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YEAR 3 TCD > WEEK 10 - Epigastric Abdominal Pain > Flashcards

WEEK 10 - Epigastric Abdominal Pain Flashcards

1
Q

Colic is an example of what kind of pain, caused by contraction/distention (such as renal, biliary or bowel colic)?

A

Visceral

Colic causes distention of the colon that is felt as visceral pain

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2
Q

What is visceral pain stimulated by?

A

Contraction, tension, stretching or ischaemia

—> visceral structures are highly sensitive to distention (stretch), ischaemia and inflammation

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3
Q

What is visceral pain like?

A

Dull and poorly localised

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4
Q

Visceral pain is pain that results from the activation of _________ of the thoracic, pelvic, or abdominal viscera (organs). Visceral pain is diffuse, difficult to localise and often referred to a distant, usually superficial, structure. Pain from foregut structures is experienced in the __________, midgut structures in the _________ region and hindgut structures in the ___________ region.

A
  • nociceptors
  • epigastrium
  • periumbilcal
  • hypogastric
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5
Q

Somatic pain is stimulated by a direct _______ substance causing inflammation of the ________ peritoneum

A
  • noxious
  • parietal

Stretching of the peritoneum from movement causes somatic pain

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6
Q

What does the term peritonitic mean?

A

Inflammation of the peritoneum by a noxious substance

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7
Q

What is meant by the term rebound tenderness?

A

Pain when releasing pressure from palpation (sign of peritonism)

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8
Q

What is meant by the term guarding?

A

Involuntary tensing of abdominal wall muscle on palpation (sign of local peritonism if in one quadrant only)

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9
Q

What is meant by the term rigid abdomen?

A

Involuntary guarding in all 4 quadrants (sign of general peritonitis)

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10
Q
A
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11
Q

What do each secrete?

  1. Chief cells
  2. G cells
  3. Parietal cells
  4. Mucous cells
A
  1. Pepsinogen
  2. Gastrin
  3. HCl
  4. Alkaline mucus (for protection of the stomach lining)
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12
Q

Where is trypsinogen activated into its active form, trypsin, by enterokinase?

A

Duodenum

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13
Q

Where is elastin broken down by elastases?

A

Exocrine pancreas

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14
Q

Where does lipase break down triglycerides into fatty acids and monoglycerides?

A

Exocrine pancreas

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15
Q

What are Caput medusae?

A

periumbilical varices that branch out from the umbilicus that occurs with portal hypertension from liver cirrhosis.

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16
Q

What is this?

A

Cullen’s sign = Periumbilical ecchymosis

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17
Q

What is grey-turner’s sign?

A

Ecchymosis in either flank

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18
Q

What is Murphy’s sign?

A

Pain in the RUQ from local peritonism from acute cholecystitis

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19
Q

What is Rovsing’s sign?

A

Pain felt in the right iliac fossa on palpation in the left iliac fossa from local peritonism from acute appendicitis

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20
Q

What do Cullen’s sign and Grey-Turner’s sign indicate?

A

Internal haemorrhage which can present in acute pancreatitis, splenic rupture or perforated peptic ulcer disease. When these signs result from a cute haemorrhagic pancreatitis, this can indicate severe disease and higher mortality

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21
Q

Acute pancreatitis is an inflammation of the pancreas caused by an activation of __________ + __________. It can often cause a _______ which can in turn cause organ failure, such as an acute kidney injury (renal failure) and ______ (respiratory failure). Although it is a self-limited condition, there is a wide spectrum of disease severity, ranging from very mild cases where patients experience only upper abdominal discomfort, to very severe cases that require a prolonged hospital stay with Critical Care support and death. Thus, an important facet of care is to determine the cause of the acute pancreatitis, so treatment to minimise (or eliminate) the risk factors will prevent future episodes of acute pancreatitis.

A
  • pancreatic enzymes + autodigestion
  • SIRS (systemic inflammatory response syndrome)
  • ARDS (acute respiratory distress syndrome)
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22
Q

What does a diagnosis of acute pancreatitis require?

A

At least 2/3 of the following:

  • abdominal pain (acute, persistent, epigastric pain radiating into the back)
  • serum lipase/amylase levels greater than 3X THE UPPER LIMIT OF NORMAL
  • radiological evidence of pancreatitis (CT/MR)
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23
Q

During the acute pancreatitis disease process, what 2 digestive enzymes are both pathologically released into the bloodstream by acinar cells of the inflamed pancreas?

A

Lipase and amylase — this makes these 2 enzymes excellent bio markers for diagnosing AP

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24
Q

Lipase vs amylase sensitivity in identifying patients with AP

A

Lipase is more sensitive (95%) vs amylase (80%)

However, both have a specificity of 99% (i.e. the ability to correctly identify 99% of patients without acute pancreatitis – the true negative rate).

25
Q

How do the levels of amylase vs lipase rise/change in AP?

A

Amylase — rises rapidly within 2 hours of the onset of AP, and peaks between 12 and 72 hours. It is then excreted rapidly by the kidneys, with levels returning to normal as soon as 3 days

Lipase — peaks at 24 hours and can remain elevated for between 8 and 14 days as it is reabsorbed by the renal tubular;es back into the circulation.

This biochemical profile makes lipase a much better clinical test for AP

26
Q

What are the different severity levels of AP?

A
  1. Mild AP — no organ failure or local/systemic complications
  2. Moderate severe AP — transient organ failure (such as AKI) resolving within 48 hours. May have local complication (eg a peripancreatic collection)
  3. Severe AP — persistent organ failure/multi-organ failure
27
Q

What are the 2 types of acute pancreatitis?

A
  1. Interstitial oedematous pancreatitis
  2. Necrotising pancreatitis
28
Q

Describe intestinal oedematous pancreatitis

A
  • 90-95% of all cases
  • pancreatic parenchyma is inflamed/oedematous
29
Q

Describe necrotising pancreatitis

A
  • 5-10% of cases
  • necrosis of pancreatic parenchyma and/or peripancreatic tissue
  • may become infected
30
Q

Acute pancreatitis causes

A

I GET SMASHED

I - idiopathic
G - gallstones
E - ethanol
T - trauma
S - steroid use
M - mumps
A - autoimmune
S - scorpion sting
H - hypercalcaemia and hypertriglyceridaemia
E - ERCP (endoscopic retrograde cholangiopancreatography_
D - drugs/medications

31
Q

What investigation should be performed in suspected AP to exclude visceral perforation and a differential of pneumonia?

A

Erect CXR

32
Q

Where is albumin made?

A

Liver

33
Q

Who would you refer 2ww for upper GI endoscopy?

A

patients with dysphagia or those over 55 years with weight loss and either upper abdominal pain, reflux or dyspepsia

34
Q

What lifestyle changes could you suggest to a patient with GORD?

A
  • smoking cessation
  • weight reduction
  • avoiding precipitating foods such as chocolate, citrus and coffee
  • sleeping with the head of the bed raised
35
Q

Gastro-oesophgeal reflux disease (GORD) describes the symptomatic passing of gastric contents back up into the oesophagus. The pathophysiology is complex and can involve the abnormal transient __________ of the lower oesophageal sphincter, impaired oesophageal __________ and delayed gastric ___________ that increase gastric pressure. It is also associated with a _____________ where a weakness in the crural diaphragm allows the proximal stomach to pass upwards into the chest. It is estimated that up to __% of the adult population will experience GORD or dyspepsia symptoms each year.

A
  • relaxation
  • clearance
  • emptying
  • hiatus hernia
  • 40%
36
Q

What are risk factors for GORD?

A

These can include:

Smoking and alcohol
Obesity
Stress
Hiatus hernia
Pregnancy
Trigger foods
Medications that reduce the lower oesophageal sphincter tone (such as NSAIDS and beta-blockers)

37
Q

What is a Nissan fundoplication?

A

For patients where conservative management (lifestyle changes and medical management) have failed, a Nissen fundoplication can be offered to control the symptoms of GORD. This is usually performed laparoscopically, and involves wrapping the fundus of the stomach around the lower oesophagus to reinforce the lower oesophageal sphincter.

38
Q

What are the potential complications resulting from untreated GORD?

A
39
Q

What are the indications for surgery in GORD?

A
  • Failure of medical therapy (either through efficacy or side effects)
  • desire to discontinue medical therapy
  • presence of a hiatus hernia
40
Q

What are the ALARM symptoms in patients who present with symptoms of dyspepsia?

A

A - anaemia (lethargy, breathlessness)
L - loss of weight
A - anorexia
R - recent onset/progressive symptoms
M - malaena and haematemesis
S - swallowing difficulty (dysphagia)

41
Q

What is the most common histological type of gastric cancer? What are the rarer types?

A

Adenocarcinoma

Rarer types include squamous cell carcinoma, non-Hodgkin’s lymphoma, gastrointestinal stromal tumours (GIST) and neuroendocrine tumours (NETs)

42
Q

When adenocarcinoma spreads primarily through the musculature of the stomach wall, the ‘thickening’ is called _________. (a classic ‘leather bottle’ appearance)

A

Linitis plastica

43
Q

What are risk factors for gastric adenocarcinoma?

A
  • Age (75 years and over)
  • Male (2:1 – 12:1)
  • H.pylori infection
  • Familial adenomatous polyposis (FAP)
  • Ethnicity (Black, Hispanic and Asian)
  • Smoking and alcohol
  • Diet
  • Obesity – more so in men
44
Q

What are investigations for gastric adenocarcinoma?

A
  • Upper GI endoscopy
  • Minimum of 6 biopsies taken during the endoscopy
  • Initial staging CT thorax, abdomen, and pelvis
  • Discussion at the local Upper GI cancer MDT
  • If the tumour is potentially resectable, a staging laparoscopy is performed, and perioperative systemic chemotherapy is given
45
Q

What potential problems can occur that are specific to gastric cancer?

A
46
Q

A peptic ulcer is a break in the ______ lining of the stomach (gastric ulcer) or duodenum (duodenal ulcer). The disruption extends into the submucosa or muscularis propria and is usually more than __mm in diameter. It is estimated that up to 3% of the world population has PUD

A
  • mucosal
  • 5mm
47
Q

What are the risk factors for peptic ulcer disease?

A
  • alcohol
  • NSAIDs
  • smoking
  • H Pylori
  • blood group O — People with blood group O show enhanced binding of H.pylori to epithelial cells as well as a greater inflammatory response mediated by interleukin-6.
48
Q

What do each describe?

  1. Epigastric / RUQ pain that comes in waves and radiates into the back usually after food
  2. Epigastric pain that radiates up into the chest usually after eating
  3. Epigastric pain that is constant, radiates into the back when hungry
  4. Epigastric pain associated with weight loss and dysphagia
A
  1. Typical biliary colic pain from gallstones
  2. GORD
  3. PUD
  4. Oesophageal malignancy
49
Q

What can con from eradication of H.pylori?

A

Urea breath test, faecal antigen testing, and endoscopy (rapid urease test, histology and culture) can confirm eradication. H.pylori serology can confirm infection (regardless of PPI or antibiotic use), but antibodies remain following eradication.

50
Q

What kind of bacteria is H.pylori?

A

Gram-negative helical bacterium

51
Q

How can H.pylori be transmitted?

A

H.pylori can be transmitted by the oral-oral route, or faecal-oral

  • H.pylori has been isolated from saliva and faeces of infected persons
52
Q

How is H.pylori naturally resistant to stomach acid?

A

H.pylori is protected from stomach acid as it uses its flagella to migrate into the mucous lining of the stomach wall to bind to epithelial cells. It also produces urease to neutralise stomach acid into CO2 and ammonia.

53
Q

Perforated PUD

An ulcer can erode through the entire stomach/duodenal wall leading to a perforation if untreated. Patients will present with a _____ abdomen which is indicative of generalised _________ secondary to florid bowel contents in the peritoneal cavity. There is usually a ________ onset of epigastric pain before becoming more generalised in nature. Patients also experience symptoms of distention and nausea and vomiting.

An _____ CXR will show features of a perforation in 60% of patients. For those where there are clinical features of a perforation but a ‘normal’ CXR, a ______ is required to confirm the diagnosis as CT has a sensitivity to show a perforation in 98% of cases.

The management for a perforated ulcer is a _________ to repair the perforation (usually by patching _______ over the perforation to seal it up), and a washout of enteric contents from the peritoneal cavity. Patients are usually given H.pylori eradication therapy as well as being investigated for more sinister causes of a perforation, such as gastric cancer.

A
  • rigid
  • peritonitis
  • sudden
  • erect
  • CT scan
  • laparotomy
  • omentum
54
Q

What is the main cause of a distended abdomen following surgery a/

A

A postoperative ileus — this is a functional bowel obstruction resulting from any noxious insult to the bowel, and usually resolves within a week

55
Q
A

Acute pancreatitis

56
Q
A

Upper GI endoscopy

57
Q
A

PPI for 4-8 weeks and lifestyle advice

58
Q
A

CT abdomen/pelvis

Clinically, you suspect a visceral perforation. An erect CXR is only 60% sensitive to detect a perforation, and so the next appropriate investigation is a CT abdomen/pelvis.

59
Q
A

Postoperative ileus

The history is that of a functional bowel obstruction following recent surgery and peritoneal irritation

YEAR 3 TCD (15 decks)

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