Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
40 Cards in this Set
- Front
- Back
- 3rd side (hint)
|
Dyspepsia definition
|
persistent or recurrent abdominal pain or
abdominal discomfort centred in upper abdomen |
|
|
|
dyspepsia causes
|
Gastro-oesophageal reflux disease (GORD)
Peptic ulcer disease (PUD) Functional (non-ulcer) dyspepsia Gastric cancer Miscellaneous: biliary tract disease, chronic pancreatitis, intestinal angina, diabetes mellitus (causes gastroparesis), drugs |
|
|
|
what are the percentage causes of dipepsia
|
|
|
|
|
what factors when not balanced can lead to a gi acid disorder
|
|
|
|
|
Desribe some of the pathways that contribute to acid and possible drug targets
|
|
|
|
|
describe some of the clinical differences between GORD, PUD, DU
|
|
|
|
|
“Alarm” symptoms or signs:
|
Anaemia (iron-deficiency)
Loss of weight (unintentional) Anorexia Recent onset of progressive symptoms Malaena or haemetemesis |
|
|
|
Other features that may indicate further investigaiton
|
Dysphagia
Previous gastric surgery Persistent vomiting Epigastric mass Jaundice Previous peptic ulcer disease Non-steroidal anti-inflammatory drug use Age > 45 years at onset (higher risk of malignancy) |
|
|
|
The process of further investigation
|
|
|
|
|
Drugs that lower LOS
|
|
|
|
|
drugs that irritate mucosa
|
|
|
|
|
what drugs are protective
|
bottoms ones decrease opening
|
|
|
|
GORD What foods aggravate?
|
fatty foods
spicy carbonated drinks citrus caffeinated tomatoe chocolate ethanol garlic mint onion sugar |
|
|
|
GORD aggravating lifestyle?
|
overweight
too much too quickly |
|
|
|
GORD lifestyle protective?
|
eater smaller meals
higher protein elevate bed loss weight if needed loose clothes |
|
|
|
GORD incidence?
|
It is common
5-35% of adults have symptoms once a month 15% of adults have symptoms once a week 7% have it daily |
|
|
|
GORD disturbance of what factors
|
GORD is related to disturbance of normal
anti-reflux mechanisms Lower oesophageal sphincter (LOS) tone Crural diaphragm Junction below diaphragmatic hiatus |
|
|
|
GORD: consequences?
|
Oesophageal
Dyspeptic symptoms Reflux oesophagitis Erosive oesophagitis Stricture disease Barrett’s oesophagus ulceration circumferential erosions |
|
|
|
Barrett’s oesophagus features?
|
This involves metaplasia of the oesophageal
epithelium to columnar epithelium This columnar epithelium is what is normally found in the stomach and is more resistant to acid Barrett’s is a risk factor for oesophageal cancer Increases risk 40 fold |
|
|
|
GORD treatment goals
|
Relieve symptoms
Heal any erosions or ulcerations Prevent complications |
|
|
|
Treatment principles
|
Reduce (if possible) any worsening factors
drugs, such as NSAIDs, tetracyclines, bisphosphonates, potassium salts Render the refluxate less harmful Acid-neutralisation or suppression Improve oesophageal clearance Posture, pro-kinetics Protect oesophageal mucosa Posture , exercise, bed head elevation |
|
|
|
GORD: Treatment strategies?
|
Step-up
Start with low potency treatments and increase if necessary E.g. Antacid / alginate> H2RA > PPI* Step-down Start with high potency treatments and decrease if possible E.g. PPI* > H2RA > Antacid / alginate * may step-up or down between high and low dose PPIs |
|
|
|
GORD: Treatment strategies pros and cons
|
Step-down
May use higher potency treatment than needed Rapid resolution of symptoms Minimises consultations, but ? treat and forget Step-up Uses therapy of minimum force May delay resolution of symptoms May involve more consultations Costs may also vary between approaches, although now with generic PPIs this is less of an issue |
|
|
|
barrets treatment
|
Note however that potent and long-term acidsuppression
with PPIs is indicated where Barrett’s Oesophagus has been confirmed Reduced exposure to acid is considered essential to reduce the risk of progression to malignancy |
|
|
|
GORD prokinetics
|
By encouraging gastric emptying (downwards !)
they reduce the risk of regurgitation of acid stomach contents into the oesophagus Dopamine antagonists The anti-emetics metoclopramide and domperidone possess useful pro-kinetic effects Other agents Cisapride stimulates acetylcholine release to increase GI motility. Now only available through Special Access Scheme due to the risk of prolonging the QT interval |
|
|
|
Peptic Ulcer Disease (PUD)
freq ratio mortality risk for? |
Peptic Ulcer Disease
Ulceration present, may be either in Small intestine e.g. duodenum (DU) Stomach (GU) Peptic ulcer disease is common 12% of men and 9% of women have PUD at some time in their lives Duodenal Ulcer: Gastric Ulcer ratio 1.5:1 Mortality highest >75 years Rare in children and juveniles |
|
|
|
Aetiology of PUD?
|
|
|
|
|
PUD: quantifying factors
that increase risk |
Some viral infections (CMV, herpes)
Cancer therapy: chemo- and radio- therapy Genetic pre-disposition Illicit drug use (crack cocaine) Helicobacter pylori infection is the most common cause of PUDH.Pylori associated with >90% of DU and >80% of GU |
|
|
|
PUD: complications?
|
Perforation
into peritoneal cavity Penetration into a solid organ eg. Pancreas Fistulation into a hollow organ eg. large bowel Bleeding acute or chronic, leading to anaemia Death most ulcers are oval shape most only have one at a time |
|
|
|
H.pylori characteristics
|
Infection acquired by oral-oral,
oral-faecal transmission Commonly transmitted between family members, especially in overcrowded homes Effects include: Secretion of enzymes which cause tissue damage Hypergastrinaemia Activated inflammatory cascade H.Pylori is also associated with certain lymphomas and is classed as a carcinogen can cause asymptomitic colonisation |
|
|
|
Helicobacter pylori: tests
|
|
|
|
|
SNAIDS PUD cause
treatment different SNAIDS |
Reduction in normal gastric cytoprotective
mechanisms through Cyclooxygenase inhibition is the main issue here Local irritation of GI mucosa by NSAIDs is of less importance Clinically diagnosed peptic ulcers will develop in 2-4% of patients per year treated with an NSAID (higher when other risk factors co-exist) Greatest risk within the first month of treatment (especially between days 7-30), whilst risk declines slightly thereafter, it still remains |
COX 2 rates of ulcer same at 12 months, low dose aspirin negates lower risk
|
|
|
NSAIDs – GI toxicity avoidance
|
If NSAIDs must be used, options to reduce GI risk are:
Proton Pump Inhibitors (PPIs) Omeprazole 20mg daily or equivalent, effective, convenien usually well tolerated Prostaglandin analogue Misoprostol, 200mcg QDS most effective, poorly tolerated H2 Receptor Antagonists Ranitidine, evidence less impressive unless double dosed H.Pylori eradication controversial ? effective for low risk patients, but not high risk patients |
|
|
|
PUD: Treatment principles
|
Remove aggravating factors where possible
Drugs, smoking, alcohol Treat complications Anaemia, other acute complications Heal ulcer Prevent recurrence Eradication of H.pylori leads to a lower recurrence rate of PU than maintenance treatment with H2 antagonists or PPIs |
|
|
|
PUD: Treatment options
|
Antisecretory Agents
H2 receptor antagonists Proton pump inhibitors H.Pylori eradication Mucosal Protective Agents Antacids Alginates |
|
|
|
PUD treatment flowchart
|
|
|
|
|
H.Pylori Eradication
|
1
esomeprazole 20 mg orally, twice daily for 7 days OR 1 omeprazole 20 mg orally, twice daily for 7 days PLUS amoxycillin 1 g orally, twice daily for 7 days PLUS clarithromycin 500 mg orally, twice daily for 7 days. |
Helicobacter pylori is able to withstand the
acid environment usually present in the stomach However growth of H.Pylori occurs when acid levels are lower i.e. at a higher pH Effectiveness of antibiotic therapy is increased when growth of the bacterium is occurring Therefore acid-lowering therapy (e.g. with PPI) acts synergistically with antibiotics to kill H.Pylori Standard approach is to give PPI plus two Antibiotics (“Triple Therapy”) Adherence is poor packs can help, treatment failure common |
|
|
H.Pylori Eradication failure
|
Failure of eradication therapy is not uncommon
If clarithromycin was used in initial regime, it is likely to have induced resistance, so should not be used in the repeat attempt at eradication Options quite limited, need specialist advice Regimens used may include: Tetracyclines Metronidazole Rifabutin Bismuth May need longer course or “quadruple therapy” |
|
|
|
PUD: Treating Complications
|
Complicated Ulcers
Bleeding Ulcers haemodynamic stabilisation endoscopy +/-adrenaline injection cautery for obviously bleeding vessels IV PPIs |
1
esomeprazole 80 mg IV, as a bolus, FOLLOWED BY esomeprazole 8 mg/hour by IV infusion, for up to 3 days OR 1 pantoprazole 80 mg IV, as a bolus, FOLLOWED BY pantoprazole 8 mg/hour by IV infusion, for up to 3 days. Costs can be reduced by switching to oral proton pump inhibitor therapy, twice daily, once the patient is permitted to drink, but efficacy may be less. |
|
|
Antiacids
|
Some antacid preparations also contain alginate salts
These are intended to exert a “rafting effect”to reduce exposure of mucosa to acidic gastric contents May be useful for some patients with GORD Popular in GORD related to pregnancy as established safety As with simple antacids, some care needed where Sodium content is significant Some evidence that may help laryngopharyngeal reflux where reflux associated with hoarseness and other voice disorders, sore throats and cough may also contain sugar care with diabetics |
|
