemoreceptor trigger zone located?

A

In the medulla, outside the blood brain barrier -> more permeable to circulating substances such as cytotoxic chemotherapy

81
Q

What structure is responsible for motion sickness?

A

Labyrinth (found in the inner ear), in particular, the vestibule which is a part of the labyrinth

82
Q

What is the vestibule responsible for?

A

Balance and space

83
Q

Explain the pathophysiology of motion sickness

A

Problems in the vestibule -> electrical signals sent to the brain stem via the vestibulocochlear nerve -> signals sent to the vestibular nuclei, located in the pons of the brain stem

The vestibular nuclei contain histamine-1 and muscarinic receptors. When stimulated, these signals will then be passed to the chemoreceptor trigger zone, which will be sent to the vomiting center to trigger vomiting reflex

84
Q

What are the 3 main causes of vomiting?

A

1) Motion sickness
2) From the cerebrum: sensed by higher brain centers-> signal is sent to vomiting center to initiate vomiting reflex
3) Stomach: enterochromaffin cells in stomach releases serotonin in response to cytotoxic agents which is thought to stimulate serotonin receptors on nerve fibers around the area. Stimulation of sensory nerve fiber (vagus nerve) will bring information to the vomiting center to trigger vomiting reflex

85
Q

How does antihistamines (e.g. promethazine) help with nausea and vomiting and what are some of its side effects?

A
  • Blocks histamine-1 receptors, aids in motion and morning sickness
  • S.E: drowsiness, sedation
86
Q

Explain the role of 5HT3 antagonists e.g. ondansetron in treatment of nausea and vomiting

A
  • Antagonizes serotonin receptors
  • Controls nausea and vomiting by working at the CTZ and GI tract
  • Good for patients undergoing chemotherapy, radiation and post surgery
  • Also works locally on GI tract due to serotonin receptors on sensory nerve fibers in that location
87
Q

What is the MOA of metoclopramide in treatment of nausea and vomiting?

A
  • Inhibits dopamine-2 receptors, also increase gut motility as it stimulates GI tract activity
  • Good for chemotherapy, radiation, patients with reflux and biliary disorders
88
Q

What are some side effects of domperidone

A

PECT (17 decks)

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