GORD Flashcards

1
Q

How can acute HF be managed?

A

Initial Management of acute heart failure (pulmonary oedema)

Sit the patient up
Oxygen therapy (aiming saturations >94% in normal circumstances)
IV furosemide 40mg or more (with further doses as necessary) and close fluid balance (aiming for a negative balance)
SC morphine - this is contentious with some studies suggesting that it might increase mortality by suppressing respiration
Advanced management of acute heart failure (pulmonary oedema)

The following usually occurs in a high dependency or ITU setting.

CPAP - reduces hypoxia and may help push fluid out of alveoli
Intubation and ventilation
Furosemide infusion - continuous IV furosemide given over 24 hours to maximise diuresis
Dopamine infusion - Continuous IV dopamine given over 24 hours. It works by inhibiting sympathetic drive and thereby increasing myocardial contractility.
Intra-aortic balloon pump - if the patient is in cardiogenic shock
Ultrafiltration - If resistant to or contraindicated diuretics
Note that GTN infusion is no longer routinely used in acute heart failure

Adverse effects of heart failure medications

Common adverse effects for different medications are listed below

Beta blockers: Bradycardia, hypotension, fatigue, dizziness
ACE inhibitors: Hyperkalaemia, renal impairment, dry cough, lightheadedness, fatigue, GI disturbances, angioedema
Spironolactone: Hyperkalaemia, renal impairment, gynaecomastia, breast tenderness/hair growth in women, changes in libido
Furosemide: Hypotension, hypoatraemia/kalaemia,
Hydralazine/nitrate: Headache, palpitation, flushing
Digoxin: Dizziness, blurred vision, GI disturbances

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2
Q

How can HF be managed?

A

Lifestyle modification

Smoking cessation
Salt and fluid restriction (this improves mortality)
Supervised cardiac rehabilitation
Pharmacological management

ACE-inhibitor and beta-blocker (these improve mortality)
Consider angiotensin receptor blocker (ARB) if intolerant to ACE inhibitors
Consider hydralazine and a nitrate intolerant to ACE-I and ARB.
Loop diuretics such as furosemide or bumetanide improve symptoms (but NOT mortality)
If symptoms persist and NYHA Class 3 or 4 consider:
Aldosterone antagonists such as spironolactone or eplerenone. These drugs also improve mortality.
Hydralazine and a nitrate for Afro-Caribbean patients
Ivabradine if in sinus rhythm and impaired ejection fraction
Angiotensin receptor blocker
Digoxin - useful in those with AF. This worsens mortality but improves morbidity.

Surgical/device management options

Cardiac resynchronisation therapy
ICDs are indicated if the following criteria are fulfilled:
QRS interval <120ms, high risk sudden cardiac death, NYHA class I-III
QRS interval 120-149ms without LBBB, NYHA class I-III
QRS interval 120-149ms with LBBB, NYHA class I

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3
Q

What are the causes go GORD?

A

OXFORD

Pathophysiology

Reflux of stomach content into oesophagus, usually due to lower oesophageal sphincter dysfunction.

Risk factors

Medical:

Hiatus hernia.

Gastric acid hypersecretion.

Pregnancy

Lifestyle:

Obesity

Overeating

Smoking

Alcohol

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4
Q

What are the symptoms of GORD?

A

OXFORD

Signs and symptoms

Heartburn, a burning chest/epigastric pain. Worse after eating, on lying, and bending forward. Relieved by antacids.

Cough, hoarseness, nocturnal asthma.

Belching, acid brash (acid regurgitation).

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5
Q

What are differentials for GORD?

A

OXFORD

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6
Q

How is GORD investigated?

A

OXFORD

Investigations

Diagnosis is usually clinical, involving a PPI trial.
Refer for urgent endoscopy if there is suspicion of malignancy:

Alarm signs for gastric or oesophageal cancer: >55 years old at onset of dyspepsia (and persistent), persistent vomiting, dysphagia, weight loss, upper GI bleeding (or iron-deficiency anaemia), epigastric mass.

Endoscopy may show oesophagitis (erosions, strictures, ulceration), Barret’s oesophagus, or oesophageal cancer.

Stop PPIs 2 weeks before test.

pH monitoring if clinical picture and endoscopy not diagnostic:

Naso-oesophageal catheter or wireless radiotelemetry.

pH <4 for >4% of 24 hour period is diagnostic.

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7
Q

How is GORD treated ?

A

Lifestyle
Drugs
Surgery

OXFORD

Management

Management of dyspepsia:

Review meds and try lifestyle changes for 1 month. Endoscopy if there are alarm signs.

Empirical PPI therapy for 1-2 months if GORD suspected (rather than ulcer) i.e. heartburn predominates.

H. pyloritesting if still symptomatic. Needs 2 weeks PPI washout first.

If GORD confirmed on endoscopy, go straight to PPI.
Lifestyle changes:

Reduce alcohol and smoking.

Lose weight and exercise.

Reduce spicy and fatty foods.

Have small, regular meals.

Long-term:

Low dose PPI if symptoms recur, but ideally aim to just use antacids.

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8
Q

What are the complications of GORD?

A

OXFORD

Oesophagitis

Oesophageal ulcers.

Benign oesophageal strictures (aka peptic stricture).

Barrett’s oesophagus in 10%.

All are potential causes of dysphagia.

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9
Q

How can H-pylori be treated?

A

Helicobacter pylori is a Gram-negative bacteria associated with a variety of gastrointestinal problems, principally peptic ulcer disease

Associations
peptic ulcer disease (95% of duodenal ulcers, 75% of gastric ulcers)
gastric cancer
B cell lymphoma of MALT tissue (eradication of H pylori results causes regression in 80% of patients)
atrophic gastritis

The role of H pylori in Gastro-oesophageal reflux disease (GORD) is unclear - there is currently no role in GORD for the eradication of H pylori

Management - eradication may be achieved with a 7 day course of
a proton pump inhibitor + amoxicillin + (clarithromycin OR metronidazole)
if penicillin allergic: a proton pump inhibitor + metronidazole + clarithromycin

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10
Q

When is an endoscopy recommended in GORD?

A

Overview
poor correlation between symptoms and endoscopy appearance

Indications for upper GI endoscopy:
age > 55 years
symptoms > 4 weeks or persistent symptoms despite treatment
dysphagia
relapsing symptoms
weight loss

If endoscopy is negative consider 24-hr oesophageal pH monitoring (the gold standard test for diagnosis)

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11
Q

Hoe does a upper GI bleed present?

A

The symptoms of an upper gastrointestinal bleed include haematemesis (vomiting of blood or coffee-ground-like material) and/or melena (black, tarry stools).

The observations can assess the extent of blood loss. Resting tachycardia suggests mild to moderate hypovolaemia (less than 15% of blood volume lost). Orthostatic hypertension, as seen in this question, suggests at least 15% blood volume loss. Supine hypotension suggests over 40% blood volume loss.

Causes of Upper GI bleeds

Oesophageal/gastric varices
Peptic ulcer disease (H. pylori, NSAID use, smoking)
Malignancy
Aorto-enteric fistula (previous abdominal aortic aneurysm or an aortic graft)
Angiodysplasia
Mallory Weiss tear
Further considerations in Upper GI bleeds

Is the patient more susceptible to the effects of anaemia, such as coronary artery disease?
Is the patient at risk of fluid overload with aggressive resuscitation (such as renal disease)?
Will the bleeding be harder to control, owing to anticoagulation, liver disease or thrombocytopaenia?

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12
Q

How is a upper Gi bleed managed?

A

Management

Initial management involves an A-E assessment, focussing on IV fluid resuscitation and blood transfusion (if Hb <7) with or without platelets and fresh frozen plasma (every 4th unit of blood).
Recent evidence suggests that overtransfusion increases mortality therefore patients should not be transfused to a normal haemoglobin.
The patient should be NBM and supplemental oxygen given.
IV PPI may also be initiated.
In variceal bleeding, IV terlipressin and antibiotics are used.
Once stable, upper GI endoscopy is carried out to locate the source of the bleeding and attempt to stop further bleeding through various mechanisms, such as adrenaline injection and ulcer clipping.
The Rockall Score

The Rockall score is a risk assessment tool that predicts mortality in these patients. It can be calculated pre-endoscopy (maximum score 7) or post endoscopy (maximum score 11).
Patients who score >0 are recommended to have an inpatient OGD whereas those scoring 0 can have an urgent outpatient OGD.
0 points 1 point 2 points 3 points
Age (years) <60 60-79 >80
Systolic blood pressure/pulse rate (mmHg) SBP>100, HR<100 SBP>100, HR>100 SBP<100
Comorbidities none Ischemic heart disease or cardiac failure Liver failure, renal failure or metastases
Post endoscopy diagnosis Mallory Weiss tear All other diagnoses Upper GI malignancy
Signs at endoscopy No blood or dark red spot Blood in upper GI tract, spurting vessel or adherent clot.
Glasgow-Blatchford Score

The Glasgow-Blatchford score is preferred by NICE pre-endoscopy for deciding upon timing of the procedure.
Again those scoring<0 may be suitable for outpatient OGD.
It is formed by giving scores for the following paratmeters:
Urea
Haemoglobin (different for men and women)
Systolic blood pressure
Other paremeters:
Tachycardia
Clincally observed malaena
Syncope
Liver disease
Heart failure

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13
Q

What are the risk factors and causes of PUD?

A

Peptic ulcer disease includes duodenal and gastric ulcers; duodenal ulcers and four-times more common. The stomach lining protects itself with mucin and bicarbonate secretion and mucosal blood flow; however, damage can occur if these barriers are not sufficient, or if external factors such as Helicobacter pylori (H. Pylori) are present.

Causes of peptic ulcer disease

Approximately 90% of duodenal ulcers are caused by H. Pylori infection.

Other risk factors for duodenal ulcers include:

NSIADS
Chronic steroid use
SSRIs
Increase in gastric acid secretion
Smoking
Blood group O
Increased gastric emptying (more acid in the duodenum)
Risk factors for gastric ulcers
NSAIDs
H. Pylori
Smoking
Delayed gastric emptying
Severe stress.
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14
Q

How can PUD be managed?

A

Management

H. Pylori-negative peptic ulcer disease is managed with 4-8 weeks of full dose PPI treatment and lifestyle advise, including:

Stop smoking
Cut down on alcohol
Have more regular, smaller meals and eat 4 hours before bed
Avoid acidic foods, coffee, fatty or spicy foods
Encourage weight loss if obese
Try to avoid stress
Avoid NSAIDs, steroids, bisphosphonates, potassium supplements, SSRIs and crack cocaine
Try over the counter antacids
Follow-up of patients with peptic ulcers

Patients with a gastric ulcer should have a repeat endoscopy 6-8 weeks after the start of PPI treatment to ensure ulcer healing and rule out malignancy.
Patients with a duodenal ulcer should be asked about adherence and lifestyle factors should be enforced. If symptoms continue, other rarer causes of duodenal ulcers should be considered, such as malignancy, use of ulcer-promoting drugs, missed H. pylori infection, Zollinger-Ellison syndrome, or Crohn’s disease. If these are ruled out, a low-dose PPI can be prescribed.
References

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15
Q

What are the drug causes of GORD?

A

Drugs, BACON:

β-blockers

Anticholinergics

Calcium channel blockers.

Oral contraceptives.

NSAIDs

Bisphosphanates

Antidepressants

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16
Q

How do PPI’s work and what are the side effects?

A

Proton pump inhibitors (PPIs)

Drugs

Omeprazole, esomeprazole, lansoprazole, and pantoprazole.

Mechanism

Inhibits the H+/K+ATPase (proton pump) of gastric parietal cells.

Side effects

GI (common): diarrhoea, constipation, nausea, vomiting, abdo pain.

CNS: headache, dizziness.

C. diff, especially if taken with antibiotics.

↓Mg2+, ↓Na+.

Osteoporotic fracture.

Acute interstitial nephritis.

Interactions

Inhibits CYP3A4 → ↑warfarin, ↑BZD, ↑tramadol.

Inhibits CYP2C19 → ↓clopidogrel efficacy.