Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Y3 CBLs > CBL_dyspepsia > Flashcards

CBL_dyspepsia Flashcards

1
Q

What is dyspepsia? (definition)

A

Dyspepsia = a range of upper gastrointestinal (GI) symptoms l_asting 4 weeks_ or more including heartburn (burning retrosternally), indigestion, upper abdominal pain or discomfort, gastric reflux, nausea or vomiting.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Definition of the following symptoms:

  • heartburn
  • gastric reflux
A

•Heartburn

–Typically a burning retrosternal sensation

•Gastric Reflux

–Describes the movement of stomach contents (usually acid) into the oesophagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Definition of the following symptoms:

  • indigestion
  • dysphagia
  • odynophagia
A

•Indigestion

–Pain or discomfort in the stomach associated with difficulty digesting food

•Dysphagia

–Difficulty swallowing

•Odynophagia

–Painful swallowing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What’s functional dyspepsia?

A

Functional dyspepsia

One or more of:

  • Bothersome postprandial (after meal) fullness
  • Early satiety
  • Epigastric pain
  • Epigastric burning

And: No evidence of structural disease (including normal OGD) that is likely to explain the diagnosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What’s GORD?

A

Gastro Oesophageal**Reflux Disease (GORD)

–A condition which develops when the reflux of gastric content causes troublesome symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

The differential diagnosis for dyspepsia

A

Dyspepsia differentials

  • GORD (A condition which develops when the reflux of gastric content causes troublesome symptoms)
  • Peptic/duodenal ulcer disease
  • Gastritis
  • Duodenal obstruction (e.g. pancreatic malignancy)
  • Gallbladder disease/Gallstones
  • Hiatus hernia = sliding vs oesophageal
  • Medication (NSAIDs, bisphosphonates, Ca2+ channel blockers, steroids)
  • Functional dyspepsia
  • IBS/IBD
  • Eosinophilic oesophagitis = autoimmune - allergy to precipitating foods
  • Cardiac causes
  • Cancers (oesophageal, gastric, pancreatic)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Initial consideration in management in the patient with dyspepsia

(3 likely scenarios)

A

Consider if:

A. Patient needs an urgent OGD (oesophago-gastroduodenoscopy) -> if there is any GI bleed: hematemesis or malena -> refer to hospital

B. Red flag symptoms -> 2 weeks referral cancer pathway

C. If not above -> consider most likely clinical diagnosis and trial of treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Who to refer for direct access (2 weeks wait) upper GI endoscopy?

A

•With dysphagia

•Aged 55 and over with weight loss and any of the following:

–Upper abdominal pain

–Reflux

–Dyspepsia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

In what group of patients (age and symptoms) we consider non-urgent direct access upper GI endoscopy?

(2 weeks oesophageal cancer referral)

A

Patients 55 years old or more

Symptoms:

  • failed dyspepsia treatment
  • upper abdo pain + anaemia
  • raised platelets + nausea/vomiting/weight loss/reflux/dyspepsia/upper abdo pain
  • N+V + weight loss/reflux/dyspepsia/upper abdo pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Dyspepsia management

  • lifestyle advice
A

Lifestyle advice:

  • No spicy, citrus foods
  • No smoking/alcohol
  • Lose weight
  • No lying down after meals
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

H. Pylori

  • type of an organism
  • transmission
A

H. Pylori:

  • gram negative bacteria (rod shaped)
  • oral-faecal or oral-oral route

-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

H. Pylori

  • is it usually symptomatic?
A
  • 90% of patients do not have symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What diseases does H. Pylori increase the risk of?

A
  • gastric cancer
  • doudenal ulcer
  • gastric ulcer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Investigations for H. Pylori

A

H. pylori testing

  • Breath test: looks at breakdown of urea in breath (urease activity by the bacteria) - requires 2+ weeks off PPI
  • Faecal antigen test
  • Biopsy on OGD (multiple biopsies)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Treatment for H. Pylori

A

_H. pylori treatmen_t

Triple therapy: Amoxicillin + metronidazole + PPI

for 2 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Management of dyspepsia (pharmacological classes)

A

A. H. pylori testing -> if negative start treatment (below)

B. PPI for 4-8w

C. If symptoms reoccur - low dose PPI, H2A - PRN

D. Consider H2 receptor antagonist therapy if there is an inadequate response to PPI

*Probably should be reviewing the diagnosis and the need for endoscopy at this point

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the components of Gaviscon?

A

Sodium alginate and sodium bicarbonate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Mechanism of action of Gaviscon and its components

A
  • Anti-acid -> it is alkali based; neutralises the gastric acid -> symptoms relief
  • Alginate -> forms a protective layer that floats on the top of gastric content
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Mode of action of Histamine 2 Receptor Antagonist? (in terms of dyspepsia)

Examples of H2RA drugs

A

Mode of action:

  • Histamine (H2) stimulates parietal cells to produce gastric acid
  • H2RA competitively block this receptor -> decrease in gastric acid production

Examples: Cimetidine, Ranitidine, Famotidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Side effects of H2 receptor antagonists

A

Side effects:

  • Cimetidine > Ranitidine > others -> inhibit cytochrome P450 pathway
  • Diarrhoea, headache, dizziness, rash
  • Increased risk of pneumonia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

PPI

  • mode of action
  • examples of drugs
A

Mode of action of PPI:

  • Irreversibly inhibit the proton pump (H+/K+/ATPase) of the gastric parietal cells
  • Stops H+ ions from being secreted into the gastric lumen

•Reduces acid production by 95-99%

Examples: Omeprazole, Lansoprazole, Pantoprazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

General side effects of PPI

A

General side effects PPI

•Nausea, vomiting, abdominal pain, flatulence, diarrhoea, constipation and headache

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Concerns associated with PPI use

A

Specific PPI Concerns

  • Increased risk of Clostridium difficile infection (and recurrence)
  • Osteoporosis (long term use)
  • Pneumonia
  • Rebound acid hyper-secretion (after stopping)
  • Iron deficiency anaemia
  • Electrolyte disturbance (Mg/Ca/K)
  • Microscopic colitis
  • Drug induced Subacute Cutaneous Lupus Erythematosus (SCLE)

*generally PPI are safe to use, but try to minimase a long-term and large dose use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Risk factors and associations in gastric ulcer

A

Gastric ulcers

  • Middle aged/older aged population
  • Pain worse with food
  • Gastro-toxic medications often implicated (Aspirin/NSAIDs/Steroids) & smoking
  • H.Pylori implicated in >60%
  • Malignancy must be considered 1-2%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Risk factors and associations with duodenal ulcers

A

Duodenal ulcers

  • Younger and usually male
  • Food relieves the pain
  • Nocturnal pain more common
  • H.Pylori implicated in >90%
  • Malignancy is very rare
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Examples of rare ulcers

A
  • Gastrinoma/Zollinger Ellison Syndrome
  • Crohn’s disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Symptoms of Zollinger Ellison syndrome

A

refractory diarrhoea + persistent/multiple ulcers

28
Q

What, when and why do we need to do if a gastric ulcer is identified on OGD?

A

Repeat OGD in 6-8 weeks

It is to asses the healing of the ulcer and for malignancy

29
Q

Management of ulcers

A
  • If Pylori positive – repeat testing after treatment should be considered to confirm eradication
  • Carefully consider NSAIDs

–Can they be stopped (ideally) or if not co-prescribe PPI with NSAID or COX-2 specific NSAID

30
Q

Complications of ulcers

A. Immediate

B. Long term

A

Immediate

Long term

  • Perforation (gastric/duodenal)
  • Bleeding
  • Obstruction/stricture
  • Fistula formation
  • Malignant transformation
31
Q

Management of GORD

  • lifestyle
A

Conservative/lifestyle Measures

–Diet

–Weight loss

–Smoking cessation

–Meal times/elevating bed

32
Q

Management of GORD

  • medication
A

Medication

  • Reviewing potentially exacerbating medications

Meds to relieve symptoms:

  • Antacids
  • PPI’s
  • H2RA’s
33
Q

Management of GORD

  • surgery
A

Surgery:

Anti-reflux surgery i.e. Laparoscopic Nissen Fundoplication

*fundus of the stomach is wrapped around the oesophagus -> when stomach contracts releasing its gastric acid content -> oesophagus closes so the acid cannot irritate it

34
Q

Pancreatic juice

  • content
  • how much is secreted each day
  • where does it go?
A

Pancreatic juice

Content: amylase, lipase, colipase and other proteases

  • 1.5 L a day

Secreted via pancreas -> pancreatic duct -> ampulla of Vater -> sphincter of Oddi -> duodenum

35
Q

What’s the role of bile acids?

How much is secreted?

A

Bile acids breakdown and dispose of fat and recycle products of haemolysis (e.g. bilirubin and biliverdin)

1-2 L bile secreted a day

36
Q

Where parietal cells are located?

What’s their role?

A

Parietal cells -> located in fundus and body of the stomach

Role: secrete intrinsically factor and gastric HCl

37
Q

What is the role of chief cells in the stomach?

A

They secrete pepsinogen, mucin and gastric lipase -> to digest food components

38
Q

What’s the role of H2 receptors and Vagus nerve in the stomach?

A
  • Histamine -> H2 receptor and vagus nerve (acetylcholine) -> stimulate acid secretion
  • Vagus nerve-> stimulates the hypothalamic nuclei -> satiety feeling when stomach is distended
39
Q

What do cardia and pyloric regions secrete?

A
  • Cardia and pyloric regions secrete mucus and bicarbonate ions
40
Q

What does antrum of stomach secrete?

A

antrum stomach -> gastrin secretion -> goes via blood stream to parietal cells to stimulate HCl secretion

41
Q

Why does the patient with GORD usually wake up around 2 AM?

A
  • no food buffering of pH (pH is not neutralised)
  • lowest acidity at about 2am
  • lying down position may aggravate GORD

Patient can wake up with heartburn.

42
Q

What is definition of GORD?

A

Gastro-oesophageal reflux disease (GORD) refers to gastroscopy proven oesophagitis and gastric acid sometimes regurgitates into the mouth

43
Q

Drugs that are common to cause dyspepsia

A

—NSAID’S

—Bisphosphonates

—Steroids

—Metformin

—Calcium antagonists

—Theophylline

—Nitrates

44
Q

Red flag symptoms for 2 weeks referral for gastroscopy

A
  • Acute GI bleeding
  • Progressive dysphagia
  • unintentional weight loss
  • persistent vomiting
  • iron deficiency anaemia
  • epigastric mass
  • aged over 55 yrs with new persistent dyspepsia
45
Q

Management of dyspepsia algorithms (2)

A. New onset - needing referral

B. New onset - not needing referral

A
46
Q

What cellular changes and what type of cancer is involved in Barrett’s oesophagus?

A

Metaplasia: squamous epithelium into columnar epithelium

Cancer type: oesophageal adenoma

47
Q

Management of Barrett’s oesophagus

  • surveillance
  • medication
  • endoscopic intervention
A

‘

  • endoscopic surveillance with biopsies
  • high-dose proton pump inhibitor: whilst this is commonly used in patients with Barrett’s

*the evidence base that this reduces the change of progression to dysplasia or induces regression of the lesion is limited

Endoscopic surveillance

  • for patients with metaplasia (but not dysplasia) endoscopy is recommended every 3-5 years

If dysplasia of any grade is identified endoscopic intervention is offered. Options include:

  • endoscopic mucosal resection
  • radiofrequency ablation
48
Q

Side effects of H2 antagonists (Cimetidine, Ranitidine) used for dyspepsia

A

Can cause:

  • diarrhoea
  • headache
  • rarely rash
  • liver problems
  • cimetidine -> causes gynaecomastia and erectile dysfunction (probably by blocking androgen receptors)
49
Q

PPI

  • examples
  • side effects
  • what does long term use may cause?
A

PPI

Examples: omeprazole, lansoprazole

Side effects: diarrhoea, nausea, vomiting, headache and abdo pain

Long term use: hyponatraemia, increased risk of C Diff contraction, reduced Mg levels, increased fracture risk

50
Q

What’s CLO test?

A

C ampylobacter like organism test

  • Rapid diagnostic test
  • Ability of H pylori to secrete the urease enzyme, which catalyse the conversion of urea to ammonia and carbon dioxide

*it is done during gastroscopy -> gastric mucose is placed onto medium containing urea

51
Q

1st and 2nd line treatment to eradicate H Pylori

A

First line

◦7 days, twice daily course of PPI, Amoxicillin & either clarithromycin or metronidazole

*Allergic to Penicillin – PPI, clarithromycin or metronidazole

Second line

◦7-days twice day course of PPI, Amoxicillin & clarithromycin or metronidazole (whihever was not used before)

◦ could use tetracycline or Quinolone

◦Levofloxacin, PPI & metronidazole – Penicillin allergy

52
Q

Gastric vs duodenal ulcer

A
53
Q

Classical signs of pancreatitis

A
  • Classically epigastric pain radiating to the back
  • Grey-Turner’s sign (flank ecchymoses)
  • Cullen’s sign (peri-umbilical ecchymoses)
54
Q

Two most common causes of pancreatitis

A

80% of causes:

  • alcohol
  • gallstones
55
Q

What is used to predict the outcomes of pancreatitis?

A
  • Marker for prognostic severity = CRP (high at 48h –> bad prognosis)
  • Modified Glasgow score = pancreatitis severity scoring system
56
Q

Markers (2) for pancreatitis

  • how long are they raised for?
A
  • Amylase = can rise rapidly within 3–6 hours of the onset of symptoms, and may remain elevated for up to five days (normally 3-4 days)
  • Lipase = elevated for longer and more sensitive marker
57
Q

Initial imaging in suspected acute pancreatitis

A
  • Initial investigation in acute pancreatitis = USS -> identification of gallstones
  • If diagnostic uncertainty = CT
58
Q

Hypocalcaemia and pancreatitis - what does it tell us?

A

poor prognostic sign in pancreatitis –> extensive retroperitoneal necrosis

59
Q

Complications of pancreatitis

A. before 4 weeks

B. after 4 weeks

A

Before 4w

After 4w

  • Peripancreatic fluid collections
  • Necrosis
  • Pseudocyst
  • Abscess
60
Q

What’s Courvoisier’s sign?

A

Courvoisier’s sign:

palpably enlarged gallbladder + nontender + painless jaundice -> the cause is unlikely to be gallstones

*possible malignancy of the gallbladder or the pancreas

61
Q

Interpretation of AST:ALT

  • AST:ALT = 1
  • AST:ALT >2.5
  • AST:ALT <1
A

Aminotransferases (AST, ALT) - generally associated with hepatocellular damage

  • AST: ALT =1
    • Associated with ischaemia (CCF and ischaemic necrosis and hepatitis)
  • AST: ALT >2.5
    • Associated with Alcoholic hepatitis
    • Alcohol induced deficiency of pyridoxal phosphate
  • AST: ALT <1
    • High rise in ALT specific for Hepatocellular damage
    • Paracetamol OD with hepatocellular necrosis
    • Viral hepatitis, ischaemic necrosis, toxic hepatitis
62
Q

What’s the role of ALP and GGT?

A

ALP, γ**GT - generally associated with cholestasis

  • ALP primarily associated with cholestasis and malignant hepatic infiltration
    • Marker of rapid bone turnover and extensive bony metastasis
  • GGT sensitive to alcohol ingestion
    • Marker of Hepatocellular damage but non-specific
    • Sharpest rise associated with biliary and hepatic obstruction
63
Q

What is Whipple’s procedure?

A

Whipple’s procedure = pancreaticoduodenectomy - removal of the head of the pancreas, the first part of the small intestine (duodenum), the gallbladder and the bile duct.

64
Q

The most common pancreatic cancer

A. adults

B. children

A

95% of pancreatic cancers are exocrine tumours

A. adults: ductal adenocarcinoma

B. children: pancreatoblastoma

65
Q

What set of symptoms does need an urgent referral for endoscopy?

A

Urgent (2ww endoscopy)

  • dysphagia
  • an upper abdominal mass consistent with stomach cancer
  • Patients aged >= 55 years who’ve got weight loss, AND any of the following:
  • upper abdominal pain
  • reflux
  • dyspepsia
66
Q

Set of symptoms for non-urgent referral for endoscopy

  • all age patient + what symptoms
  • if a patient is >=55 + what symptoms
A

Non-urgent

Patients with haematemesis

Patients aged >= 55 years who’ve got:

  • treatment-resistant dyspepsia or
  • upper abdominal pain with low haemoglobin levels or
  • raised platelet count with any of the following: nausea, vomiting, weight loss, reflux, dyspepsia, upper abdominal pain
  • nausea or vomiting with any of the following: weight loss, reflux, dyspepsia, upper abdominal pain
67
Q
A

Y3 CBLs (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions