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Semester 1 ( 3rd Year) > Case 10: Epigastric Pain > Flashcards

Case 10: Epigastric Pain Flashcards

1
Q

what is visceral pain

A

it is dull and poorly localised

is due to activation of nociceptors in organs (viscera)

stimulated by contraction, tension, stretching or ischaemia

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2
Q

what is somatic pain

A

originating from muscle, bone, joints, tendons, or blood vessels

pain receptors are in tissues and are activated by noxious substance causing inflammation of the parietal peritoneum

stimuli typically is force, temperature, vibration or swelling

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3
Q

what is colic

A

visceral pain caused by contraction/distension (renal, biliary, bowel)

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4
Q

what is a tympanic abdomen

A

distended abdomen (air) like balloon

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5
Q

what is a tender abdomen

A

abdominal pain present in response to touch/pressure

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6
Q

what is a peritonitic abdomen

A

there is inflammation of the peritoneum by a noxious substance

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7
Q

which cells of the stomach secrete hydrochloric acid

A

parietal cells

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8
Q

which cells of the stomach secrete gastrin

A

G cells

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9
Q

which cells of the stomach secrete mucous

A

mucous cells (goblet?)

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10
Q

which cells of the stomach secrete pepsinogen

A

chief cells

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11
Q

what are the functions of the exocrine pancreas

A

elastases break down elastin

chymotrypsin (chymotrypsinogen is inactive form) breaks down protein into amino acids

amylase breaks down starch and glycogen

lipase breaks down triglycerides into fatty acids and monoglycerides

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12
Q

what is the acceptable weekly unit of alcohol

A

less than 14 units

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13
Q

what is Cullens sign

A

periumbilical (below belly button) ecchymosis (redness/brusing) due to retroperitoneal bleed

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14
Q

what is peritonitis

A

inflammation of the peritoneum (can be generalised or localised)

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15
Q

what is peritonism

A

an indirect activation of the entire abdominal musculature due to peritoneal irritation and is called peritonism

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16
Q

what causes guarding

A

peritonism

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17
Q

2 conditions which may cause local peritonism in the upper abdomen (umbilical)

A

acute pancreatitis
acute cholecystitis

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18
Q

what type of peritonitis would a visceral perforation cause

A

generalised

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19
Q

do peptic ulcers cause guarding

A

no as there is no peritonism

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20
Q

what is acute pancreatitis

A

inflammation of the pancreas caused by activation of pancreatic enzymes and auto digestion

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21
Q

what can the consequences of acute pancreatitis be

A

systemic inflammatory response syndrome (SIRS) which can in turn causes organ failure such as:

acute kidney injury (AKI)
respiratory distress syndrome (respiratory failure)

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22
Q

causes of pancreatitis pneumonic

A

Idiopathic

Gallstones
Ethanol
Trauma (penetrating)

Steroids
Mumps
Autoimmune
Scorpion venom
Hyperlipidaemia/hypercalxaemia
ERCP
Drugs

also family history/genetic factors

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23
Q

most common cause of acute pancreatitis

A

gallstones

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24
Q

most common cause of chronic pancreatitis

A

alcohol abuse

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25
Q

how to diagnose acute pancreatitis

A

abdominal pain (acute, persistent, epigastric pain radiating to the back)

serum lipase/amylase over 3 times the upper limit

radiological evidence of pancreatitis (MR/CT)

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26
Q

which cells of the pancreas release enzymes

A

acinar cells

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27
Q

why are amylase and lipase used for pancreatitis diagnosis

A

they are pathologically released by acinar cells of the inflamed pancreas

lipase is more sensitive

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28
Q

how do lipase levels rise during acute pancreatitis

A

peaks at 24hrs
can remain elevated between 8-14 days as it is reabsorbed by the renal tubules back into circulation

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29
Q

how do amylase levels rise during acute pancreatitis

A

rises rapidly within 2hrs of onset of acute pancreatitis
peaks between 12-72hrs
is then excreted rapidly by the kidneys
levels can return to normal as soon as 3 days

30
Q

what is considered mild acute pancreatitis

A

no organ failure or local/systemic complications

31
Q

what is considered moderate severe acute pancreatitis

A

transient organ failure (such as AKI) resolving within 48hrs

may have local complications (peripancreatic collection)

32
Q

what is considered severe acute pancreatitis

A

persistent organ failure/ multi-organ failure

33
Q

what are the two main types of acute pancreatitis

A

interstitial oedematous pancreatitis (90-95%)
necrotising pancreatitis (5-10%)

34
Q

what can be the consequences of interstitial oedematous pancreatitis

A

acute peripancreatic fluid collection (APFC)- occurs within 4 weeks and fluid is extra pancreatic

if the above is not resolved within 4 weeks it may organise and become a pseudocyst

pseudocyst- this is a homogenous fluid-filled collection with a cyst wall, can compress the surrounding structures such as the stomach

35
Q

what can be the consequences of necrotising pancreatitis

A

acute necrotic collection (ANC)- occurs within 4 weeks, fluid is intra and/or extra pancreatic, there is a homogenous collection of fluid and solid components and no wall

walled off necrosis (WON)- occurs after 4 weeks of onset of pain, is homogenous collection of fluid and solid components/necrotic tissue within a cyst wall

36
Q

what is the name of the criteria for diagnosing acute pancreatitis

A

Atlanta criteria

37
Q

raised what in the blood may suggest AKI

A

urea and creatinine

38
Q

what on chest x-ray would suggest visceral perforation

A

free air under the diaphragm

39
Q

what investigation is done with suspected pancreatitis

A

ultrasound of the abdomen- gallstones need to be ruled out/in as a cause

40
Q

how to manage acute pancreatitis

A

analgesia
antiemetics (NG tube if vomiting)
fluid balance (IV fluid resuscitation and urinary catheter)
venous thromboembolism prophylaxis

41
Q

under what circumstances would you 2 week wait someone for endoscopy

A

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

42
Q

what lifestyle changes would you recommend with GORD

A

smoking cessation
weight loss
avoid precipitating foods- chocolate, citrus, coffee
sleeping with head of the bed raised

43
Q

what is GORD

A

symptomatic back flow of acid and stomach contents into the stomach causing heartburn

44
Q

what can be the pathophysiology of GORD

A

abnormal transient relaxation of the LOS
impaired oesophageal clearance
delayed gastric emptying that increases gastric pressure
also associated with hiatus hernia

45
Q

GORD risk factors

A

smoking and alcohol
obesity
stress
hiatus hernia
pregnancy
trigger foods
NSAIDs and beta-blocker use- these reduce the LOS tone

46
Q

what can you offer patients with GORD who do not respond to acid suppression therapy

A

OGD- oesophago-gastro duodenoscopy

also:
oesophageal manometry
ambulatory 24hr oesophageal pH monitoring

47
Q

surgical options for GORD

A

nissen fundoplication- laprascopic
fundus of the stomach is wrapped around lower oesophagus to reinforce the LOS

48
Q

complications of ongoing GORD

A

barrets oesophagus- metaplastic changes to lower oesophagus from squamous cells to columnar

oesophagitis

recurrent chest infections- reflux can go into respiratory system potentially giving rise to aspiration pnuemonia, bronchitis and bronchial asthma

chronic cough- acid affects the larynx especially when lying down at night

benign stricture- ongoing oesophageal inflammation damages the epithelium causing a stricture, circular band of mucosa can form (Schazki ring) which can cause dysphagia

49
Q

what would indicate surgery for GORD

A

failure of therapy (efficacy or side effects)
desire to discontinue medical therapy
hiatus hernia

50
Q

ALARMS red flag symptoms for dyspepsia

A

Anemia
Loss of weight
Anorexia
Recent onset/progressive symptoms
Malena and haematemesis
Swallowing difficulties (dysphagia)

51
Q

what is the most likely diagnosis given weight loss and dyspepsia

A

upper GI malignancy

52
Q

what is the most common type of gastric cancer

A

adenocarcinoma- when it spreads primarily through the musculature of the stomach wall, the ‘thickening’ is called linitis plastica- ‘leather bottle appearance’

53
Q

other types of gastric cancers

A

squamous cell carcinoma
non-Hodgkin’s lymphoma
gastrointestinal stromal tumours (GIST)
neuroendocrine tumours (NET)

54
Q

risk factors for gastric adenocarcinoma

A

age (over 75)
male
H.pylori
FAP
ethnicity- black, hispanic, asian
smoking and alcohol
diet
obesity (more so in men)

55
Q

investigations for gastric adenocarcinoma

A

upper GI endoscopy- minimum of 6 biopsies taken
staging- CT thorax, abdomen and pelvis
MDT discussion
staging laparoscopy surgery + chemotherapy if tumour is potentially resectable

56
Q

what potential problems specific to gastric cancer may occur during end of life

A

nausea
vomiting
haematemesis- bleeding from the tumour
ascites
pain

57
Q

what is a perforated viscus

A

intestinal/bowel perforation
enteric contents leak into the peritoneal cavity therefore causing severe abdominal pain

58
Q

which blood tests are useful for perforated viscus

A

FBC (WCC)
lipase
CRP

urea and creatinine are also useful

59
Q

what is SIRS

A

systemic inflammatory response syndrome (as a result of sepsis)

60
Q

what would you see on chest xray with visceral perforation

A

on erect chest xray would see free air under the diaphragm

61
Q

history of what disease could increase risk of gastric/duodenal perforation

A

peptic ulcer disease

62
Q

what is peptic ulcer disease

A

a peptic ulcer is a break in the mucosal lining of the stomach (gastric ulcer) or duodenum (duodenal ulcer)

distribution extends into submucosa or muscularis propria and is usually more than 5mm in diameter

63
Q

what % of world have peptic ulcer disease

A

3%

64
Q

risk factors for peptic ulcer disease

A

h.pylori
smoking
alcohol
NSAIDs- ibuprofen, naproxen

65
Q

symptoms of peptic ulcer disease

A

epigastric pain that is constant and radiates into the back usually when hungry

early satiety

reflux symptoms

nausea

66
Q

properties of h pylori

A

patients with infection can be asymptomatic

is naturally resistant to stomach acid

can be transmitted by oral-oral or faecal-oral route

67
Q

triple therapy for h pylori

A

PPI + 2 antibiotics

PPI= omeprazole, lansoprazole, esomeprazole
clarythromycin
amoxicillin (metronidazole if penicillin allergy)

68
Q

usual presentation of perforated peptic ulcer disease

A

rigid abdomen- indicative of generalised peritonitis (secondary to florid bowel contents in peritoneal cavity)

sudden onset of epigastric pain before becoming more generalised in nature

symptoms of distention and nausea and vomiting

69
Q

what to do if perforation cannot be seen on chest xray

A

CT

70
Q

treatment and management of perforated peptic ulcer disease

A

nil by mouth
analgesia
antibiotics
fluid balance (IV fluids and urinary catheter)
refer to on-call general surgery team for further management
VTE prophylaxis
antiemetics (with NG tube if actively vomiting)

71
Q

what surgery is performed for perforated peptic ulcer disease

A

laparotomy- some omentum is sutured over perforation along with a thorough was out of the peritoneal cavity

72
Q

common post operative complications of laparotomy

A

lower respiratory tract infections/pneumonia
postoperative ileus
UTIs
DVT
ongoing leak from site of perforation

Semester 1 ( 3rd Year) (12 decks)

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