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Block 32 GI and surgery > Dyspepsia/Indigestion > Flashcards

Dyspepsia/Indigestion Flashcards

1
Q

what is achalasia?

A

An oesophageal motor disorder. Loss of oesophageal peristalsis and failure of lower oesophageal sphincter to relax

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2
Q

what are the presenting symptoms of achalasia?

A

dysphagia to solids and liquids, regurgitation and retrosternal pain which is slowly progressive over months or years. Patients may alter posture to enable swallowing.

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3
Q

what are oesophageal strictures?

A
  • Abnormal narrowing of the oesophageal lumen, often presents as dysphagia.
  • It can be due to inflammation, fibrosis or neoplasia.
  • The oesophagus loses distensibility and the stricture may be localised or diffuse.
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4
Q

what are the types of oesophageal strictures?

A

benign or malignant
most are a result of benign peptic strictures from GORD (risk reduced with PPIs). There is damage to the mucosal lining which over time leads to chronic inflammatory changes.
Malignant strictures develop from intrinsic direct proliferation and invasion of cancer cells from luminal mucosa.

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5
Q

what is the aetiology of benign strictures?

A
  • Corrosive substance ingestion
  • Eosinophilic oesophagitis
  • Drug induced oesophagitis
  • Radiation injury
  • Iatrogenic stricture post-endoscopic therapy
  • Anastomotic stricture
  • Chemotherapy induced oesophageal stricture
  • Thermal injury
  • Infectious oesophagitis
  • Other causes: (prolonged use of nasogastric tube, collagen vascular diseases such as scleroderma, benign mucosal pemphigoid, graft versus host disease, oesophageal web in plummer-vinson syndrome, Crohn disease, tuberculosis)
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6
Q

what is the aetiology of malignant strictures?

A
  • Oesophageal adenocarcinoma
  • Oesophageal squamous cell carcinoma
  • Metastatic oesophageal neoplasm (usually lung cancer)
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7
Q

what are the important things to ask for in a patient with strictures?

A
  • Dysphagia (progressive dysphagia)
  • Food impaction
  • Odynophagia
  • Chest pain
  • Weight loss
  • Rate and type of symptom progression correlates with underlying type of stricture
  • Physical examination not significant
  • Malignant stricture (Develop rapidly)
  • Benign stricture (Slow and insidious course)
  • history of GORD, barrets, hiatus hernia, medication
  • prior endoscopic treatment or oesophageal surgery
  • radiation therapy
  • meds (alendronate, tetracycline, antibiotics, NSAIDs)
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8
Q

what is the clinical presentation of peptic ulcer disease?

A

Usually present as chronic, upper abdominal pain related to eating a meal.
Due to NSAIDs and H.pylori
May be epigastric tenderness

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9
Q

what is the clinical presentation of GORD?

A

Risk factors such as family history of heartburn or GORD, obesity, older age, hiatus hernia.
Heartburn-burning sensation in chest after meals, worse when lying down, can occur at night but not usually exertional.
Reflux of acid into mouth with sour taste after meals

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10
Q

what is the clinical presentation of functional dyspepsia?

A

Sensation in upper gut and pain. Heartburn, sour taste in mouth, excessive burping, nausea and vomiting

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11
Q

what are the investigations for peptic ulcer disease?

A

H. Pylori urea breath test or stool antigen test. (patients <60)
Upper GI endoscopy-most specific and sensitive (patients over 60 or over 55 if weight loss). Endoscopy repeated 6-8 weeks later in patients with gastric ulcer to ensure healing
FBC-only if patient looks clinically anaemic or evidence of GI bleeding

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12
Q

what are the investigations for GORD?

A

PPI trial-further tests if no symptom relief after 8 weeks
OGD-with alarm symptoms
Ambulatory pH monitoring-can demonstrate abnormal exposure to oesophageal acid
Oesophageal manometry-evaluate oesophageal contractions and lower sphincter function
Combined impedance pH testing-quantify exposure to acid
Barium swallow-may be complementary to endoscopy for dysphagia
Oesophageal capsule endoscopy-visualise oesophagus without sedation

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13
Q

what are the investigations for functional dyspepsia?

A

No definitive diagnostic test. Cannot confirm dysmotility with any test. Normal X-ray or gastroscopy doesn’t mean there is nothing wrong

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14
Q

what are the investigations for H.pylori?

A

Blood test
Breath test-swallow pill containing tagged carbon molecules. With H.pylori carbon is released when solution is broken down
Stool test-stool antigen test
Scope test-upper endoscopy exam, biopsy which is analysed for H.pylori

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15
Q

what is the management for an active bleeding peptic ulcer?

A

mostly treated endoscopically, PPI reduce rebleeding. Stop NSAIDs, blood transfusion if needed, assess for H.pylori.

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16
Q

what is the management for a none active bleeding peptic ulcer?

A

eliminate underlying cause, ulcer healing therapy. Assess for H.pylori

H.Pylori negative-stop NSAIDs, ulcer healing therapy (PPIs), sucralfate, misoprostol
H.Pylori positive-eradication therapy

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17
Q

what is the management for mild typical GORD?

A

antacids, H2 antagonists, lifestyle changes. PPIs plus lifestyle changes are first line. Start with lowest effective dose of PPI. bedtime adjunctive H2 antagonists for people with nocturnal symptoms

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18
Q

what is the management for atypical/complicated GORD?

A

immediate endoscopy and also treated with PPIs

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19
Q

what is the management for functional dyspepsia

A

Treat for H.pylori if present. Low doses of antidepressants might reduce syptoms, PPIs

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20
Q

what treatment is used if a patient tests positive for H.pylori?

A

Eradication therapy should be started. Stop NSAIDs. This causes ulcer healing and a dramatic decrease in ulcer recurrence.. Therapy shouldn’t be started without infection. Triple therapy (a PPI plus two antibiotics) is recommended first-line in select patients.

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21
Q

describe H.pylori triple therapy?

A

Clarithromycin-based triple therapy (a PPI plus clarithromycin plus either amoxicillin or metronidazole) is a first-line treatment option in regions where clarithromycin resistance is known to be low (<15%) and in patients who have no previous history of macrolide antibiotic exposure. In patients who are allergic to penicillin, metronidazole should replace amoxicillin.

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22
Q

what is quadruple therapy for H.pylori?

A

Quadruple therapy (a PPI plus bismuth plus tetracycline plus a nitroimidazole such as metronidazole or tinidazole) is recommended for patients with previous macrolide exposure. Quadruple therapy is also an option for patients with penicillin allergy.

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23
Q

what are bismuth based regimens and sequential therapy for H.pylori eradication?

A

Bismuth-based regimens and sequential therapy (i.e., 5 days PPI plus amoxicillin, followed by 5 days PPI plus clarithromycin and a nitroimidazole) may have comparable eradication rates to standard triple first-line therapy.

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24
Q

H.pylori eradication

  1. concominant therapy
  2. hybrid therapy
  3. levofloxacin triple therapy
  4. fluoroquinolone sequential therapy
A
  1. Concomitant therapy (PPI, clarithromycin, amoxicillin, and a nitroimidazole)
  2. hybrid therapy (PPI and amoxicillin for 7 days, followed by a PPI, amoxicillin, clarithromycin, and a nitroimidazole for 7 days),
  3. levofloxacin triple therapy (PPI, levofloxacin, and amoxicillin),
  4. fluoroquinolone sequential therapy (PPI and amoxicillin for 5-7 days followed by a PPI, fluoroquinolone, and nitroimidazole for 5-7 days)

alternative first-line treatment strategies.

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25
Q

what are the principles of all types of H.pylori eradication?

A

All regimens contain antibiotics and therefore may cause diarrhoea, promote opportunistic infections, and interfere with absorption of many other drugs, including oral contraceptives.
Check for eradication of H pylori 1 month after the end of therapy. Continuation of acid suppressive therapy after treatment of infection is not necessary in most patients.
If the first treatment fails, at least one alternative regimen should be tried. Second-line regimens should avoid the antibiotics that were given in the first-line regimen. If the organism cannot be eradicated despite repeated attempts, long-term acid suppression therapy may be necessary to control symptoms.
In areas with high rates of multiple drug resistance, pre-treatment antimicrobial susceptibility-guided therapy may be more effective than clarithromycin-based triple therapy alone for H pylori eradication. However, H pylori culture and molecular testing is not widely available in all countries.

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26
Q

Gastric Cancer

  1. symptoms
  2. investigations
  3. treatments
  4. complications
A
  1. weight loss, abdominal pain. If proximal or gastro-oesophageal junction tumour can be dysphagia. Mainly adenocarcinomas but can also be lymphoma, leoimyosarcoma, neuroendocrne tuours, squamous cell carcinomas
  2. OGD with biopsy and staging based on imaging
  3. Early stage disease is treated with surgery alone. Locally advanced disease is treated with multimodality approach including surgery and postoperative chemoradiation. Metastatic disease is treated with chemotherapy, immunotherapy, chemoradiation.
  4. Complications include gastric bleeding and gastric outlet obstruction.
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27
Q

what is the epidemiology of gastric cancer?

A

Twice as likely in men than women and more common with older people. In recent years the incidence has decreased but tumours from cardia are increasing. More common in japan, china, finland and columbia than west.

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28
Q

what is the aetiology of gastric cancer?

A

Associated with consumption of smoked and salted foods and lack of refrigeration. Association with H.pylori, blood group A, gastric adenomatous polyps, pernicious anaemia, smoking.

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29
Q

describe the pathophysiology of gastric cancer?

A

loss of tumour supression gene p53. proto-oncogenes such as ras, c-myc, erbB2 (HER2/neu) overexpressed

There are 4 main genomic subtypes:

  • Tumours positive for epstein barr
  • Microsatellite unstable tumours
  • Genomically stable tumours
  • Chromosomal unstable tumours
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30
Q

what are signet ring cells?

A

large vacuole of mucin displaces nucleus to one side
the more signet the patient has the worse the prognosis
associated with gastric cancer

31
Q

what are the appropriate investigations to perform if suspect gastric cancer?

A

-FOB (->FIT)-more indicative of colorectal cancer though digested blood from stomach could still pass into stools
-Diagnosis with endoscopy and biopsy
Bloods (FBC, CRP, Serum amylase, LFT’s)

32
Q

what investigations are used to aid with staging of gastric cancer?

A

TMN-CT TAP=routine first line staging investigation/endoscopic ultrasound (better than CT)
Laparsocopy-identify occult peritoneal disease
PET CT-for junctional tumours

33
Q

what are the features of a type 1 gastric carcinoid?

A
  • mainly in women
  • multiple small (<1cm)
  • rare metastasis
  • submucosal, non invasive, gastric fundus and body
  • associated with chronic atrophic gastritis, hyperplasia of enterochromaffin like cells
  • good prognosis
34
Q

what are the features of type 2 gastric carcinoids?

A
  • multiple, variable sized
  • local lymph node metastasis
  • gastric fundus and body
  • associated with ZES, ZES with MEN
  • good prognosis
35
Q

what are the features of type 3 gastric carcinoids?

A
  • large solitary lesions
  • most have nodal and liver metastases
  • aggressive and invasive
  • over expression of TP53
  • poor prognosis
36
Q

what are the initial investigations for a patient with upper abdominal pain?

A

-Erect chest x-ray if perforation suspected (Rule out presence of free air)
-CT abdomen (Obstruction, diverticulitis, pancreatitis, acute appendicitis, suspected AAA
In pregnant women)
-Ultrasound (Right upper quadrant-cholecystitis-gallstones, Ectopic)
-MRI (Limited role)
-laproscopy
-Plain abdominal X-ray (Initial test, fast to perform, inexpensive, narrows diagnosis
Aortic wall calcification on kidney, ureters, bladder may suggest AAA)

37
Q

what increases the risk of gallstones?

A

4Fs: Female, fat, fair, fourty

12% in CBD

38
Q

what other condition increases the risk of obstructive ascending cholangitis?

A

obstructive ascending cholangitis more common in patients with gallstones

39
Q

what is primary biliary cholangitis associated with?

A

Associated with: Sjogren’s syndrome
RA
Systemic sclerosis
Thyroid disease

40
Q

what is gallbladder abscess a consequence of?

A

Consequence of acute cholecystitis

41
Q

what increases risk of gallstone ileus?

A

History of previous cholecystitis/ known gallstones

42
Q

what is the epidemiology of acalculous cholecystitis?

A

Complication of other medical & surgical conditions

Causes 5-10% of all acute cholecystitis.

43
Q

what are the clinical features of gallstones?

A

Colicky RUQ pain

Post-prandial (worst after fatty meal)

44
Q

what are the clinical features of cholangitis?

A 
Charcot’s triad:
Fever
RUQ pain
Jaundice
Murphy’s sign
45
Q

what are the clinical features of primary biliary cholangitis?

A

Fever
RUQ pain
Jaundice
Systemically unwell

46
Q

what are the clinical features of gallbladder abscess?

A

RUQ pain
Swinging pyrexia
Systemic illness

47
Q

what are the clinical features of gallstone ileus?

A

Fistula between gallbladder and duodenum

Abdominal pain

48
Q

what are the clinical features of acalculous cholecystitis?

A

High fever
There’ll be another co-morbidity
Systemically unwell
Gallbladder inflammation in absence of stones

49
Q

what pathogens are associated with cholangitis?

A

E. coli
Klebsiella
Enterococcus
Streptococcus

50
Q

what investigations are performed in a patient with suspected gallstones?

A

Abdominal USS
LFTs
MRCP

51
Q

what investigations are performed in a patient with suspected cholangitis?

A

Blood culture
USS
CT
ERCP

52
Q

what investigations are performed in a patient with suspected primary biliary cholangitis?

A

Anti-mitochondrial antibodies M2 subtype
Smooth muscle antibodies
IgM (expect to be raised)

53
Q

what investigations are performed in a patient with suspected gallbladder abscess?

A

USS +/ - CT scan

54
Q

what investigations are performed in a patient with suspected gallstone ileus?

A

Abdo X ray

USS +/- CT

55
Q

what investigations are performed in a patient with suspected acalculous cholecystitis?

A

Blood culture
USS
CT
MRCP/ERCP

56
Q

what are the complications of gallstones?

A

Gallbladder rupture
Cholangitis
Pancreatitis

57
Q

what are the complications of cholangitis?

A

Reynold’s pentad (adds confusion & hypotension to Charcot’s triad); can point to sepsis

58
Q

what are the complications of primary biliary cholangitis?

A

Cirrhosis
Osteomalacia & osteoporosis
Hepatocellular carcinoma risk significantly increased

59
Q

what are the complications of gallbladder abscess

A

Sepsis

60
Q

what are the complications of gallstone ileus?

A

Small bowel obstruction

61
Q

what are the complications of acalculous cholecystitis?

A

More serious morbidity & mortality than calculous cholecystitis

62
Q

what is the treatment for gallstones?

A

Laparoscopic cholecystectomy

63
Q

what is the treatment for obstructive ascending/acute cholangitis?

A

IV Abx
ERCP (usually 24-48 hrs after Abx)

64
Q

what is the treatment for primary biliary cholangitis

A 
Broad spectrum IV abx
Cholestyramine for pruritis
Fat-soluble vitamin supplementation
Ursodeoxycholic acid
Liver transplant where bilirubin >100
65
Q

what is the treatment for gallbladder abscess?

A

surgery

66
Q

what is the treatment for gallstone ileus?

A

Laparotomy & removal of gallstone from small bowel

67
Q

what is the treatment for acalculous cholecystitis?

A

Fitness determines surgery:
Fit – cholecystectomy

Unfit – percutaneous cholecystostomy

68
Q

what investigations would be used to assess acute pancreatitis?

A
  • Serum lipase or amylase
  • Aspartate -aminotransferase/alanine aminotransferase-
  • FBC
  • CRP
  • Haematocrit
  • Abdominal plain film
  • CXR
  • Trans-abdominal ultrasound
  • Ratio of serum lipase:amylase
69
Q

what would serum lipase or amylase levels be in a patient with acute pancreatitis?

A

3 times upper limit of normal range

70
Q

what is the role of testing CRP in patients with acute pancreatitis?

A

indicator of severity and progression of inflammation

71
Q

what is the role of testing haematocrit in patients with acute pancreatitis?

A

indicate severity and prognosis

72
Q

what is the role of testing arterial blood gas in patients with acute pancreatitis?

A

hypoxaemia and disturbances in acid base balance

73
Q

what investigations are performed in patients with suspected chronic pancreatitis and what would they show?

A

Blood glucose-may be elevated

CT scan – pancreatic calcifications, focal or diffuse enlargement of pancreas, ductal dilation and/or vascular complications

Abdominal ultrasound-structural/anatomical changes eg cavities, duct irregularity, contour irregularity of head/body, calcification

Abdominal x-ray –calcification present 30-70% of the time

Block 32 GI and surgery (12 decks)

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