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Core clinical problems > 61. Abdominal pain > Flashcards

61. Abdominal pain Flashcards

1
Q

History taking abdominal pain

A
  • Pain, SOCRATES
  • Abdominal distension
  • Nausea and vomiting
  • Dysphagia (difficulty swallowing)
  • Dyspepsia (indigestion / heartburn), hiatus hernia and peptic ulceration
  • History of gallstones or previous pancreatitis
  • Jaundice
  • Altered bowel habit, diarrhoea, constipation or alternating diarrhoea and constipation
  • Blood loss (haematemesis or rectal bleeding)
  • Mucus or slime per rectum
  • Appetite
  • Weight change
  • Continence
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2
Q

DDX RUQ pain inc epigastric

A

Hepatobiliary:
Biliary colic
Acute cholecystitis
Chronic cholecystitis
Acute cholangitis
Bile duct gall stone
Primary biliary cholangitis (PBC)
Primary sclerosing cholangitis (PSC)
Hepatitis : viral and autoimmune
as usually painless jaundice)

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3
Q

DDX epigastric pain

A

Oesophagus and stomach/Dyspepsia
- GORD
- Gastritis
- Peptic ulcer: gastric, duodenal. H.pylori, iatrogenic, idiopathic
- Oesophageal cancer

  • pancreatitis
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4
Q

DDX generalised abdo pain/ stiff to consider in every part of abdo?

A

Peritonitis
Ruptured abdominal aortic aneurysm
Intestinal obstruction
Ischaemic colitis
Medical - sepsis, diabetic ketoacidosis, sickle cell crisis, hypercalcaemia

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5
Q

DDX iliac fossa pain

A

Either iliac fossa pain:
Ectopic pregnancy
Ruptured ovarian cyst
Ovarian torsion

Right iliac fossa pain:
Acute appendicitis
Meckel’s diverticulitis

Left iliac fossa pain:
Diverticulitis

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6
Q

DDX suprapubic pain

A

Lower urinary tract infection
Acute urinary retention
Pelvic inflammatory disease
Prostatitis

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7
Q

What are the symptoms of dyspepsia

A

Pain:
Acid regurgitation
Retrosternal or epigastric pain

abdo:
Bloating

Cough and voice:
Nocturnal cough
Hoarse voice

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8
Q

Invetsigations dyspepsia

A

H.pylori urea breath test/stool antigen test

Immediate endoscopy if evidence eg GI bleed (melena, coffee ground vomit)

2ww urgent direct access upper GI endoscopy if:
- dysphagia
- aged 55 and over with weight loss and any of the following:
- upper abdominal pain
- reflux
- dyspepsia.

Consider non‑urgent direct access upper GI endoscopy if:
- haematemesis

Consider non‑urgent direct access upper gastrointestinal endoscopy to assess for stomach cancer in people aged 55 or over with:
- treatment‑resistant dyspepsia
- upper abdominal pain with low haemoglobin levels
- 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.
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9
Q

Management of ‘undiagnosed dyspepsia’

A
  • Lifestyle advice
  • Acid neutralising medications
  1. Full dose PPI for 4 weeks
  2. If symptoms return after treatment, step down to lowest dose that controls dyspepsia
  3. H2 receptor antagonist eg Ranitidine
  4. Laparoscopic fundoplication
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10
Q

Causes of GORD

A

dysfunction of lower esophageal sphincter (LES), hiatus hernia, delayed gastric emptying

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11
Q

Typical history GORD

A

PC: heartburn, regurgitation, retrosternal or epigastric pain, bloating, nocturnal cough, hoarse voice

SHx: obesity, high caffeine intake, smoking, alcohol, meal soon before bed

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12
Q

typical history peptic ulcers

A

PC: Epigastric discomfort or pain, Nausea and vomiting, Dyspepsia, Bleeding causing haematemesis, “coffee ground” vomiting and melaena, Iron deficiency anaemia (due to constant bleeding), eating typically worsens the pain of gastric ulcers and improves the pain of duodenal ulcers

DHx: NSAIDs, steroids

SHx: Stress, Alcohol, Caffeine, Smoking, Spicy foods

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13
Q

what type of bacteria is h.pylori

A

gram negative aerobic, fastidious growth reqs

spiral-shaped

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14
Q

pathophysiology h.pylori

A

It damages the epithelial lining of the stomach resulting in gastritis, ulcers and increasing the risk of stomach cancer. It avoids the acidic environment by forcing its way into the gastric mucosa.

The breaks it creates in the mucosa exposes the epithelial cells underneath to acid.
It also produces ammonia to neutralise the stomach acid. The ammonia directly damages the epithelial cells. Other chemicals produced by the bacteria also damage the epithelial lining.

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15
Q

investigation ?peptic ulcer

A

Endoscopy with rapid urease test (CLO test) to check for H. pylori, biopsy ?ulcer to exclude malignancy

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16
Q

management h.pylori

A

triple therapy

proton pump inhibitor (e.g. omeprazole)

plus 2 antibiotics (e.g. amoxicillin and clarithromycin) for 7 days.

ABC
Amoxicillin
PPI looks like B
Clarithromycin

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17
Q

Management peptic ulcer caused by drugs/lifestyle

A

Stop/reduce causative agent
Full course PPIs (4 or 8 weeks)
H2 receptor antagonist Ranitidine
Can monitor healing using endoscopy

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18
Q

Complications peptic ulcer

A
  • Bleeding - common and potentially life threatening
  • Perforation “acute abdomen” and peritonitis. This requires urgent surgical repair (usually laparoscopic).
  • Scarring and strictures of the muscle and mucosa - narrowing of the pylorus - pyloric stenosis.
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19
Q

pathophysiology barretts oesophagus

A

chronic reflux → metaplasia from a squamous to a columnar epithelium
A “premalignant” condition and is a risk factor for the development of adenocarcinoma of the oesophagus (3-5% lifetime risk with Barretts).

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20
Q

lifetime risk adenocarcinoma of oesophagus with barretts oesophagus

A

3-5%

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21
Q

Management barrets

A
  • regular endoscopy
  • PPI
  • ablation therapy if low/high grade dysplasia
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22
Q

typical history simple gallstones/ bilairy colic

A

PC: pain starting suddenly in epigastrium or RUQ and may radiate round to the back in the interscapular region.
HoPC: often doesn’t fluctuate as name suggests but instead persists from 15 mins to 24 hours, nausea and vomiting. Pain may be pptated by fatty food consumption.
Red flags: no fever,
Environment:
MHx: diabetes
DHx: oral contraception
FHx: may have family history
SH: “fair, fat, fertile, female, forty”, after sudden weight loss or abdominal surgeries
ICE:

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23
Q

pain starting suddenly in epigastrium or RUQ and may radiate round to the back in the interscapular region.

A

bliary colic

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24
Q

examination bilairy colic

A

no fever
no abdominal tenderness
no jaundice

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25
Q

pathophysiology bilairy colic

A

Gallbladder neck is impacted by a gallstone. No inflammatory response, yet the contraction of the gallbladder against the occluded neck will result in pain

worse after eating as Fatty acids stimulate the duodenum endocrine cells to release cholocystokinin (CCK) which in turn stimulates the contraction of the gallbladder

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26
Q

plan ?gallstones

A

Investigations:
- USS (90-95% sensitive)
- LFTs and inflammatory marker normal
- Lipase normal
- Gold standard investigation for gallstones: magnetic resonance cholangiopancreatography (MRCP)- can show potential defects in biliary tree

Management:
Analgesia:

for severe pain : diclofenac 75mg IM. A second dose can be given after 30 minutes if necessary.if CI IM opioid

For mild to moderate pain : paracetamol or NSAID ef diclofenac which can be given orally or rectally if nausea is a problem

  • Lifestyle factors (reduce fatty foods especially before surgery, don’t need to as much after surgery)
  • Referral for elective laparoscopic cholecystectomy
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27
Q

gold standard investigation for gallstones

A

magnetic resonance cholangiopancreatography (MRCP)- can show potential defects in biliary tree

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28
Q

steady non-paroxysmal pain in epigastrium/RUQ that radiates to back PLUS fever and tenderness

A

acute cholecystitis

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29
Q

o/e acute cholecystitis

A

fever
tenderness
murphys sign positive
no jaundice

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30
Q

Plan acute cholecystitis

A

Investigations:
Carried out in hospital
- abdominal USS
- Bloods (raised WCC, raised CRP, serum amylase)

Management:
Admit to hospital
Analgesia
Monitoring
IV fluids
Antibiotics
Surgical assessment for cholecystectomy (to be done within 1 week of presentation, ideally within 48 hours)

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31
Q

What is mirizzi syndrome

A

A stone located in Hartmanns pouch (an out-pouching of the gallbladder wall at the junction with the cystic duct) or in the cystic duct itself can cause compression on the adjacent common hepatic duct.

This results in an obstructive jaundice, even without stones being present within the lumen of the common hepatic or common bile ducts.

Investigation:
MRCP
Management:
Laparoscopic cholecystectomy

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32
Q

What is chronic cholecystitis

A

PC: recurrent or untreated acute cholecystitis —> persistent inflammation of gallbladder wall
Management:
Elective cholecystectomy

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33
Q

What is gallbladder empyema

A

Gallbladder fills with pus and patient may become septic
PC: similar to acute cholecystitis

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34
Q

Pathophysiology ascending cholangitis

A

Infection of biliary tract caused by biliary outflow obstruction and biliary infection. Stasis of fluid allows bacterial colonisation.
Main organisms are: e.coli, klebsiella and enterococcus

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35
Q

fever, jaundice, RUQ pain

A

charcots triad - indicates ascending cholangitis

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36
Q

typical history ascending cholangitis

A

PC: fever, jaundice, RUQ pain (charcots triad)
HoPC: may have pyrexia, rigours, jaundice, RUQ tenderness, confusion, hypotension, tachycardia
Red flags:
Environment:
MHx: gallstones, recent ERCP procedure, previous cholangitis
DHx: oral contraceptive pill and fibrates
FHx:
SHx: diet rich in fatty foods

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37
Q

Plan ?ascending cholangitis

A

Initial management:
IV access
Fluid resuscitation
Antibiotics broad spectrum eg co-amoxiclav +metronidazole

Investigation/management:
blood cultures
USS first line - bile duct dialtation
ERCP with or without sphincterotomy and stunting

Long term may require cholecystectomy of gallstones were the cause

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38
Q

o/e ascending cholangitis

A

fever
tenderness
jaundice

confusion
hypotension
tachycardia

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39
Q

pathophysiology pancreatitis

A

inflammation of the pancreas. Autodigestion of pancreatic tissue by the pancreatic enzymes, leading to necrosis, caused most commonly by gallstones or alcohol

Each cause will trigger a premature and exaggerated activation of the digestive enzymes within the pancreas. The resulting pancreatic inflammatory response causes an increase in vascular permeability and subsequent fluid shifts (often termed “third spacing”).
Enzymes are released from the pancreas into the systemic circulation, causing autodigestion of fats (resulting in a ‘fat necrosis’) and blood vessels (sometimes leading to haemorrhage in the retroperitoneal space). Fat necrosis can cause the release of free fatty acids, reacting with serum calcium to form chalky deposits in fatty tissue, resulting in hypocalcaemia.

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40
Q

causes pancreatitis

A

GET SMASHED
Gall stones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpion stings
Hypertriglyceridemia, hypercalcaemia and hyperparathyroidism
ERCP – endoscopic retrograde cholangiopancreatography
Drugs – such as sodium valproate, azathioprine and sulphonamides

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41
Q

sudden onset severe constant epigastrium pain radiating to the back/flanks with profuse vomiting

worsen with movement and improve by leaning forwards/in foetal position

A

pancreatitis

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42
Q

typical history pancreatitis

A

PC: sudden onset severe constant epigastrium pain radiating to the back/flanks with profuse vomiting
HoPC: worsen with movement and improve by leaning forwards/in foetal position. If caused by gallstones, pain may be described as sudden and knife-like, and may be worse after food.
If alcohol-related, pain may be of less abrupt onset and poorly localized.
Red flags:
Environment: alcohol intake
MHx:
DHx: sodium valproate, azathioprine and sulphonamides

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43
Q

o/e pancreatitis

A
  • pain better on leaning forwards
  • fever (inflammation or sepsis)
  • signs of shock
  • Cullen’s sign (bruising around the umbilicus) and Grey Turner’s sign (bruising in the flanks) , representing retroperitoneal haemorrhage.
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44
Q

plan ?pancreatitis

A

Plan:
Investigation:
Admit to hospital
Fluid resus, access, abx, o2, parenteral feeding
Bloods: lipase, amylase (3x upper limit), liver and renal function, and inflammatory marker levels.

Imaging: contrast CT is best for pancreatitis.

Investigating cause:
USS for gallstones

Management:
ERCP if gallstones is the cause
Cholecystectomy

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45
Q

which is better amylase or lipase

A

Lipase is lit !!

raised serum lipase is more accurate for acute pancreatitis, as it remains elevated longer than amylase

Serum amylase or serum lipase – diagnostic of acute pancreatitis if 3x the upper limit of normal*

Amylase can also be marginally raised in pathologies such as bowel perforation, ectopic pregnancy, or diabetic ketoacidosis

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46
Q

LFTs pancreatitis

A

assess for any concurrent cholestatic element to the clinical picture. Patients with acute pancreatitis noted that an alanine transaminase (ALT) level >150U/L has a positive predictive value of 85% for gallstones as the underlying cause

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47
Q

causes hepatitis

A

alcoholic hepatitis
non alcoholic fatty liver disease
viral hepatitis
autoimmune hepatitis
drug induced hepatitis

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48
Q

Presentation hepatitis

A

abdominal pain, fatigue, pruritus, muscle and joint aches, N+V, jaundice, fever (viral hepatitis)

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49
Q

LFTs and bilirubin in hepatitis

A

LFTS: “hepatitic picture” - high transaminases (AST/ALT) with proportionally less of a rise in ALP.

Transaminases are liver enzymes released into the blood as a result on inflammation of the liver cells
Bilirubin can also rise as a result of inflammation of the liver cells—> jaundice

Elevation in unconjugated bilirubin indicates pre-hepatic or hepatic jaundice eg hepatitis. Whereas conjugated indicates he pato cellular or cholestasis.

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50
Q

Which viral hepatitis’ are faecal oral

A

A - ass
E - eating

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51
Q

viral hepatitis mneumonic

A

A - ass (F-O)
B - blood-borne (PP)
C - cerious and circulation (PP)
D - depends on B (PP)
E - eating (F-O)

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52
Q

Prognosis/management each viral hepatitis

A

A - self-resolves usually within 1-2 months, worse outcome rare

B- 90% of people self-resolve, 10% chronic, antiviral medication can slow progression

C- 25% self resolve, Direct acting antiviral medication for 8-12 weeks (curative in 90% of patients)

D- Increases complications and severity of Hep B

E- Usually self-resolve within 1 month, can become chronic if immunocompromised

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53
Q

why is the liver scanned in hepatitis, what are you looking for?

A

Cirrhosis : fibroscan
Hepatocellular carcinoma : USS

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54
Q

initial testing for hepatitis B

A

Surface antigen (HBsAg) – active infection
Core antibodies (HBcAb) – implies past (or current) infection

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55
Q

Which viral hepatitis is a DNA virus

A

hepatitis B

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56
Q

Autoimmune hepatitis type 1 typical history

A

PC Type 1: adults, typically women in late 40s and 50s, around or after menopause. fatigue and features of liver disease

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57
Q

antibodies type 1 autoimmune hepatitis

A

Anti-nuclear antibodies (ANA)
Anti-smooth muscle antibodies (anti-actin)
Anti-soluble liver antigen (anti-SLA/LP)

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58
Q

typical history type 2 autoimmune hepatitis

A

children in their teenage or early twenties present with acute hepatitis with high transaminases and jaundice

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59
Q

autoantibodies for type 2 autoimmune hepatitis

A

Anti-liver kidney microsomes-1 (anti-LKM1)
Anti-liver cytosol antigen type 1 (anti-LC1)

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60
Q

Plan ?autoimmune hepatitis

A

Invetsigations
Bloods:
Raised transaminases (ALT and AST), IgG levels and it is associated with many autoantibodies such as ANA,LKM1
Big:
Diagnosis confirmed using liver biopsy

Management
1. High dose steroids (prednisolone)
1b. Taper steroids and introduce immunosuppressants such as azathioprine
2. Liver transplant in end stage disease, however can recur in transplanted livers

61
Q

are there complications from hep A

A

complications are rare and there is no increased risk of hepatocellular cancer

62
Q

who should be vaccinated for hep A

A

people travelling to or going to reside in areas of high or intermediate prevalence, if aged > 1 year old

people with chronic liver disease

patients with haemophilia

men who have sex with men

injecting drug users

individuals at occupational risk: laboratory worker; staff of large residential institutions; sewage workers; people who work with primates

63
Q

HBsAG

A

hep B surface antigen

= active infection /chronic infection

64
Q

HBsAb

A

hep B surface antibody

= immunised
= infection cleared after exposure
= current infection

65
Q

HBcAb

A

core antibodies

= past infection cleared after exposure
= chronic infection

66
Q

E antigen (HBeAg)

A

marker of viral replication and implies high infectivity

67
Q

E antibody

A

evidence of immune response

68
Q

Hepatitis B virus DNA (HBV DNA)

A

this is a direct count of the viral load

69
Q

what are the treatments for hep B

A
  1. Pegylated Interferon alpha (weekly injectable for 48 weeks) which aims to stimulate the immune system to fight the virus,
  2. oral anti-viral agent which suppresses viral replication (Tenofovir or Entecavir once a day, long term)
70
Q

lifestyle advice to reduce infecting others at hep B diagnosis

A
  • Avoid having unprotected sex, unless the partner has been vaccinated and is immune
  • Avoid sharing needles in inject drugs
  • Avoid sharing toothbrushes or razors with people in the house
  • Avoid drinking alcohol
71
Q

Hep B summary

A

Type: DNA virus
Transmission: Blood or bodily fluids (sexual intercourse, sharing needles, tattoos, toothbrushes, surgical procedures, vertical transmission)
Vaccine available: yes

Acute infection self resolves in 90% of patients, 10% become chronic as it integrates DNA into own DNA so carrier continues to produce viral proteins

Not curable but can use pegylated interferon alpha or oral anti-virals such as tenofovir or entecavir to keep virus at bay if it is affecting the liver

72
Q

Hep A summary

A

Type: RNA virus
Transmission: faecal-oral route, contaminated water or food
Vaccination available: yes
PC: N+V, anorexia, jaundice
Can cause cholestasis —> dark urine and pale stools and moderate hepatomegaly

Management
resolves without treatment in around 1-3 months.

73
Q

what is main risk factor for hep C

A

IVDU

74
Q

invetsigation hep C

A

Hepatitis C antibody test: will be positive if the patient has ever been exposed to the hepatitis C virus, but DOESN’T mean they are actively infected

HCV RNA is done in patients with a positive HCV antibody to confirm current infection, by means of a PCR.

75
Q

normal course of hep C?

A

1/4 self resolve, rest chronic hep C

76
Q

what is aim of hep C tretament

A

cure

All patients with current HCV infection (HCV RNA detected) should be offered a course of potentially curative treatment.
Cure is defined as an undetectable HCV RNA in blood 12 weeks after the end of treatment (sustained virological response – “SVR12”).

77
Q

what drugs are used to treat hep C

A
  1. NS3/4A protease inhibitors (end in –previr) e.g. grazoprevir
  2. NS5A inhibitors (end in –asvir) e.g. elbasvir
  3. NS5B inhibitors (end in –buvir) e.g. sofosbuvir
78
Q

side effects interferon alpha

A

flu-like symptoms, depression, fatigue, leukopenia, thrombocytopenia

79
Q

complications of chronic hep C

A

rheumatological problems: arthralgia, arthritis
eye problems: Sjogren’s syndrome

cirrhosis (5-20% of those with chronic disease)
hepatocellular cancer

cryoglobulinaemia: typically type II (mixed monoclonal and polyclonal)

porphyria cutanea tarda (PCT): it is increasingly recognised that PCT may develop in patients with hepatitis C, especially if there are other factors such as alcohol abuse

membranoproliferative glomerulonephritis

80
Q

hep C summary

A

Type: RNA virus
Transmission: blood and bodily fluids, At risk groups include intravenous drug users and patients who received a blood transfusion prior to 1991 (e.g. haemophiliacs).
Vaccine available: no
test: hep C antibody test- if positive test for RNA to confirm current infection

treatment:
antiviral medication for 8-12 weeks (curative in 90% of patients) grazoprevir, elbasvir, sofobuvir

81
Q

summary hep D

A

Type: RNA virus
Occurs only in people with hepatitis B infection (attaches to HBsAg)
Increases complications and severity of Hep B
Notifiable disease
test: PCR of hep D RNA

no treatment, inteferon sometimes used but poor evidence

82
Q

what is hepB/hepD co-infection vs superinfection

A

Co-infection: Hepatitis B and Hepatitis D infection at the same time.
Superinfection: A hepatitis B surface antigen positive patient subsequently develops a hepatitis D infection.

Superinfection is associated with high risk of fulminant hepatitis, chronic hepatitis status and cirrhosis.

83
Q

hep E summary

A

Type: RNA virus
Transmission: faecal oral
Vaccination: no
causes a similar disease to hepatitis A, but carries a significant mortality (about 20%) during pregnancy

Management
Usually self-resolve within 1 month
Rarely → chronic hepatitis esp if immunocompromised

84
Q

what is fulminant hepatitis

A

Fulminant hepatitis (FH) or acute liver failure (ALF) is defined by an INR > 1.5 and the presence of hepatic encephalopathy but the absence of chronic, underlying (or prior) disease.

85
Q

presentation perforation secodnary to peptic ulcer disease

A

epigastric pain, later more generlaised
syncope

86
Q

invetsigation acute upper abdo pain ?bowel perforation secondary to peptic ulcer

A

An upright (‘erect’) chest x-ray is usually required when a patient presents with acute upper abdominal pain

This is a useful test, as approximately 75% of patients with a perforated peptic ulcer will have free air under the diaphragm

87
Q

Presentation primary biliary cirrhosis/cholangitis

A

PC: pruritus, fatigue, GI disturbance and abdo pain, jaundice, cardiovascular disease, xanthelasma, pale stools, signs of cirrhosis and failure (ascites, splenomegaly, spider naevi)
HoPC:
Red flags:
Environment:
MHx: other autoimmune conditions (thyroid, coeliac), rheumatoid conditions (systemic scleorisis, sjorgrens, rheumatoid arthritis)
DHx:
FHx:
SHx: middle aged women (think b for boobs)
ICE:

88
Q

pathophysiology PBC

A

immune system attacks the small bile ducts within the liver → cholestasis → back pressure causes fibrosis, cirrhosis and liver failure. Bile acids, bilirubin and cholesterol build up in the bloodstream and cause symptoms.

89
Q

Investigations PBC

A

LFTs: alkaline phosphatase is the first liver enzyme to be raised (as with most obstructive pathology), other liver enzymes and bilirubin are raised later in disease

Autoantibodies: anti-mitochondrial antibodies (AMA) is most specific to PBC, anti-nuclear antibodies are present in 35% of patients

Scan: required before diagnosis to exclude an extrahepatic biliary obstruction (typically a right upper quadrant ultrasound or magnetic resonance cholangiopancreatography (MRCP)

ESR raised
IgM raised
Liver biopsy is used for diagnosing and staging disease

Primary biliary cholangitis - the M rule
IgM
anti-Mitochondrial antibodies, M2 subtype
Middle aged females
MRCP

90
Q

Management PBC

A

Ursodeoxycholic acid reduces the intestinal absorption of cholesterol (slows disease progression and improves symptoms)

Colestyramine is a bile acid sequestrate in that it binds to bile acids to prevent absorption in the gut and can help with pruritus due to raised bile acids

Liver transplant in end stage liver disease (bilirubin >100)

Immunosuppression (e.g. with steroids) is considered in some patients

91
Q

complications/issues with PBC

A

cirrhosis → portal hypertension → ascites, variceal haemorrhage

osteomalacia and osteoporosis (decreased bone formation due to impaired calcium and vitamin d absorption resulting from cholestasis)

significantly increased risk of hepatocellular carcinoma (20-fold increased risk)

Distal renal tubular acidosis

Hypothyroidism

92
Q

presentation primary sclerosing cholangitis

A

PC: jaundice, chronic RUQ pain, pruritis, fatigue, hepatomegaly
HoPC:
Red flags:
Environment:
MHx: ulcerative colitis
DHx:
FHx: FH of UC or PSC
SHx: male aged 30-40
ICE:

93
Q

Pathophysiology priamry sclerosing cholangitis

A

intrahepatic or extrahepatic ducts become structured and fibrotic → obstruction to the flow of bile out of the liver and into the intestines. Chronic bile obstruction leads to liver inflammation (hepatitis), fibrosis and cirrhosis

94
Q

gold standard invetsigation for PSC

A

MRCP (magnetic resonance cholangiopancreatography) - MRI scan of the liver, bile ducts and pancreas. In primary sclerosis cholangitis it may show bile duct lesions or strictures.

95
Q

autoantibodies PSC

A

p-ANCA

Autoantibodies: No antibodies are highly sensitive or specific to PSC. They aren’t very helpful in diagnosis but they can indicate where there is an autoimmune element to the disease that may respond to immunosuppression.
Antineutrophil cytoplasmic antibody (p-ANCA) in up to 94%
Antinuclear antibodies (ANA) in up to 77%
Anticardiolipin antibodies (aCL) in up to 63%

96
Q

autoantibodies PBC

A

anti-mitochondrial antibodies (AMA) is most specific to PBC, anti-nuclear antibodies are present in 35% of patients

97
Q

associations PSC

A

ulcerative colitis

Acute bacterial cholangitis
Cholangiocarcinoma develops in 10-20% of cases
Colorectal cancer
Cirrhosis and liver failure
Biliary strictures
Fat soluble vitamin deficiencies

98
Q

management psc

A

Liver transplant can be curative but is associated with its own problems (around 80% survival at 5 years).

ERCP can be used to dilate and stent any strictures

Colestyramine is a bile acid sequestrate in that it binds to bile acids to prevent absorption in the gut and can help with pruritus due to raised bile acids
Monitoring for complications (such as cholangiocarcinoma, cirrhosis and oesophageal varices)

99
Q

referral criteria ?upper GI malignancy

A

2ww urgent direct access upper GI endoscopy if:
- dysphagia
- aged 55 and over with weight loss and any of the following:
- upper abdominal pain
- reflux
- dyspepsia.

Consider non‑urgent direct access upper GI endoscopy if:
- haematemesis

Consider non‑urgent direct access upper gastrointestinal endoscopy to assess for stomach cancer in people aged 55 or over with:
- treatment‑resistant dyspepsia
- upper abdominal pain with low haemoglobin levels
- 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.
100
Q

Gall bladder pathology worrying signs

A

Tenderness (Murphy) suggests cholangitis

Fever - suggests ascending cholangitis or cholecystitis (could have empyema etc)

Deranged LFTs - bile duct stone - ascending cholangitis

Pancreatitis - bile duct stone - ascending cholangitis

101
Q

ddx loin to groin pain

A

Renal colic (kidney stones)
Ruptured abdominal aortic aneurysm
Pyelonephritis

102
Q

what is peritonitis

A

Peritonitis refers to inflammation of the peritoneum, the lining of the abdomen.

  • local peritonitis is caused by underlying organ inflammation, for example, appendicitis or cholecystitis.
  • Generalised peritonitis may be caused by perforation of an abdominal organ (e.g., perforated duodenal ulcer or ruptured appendix) releasing the contents into the peritoneal cavity and causing generalised inflammation of the peritoneum.
103
Q

presentation peritonitis

A

sudden onset acute abdo pain exacerbated by movement eg coughing. Often pain may be generalised and then become localised, shock, fever, sinus tachycardia, nausea and vomiting, abdo swelling,

o/e:
- gurading
- rigidity
- rebound tenderness
- pain on coughing
- percusiion tenderness
- absence of bowel sounds suggests paralytic ileus

104
Q

what is the difference between guarding and rigidity?

A

Guarding refers to voluntary contraction of the abdominal wall musculature, usually the result of fear, anxiety, or the laying on of cold hands.

Rigidity refers to involuntary contraction of the abdominal musculature in response to peritoneal inflammation, a reflex that the patient cannot control.

105
Q

Causes of periotnitis?

A

Infected:
- Perforation of part of the GI tract, or, in women, of the reproductive system
- distruption of peritoneum by surgery or trauma : bacteria frome xternal environemnt
- spontaenous bacterial peritonitis
- systemic infections sucha s TB

Non-infected:
- leakage of sterile body fluids such as blood/bile - they will usually become infected once in the peritoneal cavity, causing full blown peritonitis within 24-48 hours.
- autoimmune disease sucha s lupus

106
Q

what types of bacteria are usually involved in infetcive peritonitis

A
  • perforation of GI tract –> Gram negative bacteria and anaerobic bacteria eg E. coli.
  • Disruption of the peritoneum – e.g. by surgery or trauma –> external environemnt –> staph aureus
107
Q

complications of peritonitis

A

sepsis
loss of fluid and electrolyte disturbance
abscess
Difficulty breathing – due to pressure of fluid on diaphragm.

108
Q

when should you susepct and abscess after surgery

A

if the patient’s condition does not improve and there is continuing fever and high white cell count.

109
Q

plan ?peritonitis

A

inform a senior

Erect CXR to check for air under the diaphragm
Serum amylase to rule out pancreatitis.
Ultrasound / CT to confirm diagnosis

IV fluids and electrolytes
IV abx
Surgery - laparotomy

110
Q

features SBP

A

ascites
abdominal pain
fever

111
Q

how to diagnose SBP

A

paracentesis: neutrophil count > 250 cells/ul

112
Q

most common organism found on ascitic fluid culture

A

e.coli

113
Q

management SBP

A

intravenous cefotaxime is usually given

114
Q

what is marker of poor prognosis SBP

A

Alcoholic liver disease

115
Q

who should get antibiotic prophylaxis for SBP

A

patients who have had an episode of SBP
patients with fluid protein <15 g/l (low protein = low wcc etc to fight off infection)

and either Child-Pugh score of at least 9 or hepatorenal syndrome
NICE recommend: ‘Offer prophylactic oral ciprofloxacin or norfloxacin for people with cirrhosis and ascites with an ascitic protein of 15 g/litre or less until the ascites has resolved’

116
Q

most common cause/s of small bowel obstruction

A

Adhesions (e.g. following previous surgery) are the most common cause of small bowel obstruction, followed by hernias.

117
Q

most common cause/s of large bowel obstrution

A

tumour - this accounts for 60% of cases of large bowel obstruction

volvulus
diverticular disease

118
Q

first line invetsigation ?bowel obstruction

A

abdominal xray

119
Q

features of bowel obstruction? small vs large?

A

common in both:
- ‘constipation’ with complete obstruction and lack of flatulence
- diffuse, central abdominal pain
- tinkling bowel sounds more so early on

more in small bowel
- nausea and vomiting
typically bilious vomiting
- ask abt previous surgeries (adhesions)

more in large bowel:
- distension
- signs of perforation
- ask abt symptoms of undelrying cause eg colon cancer, diverticualr

120
Q

definitive scan bowel obstruction

A

CT

121
Q

management ?bowel obstruction

A

initial steps:
NBM
IV fluids
nasogastric tube with free drainage
“drip and suck”

small bowel obstruction:
some patients settle with conservative management but otherwise will require surgery

large bowel obstruction:
EMERGENCY SURGERY IF SIGNS OF PERFORATION
may have a period (72hr) of conservative management but around 75% will eventually require surgery.
IV abx if perforation or sugrery planned

122
Q

what is ischaemic colitis

A

IIschaemic colitis describes an acute but transient compromise in the blood flow to the large bowel. This may lead to inflammation, ulceration and haemorrhage.

123
Q

what region of the bowel is most likely to be affected by ischaemic colitis

A

‘watershed’ areas such as the splenic flexure

124
Q

presentation ischaemic colitis

A

acute/subacute onset
- abdo pain,
- rectal bleeding: Haematochezia usually occurs within 24 hours after the onset of abdominal pain.
- diarrhoea, urgency, tenesmus, or less commonly constipation.

Fever and tachycardia might be present in severe cases, indicating systemic involvement or progressing towards gangrenous colitis. fluid/electrolyte loss → dehydration, shock, metabolic acidosis

125
Q

what are the subtypes of ischamic colitis? blood supply affected?

A

acute mesenteric ischaemia
- superior mesenteric artery

colonic ischaemia
- superior and inferior mesenteric arteries (switch is 2/3 along TC) here is watershed area splenic flexure (Griffiths point) and rectosigmoid junction (Sudek’s point) supplied by MARGINAL ARTERY (where 70% of colonic ischaemia occurs)

The SMA supplies the bowel from the lower part of the duodenum to two-third of the transverse colon. The IMA supplies a large intestine from the distal one-third of the transverse colon to the rectum.

126
Q

features of acute mesenteric ischaemia?

A

The abdominal pain is typically severe, of sudden onset and out-of-keeping with physical exam findings (not as tender as youd expect at first)

Bleeding occurs late
Classically patients have a history of atrial fibrillation.

127
Q

imaging acute mesenteric ischaemia

A

ct with contrast

128
Q

what condition is associated with aucte mesenteric ischaemia

A

atrial fibrillation

129
Q

management of ischameic colitis

A

urgent surgery - bowel resection

IV abx more so if colonic

130
Q

features of colonic ischaemia

A

Mild crampy pain, tenderness
Prominent bloody diarrhoea

131
Q

what is chronic mesenteric ischameia?what investigation?

A

may be thought of as ‘intestinal angina’. It is most commonly seen in elderly patients with a history of smoking, hypertension, and hyperlipidemia. The symptoms of CMI include abdominal pain, weight loss, nausea, vomiting, and diarrhoea. The diagnosis of CMI is made through imaging studies such as CT angiography or magnetic resonance angiography. Treatment options for CMI include medical management, endovascular interventions, and surgical revascularization.

132
Q

what condition is associated with the classic triad of postprandial abdominal pain, weight loss, and food aversion

A

chronic mesenteric ischameia

133
Q

what is an ectopic pregnancy

A

Ectopic pregnancy is when a pregnancy is implanted outside the uterus. The most common site is a fallopian tube. An ectopic pregnancy can also implant in the entrance to the fallopian tube (cornual region), ovary, cervix or abdomen.

134
Q

risk factors ectopic pregnancy

A

Previous ectopic pregnancy
Previous pelvic inflammatory disease
Previous surgery to the fallopian tubes
Intrauterine devices (coils)
Older age
Smoking

135
Q

Presentation ectopic pregnancy

A

Constant lower abdominal pain in the right or left iliac fossa
Vaginal bleeding
Lower abdominal or pelvic tenderness
Cervical motion tenderness (pain when moving the cervix during a bimanual examination)
Missed period

It is also worth asking about:
Dizziness or syncope (blood loss)
Shoulder tip pain (peritonitis)

136
Q

investigation ?ectopic pregnancy

A

transvaginal USS

positive pregnancy test

137
Q

what may transvaginal uss show ectopic

A

A gestational sac containing a yolk sac or fetal pole may be seen in a fallopian tube.

Sometimes a non-specific mass may be seen in the tube. When a mass containing an empty gestational sac is seen, this may be referred to as the “blob sign”, “bagel sign” or “tubal ring sign” (all referring to the same appearance).

138
Q

most common site ectopic pregnancy? most damgerois site?

A

Most common site: ampulla

More dangerous : isthmus

139
Q

what is the adenexa?

A

The adnexa is the region adjoining the uterus that contains the ovary and fallopian tube, as well as associated vessels, ligaments, and connective tissue.

140
Q

what is a pregnancy of unknown location?

A

A pregnancy of unknown location (PUL) is when the woman has a positive pregnancy test and there is no evidence of pregnancy on the ultrasound scan.

141
Q

management of pregnancy of unknown location?

A

monitor hCG and chanegs in symptoms
- In an intrauterine pregnancy, the hCG will roughly double every 48 hours. A rise of more than 63% after 48 hours is likely to indicate an intrauterine pregnancy. A repeat ultrasound scan is required after 1 – 2 weeks to confirm an intrauterine pregnancy. A pregnancy should be visible on an ultrasound scan once the hCG level is above 1500 IU / l.

  • A rise of less than 63% after 48 hours may indicate an ectopic pregnancy. When this happens the patient needs close monitoring and review.
  • A fall of more than 50% is likely to indicate a miscarriage. A urine pregnancy test should be performed after 2 weeks to confirm the miscarriage is complete.
142
Q

what are the three types of management for an ectopic pregnancy?

A

Expectant management (awaiting natural termination)

Medical management (methotrexate)

Surgical management (salpingectomy or salpingotomy)

143
Q

criteria for expectant management of an ectopic pregnancy?

A

Patient:
Follow up needs to be possible to ensure successful termination

Symptoms:
No significant pain

Bloods:
HCG level < 1500 IU / l

USS:
The ectopic needs to be unruptured
Adnexal mass < 35mm
No visible heartbeat

144
Q

criteria for medical management of ectopic pregnancy?

A

The ectopic needs to be unruptured
Adnexal mass < 35mm
No visible heartbeat
No significant pain

+ HCG level must be < 5000 IU/l
+ Confirmed absence of intrauterine pregnancy on ultrasound

145
Q

what is used as the medical manageemnt for ectopic pregnancy?

A

methotrexate

146
Q

criteria for surgical management of ectopic pregnancy

A

Anyone that does not meet the criteria for expectant or medical management requires surgical management. Most patients with an ectopic pregnancy will require surgical management. This include those with:
Pain
Adnexal mass > 35mm
Visible heartbeat
HCG levels > 5000 IU / l

147
Q

what is used as surgical management of ectopic pregnancy? when is each used?

A

Laparoscopic salpingectomy is the first-line treatment for ectopic pregnancy. This involves a general anaesthetic and key-hole surgery with removal of the affected fallopian tube, along with the ectopic pregnancy inside the tube.

Salpingotomy should be considered for women with risk factors for infertility such as contralateral tube damage
around 1 in 5 women who undergo a salpingotomy require further treatment (methotrexate and/or a salpingectomy)

148
Q

what is given to women having a surgical management of ectopic

A

Anti-rhesus D prophylaxis is given to rhesus negative women having surgical management of ectopic pregnancy.

149
Q
A

Core clinical problems (94 decks)

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