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PHCY220 > GI WORKSHOPS > Flashcards

GI WORKSHOPS Flashcards

1
Q

what does GORD stand for?

A

gastro oesophageal reflux disease
(sometimes refered to as GERD)

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2
Q

What is Gastro oesophageal reflux disease?

A
  • Gastro-oesophageal reflux is the retrograde, effortless movement of stomach contents into the oesophagus.
  • When troublesome symptoms or mucosal damage occurs as a result of this process, this is defined as gastrooesophageal reflux disease (GORD)
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3
Q

diagnosis of GORD

A
  • diagnosis of GORD is **suggested when heartburn or regurgitation symptoms occur two or more times per week **
  • Endoscopy is preferred for assessing mucosal injury and to identify complications such as esophageal strictures (which can cause difficulty swallowing) and erosive esophagitis due to repeated and prolonged exposure to gastric refluxate.
  • A mucosal biopsy should be taken to identify Barrett esophagus, which is associated with an increased risk of developing esophageal cancer
    *
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4
Q

Clinical presentation of GORD (typical symptoms)

A

may be aggravated by activities that worsen reflux such as recumbent position, bending over, or eating a high-fat meal
* heartburn - often described as a substernal sensation of burning
* hypersalivation
* regurgitation
* belching

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5
Q

atypical symptoms of GORD

A

these are associate with GORD, but causality should only be considered if typical symptoms are also present
* chronic cough
* larngitis
* hoaresness
* wheezing
* noncardiac chest pain
* asthma (approx. 50% with asthma have GORD)

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6
Q

alarm symptoms of GORD

A

may indicate GORD complications such as Barrett esophagus, esophageal strictures, or esophageal adenocarcinoma and require further diagnostic evaluation
* dysphagia
* odynophagia
* weight loss
* bleeding

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7
Q

General approach to treatment of GORD

A

treatment for GERD involves one or more of the following modalities:
1. patient-specific lifestyle changes (non pharmacological therapy)
2. pharmacologic intervention primarily with acid-suppressing therapy
3. **antireflux surgery ** (surgical treatment)

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8
Q

Nonpharmacologic therapy for GORD

A

lifestyle modifications
* many won’t respond adequately to just lifestyle changes alone - it is still helpful to reduce need for long-term pharmacologic therapies
* losing weight if overweight or obese (particulary a reduction in waist circumference)
* elevating head of the bed with a foam wedge if symptoms are worse when recumbent
* smaller meals & avoiding meals 3h before sleeping
* avoiding food or medications that exacerbate GORD
* smoking cessation
* avoiding alcohol

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9
Q

why is elevating the head of the bed a helpful lifestyle modification for patients with GORD

A

decreases the contact time of gastric acid with the oesophageal mucosa at night

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10
Q

Surgical treatment of GORD

A

generally last resort BUT antireflux surgical options may be considered when there is a large hiatal hernia, evidence of aspiration or cardia dysfunction, or when pharmacologic management is undesirable due to side effects or adherence challenges in patients with well-documented GORD
* GOAL OF SURGERY → to reestablish the antireflux barrier, position the LES within the abdomen where it is under positive (intra-abdominal) pressure, and close any associated hiatal defect.

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11
Q

pharmacological therapies for treatment of GORD

A

Pharmacologic therapies for GERD typically involve **increasing the pH of gastric contents **through either direct gastric acid neutralization OR reducing acid production through inhibition of stimulation pathways, thereby reducing GERD symptoms and tissue damage.
* antacids & alginic acid
* histamine-2 receptor antagonists (H₂RAs)
* proton pump inhibitors (PPIs)

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12
Q

Effectiveness ranking of pharmacologic therapies for GORD

A

antacids are inferior to histamine-2 receptor antagonists (H2RAs), and H2RAs decrease acid secretion less than PPIs.
i.e. PPIs are best!

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13
Q

antacids & alginic acid for treatment of GORD

A

ANTACIDS:
* useful for intermittent treatment of GORD symptoms and can be used for patients with infrequent typical reflux symptoms
* effective for immediate, symptomatic relief, BUT require frequent dosing
* usually well tolerated, and potential side effects include constipation or diarrhea depending on the formulation being used
ALGINIC ACID:
* creates a viscous barrier that can aid in acid neutralization & is often used in combo with antacids

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14
Q

histamine-2 receptor antagonists for the treatment of GORD

A
  • examples → cimetidine, famotidine, nizatidine
  • decrease acid secretion by blocking histamine-2-receptors in gastric paretial cells
  • provide relief from typical acute GERD symptoms and can also be administered prophylatically (as prevention treatment)
  • more effective than antacids at controlling chronic GERD symptoms but less effective than PPIs
  • may be dosed intermittently or on a scheduled basis depending on the degree of symptom control
  • generally well tolerated; side effects are mild and include headache and nausea
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15
Q

Proton pump inhibitors (PPIs) for the treatment of GORD

A
  • eg → omeprazole, lansoprazole
  • block gastric acid secretion by inhibiting gastric H+/K+-ATPase in gastric parietal cells
  • Primary uses of PPIs are treating frequent reflux symptoms and healing of gastric or esophageal ulcerations
  • PPIs provide significant reduction in gastric acid and the greatest relief of symptoms, especially in patients with moderate-to-severe GERD, with high rates of healing erosive disease
  • typically formulated in delayed-release capsules or tablets
  • Most patients should be instructed to take their PPI in the morning, 30 to 60 minutes before breakfast to maximize efficacy.
  • Due to their slow onset of action, PPIs are most effective when taken on a scheduled basis. Patients requiring a second dose if nighttime symptoms are predominant should take the dose before the evening meal
  • PPIs are generally well tolerated; the most common side effects are headache and GI effects such as diarrhea and nausea
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16
Q

what is heartburn?

A
  • common term to describe a burning feeling in the chest or throat caused by stomach acid.
  • This feeling is a symptom of a condition, not a condition itself
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17
Q

what is gastric/acid reflux?

A
  • common term to describe the movement of stomach acid up the oesophagus
  • used interchangeably with GORD sometimes
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18
Q

what is dyspepsia?

A
  • A term to represent a group of symptoms of upper GI discomfort including: bloating, belching, nausea, early satiety after meals. Symptoms usually associated with eating.
  • also known as/called indigestion
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19
Q

what is emesis?

A
  • the clinical word for vomiting
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20
Q

what is nausea?

A

unpleasant sensation of an urge to vomit

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21
Q

GI or intraperitoneal causes of vomiting

A
  • obstructing disorders
  • achalasia
  • enteric infections
  • appendicitis
  • pancreatitis
  • inflammatory bowel disease (IBS)
  • cholecystitis
  • gastroparesis
  • gastroesophageal reflux (GORD)
  • peptic ulcer disease
  • peritonitis
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22
Q

cardiac causes of nausea & vomiting

A
  • cardiomyopathy
  • myocardial infarction
  • heart failure
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23
Q

neurologic causes of nausea & vomitting

A
  • vestibular disease
  • motion sickness
  • labryinthitis
  • head trauma
  • migraine headache
  • increased intercranial pressure
  • meningitis
  • hydrocephalus
  • psychological distress
  • self-induced
  • depression
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24
Q

other causes of nausea & vomiting

A
  • bulimia
  • anorexia nervosa
  • cyclic vomiting syndrome
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25
Q

therapy induced causes of nausea & vomiting

A
  • cancer chemotherapy
  • antibiotics
  • antiarrythmics
  • digoxin
  • oral hypoglycemics
  • oral contraceptives
  • theophylline
  • anticonvulsants
  • radiation therapy
  • ethanol
  • toxins
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26
Q

endocrine/metabolic causes of nausea & vomiting

A
  • pregnancy (NVP)
  • hyperemesis gravidarum
  • renal disease (uremia)
  • diabetes (ketoacidosis)
  • thyroid disease
  • parathyroid disease
  • adrenal insufficiency
  • hyponatremia
  • hypercalcemia
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27
Q

what are common causes of acute nausea & vomiting

A
  • infection
  • motion sickness
  • alcohol
  • poisioning
  • anaesthesia
  • over-eating
  • pregnancy
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28
Q

what are common causes of chronic nausea & vomiting
(these can also be causes of acute)

A
  • migraine
  • severe pain
  • emotional distress
  • gastroparesis
  • traumatic brain injury/concussion
  • food intolerance
  • vertigo
  • drug-induced
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29
Q

what are the most likely causes of vomiting in a young child?

A

the most common cause of vomiting in both adults & children is gastroenteritis, which is commonly known as ‘gastro’ or tummy bug

other causes include:

  1. food allergy
  2. poisoning
  3. reflux
  4. meningitis
  5. overeating
  6. stress
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30
Q

what is the most important (possible) medical complication associated with vomiting to manage in the short term?

A

dehydration
manage by rehydrating!

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31
Q

desired outcomes of treatment for nausea & vomiting

A
  • The primary goals of treatment → relieve the symptoms of nausea and vomiting,** increase quality of life**, and prevent complications such as dehydration or malnutrition
  • Drug therapy for nausea and vomiting should be safe, effective, and economical.
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32
Q

nonpharmacologic therapy for nausea & vomiting

A
  • include dietary, physical, and psychological measures
  • Dietary management is important when treating NVP due to concern for teratogenic effects with drug therapies
  • eating frequent, small meals
  • avoiding spicy or fatty foods
  • eating high-protein snacks
  • avoiding iron-containing pills
  • eating bland or dry foods the first thing in the morning
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33
Q

signs of nausea and vomiting

A

with complex & prolonged nausea & vomiting, patients may show signs of malnourishment, weight loss, & dehydration (dry mucous membranes, skin tenting, tachycardia, & lack of axillary moisture)

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34
Q

laboratory tests for nausea & vomiting

A

Dehydration, electrolyte imbalances, and acid–base disturbances may be evident in complex and prolonged nausea and vomiting.
* Dehydration is suggested by elevated blood urea nitrogen (BUN), serum creatinine (SCr), and BUN-to-SCr ratio (20:1 or greater using traditional units of measurement [100:1 or greater using SI units of mmol/L]).
* Calculated fractional excretion of sodium (FeNa) less than 1% (0.01) indicates dehydration and reduced renal perfusion.
* Low serum chloride and elevated serum bicarbonate levels indicate metabolic alkalosis.
* Hypokalemia may occur from GI potassium losses and intracellular potassium shifts to compensate for alkalosis.

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35
Q

what are antimetic drugs, and what are the most common classes?

A

antimemetic drugs = drugs effective against nausea & vommiting
* anticholinergics
* dopamine antagonists
* corticosteriods
* cannabinoids
* benzodiazepines
* serotonin antagonists
* neurokinin-1 receptor antagonists
* olanzapine

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36
Q

anticholinergics (scopolamine) for nausea & vomiting

A
  • scopolamine blocks muscarinic receptors
  • effective for prevention & treatment of motion sickness, & some efficacy in preventing PONV
  • adhesive transdermal (TD) patch, effective for up to 72 hours after application
  • should be applied 4 hours prior to motion sickness triggers and the evening before surgery if used to prevent PONV
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37
Q

what does PONV stand for

A

Post-operative nausea & vomiting

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38
Q

what does CINV stand for

A

chemotherapy induced nausea & vomiting

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39
Q

antihistamines for nausea & vomiting

A
  • used to prevent and treat nausea and vomiting due to motion sickness, vertigo, or migraine headache
  • 2nd Gen → cyclizine, fexofenadine
  • 1st Gen → meclizine, hydroxyzine, dimenhydrinate
  • First-generation antihistamines cause undesired effects including drowsiness, blurred vision, and urinary retention
  • available in a variety of dosage forms, including oral capsules, tablets, and liquids
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40
Q

what are the 3 main groups of dopamine antagonists (antiemetic drugs)

A
  • phenothiazines
  • butyrophenones
  • prokinetic agents
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41
Q

phenothiazines for nausea & vomiting

A
  • dopamine antagonist
  • e.g. promethazine, prochlorperazine, chloropromazine
  • Availability in multiple dosage forms (ie, oral, parenteral, rectal)
  • use in a variety of settings including severe motion sickness or vertigo, gastritis or gastroenteritis, NVP, PONV, and CINV
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42
Q

what does NPV stand for

A

nausea & vomiting in pregnancy

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43
Q

butyrophenones in nausea & vomiting

A
  • dopamine antagonist
  • e.g. droperidol, haloperidol
  • effective for preventing PONV
  • may also be used in for treating CINV for patients who are intolerant to serotonin receptor antagonists and corticosteroids
  • RARE BUT SERIOUS: QT prolongation, cardiac arrymthimias
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44
Q

Prokinetic agents in nausea & vomiting

A
  • dopamine antagonists
  • e,g, metoclopramide & domperidone
  • Their antiemetic and prokinetic effects are useful in PONV, CINV, gastroparesis, and gastroesophageal reflux disease (GORD)
  • Metoclopramide is available in injectable, oral solid, and oral liquid dosage forms
  • metoclopramide crosses BBB, so has centrally mediated adverse effects!
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45
Q

corticosteriods for nausea & vomitting

A
  • e.g. dexamethasone, methylprednisolone
  • used alone or in combo for preventing & treating PONV, CINV, or radiation-induced nausea & vomiting
  • Efficacy is thought to be due to release of 5-HT, reduced permeability of the blood–brain barrier, and decreased inflammation
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46
Q

cannabinoids for nausea & vomiting

A
  • e.g. dronabinol, nabilone
  • used for prevention & treatment of refractory or delayed CINV
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47
Q

benzodiazepines for nausea & vomiting

A
  • e.g. lorazepam, alprazolam
  • used to prevent & treat CINV
  • used as an adjunct to antiemetic agents
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48
Q

serotonin antagonists for nausea & vomiting

A
  • e.g. ondansetron, granisetron, dolasetron, tropisetron, palonosetron
  • most useful for PONV
  • also CIVN, radiation induced nausea
  • most well tolerated, dose-related QT changes have been reported (so ECG monitoring recommended for at risk patients)
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49
Q

neurokinin-1 receptor antagonists for nausea & vomiting

A
  • e.g. aprepitant, rolapitant, netupitant
  • effective for preventing acute and delayed CINV, PINV
  • numerous drug interactions! (as CYP inhibitor)
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50
Q

olanzapine for nausea & vomiting

A
  • antipsychotic agent that has effects at D2, 5-HT2c, and 5-HT3 receptors
  • combination therapy for prevention of CINV in patients receiving highly emetogenic chemotherapy
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51
Q

Sea-legs product

A
  • sold for the prevention of travel sickness
  • contains meclozine, an antihistamine which is generally less sedating than promethazine
  • Meclozine is a Pharmacy Only Medicine and not for use in children under six years old.
  • Taken the night before travel or one hour before travel and the dose can repeated every 24 hours if necessary.
  • Can cause drowsiness thus making it dangerous to drive or operate machinery. Limit alcohol intake
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52
Q

Scopoderm TTS product

A
  • sold for the prevention of motion sickness
  • contains hyoscine (scopolamine) (an antichlonergic medicine)
  • a topical patch, needs to be placed behind the ear at least five hours before travelling (though eight hours produces the best effect)
  • wash hands after handling the patch, & to wash area after patch removal
  • Drowsiness can occur with this medicine and patients must be warned about driving or operating machinery
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53
Q

sea band product

A
  • sold for “the control of nausea & motion sickness without drugs”
  • is homeopathic and may be of benefit to those who cannot take other medicines
  • bands aim to apply constant pressure to the Nei-Kuan pressure points in the wrists which may help reduce the feelings of nausea
  • Patients should be advised to place the bands in the middle of the inner wrist, about three finger widths from the crease where the wrist joins the hand.
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54
Q

Phenergan product

A
  • 1st gen antihistamine
  • PHARMACIST ONLY
  • Phenergan is a **brand name of the generic promethazine **which is a sedating antihistamine
  • pharmacists must be wary about the potential abuse of this type of medicine
  • Patients should be warned about drowsiness and avoiding driving and operating machinery.
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55
Q

nausicalm product

A
  • sold for the treatment of nausea and prevention of travel sickness
  • contains cyclizine, an antihistamine which is generally less sedating than promethazine
  • PHARMACIST ONLY (max 6 tablets)
  • adult dose: 1 tablet (50mg) taken 1–2 hours before travel
  • Warnings: Drowsiness - do not drive or use tools or machines. Do not drink alcohol.
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56
Q

what is the likely mechanism that causes motion sickness?

A

conflicting sensory input to brain due to differences between actual and expected patterns of movement or vision

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57
Q

heartburn

A
  • Heartburn is a burning feeling that rises from the stomach or lower chest up towards the neck and is often a symptom of GORD.
  • Heartburn does not refer to pain of cardiac origin although pharmacists should be alert for symptoms that might indicate heart disease.
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58
Q

what are some conditions you should try rule out when questioning a patient with dyspepsia?
(i.e. differential diagnoses for dyspepsia)

A
  • gastric ulcer
  • duodenal ulcer
  • medicine-induced dyspepsia
  • irritable-bowel syndrome (IBS)
  • gastric or oesophageal cancer
  • heart disease
  • galstones
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59
Q

what are some questions you might ask a patient complaining of dyspepsia?

A
  • AGE? The age of the patient is relevant as pathological conditions are more likely to occur in older patients (e.g. >50 years of age)
  • DESCRIPTION OF THE PAIN? Both the location of the pain and it’s intensity may point towards a possible cause. Pain described as gnawing, sharp or stabbing may indicate more serious pathology. Intense or severe pain should be referred to exclude more serious conditions
  • DOES PAIN RADIATE? Pain that radiates to other parts of the body may indicate more serious disease & should be referred e.g. cardiovascular pain may radiate to the left arm, shoulder or jaw
  • ASSOCIATED SYMPTOMS? Symptoms such as persistent vomiting, altered bowel habit or black & tarry stools may indicate serious disease & should be referred
  • WHAT MAKES IT WORSE (OR BETTER)? does eating make it better, or worse? Is it relieved by antacids? Certain types of food may aggravate symptoms for some people
  • SOCIAL HISTORY? stress or rushed eating may worsen symptoms. Alcohol consumption often causes dyspepsia.
  • HOW LONG has this been a problem?
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60
Q

what are some symptoms associated with heart burn?

A
  • burping & regurgitation of food
  • pain relieved by antacids
  • burning sensation at front of chest after meals
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61
Q

what are 3 OTC products a patient can purchase for the treatment of GORD

A
  • mylanta (antacid)
  • gaviscon (anginate)
  • losec (omeprazole) (proton pump inhibitor)
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62
Q

what is gastroenteritis?

A
  • Gastroenteritis is a bowel infection causing diarrhoea, and sometimes vomiting.
  • common in children
  • a virus commonly causes gastro, common viruses are rotavirus & adenovirus
  • the virus is easily spread in homes, day cares, kidergartens and schools
  • Acute gastroenteritis may be defined as diarrhoea of rapid onset, with or without vomiting, fever or abdominal pain. There is often a history of contact with another person with the same symptoms.
63
Q

what is the treatment of choice for dehydration from gastroenteritis?

A
  • oral rehydration therapy (ORT)
  • can purchase OTC electrolyte solutions i.e. gastrolyte or pedialyte
  • rehydrate!! water, fluids
64
Q

signs & symptoms of gastroenteritis

A
  • feeling sick (nausea)
  • diarrhoea (runny, watery poo)
  • vomiting
  • fever
  • stomach pains
65
Q

food/dietary recommendations for a child with gastroenteritis

A
  • starchy simple foods are best - bread, porridge, rice, potatoes, plain biscuits, yogurt
66
Q

red flags for gastroenteritis

A
  • vomiting and/or diarrhoea and is less than 6 months old – babies can become dehydrated and unwell quickly.
  • drowsy and difficult to rouse.
  • lots of diarrhoea (8 to 10 watery motions in 1 day).
  • blood or mucus in poo.
  • Vomiting is increasing or child cannot keep fluids down.
  • vomiting green fluid (bile).
  • child develops severe stomach pains.
  • child shows signs of dehydration.
  • bloody or dark coffee ground looking vomit
  • black or tarry stool
67
Q

signs of dehydration in a child

A
  • dry mouth and tongue
  • sunken eyes
  • cold hands & feet
  • Unusual sleepiness or lack of energy.
68
Q

what is a duodenal ulcer

A
  • A duodenal ulcer is a sore that forms in the lining of the duodenum. Your duodenum is the first part of your small intestine. This is the part of yourdigestive systemthat food travels through, after it leaves your stomach
  • is a type of peptic ulcer
  • Your stomach makes a strong acid that helps you digest food and kills germs. The cells of the stomach and duodenum make a barrier from mucus, to protect themselves against this acid. If the mucus barrier is damaged, an ulcer can form.
69
Q

causes of duodenal uclers

A
  • The main cause of this damage is infection with bacteria calledHelicobacter pylori, orH. pylori. The bacteria can cause the lining of your duodenum to become inflamed and an ulcer can form.
  • Some medications can also cause duodenal ulcers, particularlyanti-inflammatory medicinessuch as ibuprofen and aspirin. It is rare that other medicines or medical conditions cause an ulcer.
70
Q

what is an endoscopy?

A
  • An endoscopy is a procedure used in medicine to look inside the body.
  • The endoscopy procedure uses an endoscope to examine the interior of a hollow organ or cavity of the body.
  • Unlike many other medical imaging techniques, endoscopes are inserted directly into the organ.
  • There are many types of endoscopies.
71
Q

what is epigastric pain?

A
  • The upper part of your abdomen, which sits below your rib cage, is known as the epigastrium. Your pancreas sits within the epigastrium, as well as parts of your small intestine, stomach and liver.
  • Pain or discomfort below your ribs in this area of the upper abdomenis called epigastric pain
72
Q

what is gastritis & what are causes, symptoms & treatment

A
  • aka stomach inflammation
  • Any of a group of conditions in which the stomach lining is inflamed.
  • CAUSES: include infection, injury, regular use of pain pills called NSAIDs and too much alcohol.
  • SYMPTOMS: include upper stomach pain, nausea and vomiting. Sometimes, there are no symptoms.
  • TREATMENT: depends on the cause. Antibiotics and antacids might help.
73
Q

what are peptic uclers?

A
  • are open sores that develop on the inside of your stomach & the upper portion of your small intestine
  • the most common symptom is stomach pain
  • peptic uclers include both duodenal and gastric uclers
74
Q

what are the most common causes of peptic ulcers?

A
  • infection with the bacterium Helicobacter pylori (H. pylori)
  • long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen (Advil, Motrin IB, others) and naproxen sodium (Aleve).
  • Stress and spicy foods do not cause peptic ulcers. However, they can make your symptoms worse.
75
Q

what is Peptic ulcer disease?

A
  • Peptic ulcer disease (PUD) is a condition in which there is a break in the mucosal lining of the stomach or the first part of the small intestine (the duodenum)
  • these breaks are more than 5mm in diameter, with depth to the submucosa
  • results in painful sores or ulcers in the lining
  • normally, a thick layer of mucus protects the stomach lining from the effect of its digestive juices, but for various reasons, this protective layer can be compromised, allowing stomach acid to damage the tissue and erode the lining of the digestive tract, resulting in an ulcer.
76
Q

why do peptic ulcers occur?

A

can occur when there is excess acid in the system OR when the protective layer of the mucus on the lining is broken down (making it more susceptible to damage)
* caused by an imbalance between factors promoting musocal damage (gastric acid, pepsin, helicobacter pylori infection, non-steriodal anti-inflammatory (NSAID) drug use) AND those mechanisms promoting gastroduodenal defence (prostaglandins, mucus, bicarbonate, mucosal blood flow)

77
Q

differences between the root cause of duodenal & gastric ulcers?

A

Duodenal ulcers result from an excess amount of acid being produced
gastric ulcers occur due to a reduced protective muscosal barrier, which allows acid and pepsin to get in and erode the mucosa.

78
Q

what are the most common causes of peptic ucler disease?

A
  • Helicobacter pylori → can increase amount of acid, can cause inflammation of lining of digestive tract, can breakdown protective mucous layer
  • NSAIDs → wear away the protective mucous layer of the digestive tract, leading to uclers
79
Q

risk factors for peptic ulcer disease

A
  • genetics - having a family member with peptic ulcers make a person more likley to develop ulcers aswell
  • cigarette smoking
  • alcohol abuse can interfere with ulcer healing
  • stress (although controversial & difficult to measure)
80
Q

signs of ulcers (in general)

A
  • Constant’, ‘annoying’ or ‘gnawing’ or burning pain in your middle or upper stomach between meals or at night
  • Chronic upper abdominal pain
  • Pain that temporarily disappears if you eat something or take an antacid
  • Bloating
  • Heartburn
  • Nausea or vomiting
    peptic ulcers most commonly occur in patients 30-50 years old!
81
Q

specific gastric ulcer symptoms

A
  • non-specific pain in upper abdomen
  • aggrevated by food
  • nausea & vomiting
  • reduced appeptite
  • persistent & severe
82
Q

specific symptoms of duodenal ulcers

A
  • ** specific pain** in upper abdomen
  • dull pain
  • occurs on empty stomach
  • relieved by food
  • relieved by antacids
83
Q

how do you diagnosis a peptic ucler?

A

depending on the patients history & symptoms, further tests wll be carried out to determine if there is a peptide ulcer
* upper endoscopy
* h. pylori testing

84
Q

what are the 3 main complications with peptic ulcer disease?

A

The risk of serious complications depends on the cause of the ulcer, the size and location of the ulcer, and the person’s age and health. There are three main complications:
1. bleeding → bleeding ulcers most often affect older people. Symptoms may include blood in the vomit or in the stool (black, tar-like appearance)
2. perforation → when an ulcer leads to a hole or puncture in the wall of the stomach or duodenum. Symptoms include sudden, severe abdominal pain, a rapid heart beat and a low body temperature. Pain may radiate to one or both shoulders and the abdomen may become rigid. Treatment needs to be given immediately, and includes insertion of a nasogastric tube, IV fluids, medications and/or surgery
3. obstruction → gastric outlet obstruction refers to a blockage of the outlet of the stomach, which leads to the small intestine. Vomiting is the most common symptom. Treatments include nasogastric tube, IV fluids for hydration, endoscopy or surgery.

85
Q

treatment considerations for peptic ulcer disease

A
  • identify the cause
  • treatment of H. pylori = 2x antibiotics + PPI (i.e. triple-therapy regimen)
  • treatment of ulcers not due to H.pylori = PPI or H₂-receptor antagonist
  • stop NSAIDs → if this is not possible, then co-prescribe a PPI
  • other methods of symptom relief → quit smoking, limit alcohol, antacids
86
Q

what are the likely conditions a patient presenting with dyspepia is suffering?

A
  • GOR
  • gastritis
  • non-ulcer dyspepsia
87
Q

what symptoms are characteristic of straight forward dsypepsia?

A

Patients with dyspepsia present with a range of symptoms commonly involving:
* vague abdominal discomfort (aching) above the umbilicus associated with belching
* bloating
* flatulence
* a feeling of fullness
* nausea or vomiting
* heartburn
although dyspeptic symptoms are a poor predictor of disease severity or underlying pathology!

88
Q

what is the most classicial symptom of GORD?

A
  • retrosternal heartburn
89
Q

in a patient presenting with dyspepsia - what symptoms would be ‘red flag symptoms’, warranting referral?

A

ALARM Symptoms:
* Anemia
* Loss of Weight
* Anorexia
* Recent onset of progressive symptoms
* Melaena, dysphagia, & haematemesis
* Pain described as severe, debilitating or that wakes the patient in the night; Persistent vomiting; Referred pain

90
Q

what are the differential diagnoses of dyspepsia (i.e. the conditions to eliminate)

A
  • Peptic ulceration
  • Medicine-induced dyspepsia
  • Irritable bowel syndrome
  • Biliary disease
  • RARE:Gastric carcinoma,Oesophageal carcinoma,Atypical angina
91
Q

what diagnostic tests are available to test for the presence of H. plyori infection?

A
  1. biopsy via upper endoscopy
  2. serology test (blood test)
  3. faecal antigen test
    * Internationally, Carbon-13 urea breath testing is commonly used for diagnosis of infection, but this test is not freely available in New Zealand.
92
Q

which H. pylori diagnostic test can generate a false positive reading, & how?

A
  • serology test
  • an generate a false positive reading asantibodies can be found for a prolonged period (up to five years), making it impossible to distinguish active from past infection
93
Q

Faeacel antigen test for diagnosis of H pylori infection:

A
  • is the recommended non-invasive test forH. pyloriinfection in New Zealand. Faecal antigen testing can be used to diagnose active infection withH. pyloriand, if required, to confirm that eradication treatment has been successful
  • has a reported sensitivity of 94% and specificity of 97%
  • False negative results can occur if the patient has been taking medicines that decrease the load ofH. pyloriin the stomach, e.g. antibiotics, or the contents of the stomach are less acidic, e.g. if a patient has been taking a PPI
  • Patients should be advised not to take PPIs within two weeks, or antibiotics or bismuth compounds (found in some indigestion remedies) within four weeks prior to faecal antigen testing to prevent false negative results
94
Q

which H. plyori test is fully funded & widely available in NZ?

A

faecal antigen test

95
Q

serology test for diagnosis of H pylori infection

A
  • Serology cannot distinguish between infection that is past or current, and because antibody levels decrease slowly over 6 – 12 months or longer after eradication treatment, it cannot be used as a test of treatment success.
96
Q

Urea breath test for diagnosis of h pylori infection

A
  • is still regarded in the literature as the gold standard for clinical diagnosis ofH. pyloriinfection
  • However, this test has limited availability in New Zealand due in part to the specialist laboratory equipment and training required
  • Both the sensitivity and specificity for carbon-13 urea breath testing is reported to be comparable to faecal antigen testing
  • False-negative results can be generated, however, by other urease-producing bacteria in the mouth and intestine.
97
Q

stomach biopsy during a gastroscopy as a diagnostic test for H pylori infection

A

the most accurate way to tell if you have anH pyloriinfection - however also the most innvasive
A tissue sample, called abiopsy, is taken from the stomach lining.
To remove the tissue sample, you have a procedure calledendoscopy. The procedure is done in the hospital or outpatient center.
Usually, a biopsy is done if endoscopy is needed for other reasons. Reasons include diagnosing the ulcer, treating bleeding, or making sure there is no cancer.

98
Q

what is triple therapy in terms of H. plyori infection treatment

A
  • the eradication treatment regimen for H pylori infection
  • GOALS = to provide symptmatic relief & to encourage ulcer healing
  • made up of 3 different medications → 1 PPI and 2 antibiotics (commonly amoxicillin & clarithromycin)
99
Q

what does the triple therapy for H pylori infection consist of?

A
  • 1x PPI (proton pump inhibitor, e.g. omeprazole) - ulcer healing medication
  • 2x antibiotics (commonly amoxicillin & clarithromycin) - to eradicate H. pylori
  • two antibiotics are used to reduce the chances of developing bacterial resistance
100
Q

How long should eradication treatment (triple-treatment regimen) for H pylori infection last?

A

14 days duration

101
Q

what is the first line H pylori eradication dosing regimen?

A
  • omeprazole, 20 mg twice daily; and
  • clarithromycin, 500 mg twice daily; and
  • Amoxicillin, 1,000 mg twice daily; or Metronidazole, 400 mg twice daily
    duration of 14 days
    metronidazole can be used if patient allergic to penicillin
102
Q

how do NSAIDs cause gastrointestinal toxicity?

A

NSAIDs can cause GI toxicity and peptic uclers as they →** cause mucosal injury due to cyclo-oxygenase (COX)-1 inhibition** by reduction of cytoprotective mucosal prostaglandins and reduction of the secretion of a protective bicarbonate mucus barrier in the stomach and small bowel

103
Q

what are the risk factors that increase the risk of gastrointestinal toxicity with NSAIDs?

A
  • aged over 65 years
  • those with a history ofpeptic ulcer diseaseor serious gastro-intestinal complication
  • those taking other medicines that increase the risk of gastro-intestinal adverse effects
  • those with serious co-morbidity (e.g. cardiovascular disease, diabetes, renal or hepatic impairment)
104
Q

rank non-selective NSAIDs & their risk of GI adverse effects

A
  • ibuprofen (lowest risk)
  • indometacin, naproxen, diclofenac (intermediate risk)
  • ketoprofen (highest risk)
105
Q

are NSAIDs that are selective COX-2 inhibitors associated with lower GI risk? (& give an example)

A
  • yes, they do have a lower risk
  • e.g. celecoxib
106
Q

what treatment strategies are used to reduce NSAID-induced GI toxicity?

A
  • if theNSAID can be discontinuedin a patient who has developed an ulcer, a proton pump inhibitor usually produces the most rapid healing; alternatively, the ulcer can be treated with a H2-receptor antagonist or misoprostol.

Iftreatment with a non-selective NSAID needs to continue, the following options are suitable:
* Treat ulcer with a proton pump inhibitor and on healing continue the proton pump inhibitor (dose not normally reduced because asymptomatic ulcer recurrence may occur);
* Treat ulcer with a proton pump inhibitor and on healing switch to misoprostol for maintenance therapy (colic and diarrhoea may limit the dose of misoprostol);
* Treat ulcer with a proton pump inhibitor and switch non-selective NSAID to a cyclo-oxygenase-2 selective inhibitor, but seeNSAIDs and cardiovascular events; on healing, continuation of the proton pump inhibitor in patients with a history of upper gastro-intestinal bleeding may provide further protection against recurrence.

  • Iftreatment with a cyclo-oxygenase-2 selective inhibitor needs to continue, treat ulcer with a proton pump inhibitor; on healing continuation of the proton pump inhibitor in patients with a history of upper gastro-intestinal bleeding may provide further protection against recurrence.
107
Q

what is the pH and typical transit time of the mouth?

A
  • pH = 5-7
  • transit time = 5-60 seconds
108
Q

what is the pH and typical transit time of the stomach?

A
  • pH = 1- 3
  • transit time = 0.5 - 4 hours
109
Q

what is the pH and typical transit time of the small intestine?

A
  • pH = 6.5 (proximal), 7.4 (distal)
  • transit time = 1-2 hours
110
Q

what is the pH and typical transit time of the large intestine?

A
  • pH = 5.7 (proximal colon), 7 (distal colon)
  • transit time = 12-24 hrs
111
Q

what is omperazole and what is it used to treat?

A
  • a proton pump inhibitor which leads to decreased amount of acid in the stomach
  • treatment of gastric ulcers
112
Q

what is mesalazine and what is it used to treat?

A
  • measlazine (aka mesalamine) is a 5-aminosalicyclic acid
  • anti-inflammatory drug
  • used to treat inflammatory bowel disease (IBD) including ulcerative colitis & crohn’s disease
113
Q

what part of the GIT is the primary site for omeprazole absorption?

A

the absorption of omeprazole takes place in the small intestine and is usually completed within 3-6 hours

114
Q

what is the release profile for omeprazole (Losec enteric coated) and how it is desirabe for the delivery of this drug?

A
  • delayed release (which is triggered by pH)
  • does not release in the acid pH environment of the stomach, will only release once the pH is increased in the small intestine
  • provides targeted drug delivery to the small intestine, bypassing the harsh environment of the stomach (protects the underlying dosage form and drug substance)
115
Q

if a patient cannot swallow whole omeprazole capsules, why is it recommeneded to mix the contents with slightly acidic food/liquid?

A
  • omeprazole is designed to not degraded in acidic conditions and instead be degraded in the more basic conditions of small intestine.
  • If you take with slightly acidic food - the granules will not get degraded within the food or the stomach - and then will get degraded in small intestine

want to maintain that enteric coat,to ensure the same therapeutic efficacy

116
Q

if a patient cannot swallow whole omeprazole capsules, they should mix the contents with slightly acidic food/liquid, and consume within 30mins - why shouldn’t the patient take the liquid dispersion if it has been standing for longer than 30 min?

A
  • drug can degrade over time
  • drug will till be slowly degrading in acidic food/liquid - therefore will need to put a time limit to ensure it doesn’t degrade too much
117
Q

It is strongly advised not to break, crush or chew the omperazole tablets. Explain why this is important?

A

Omeprazole is formulated as an enteric-coated tablet to avoid inactivation of the drug by gastric acid.
Crushing the tablet compromised the protective enteric coating, which resulted in loss of efficacy.

118
Q

what is Crohn’s disease and what part(s) of the intestine is affected?

A
  • Crohn’s disease is a type of inflammatory bowel disease (IBD). It causes swelling of the tissues (inflammation) in your digestive tract, which can lead to abdominal pain, severe diarrhea, fatigue, weight loss and malnutrition.
  • Most commonly, Crohn’s affects yoursmall intestineand the beginning of yourlarge intestine. However, the disease can affect any part of your digestive tract, from your mouth to youranus.
119
Q

what part(s) of the intestine are affected in ulcerative colitis?

A
  • Ulcerative colitis is a condition in which the lining of thelarge intestine (colon) and rectumbecome inflamed. It is a form of inflammatory bowel disease (IBD).
  • The inflammation in ulcerative colitis usually starts in yourrectum, which is close to your anus (where poop leaves your body). The inflammation can spread and affect a portion of your entire colon.
  • When the inflammation occurs in your rectum and lower part of your colon, it’s called ulcerativeproctitis.
  • If your entire large intestine is affected, it’s called pancolitis.
  • If only the left side of your colon is affected, it’s called limited or distal colitis.
120
Q

pharmacokinetics of mesalazine

A
  • Mesalazine (5-aminosalicylic acid, 5-ASA) is an anti inflammatory drug that works by coming in direct contact with the inflamed tissue.
  • Systemic absorption of mesalazine causes toxicity.
  • Mesalazine possesses good permeability in the small intestine, ~ 80% of unformulated mesalamine is absorbed in the small intestine but only poorly permeable in the colon.
  • Mesalazine is usually formulated as a modified release dosage form to ensure high local drug concentrations at the site of inflammation and to minimize its systemic exposure, which may contribute to potential side effects.
121
Q

mesalazine as modified release dosage forms

A
  • Microspheres, which release the drug via diffusion controlled mechanisms.
  • Gastro-resistant, pH sensitive polymers that release their contents rapidly or slowly over time after a certain pH is reached in the gut.
  • Azo-bond prodrugs that liberate mesalamine through bacterial cleavage once entering the colon.
122
Q

Pentasa

A
  • active ingrediant = Mesalazine
  • Prolonged release tablets, granules (time-dependent delivery)
  • Delivery site: duodenum, jejunum, ileum, colon
123
Q

Asacol

A
  • Active ingredient: Mesalazine
  • Gastro-resistant tablets (pH-dependent delivery at pH≥7)
  • Delivery site: terminal ileum & colon
  • display delayed release
  • Consist of a core of 5-ASA enveloped by a pH-dependent acrylic resin (Eudragit-S) coating, designed to deliver effective doses of 5-ASA to the colon with low systemic absorption. Coat dissolution occurs above pH 7.
124
Q

Salazopyrin EN enteric coated tablets

A
  • Active ingredient: Sulfasalazine where 5-ASA linked to sulfapyridine by azo bond
  • Gastro-resistant tablets (pH-dependent delivery at pH≥7)
  • delivery site = colon
  • Sulfasalazine is still used, however, some patients experience side effects due to the sulfur component
    use of sulfasalazine, however, is mainly limited by side effects associated with allergic reactions and high rates of
    intolerance (up to 20%) to the sulfapyridine component.
125
Q

It is recommended that patients take Asacol tablets before food. Explain why this is important for ensuring therapeutic success of the medicine?

A
  • food increases pH of the stomach - which will mean premature release of drug. food will also increase gastric residence time
  • by taking before food, it allows the medication to be properly absorbed in the intestines without interference from a large meal. This helps ensure the optimal therapeutic effectiveness of Asacol by allowing the active ingredients to reach their target sites and exert their anti-inflammatory effects more efficiently.
126
Q

PENTASA SACHETS - what region of the intestine is the 5-ASA released from the microgranules?

A
  • Pentasa’s micro granules have an ethyl cellulose coating. The drug is delivered continuously throughout the colon at all pH conditions in the GI tract.
  • When Pentasa granules are swallowed they travel from the stomach through the small bowel and large bowel to the rectum, releasing mesalazine continuously as they go (called prolonged release), treating the inflammation.
  • Pentasa’s micro granules allow a predictable and continuous diffusion-controlled release of mesalazine. Pentasa release mesalazine at all pH conditions in the colon making it also suitable for the treatment of left-sided colitis and pancolitis
127
Q

Pentasa tablets - at what point in the GI does the tablet disperse into microgranules?

A

When the Pentasa tablet is swallowed it breaks down in the stomach. The microgranules then start their journey through both the small and large bowel to the rectum, releasing mesalazine continuously as they go (called prolonged release), treating the inflammation.

128
Q

Pentasa enemas - what region of the GIT does pentasa enema deliver mesalazine to?

A

Pentasa enemas are a prescription medicine that treat Ulcerative Colitis in the last part of the large bowel, known as Distal Ulcerative Colitis (left sided colitis).

129
Q

pentasa suppositories - what region of the GIT does the pentasa suppository deliver mesalazine to?

A

Pentasa suppositories contain mesalazine (also known as 5-aminosalicylic acid or 5-ASA), and work by coming into direct contact with inflamed tissue in the rectum, treating the inflammation.

130
Q

definition of colitis

A

inflammation in the colon

131
Q

definition of distal colitis

A

Left-sided (distal) colitisis a form of ulcerative colitisthat begins at the rectum and extends up to the left colon (sigmoid colonand descending colon)

132
Q

definition of recto-sigmoid

A

The distal part of the sigmoid colon and the proximal part of the rectum

133
Q

definition of proctitis

A

inflammation of the rectum

134
Q

definition of diffuse disease

A

widespread to different parts of the bowel

135
Q

definition of refractory

A

not responding to current treatment

136
Q

definition of fistula

A

an abnormal or surgically made passage between a hollow or tubular organ & the body surface, or between two hollow or tubular organs

137
Q

definition of stricture

A

Narrowing in a tubular organ

138
Q

definition of crohn’s disease

A

An inflammatory disease of the bowel that can occur anywhere from the tip of the tongue to the anus. It is characterised by areas of normal tissue and areas of inflammation (skip lesions).

139
Q

definition of ulcerative colitis

A

Inflammatory disease that affects the colon and rectum. Inflammation is continuous from where it starts to where it ends – no skip lesions.

140
Q

cells and cytokines involved (patholophysiology) in crohns disease

A
  • Type 1 T-helper cells promote an inflammatory response via interferon-γ, TNF-α (major contributor), and IL-1, IL-6, IL-8, and IL-12.
  • CD involves the release of many proinflammatory cytokines.
  • the inflammation in CD may affect any part of the entire GI tract from the mouth to the anus. The small intestine is most commonly involved, and the terminal ileum and cecum are usually affected.
141
Q

cells and cytokines involved (pathophysiology) in ulcerative colitis

A
  • Atypical type 2 T-helper cells promote an inflammatory response viaprominflammatory cytokines: IL-1, IL-6, TNF-⍺.
  • The inflammatory process within the GI tract is limited to the colon and rectum in patients with UC
142
Q

cause of crohn’s disease

A
  • unknown - immune response to unidentifed antigens
  • thought that mycobacteruim avium subspecies paratuberculosis (MAP) could play a role
143
Q

cause of ulcerative colitis

A
  • unknown - immune response to bacteria or to unidentifed antigens
144
Q

risk factors for Crohn’s Disease

A
  • genetic predisposition
  • NSAIDs / other gastro-erosive drugs
  • oral contraceptives? (not fully proven)
  • environment
  • smoking
145
Q

risk factors for ulcerative colitis

A
  • genetic predisposition
  • NSAIDs / other gastro-erosive drugs
  • oral contraceptives? (not fully proven)
  • environment
146
Q

symptoms of crohn’s disease

A
  • diarrhoea
  • abominal cramping
  • fever
  • anemia
  • weight loss
  • fatigue
  • fistulas present
  • bloody diarrhoea rare
  • strictures common
147
Q

symptoms of ulcerative colitis

A
  • diarrhoea (bloody)
  • abominal cramping
  • fever
  • anemia
  • weight loss
  • fatigue
  • fistulas rare
  • bloody diarrhoea common
  • strictures rare
148
Q

link between nicotine & crohns disease

A
  • risk factor
  • exacerbates MAP infection in macrophages causing excessive production of pro-inflammatory cytokines
149
Q

link between nicotine & ulcerative colitis

A
  • protective factor
  • activates the cholinergic pathway providing anti-inflammatory effect
150
Q

extra-intestinal inflammatory manifestations of crohns disease & ulcerative colitis

A

various organs & systems are affected: joints, skin, liver, eye, mouth & blood (coagulation)

151
Q

complications of crohns disease

A
  • stenosis
  • abscess formation
  • fistulas
  • colon cancer
  • bowel cancer risk low
152
Q

complications of ulcerative colitis

A
  • severe bleeding
  • toxic megacolon
  • rupture of the bowel & colon cancer
  • bowel cancer risk high!
153
Q
A

PHCY220 (3 decks)

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