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Year 3 - Diseases > Gastro > Flashcards

Gastro Flashcards

1
Q

Define appendicitis

A

An acute inflammation of the vermiform appendix, most likely due to obstruction of the lumen of the appendix (by faecolith, normal stool, infective agents, or lymphoid hyperplasia).

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2
Q

Define Mallory Weiss tear and list its causes

A
  • Longitudinal muscle tear of the oesophagus (distal oesophagus/proximal stomach)
  • Caused by violent retching which increases intra-abdominal pressure.
  • Also caused by stretching, lifting, stooling and abdominal injury
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3
Q

Define haemochromatosis

A

Mutation in HFE gene (if hereditary) causing increased iron absorption from the GIT, leading to iron overload

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4
Q

List signs and symptoms of haemochromatosis

A
  • May be asymptomatic (75%)
  • Fatigue
  • Weakness
  • Lethargy
  • Arthralgias
  • Hepatomegaly
  • Diabetes mellitus (‘bronze diabetes’)
  • Impotence in males, loss of libido (due to pituitary dysfunction)
  • Skin pigmentation
  • Congestive heart failure
  • Arrhythmias
  • Porphyria cutanea tarda
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5
Q

Define wilsons disease

A
  • Liver disease where there is impaired copper secretion into the bile, therefore there is a retention of copper in the body.
  • Autosomal recessive ATP7B
  • Hepatolenticular degeneration
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6
Q

List symptoms and signs of Wilsons disease

A
  • Kayser-Flaischer rings (build up of copper around the cornea, test with slit lamp)
  • Neurologic manifestations due to atrophy of the basal ganglia (parkinsonism, dysarthria, tremor, dystonia and polyneuropathy)
  • Psychological symptoms (irritability, psychosis, emotional lability, changes in personality and difficulty concentrating)
  • GI symptoms are uncommon (bleeding, jaundice, tenderness, spider angioma, gynaecomastia, bruising)
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7
Q

Define achalasia and list its causes

A
  • Achalasia is a failure of relaxation of the lower esophageal sphincter due to loss of the myenteric (Auerbach) plexus.
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8
Q

How is achalasia investigated and what are the findings on investigation?

A
  • A barium swallow will show a dilated esophagus with an area of distal stenosis.
  • Tertiary peristalsis waves
  • This is also the characteristic ‘bird’s beak’ sign.
  • High resolution manometry is diagnostic. Shows incomplete relaxation of LOS
  • CXR shwoing absent gastric air bubble, dilated oesophagus, air fluid level above LOS
  • Oesophageal manometry is the gold standard
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9
Q

List signs of cirrhosis

A
  • Ascites (shifting dullness)
  • Asterixis
  • Confusion
  • Caput medusae (visible veins from umbilicus due to portal hypertension)
  • Splenomegaly due to portal hypertension
  • Palmar erythema (increased oestrogen)
  • Leukonychia, spider naevi
  • Oedema (lower extremity)
  • Muscle wasting
  • Testicular atrophy
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10
Q

Define cirrhosis

A

Cirrhosis is a condition due to diffuse bridging fibrosis and regenerative nodules that disrupt the normal architecture and function of the liver.

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11
Q

Define autoimmune hepatitis

A
  • Immune mediated injury of the liver
  • Caused by abhorant HLA II
  • Cause fo chronic hepatitis
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12
Q

List presentations of autoimmune hepatitis

A
  • Acute hepatitis (fever, fatigue, jaundice, upper right quadrant abdominal pain)
  • Amenorrhea
  • Epistaxis
  • Easy bruising
  • Chronic hepatitis
  • Cirrhosis
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13
Q

Describe epidemiology of autoimmune hepatitis

A
  • 10-17 people per 100000 in europe
  • 10000 people in UK
  • 3 to 4 times more common in women
  • Commonly diagnosed in women age 45, and young women
  • 30-50% have another autoimmune condition
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14
Q

How is autoimmune hepatitis diagnosed?

A
  • Elevated AST and ALT
  • Positive anti-smooth muscle antibody (most specific test)
  • Antinuclear antibody
  • Antibodies to soluble liver antigen
  • Liver/kidney microsomal antigens
  • FBC and blood film (mild leukopenia, normochromic anaemia, thrombocytopenia, eosinophilia)
  • Liver biopsy
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15
Q

Describe presentation of gallstones

A
  • Abdominal pain (right upper quadrant or epigastric)
  • Nausea
  • Vomiting
  • Cholestatic transaminitis
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16
Q

Describe the characteristics of inguinal hernias

A
  • Most common hernia
  • Medial to inferior epigastric vessels, through hesslebachs triangle is direct (acquired). Indirect hernias are lateral to the inferior epigastric vessels. They pass through both superficial and deep inguinal ring
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17
Q

List symptoms of inguinal hernia

A
  • Heaviness or dull discomfort in the groin
  • Pain when lifting
  • Severe pain may indicate strangulation
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18
Q

How are hernias diagnosed?

A
  • Ultrasound and peritoneography are most used

- CT and MRI also reliable

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19
Q

How is oral candidiasis treated?

A

Nystatin oral suspension

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20
Q

List symptoms of coelic disease

A
  • Diarrhoea
  • Abdominal cramps
  • Steatorrhea
  • Abdominal distention
  • Malabsorption
  • Loss of appetite
  • Among children, failure to grow normally.
  • Fatigue/lethargy
  • Recurrent mouth ulcers
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21
Q

How is coelic treated?

A

Lifelong gluten free diet

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22
Q

Define coelic disease

A
  • An autoimmune disorder affecting primarily the small intestine that occurs in people who have HLA-DQ2 allele or the HLA-DQ8 allele.
  • Reaction to gluten, which are various proteins found in wheat and in other grains such as barley, and rye.
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23
Q

Compare LFT in alcoholic and viral hepatits

A
  • Viral ALT>AST

- Alcoholic AST>ALT

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24
Q

How does cirrhosis affect thyroid hormones?

A
  • Decreased thyroid binding globulin
  • Decreased levels of bound thyroid hormones
  • Free thyroid hormones remain the same due to feedback induced decrease in TSH
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25
Q

Define chronic pancreatitis

A

Chronic pancreatitis is a chronic, irreversible, inflammation and/or fibrosis of the pancreas, often characterized by severe pain and progressive endocrine and exocrine insufficiency.

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26
Q

List risk factors/aetiology of chronic pancreatitis

A
  • Alcohol induced (70-80%)
  • Smoking
  • Autoimmune disease (Sjogrens, IBD, primary biliary cirrhosis)
  • CF
  • Haemochromatosis
  • Genetic abnormalities (SPINK1/PSTI gene)
  • Drugs (thiazide like diuretics, azathioprine, tetracyclines, oestrogens)
  • Obstructive causes (gallstones and strictures, cancer)
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27
Q

List symptoms of chronic pancreatitis

A
  • Recurrent epigastric pain (deep, severe, dull may radiate to back, intermittent or continuous, relieved by leaning forward, precipitated by eating, associated with nausea and vomiting)
  • Bloating
  • Abdominal cramps, flatus
  • Weight loss
  • Malnutrition
  • Steatorrhea
  • Diabetes mellitus
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28
Q

Describe management of chronic pancreatitis

A
  • Fluids
  • Pain control
  • Repletion of pancreatic enzymes
  • Low alcohol low fat diet
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29
Q

Define acute pancreatitis

A

Acute pancreatitis is an acute inflammatory process of the pancreas with varying involvement of local tissues or more remote organ systems.

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30
Q

What is the cause of indirect inguinal hernia?

A

Failure of the tunica vaginalis to fuse

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31
Q

List life threatening complications of groin hernias

A
  • Trapping of herniated intestine
  • Bowel obstruction
  • Bowel ischaemia
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32
Q

What is intrahepatic cholestasis of pregnancy?

A
  • A reversible form of cholestasis affecting some pregnant women in their second or third trimester
  • Characterised by hepatic dysfunction and pruritus of the skin caused by elevated bile acids in the blood, and bile deposition in the skin
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33
Q

Define volvulus

A
  • A subtype of malrotation, in which a loop of bowel is twisted about a focal point along the mesentery attached to the intestinal tract, that may result in a bowel obstruction.
  • A volvulus is a twisting or axial rotation of a portion of bowel about its mesentery.
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34
Q

Describe investigations of volvulus

A
  • Routine bloods
  • Erect CXR, AXR
  • Upper gastrointestinal contrast studies
  • Usually based on barium studies
  • Some are recommending CT scanning (coffee bean sign in left iliac fossa)
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35
Q

List symptoms of gastric volvulus

A
  • Sudden onset severe epigastric pain (colicky)
  • Abdominal distention
  • Constipation
  • Intractable retching without vomiting
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36
Q

Define peptic ulcer disease and gastritis

A
  • A peptic ulcer is a break in the lining of the stomach, first part of the small intestine, or occasionally the lower esophagus
  • Gastritis is inflammation of the stomach lining
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37
Q

How does perforation of peptic ulcer present?

A
  • Nausea
  • Vomiting blood
  • Bloating
  • Early satiety
  • Anaemia
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38
Q

List symptoms of acute pancreatitis

A
  • Sudden onset upper abdominal pain (epigastric radiates to back, worsens with movement and alleviated with fetal position)
  • Nausea
  • Vomiting
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39
Q

Describe diagnosis of Wilsons disease

A
  • Kayser-Fleischer ring
  • Neuropsyciatric symptoms
  • LFTs abnormal (raised transferases and bilirubin, or low albumin in failure)
  • Urinary copper levels (>100 micrograms in 24 hours)
  • Liver copper levels
  • Serum ceruloplasmin (low)
  • Genetic testing
  • Blood free copper raised but total serum copper decreased
  • MRI brain showing basal ganglia increased density (panda sign)
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40
Q

Name the common complications of cleft lip or palate

A
  • Otitis media
  • Speech problems
  • Hearing loss
  • Feeding problems
  • Psychosocial problems
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41
Q

What is the rigler triad?

A

Gallstone ileus:

  • Pneumobilia
  • Low small bowel obstruction with distended abdomen
  • Gallstone in terminal ileum
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42
Q

List causes of acute pancreatitis

A
  • Idiopathic
  • GALLSTONES (40%)
  • ETHANOL (alcohol 35%)
  • Trauma
  • Steroids
  • Mumps
  • Autoimmune
  • Scorpion stings
  • Hyperlipidaemia/hypercalcaemia
  • ERCP
  • Drugs
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43
Q

Define haemorrhoid

A
  • Haemorrhoids (also known as piles) are abnormally swollen vascular mucosal cushions that are present in the anal canal.
  • Three vascular mucosal cushions are in the anus to maintain anal continence. These become enlarged in haemorrhouds
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44
Q

Compare internal and external haemorrhoids

A
  • Internal above the pectinate line. simple columnar epithelium. Also graded 1-4 based on degree of prolapse (1 no prolapse only bleeds, 2 spntaneously reduce, 3 manual reduction, 4 cannot be reduced)
  • External inferior to pectinate line, stratified squamous epithelium
  • Above pectinate line, non-painful but more prone to bleeding
  • Below pectinate line, painful due to somatic innervation by inferior rectal nerve, but they do not generally bleed
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45
Q

What is dermatitis herpetiformis?

A
  • A manifestation of celiac disease
  • Small vesicles grouped together
  • No underlying viral cause
  • Most often lesions are on the forearms, elbows, scalp, knees and back
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46
Q

What does the double bubble sign on X ray show?

A
  • Intestinal atresia (lumen of GI tract fails to recanalize between eighth and tenth week of gestation)
  • Closely associated with down syndrome
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47
Q

What is HSP?

A
  • Henoch-Schönlein purpura

- The classic clinical triad of HSP is palpable purpura/petechia migratory arthritis, and abdominal pain

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48
Q

Describe the pain in renal colic

A
  • Loin to groin
  • Starts at the back
  • Moves down to the suprapubic region and sometimes penis as it irritates the urinary tract
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49
Q

What is caput medusa

A
  • Obstruction of vena cava

- Causes superficial veins to distend

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50
Q

What is tenesmus?

A

Sensation of needing to poo when you dont need to, due to irritation of the rectum

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51
Q

What is borborygmi?

A

Loud rumbling of the stomach

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52
Q

How is oral thrush characterised?

A

Pale plaques that can be scraped off the tongue to reveal an erythematous base

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53
Q

What is Hirschsprung and how is it diagnosed?

A
  • Failure of the neural crest to fully migrate through the gut to form the enteric nervous system.
  • The gold standard for diagnosis is biopsy of the distal colon
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54
Q

Define crohns disease

A
  • A type of IBD. Transmural granulomatous infection.
  • Unlike UC, can involve any part of the GI tract from mouth to anus
  • Skip lesions (areas of normal bowel mucosa between diseased areas)
  • Moves proximally into ileum
  • Affects the entire thickness of the colon
  • May cause fistulae, abscesses and fibrotic strictures
  • 30 times more likely if a sibling has it
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55
Q

List symptoms of Crohns disease

A
  • Fever
  • Rectal bleeding
  • Weight loss
  • Anorexia
  • Nausea
  • Vomiting
  • Malnutrition
  • Vitamin deficiencies
  • Abdominal pain (cramp or constant, most commonly right lower quadrant and peri-umbilical regions)
  • Bowel obstruction (bloating, distention, borborygmi, vomiting)
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56
Q

Describe Murphys sign

A

Where you press on the gallbladder and it makes the patient gasp with pain. Sign of acute cholecystitis

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57
Q

Describe blood from different areas of GI

A
  • Melaena is black tarry stools, caused by GI bleeding
  • Haematemesis when red blood hasnt reached stomach acid, when coffee ground it has
  • Fresh blood in stools is distal
  • Altered blood in stalls is proximal
  • Bright red blood a most commonly not cancer, fissure instead.
  • Blood smeared on stools due to anal lesion (piles, polyps, fissure)
  • Blood on toilet paper haemorrhoid or fissure
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58
Q

Describe colicky pain

A
  • Occurs in waves when peristalsis occurs

- Crescendo decreascendo

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59
Q

List symptoms and signs of bowel obstruction

A
  • Abdominal distension
  • Flatus absent
  • Absence of bowel movements
  • Vomiting (faeculent)
  • Can see peristalsis
  • Barbarigmy
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60
Q

What is a Blatchford score?

A
  • Stratifies patients presenting to hospital with haematemesis into high and low risk groups to determine who can be managed as outpatient
  • 0 is low risk, 6 is high risk
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61
Q

What is a Rockall score?

A
  • A score to predict the risk of rebleeding and mortality in patients with upper GI haemorrhage
  • Used to guide urgency of endoscopy
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62
Q

List indications for emergency endoscopy

A
  • Unstable patients with severe acute upper GI bleeding immediately after resusitation
  • Continuing upper GI bleed or Blatchford score of 6 or more
  • Patients with an aortic graft may require endoscopy to exclude aorto-enteric fistula
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63
Q

List investigations performed in haematemesis

A
  • Oesophagogastroduodenoscopy
  • Erect chest radiograph (perforated peptic ulcer, left sided pleural effusion in boerhaaves perforation)
  • CT scan of chest-abdomen (all patients with known aortic graft require this to rule out aorto-enteric fistula, provided they are haematologically stable enough)
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64
Q

Compare a mallory-weiss tear to a boerhaaves perforation

A
  • Boerhaaves perforation is transmural, surgical emergency with high mortality rate. Presents with severe chest pain after vomiting or consuming a large meal, palpable subcut emphysema at neck, dysphagia. Shock.
  • Mallory weiss tear is not, small amount of haematemesis after history of vomiting
  • Both tears to the oesophagus often caused by vomiting
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65
Q

What is dupuytrens contracture?

A
  • Thickening of a tendon resulting in contraction of a finger with visible tendon
  • A sign of liver disease
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66
Q

List the different surgical scars in the abdomen and their uses

A
  • Kochers (cholecystectomy)
  • Left paramedian (colectomy)
  • Midline (AAA, laprotomy)
  • Lanz incision (appendectomy)
  • Groin incision (inguinal hernia)
  • Pfannensteil (C section, access to bladder)
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67
Q

How is a bleeding oesophageal varix due to portal hypertension treated?

A
  • Endoscopic band ligation (use rubber band to ligate the bleeding vessel)
  • Endoscopic slerotherapy (not first line, can induce necrosis of oesophageal mucosa)
  • Balloon tamponade (tube passed into the stomach, a balloon at the end is inflated in the stomach to keep the tube in place, a second balloon along the length of the tube is inflated to apply pressure to the bleeding vein and induce haemostasis)
  • Transjugular intrahepatic portosystemic shunt (pass a catheter down the jugular vein, create a shunt from hepatic vein to portal vein to relieve portal hypertension)
  • Portiocaval shunt (place a shunt between portal and systemic circulation to bypass the liver and reduce portal hypertension)
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68
Q

Describe signs and symptoms of a bleeding peptic ulcer

A
  • Melaena
  • Haematemesis, coffee ground
  • History of heart burn/ibuprofen
  • Pain in epigastric region
  • Nausea and vomiting
  • Weight loss
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69
Q

Describe investigations for peptic ulcer disease and gastritis

A
  • Urea breath test for H pylori (patients swallow labelled urea, then take a breath sample to look for labelled carbon dioxide in the breath)
  • Serological tests for IgG
  • Stool test for H pylori
  • Endoscopy, to look for ulcer and take a sample to test for H pylori, look at histologically and antibiotic testing
  • FBC, U and E, faecal occult blood, barium meal test
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70
Q

List the main risk factors for peptic ulcers

A
  • H pylori (causes chronic gastritis by provoking an inflammatory response in the gastric epithelium)
  • Smoking
  • Alcohol
  • NSAIDS and aspirin
  • Blood group O
  • Hypercalcaemia
  • Physiological stress
  • Burns or brain trauma
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71
Q

What is an oesophageal varix?

A

Dilation of the oesophageal veins due to portal venous hypertension (often in patients with cirrhosis)

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72
Q

Describe briefly blood clotting and its measurement

A
  • Tissue damage
  • Intrinsic pathway (APTT - affected by heparin, haemophilias and VWD)
  • Extrinsic pathway (PT- affected by warfarin, liver disease)
  • factor X to Factor Xa and Va
  • Prothrombin to thrombin
  • Fibrinogen to fibrin
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73
Q

Define acute cholangitis

A
  • Ascending bacterial infection of the bilary tract related to choledocholithiasis and bile stasis
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74
Q

Describe symptoms of acute cholangitis

A

Charcot’s triad

  • Right upper quadrant pain
  • Fever
  • Jaundice
  • In severe cases, septic shock and mental confusion
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75
Q

List findings on examination in acute cholangitis

A
  • Jaundice
  • Icterus
  • Fever
  • Abdominal pain RUQ
  • Palpable gallbladder
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76
Q

How is acute cholangitis investigated?

A
  • Blood test
  • Shows leukocytosis, hyperbilirubinaemia and evelated alkaline phosphatase, elevated transaminaise and serum amylase
  • Blood cultures positive in 50% patients (e.coli, klebsiella, entercoccus and bacteriodes fragilis)
  • ERCP best first investigation
  • Consider transabdominal ultrasound
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77
Q

How is acute cholangitis managed?

A
  • Broad spectrum IV antibiotics (piperacillin, tazobactam)
  • Correction of fluid and electrolyte imbalances
  • Analgesia, oxygen
  • Biliary decompression (ERCP with or without sphincterotomy and drainage stent first line, percutaneous transhepatic cholangiography second line)
  • Lithotripsy if stone
  • Surgical decompression (second line, if risk of morbidity is high)
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78
Q

Define rectal prolapse

A
  • A condition in which the rectum loses its normal attachments inside the body, allowing it to telescope out through the anus, thereby turning it inside out.
  • It is most common in the elderly (especially women) but can occur in all ages, including children.
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79
Q

List symptoms of rectal prolapse

A
  • Pain
  • Rarely bleeding
  • Seepage
  • Constipation or incontinence
  • Mass following defecation
  • Diminished quality of life
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80
Q

List risk factors for rectal prolapse

A
  • Age over 40
  • Sex (female)
  • Multiple deliveries
  • Medial history of pelvic surgery, chronic constipation, diarrhoea or straining
  • Anatomical defects
  • In children from endemic regions, trichuris
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81
Q

List signs of rectal prolapse

A
  • Mass of tissue protruding from the rectum

- Unable to contract and relax the anal sphincter completely

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82
Q

Define hiatus hernia

A
  • Part of the stomach protrudes through the crura of the diaphragm and into the thoracic cavity.
  • At risk of ulcer formation
  • Sliding are protrusion of the gastrooesophageal junction and cardia of the stomach
  • Paraoesophageal are only the fundus of the stomach
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83
Q

List common symptoms of hiatus hernias

A
  • May be asymptomatic
  • GERD
  • Epigastric or substernal pain
  • Postprandial fullness
  • Nausea
  • May cause gastric ulcer formation, leading to haematemesis, melena, nausea and epigastric pain worsened after eating fatty foods
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84
Q

Describe odonophagia

A
  • Painful swallowing

- May be due to malignancy, more commonly a feature of infection eg. candidiasis

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85
Q

List investigations preformed in dyspagia, and their indications

A
  • Barium swallow (for patients who may have a high lesion, and patients who may have achalasia)
  • Endoscopy (visualisation of luminal and mural lesions, and opportunity to biopsy and treat lesions, used in low dysphagia)
  • Videofluoroscopy (functional high dyspagia)
  • Manometry (distinguishing between different types of motility disorders, used when endoscopy is normal)
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86
Q

Define barrets oesophagus

A

Metaplasia of the oesophageal epithelial lining, whereby normal stratified squamous epithelium is replaced by simple columnar epithelium.

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87
Q

What are risk factors for barretts oesophagus?

A
  • Family history
  • Being male
  • Being white
  • Age >50
  • Chronic heartburn and acid reflux (GORD)
  • Current or past smoking
  • Being overweight
  • Hiatus hernia
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88
Q

Describe epidemiology of Barretts oesophagus

A
  • The prevalence ranges from 0.5-2% in the Western world.
  • Around 10% of patients with GORD will have already developed Barrett’s oesophagus by the time they seek medical attention.
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89
Q

Describe symptoms of Barretts oesophagus

A
  • History of GORD (retrosternal chest pain, excessive belching, odynophagia, chronic cough and hoarseness)
  • Red flag symptoms of potential malignancy (dysphagia, weight loss, early satiety, malaise, loss of appetite, or worsening dyspepsia despite PPI treatment)
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90
Q

List signs of barretts oesophagus

A

Unremarkable on examination

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91
Q

Describe diagnosis of barretts oesophagus

A
  • Patients who undergo OGD (gastroscopy) for chronic or resistant GORD (or to exclude malignancy) should have a biopsy taken of the oesophageal epithelium and sent for histological analysis.
  • At OGD, the oesophagus appears red and velvety in cases of Barrett’s oesophagus, with some preserved pale squamous islands.
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92
Q

How is barretts oesophagus managed?

A
  • PPI
  • Diet advice (avoid acidic foods/ alcohol)
  • Stop medication eg. NSAIDS
  • Regular endoscopy due to risk of adenocarcinoma developing (radiofrequency ablation/resection)
  • Oesophagectomy
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93
Q

Describe prognosis of barretts oesophagus

A
  • High grade dysplasia has a high risk of progressing to cancer so should be resected with endoscopic mucosal resection (EMR) or endoscopic submucosal dissection (ESD).
  • Adenocarcinomas detected on routine screening for Barrett’s oesophagus are typically early-stage lesions and have a better prognosis than those discovered outside of any screening program.
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94
Q

Define GORD

A

Gastro-intestinal reflux disease (GORD) is a condition characterised by retrosternal, and sometimes epigastric pain, as a result of reflux of the acidic contents of the stomach into the oesophagus.

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95
Q

List risk factors for GORD

A
  • Hiatus hernia
  • Eating certain foods – fat, chocolate, caffeine
  • Smoking
  • Obesity
  • Dysfunction of the lower oesophageal sphincter (LOS)
  • Alcohol
  • Helicobacter Pylori
  • “Stress”
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96
Q

Describe epidemiology of GORD

A
  • GORD resulting in heartburn affects 30% of the population
  • Less common in East Asia
  • Increases with age
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97
Q

List symptoms of GORD

A
  • Dyspepsia – retrosternal chest pain radiating to the jaw back and arms, particularly after eating. May be worse on lying down, usually relieved by antacids and aggravated by drinking alcohol and hot drinks, and by bending over.
  • Regurgitation of food and acid into the mouth – this generally occurs when the patient is lying flat.
  • Waterbrash – salivation due to the presence of acid in the oesophagus.
  • Weight gain – this is a pre-disposing factor – not a symptom. Often a patient will put on a bit of weight, and shortly afterwards, the dysphagia will first present.
  • Choking at night – as gastric acid irritates the larynx
  • Dysphagia – this may be present in those people with a stricture. The stricture could be a result of mucosal damage due to reflux
  • Excess Belching
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98
Q

Describe diagnosis of GORD

A

Generally clinical, based on history and response to antacids (PPI trial 8 weeks). If patients dont respond to initial treatment…

  • H pylori testing (urea breath test)
  • Endoscopy
  • Barium swallow (hiatus hernia/strictures)
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99
Q

How is GORD treated?

A
  • Lifestyle changes (weight loss, head of bed elevation, avoid late night eating, chocolate, caffeine, alcohol, spicy foods)
  • PPI/antacids
  • Review drugs
  • If persistant, fundoplication surgery
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100
Q

Describe prognosis of GORD

A

10–15% of people with GORD will develop Barrett’s oesophagus, and 1–10% of these will develop oesophageal adenocarcinoma over the next 10–20 years.

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101
Q

Define oesophageal cancer

A
  • Tumour of the oesophagus
  • 4 types -adenocarcinoma, squamous cell carcinoma, leiomyoma and squamous papilloma.
  • Squamous cell and adenocarcinoma are by far the most common.
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102
Q

Describe epidemiology of oesophageal cancer, squamous cell carcinoma

A
  • 2-3 per 100 000 in the UK and USA. Much higher in Asia and the Middle East
  • Male:Female = 7:1
  • Peak age of incidence is 60-70
  • 15%
  • Upper 2/3 of oesophagus
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103
Q

List risk factors of oesophageal cancer, squamous cell carcinoma

A
  • Alcohol
  • Smoking
  • Dietary nitrosamines (found in mouldy foods) and nitrates
  • Alfatoxins
  • Achalasia
  • Plummer vinson syndrome
  • Coeliac
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104
Q

Describe epidemiology of adenocarcinoma of the oesophagus

A
  • 5 per 100 000 – thus in these regions it is more common than squamous cell carcinoma
  • Incidence has risen greatly in the last few decades – thought to be related to the increase in obesity (and thus the increase in reflux disease)
  • Most common presentation is in white, middle-aged males
  • Lower 2/3 of oesephagus
  • 80% cancers
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105
Q

List risk factors for adenocarcinoma of the oesophagus

A
  • Barrett’s Oesophagus.
  • Obesity
  • Smoking
  • Alcohol
  • Genetic susceptibility
  • Age (>45)
  • Male
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106
Q

List signs and symptoms of oesophageal cancer

A
  • Feeling of lump in the throat – not associated with eating
  • Progressive dysphagia – this is a very characteristic symptom
  • Regurgitation – may be misinterpreted as vomiting
  • Weight loss and anorexia
  • Possible palpable lymph nodes, such as Virchow’s node.
  • Dyspnoea
  • Odonophagia (painful swallowing suggesting local invasion)
  • FLAWS
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107
Q

How is oesophageal cancer investigated?

A
  • Endoscopy. Investigation of choice. 90% of oesophageal tumours can be imaged. Biopsy
  • Barium swallow (rare) – may be used if endoscopy cannot be tolerated
  • CT/MRI for staging
  • Rarely laproscopy
  • Metabolic profile shows volume depletion, hypokalaemia
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108
Q

List risk factors of crohns

A
  • White ancestry
  • Age 15-40 or 60-80
  • Family history
  • Cigarette smoking
  • High refined sugar diet
  • Oral contraceptive
  • Not breastfed
  • NSAIDs
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109
Q

Define gastric cancer

A

Cancer of the lining of the stomach

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110
Q

List causes of gastric cancer

A
  • The most common cause is infection by the bacterium Helicobacter pylori, which accounts for more than 60% of cases.
  • Other causes include dietary nitrosamines (smoked foods), tobacco smoking, achlorhydria, and chronic gastritis.
  • Pernicious anaemia
  • Positive family history
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111
Q

List symptoms of gastric cancer

A
  • Presents late
  • Weight loss
  • Anorexia
  • Dyspepsia
  • Dysphagia
  • Epigastric pain
  • Early satiety
  • Haematemesis (coffee ground)
  • Meleana
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112
Q

List signs on examination of gastric cancer

A
  • Palpable vircows node
  • Palpable periumbilical lymph nodes
  • Abdo mass
  • Hepatomegaly + jaundice
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113
Q

Describe epidemiology of gastric cancer

A
  • Over 7000 new stomach cancers are diagnosed each year in the UK
  • 2 times more common in males
  • Adenocarcinoma most common
  • Common in Asia
  • Age 50-70
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114
Q

How is gastric cancer investigated?

A
  • OGD, biopsy all ulcers in multiple locations.
  • endoscopic ultrasound to examine depth of invasion
  • CT/MRI for staging
  • Cytology of peritoneal wash
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115
Q

Define hepatocellular carcinoma

A

The most common type of primary liver cancer

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116
Q

List symptoms and signs of hepatocellular carcinoma

A
  • Anorexia
  • Bloating (ascites)
  • Weight loss
  • Peripheral extremity swelling
  • Hepatomegaly and upper right quadrant tenderness
  • Ascites
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117
Q

List risk factors for hepatocellular carcinoma

A
  • Cirrhosis
  • Chronic inflammation of the liver caused by hepatitis B or C
  • Alcohol
  • Non-alcoholic steatohepatitis
  • Hemochromatosis
  • Wilsons
  • A-1 antitrypsin deficiency
  • Autoimmune hepatitis
  • Male
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118
Q

Describe epidemiology of hepatocellular carcinoma

A
  • Fifth most common malignancy worldwide
  • Most common primary liver malignancy in adults
  • Highest incidence in Southeast Asia and Africa [1]
  • Peak incidence in the US: 70–75 years
  • Peak incidence in Africa and Asia: 30–40 years
  • Affects females more than males
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119
Q

Describe investigation of hepatocellular carcinoma

A
  • Raised serum alpha-fetoprotein (AFP - used to screen cirrhosis patients, raised in 80% patients)
  • Ultrasound (initial test, showing irregular mass boreders, vascular invasion, underlying cirrhosis, also used to screen cirrhosis ts)
  • Abdominal CT or MRI confirmatory (hypodense lesions, local invasion, irregular mass borders)
  • Liver biopsy for definitive diagnosis
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120
Q

Define gallstones and biliary colic

A
  • Gallstones (cholelithiasis) refers to the formation of hard stones in the gallbladder – a process which typically takes years to occur.
  • Biliary colic is pain due to gallstones which comes and goes in RUQ
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121
Q

Describe epidemiology of gallstones and biliary colic

A
  • More common in women
  • Cholesterol secretion is a massive factor in gallstone formation – particularly the amount of cholesterol secreted in relation to the concentration of bile salts. Women naturally secrete a higher proportion of cholesterol than men and thus they have a higher incidence of gallstones.
  • Incidence increases with age
  • At age 30 – 5% of women and 2% of men have / have had gallstones. Aged 55 – 20% / 10%, age 70, 30% / 20%.
  • Racial differences: More common in Scandinavia, and Native North and South American Populations.
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122
Q

List risk factors for gallstones and biliary colic

A
  • Obesity
  • Sudden weight loss
  • Family History
  • Oestrogen
  • Female gender
  • Oral contraceptive pill
  • Diet (high fat, low fibre)
  • Increasing age
  • Diabetes
  • Crohns

5F- fair, fat, female, fertile, forty

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123
Q

List presenting symptoms of gallstones and biliary colic

A
  • Gallstones usually do NOT cause flatulence, dyspepsia, fat intolerance or other vague upper abdominal symptoms, unless they are causing an acute flare-up of biliary colic (see below) or other acute manifestations
  • Symptomatic gallstones can present as either biliary colic (waves of pain in URQ after fatty meals, nausea and vomiting radiates to scapula), chtis (infection in the biliary tree – an emergency), pancreatitis, or other acute manifestations
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124
Q

List signs of gallstones and biliary colic

A
  • Murphys sign (pain when you press down on the gallbladder)
  • Rebound tenderness
  • URQ pain
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125
Q

Describe investigation of gallstones and biliary colic

A
  • An abdominal ultrasound examination and a blood test to measure liver function tests (LFTs) should be arranged for people suspected of having gallstone disease.
  • MRCP or EUS may also be used
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126
Q

Define viral hepatitis, list the causative agents

A
  • Hepatitis refers to inflammation of the liver and can be due to a number of causes. Viruses cause around half of all cases of hepatitis.
  • Viral hepatitis is most commonly caused by Hepatitis A, B and C viruses
  • Other causes include Hepatitis D (associated with hepatitis B virus) and E
  • Rarely cytomegalovirus, Epstein Barr virus, Adenovirus, HSV (very rare)
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127
Q

List risk factors for viral hepatitis

A
  • Those from highly prevalent areas; injecting drug users; sex workers (take a sexual history); those who have been sexually assaulted, sustained a needlestick injury or are HIV positive
  • At risk patients should be offered the first dose of HBV vaccine also
  • Injecting drug users and close contacts
  • Those with multiple sexual partners and sex workers
  • Those travelling to areas of high prevalence
  • Household contacts of those with HBV
  • Those receiving regular blood products
  • Those with occupational risk
  • Prison inmates and staff
  • Infants born to women with chronic HBV
  • Hep A most commonly rimming
  • Hep B most commonly vertical (can be both sexually and blood blood)
  • Hep C most commonly sharing needles (lower risk sexually)
  • Hep D infects people with hep B (not a full virus)
  • Hep E most commonly pork (immunocompromised people eg. pregnancy)
128
Q

List symptoms of viral hepatitis

A
  • Fever (often mild), arthralgia and/or rash may appear around 2 weeks before any signs of jaundice, and may resolve when jaundice appears
  • Nausea and anorexia

Acute/ Icteric phase

  • Nonspecific malaise (can be severe)
  • Pruritus
  • Pain/tenderness in the right upper quadrant
  • Fulminant hepatitis is rare (<1%)
129
Q

List signs on examination of viral hepatitis

A
  • Liver stigmata- spider naevi (chronic), finger clubbing, jaundice, hepatomegaly
  • In advanced cirrhosis- easy bruising, oedema/ascites, liver flap, encephalopathy (confusion), progressive weight loss, muscle wasting/weakness, jaundice
130
Q

Describe investigations in viral hepatitis

A
  • In acute disease- ALT and AST are usually >1000 (ALT > AST typically)
  • In chronic disease- ALT and AST are only mildly elevated (<100IU/l)
  • Hep A elevated IgM, not infective during jaundice. IgM means acute, IgG means chronic
  • Hep B anti HBe means exposure to live virus, anti HBs is given in vaccines. Can be chronic, often sub-clinical. Core IgM acute
  • HCV antibody test and RNA test
131
Q

Define primary sclerosing cholangitis

A

A disease of the bile ducts that causes inflammation and obliterative fibrosis of bile ducts inside and/or outside of the liver.

132
Q

List risk factors and aetiology for primary sclerosing cholangitis

A
  • Narrowing of the bile duct lumen usually occurs throughout the biliary tree.
  • Less commonly, changes are confined to the intra-hepatic or extra-hepatic ducts but is seldom short enough to resemble a post-traumatic or focal malignant stricture.
  • Association with inflammatory bowel disease (75 per cent of cases), particularly ulcerative colitis but also Crohn’s disease
133
Q

Describe the epidemiology of primary sclerosing cholangitis

A
  • Prevalence is estimated at 1 to 6 per 100,000.
  • Mean age at the time of diagnosis is 39 years
  • 70% of patients are men
  • Typically occurs in patients with inflammatory bowel disease, but may also occur in association with retroperitoneal or mediastinal fibrosis
  • Of the 75% of patients with primary sclerosing cholangitis who have inflammatory bowel disease, about 87% have ulcerative colitis and 13% have Crohn’s disease
134
Q

List symptoms of primary sclerosing cholangitis

A
  • Progressive fatigue, pruritus and jaundice.
  • Symptoms associated with chronic liver disease, for example, weight loss, ascites, variceal bleeding and hepatic encephalopathy.
135
Q

List signs of primary sclerosing cholangitis

A
  • Hepatomegaly is found in about 50% of patients

- Less often, there is splenomegaly, hyperpigmentation and xanthomas.

136
Q

Describe investigations performed in primary sclerosing cholangitis

A
  • Raised serum alkaline phosphatase, aspartate aminotransferase and bilirubin
  • Hypergammaglobulinaemia occurs in one third; IgM levels increased in 50% of cases
  • Raised hepatic copper levels in nearly 90% of cases
  • Liver biopsy revealing a fibrous obliterating cholangitis, and loss of interlobular and adjacent septal bile ducts (concentric onion skin fibrosis)
  • ECRP showing multiple annular strictures, separated by round or slightly dilated duct segments
    the intrahepatic and extrahepatic bile ducts have a beaded appearance
  • Raised perinuclear antineutrophil cytoplasmic antibody
137
Q

Describe management of peptic ulcer disease and gastritis

A
  • Lifestyle modification
  • Assess for stress, anxiety and depression
  • Reviewing and stopping any drugs which may be exacerbating symptoms
  • If H pylori positive, PPI prescribed for 2 months then H pylori eradication treatment. Consider H2 receptor antagonist too (triple therapy - PPI, clarithromycin and amoxicillin)
  • Long term acid suppression therapy should be considered
  • Annually review if on long term treatment
  • H pylori negative PPI and H2 antagonist eg. ranitidine
138
Q

List possible complications of peptic ulcer disease

A
  • Haemorrhage (case fatality 5-10%)
  • Perforation (may cause peritonitis 20% mortality)
  • Gastric outlet obstruction (strictures and stenosis)
  • Gastric malignancy (increased risk if H pylori positive)
  • If posterior duodenal, can infiltrate gastroduodenal artery
139
Q

Describe epidemiology of peptic ulcer disease

A
  • 5-10% lifetime prevalence
  • Incidence 0.1-0.3% per year
  • Incidence pf duodenal ulcer peaks at 45-64 years and is 2 times more common in men
  • Incidence of gastric ulcers increases with age, and is similar in men and women
140
Q

Describe prognosis of peptic ulcer disease and gastritis

A
  • If associated with H pylori, eradication may cure ulcer.
  • Lifetime gastric ulcer recurrence 60% if H.pylori positive and 5% following eradication
  • Lifetime duodenal ulcer reccurence 80% if h.pylori positive and 5% following eradication
  • If associated with NSAIDs, stopping use of drug or co-prescribing with acid suppression reduces risk of occurance
  • Mortality rate 6-8%
  • 1 in 10 people with bleeding peptic ulcer will die, and 1 in 4 people with perforated peptic ulcer will die
141
Q

Describe epidemiology of acute pancreatitis

A
  • 13-15 cases per 100000 people worldwide
  • Most hospitals admit 100 people per year
  • 80% mild
142
Q

List signs of acute pancreatitis

A
  • Abdominal tenderness
  • Abdominal distension
  • Cullens sign (bluish discolouration by umbillicus) or grey turners (bluish flank) due to retroperotineal bleed
  • Tachycardia and hypotension (shock)
  • Fever
  • Jaundice
  • Ileus
  • Rigid abdomen
143
Q

List investigations for acute pancreatitis

A
  • Lipase or amylase raised (lipase more specific, rises earlier)
  • FBC- elevated leukocyte count poor prognosis
  • ABG for oxygenation
  • AXR no psoas shadow, increased retroperitoneal fluid, sentinel loop of proximal jejunum from ileus
  • Erect CXR to exclude perforation
  • CT standard
  • US if gallstones and raised AST
  • Imaging (CT, ultrasound, MRI)
  • ERCP to check for gallstones, CRP predictor of severe pancreatitis
144
Q

Describe management of acute pancreatitis

A
  • IV fluids (crystalloid), urinary catheter
  • NJ feeding/ encourage to eat
  • Oxygen
  • Pain relief (pethidine 75-100mg/4h IM or morphine
  • Hourly obs
  • Antibiotics
  • Nutritional support
  • Cholecystectomy if gallstones, ECRP to remove a gallstone
  • ITU if worsening
145
Q

Describe prognosis of acute pancreatitis

A
  • Mild 1% mortality rate
  • Severe 10% mortality if sterile and 25% if infected
  • Average 12% mortality
146
Q

List complications of acute pancreatitis

A

Early: sepsis, ARDS, renal failure, SIC, shock, hypocalcaemia, raised glucose

Long term

  • Pancreatic necrosis with or without infection
  • Pseudocyst (thick walled collections of pancreatic fluid, drained percutaneously or using EUS)
  • Pancreatic abscess drain)
  • Fustulae (from pancreatic duct to abdominal cavity, pleural cavity or pericardial cavity, close spontaneously)
  • Pre-hepatic portal hypertension
  • Acute renal failure
  • Acute respiratory distress syndrome
  • Thrombosis causing bowel necrosis
  • Recurrent oedematous pancreatitis
147
Q

Describe epidemiology of chronic pancreatitis

A
  • 8.3 per 100000 France
  • 4.45 per 100000 US
  • India 114-200 per 100000
148
Q

List signs of chronic pancreatitis

A
  • Chronic liver disease
  • Epigastric tenderness
  • Jaundice
  • Abdominal distention (pseudocyst, pancreatic ascites or cancer)
  • Firm skin nodules due to fat necrosis)
  • SOB
149
Q

Describe investigations of chronic pancreatitis

A
  • Blood tests (liver function, may be abnormal in liver disease but serum amylase not diagnostic)
  • Abdominal ultrasonography to exclude other conditions+CT (pancreatitic calcifications)
  • Stool test for fecal elastase
  • MRCP, AXR
150
Q

Describe management of chronic pancreatitis

A
  • Stop smoking and alcohol
  • Analgesia (NSAIDs, paracetamol, weak opiod)
  • If severe pain, endoscopic therapy to remove stones and dilate strictures, surgery, adjuvant drugs (amitriptyline, gabapentin or pregabalin)
  • Screen for diabetes, osteoporosis
  • Refer to dietition
  • Pancreatic enzyme supplementation (lipase, fat soluble vitamins, insulin)
  • Corticosteroids if autoimmune chronic
  • Treat diabetes, hypercalcaemia and hypertriglyceridaemia
  • Surgery if unremitting, narcotic abuse, low weight (pancreatectomy)
151
Q

List complications of chronic pancreatitis

A
  • Maldigestion and malabsorption.
  • Diabetes mellitus.
  • Chronic pain.
  • Opioid dependency for treatment of chronic pain.
  • Low-trauma fracture due to an increased risk of osteoporosis due to malabsorption.
  • Pancreatic calcification.
  • Pseudocyst formation.
  • Duodenal or gastric outlet obstruction, gastric varices
  • Biliary obstruction.
  • Fistulae.
  • Pancreatic cancer.
  • Pseudoaneurysm.
  • Splenic or portal vein thrombosis.
152
Q

Describe prognosis of chronic pancreatitis

A
  • Chonic pain (stable, worsen or improve over time)
  • Exocrine insufficiency 91-100% of people after 26-36 years)
  • Endocrine insufficiency 28-76%
  • 50 year life expectancy if onset idiopathic around 20 years
  • 77-80 life expectency if senile idiopathic (50 years plus)
  • 55-72 year life expectancy if alcoholic
  • 44 years life expectancy if hereditary
153
Q

List what is looked for in general inspection in abdo exam

A
  • Medical paraphernalia
  • Tattoos
  • Distension or scars
  • Anaemia or jaundice
  • ASK ABOUT TATTOOS OR BRUISING
154
Q

List what is looked for in inspection of the face in abdo exam

A
  • Central cyanosis
  • Jaundice
  • Kaiser flaischer rings
  • Xanthelasma
  • Pigmentation
  • Hydration
  • Telangectasia
  • Dentition
  • Apthious ulcers
  • Angular stomatitis
  • Atrophic glossitis
  • Candidiasis
155
Q

List what is looked for in inspection of the hands and arms in abdo exam

A
  • Clubbing
  • Palmar erythema
  • Dupuytrens contracture
  • Leukonychia and koilonychia
  • Tatoos
  • Excoriation
  • Petichiae
  • Haemodialysis fistulae
156
Q

Describe epidemiology of Mallory Weiss tears

A
  • 3% to 15% of patients gastrointestinal (GI) bleed.
  • More common in adults than children (age 30-50)
  • Males 3 times more affected
157
Q

Describe symptoms of mallory-weiss tear

A
  • Haematemesis after an episode of forceful or recurrent retching, vomiting, coughing, or straining.
  • Abdominal pain
  • Melaena
  • Dizziness and syncope
158
Q

List risk factors for mallory weiss tear

A
  • Excessive alcohol ingestion.
  • Conditions predisposing to retching and vomiting. (gastroenteritis, bulimia, renal disease, hepatitis, migraine)
  • Medication such as chemotherapy.
  • Chronic cough or acute causes of prolonged coughing bouts. (eg. COPD, whooping cough)
  • Hiatus hernia. During retching or vomiting, the transmural pressure gradient is greater within the hiatus hernia than the rest of the stomach.
  • Blunt abdominal trauma and cardiopulmonary resuscitation.
  • Iatrogenic. Tears during upper gastrointestinal instrumentation are uncommon, even with the high incidence of retching during endoscopy.
  • Ingestion of aspirin or other non-steroidal anti-inflammatory drugs (NSAIDs).
159
Q

Describe investigations of Mallory Weiss tear

A
  • Oesophogastroduodenoscopy
  • FBC, haematocrit
  • Blood group serology, group and save
  • Renal function
  • ECG
160
Q

Describe management plan of a Mallory Weiss tear

A
  • Ensure patient is stable
  • Rockall score to stratify risk
  • Maintain airway, fluid levels, provide oxygen
  • Usually bleeding stops by itself
  • IV PPI
  • Sengsaken blakemore tube
  • If does not resolve itself, banding or clipping techniques used in endoscopy, or adrenaline injection
  • Monitor patients for rebleeding
161
Q

List complications of a Mallory Weiss tear

A
  • Vomiting (hypokalaemia and other metabolic disturbance, aspiration pneumonia, perforation and mediastinitis).
  • Hypovolaemic shock, and death (very rare with good care).
  • Re-bleeding. (More common in those with shock at presentation, lower haemoglobin levels, multiple transfusions or active bleeding seen at endoscopy.)
  • Myocardial ischaemia or infarction.
  • Comorbidities - MI, renal failure, liver failure, diabetic coma
  • Endoscopy (mediastinitis, aspiration pneumonia, perforation or aggravation of bleeding).
  • Angiotherapy (organ ischaemia and infarction, aggravation of bleeding).
162
Q

Describe prognosis of mallory weiss tear

A
  • Most patients usually stop bleeding spontaneously and the tears heal rapidly, usually within 48-72 hours.
  • Bleeding is variable and can range from a few specks or streaks of blood mixed with mucus to large amounts of fresh blood.
  • Re-bleeding occurs in 8-20% but is more common in those with risk factors
  • Associated diseases may have a significant effect on prognosis; for example, cirrhosis carries a very poor prognosis
163
Q

Define ulcerative colitis

A

Ulcerative colitis is a chronic, relapsing-remitting, non-infectious inflammatory disease of the gastrointestinal tract

164
Q

List risk factors for ulcerative colitis

A
  • Family history
  • Appendicectomy before adulthood is thought to be protective against the development of ulcerative colitis
  • Non-selective nonsteroidal anti-inflammatory drugs (NSAIDs) may exacerbate ulcerative colitis and increase the risk of disease flare-ups
  • Smoking appears to be protective against developing ulcerative colitis, as the risk of ulcerative colitis is decreased in smokers (in contrast to Crohn’s disease, where smoking increases the risk)
  • Conversely, smoking cessation may increase the risk of developing ulcerative colitis, and ex-smokers have an approximately 70% greater risk of developing the disease, which is often more extensive and refractory to treatment, compared with people who have never smoked
165
Q

Describe epidemiology of ulcerative colitis

A
  • Most common bowel disease
  • Within Europe, the highest incidence and prevalence rates are found in Scandinavia and the UK
  • The incidence of paediatric-onset ulcerative colitis, which represents about 15–20% of all ulcerative colitis cases, ranges from 1–4 per 100,000 per year in most North American and European regions
  • The prevalence of ulcerative colitis is estimated at 5–500 per 100,000 worldwide
  • The peak incidence occurs in late adolescence and early adulthood in the second to fourth decades of life, with a small second peak in the fifth decade
  • Ulcerative colitis affects males and females at approximately equal rates
166
Q

List symptoms of ulcerative colitis

A
  • Bloody diarrhoea persisting for more than 6 weeks, or rectal bleeding, if malignancy is not suspected.
  • Faecal urgency and/or incontinence.
  • Nocturnal defecation.
  • Tenesmus (persistent, painful urge to pass stool even when the rectum is empty).
  • Abdominal pain, particularly in the left lower quadrant.
  • Pre-defecation pain, which is relieved on passage of stool.
  • Non-specific symptoms such as fatigue, malaise, anorexia, or fever (may suggest severe disease).
  • Weight loss, faltering growth or delayed puberty in children.
167
Q

List signs of ulcerative colitis

A
  • Pallor, clubbing, or aphthous mouth ulcers.
  • Abdominal distension, tenderness or mass, for example in the left lower quadrant.
  • Signs of malnutrition or malabsorption — serial weight loss or, in children, faltering growth or delayed puberty.
  • Eye, skin, or joint signs of extra-intestinal manifestations (pauciarticular arthritis, erythema nodosum, apthous mouth ulcers, episcleritis, metabolic bone disease, ankylosing spondylitis, venous thromboembolism)
168
Q

Describe investigations of ulcerative colitis

A
  • FBC (anaemia)
  • CRP, ESR (may be raised)
  • U and E (dehydration)
  • LFT (low albumin protein losing enteropathy)
  • Thyroid function tests)
  • Ferritin, B23 folate and vit D
  • Coeliac serology
  • Stool culture to exclude infective gastroenteritis
  • Fecal calprotectin (inflammation)
  • Colonoscopy showing continuous inflammation affecting rectum upwards, limited to the mucosa, never goes further than the ileocaecal valve
  • Monitor bowel due to adenoma risk
169
Q

List complications of ulcerative colitis

A
  • Psychosocial impact
  • Toxic megacolon (>6cm, systemic upset)
  • Bowel obstruction or perforation
  • Intestinal strictures
  • Fistulas
  • Anaemia
  • Malnutrition, delayed puberty in children
  • Growth failure
  • Colorectal cancer
  • Pouchitis (colectomy)
170
Q

Describe management of ulcerative colitis

A
  • Education
  • Encourage healthy lifestyle
  • Colorectal cancer surveillance
  • Monitor child growth and development
  • Monitor flare ups (inflammatory markers)
  • Colorectal surgery for stoma
  • Vaccinations
  • Aminosalicyclates eg. mesalazine (mild to moderate)
  • Corticosteroids (induce remission, then return to 5-ASA)
  • Calcineurin inhibitors
  • Immunosuppressive drugs (thiopurines - azathioprine and mercaptourine - or methotrexate, if patients need 2 courses of steroids per year)
  • Anti TNF alpha
171
Q

Describe prognosis of ulcerative collitis

A
  • Slightly increased risk of mortality
  • 50% in remission at any one time, 90% of people have a relapsing remitting course
  • Lifetime surgery risk 20-30%
  • Poor prognosis - severe symptoms at presentation, age less than 50, poor compliance, raised inflammatory markers
172
Q

Describe epidemiology of volvulus

A
  • Malrotation affects 1 in 500 live births
  • 90% patients diagnosed in first year of life
  • Most common in the sigmoid colon
173
Q

List risk factors for developing volvulus

A
  • Increasing age
  • Neuropsychiatric disorders
  • Resident in a nursing home
  • Chronic constipation or laxative use
  • Male gender
  • Previous abdominal operations
174
Q

List signs of volvulus on examination

A
  • Inability to pass a nasogastric tube

- Tympanic abdomen to percussion

175
Q

Describe irritable bowel syndrome

A

Irritable bowel syndrome (IBS) is a chronic, relapsing, and often lifelong disorder of the lower gastrointestinal tract, with no discernible structural or biochemical cause.

176
Q

Define functional dyspepsia

A
  • Functional dyspepsia (also known as non-ulcer dyspepsia) refers to people with dyspepsia symptoms and normal findings on endoscopy (gastric or duodenal ulcer, gastric malignancy, or oesophagitis have been excluded)
  • Dyspepsia is upper GI symptoms present for four or more weeks (upper abdominal pain, discomfort, heartburn, acid reflux, nausea and/or vomiting)
177
Q

Describe epidemiology of IBS

A
  • The global prevalence of IBS in the general population is estimated to be 5–20%.
  • It most commonly affects young people aged 20–30 years, and the prevalence decreases with increasing age.
  • It is more common in women than in men
178
Q

Describe epidemiology of functional dyspepsia

A
  • About 40% of the adult population have dyspepsia symptoms each year.
  • 25% of people will consult their GP to discuss dyspepsia symptoms, and dyspepsia accounts for 1.2–4% of all primary care consultations in the UK
  • In people with dyspepsia symptoms who undergo endoscopy, 70–80% are diagnosed with functional dyspepsia
  • Consultations for functional dyspepsia increase with age, and the prevalence is similar in men and women.
179
Q

List risk factors for functional dyspepsia

A
  • Gastroduodenal dysmotility, hypersensitivity to gastric distention, gastric acid secretion abnormalities, and psychosocial factors may be contributory.
  • Infectious gastroenteritis may also increase the risk of developing subsequent functional dyspepsia.
  • H pylori may lead to abnormalities in gastroduodenal motility and sensitivity.
180
Q

List mechanisms of IBS

A
  • Visceral hypersensitivity.
  • Abnormal gastrointestinal immune function.
  • Changes in colonic microbiota.
  • Abnormal autonomic activity.
  • Abnormal central pain processing of afferent gut signals (altered ‘brain-gut interactions’).
  • Abnormal gastrointestinal motility.
181
Q

List risk factors of IBS

A
  • Genetic
  • Enteric infection (for example, following gastroenteritis)
  • Gastrointestinal inflammation (for example, secondary to inflammatory bowel disease)
  • Dietary factors (such as alcohol, caffeine, spicy and fatty foods) — up to 90% of people
  • Drugs, such as antibiotics
  • Psychosocial such as associated stress, anxiety and/or depression, PTSD, history of abuse
182
Q

List symptoms and signs of IBS

A
  • Abdominal pain, bloating or change in bowel habit for 6 months +
  • Pain related to defecation, associated with altered stool frequency or altered stool form or appearance
  • Straining, urgency or incomplete evacuation
  • Abdominal bloating
  • Symptoms worsened by eating
  • Passage of rectal mucous
  • Lethargy, nausea, balck pain, headache, bladder symptoms
  • NO PR bleed, anaemia, weight loss, nocturnal symptoms
183
Q

List symptoms and signs of functional dyspepsia

A
  • Epigastric discomfort
  • Fullness or bloating
  • Excessive flatus
  • Nausea
  • Fatty food intolerance
184
Q

Describe management of functional dyspepsia

A
  • Offering advice on lifestyle measures that may improve symptoms.
  • Assessing for stress, anxiety, and depression, and managing these appropriately.
  • Reviewing and stopping any drugs which may be exacerbating symptoms, if possible and appropriate.
  • Testing for H pylori
  • PPI or H2 receptor antagonist if ongoing
  • Acid suppression therapy with annual review
185
Q

List investigations for functional dyspepsia

A
  • Check for abdominal mass
  • FBC
  • Test for H pylori
  • Endoscopy is symptoms persist despite treatment
186
Q

Describe investigations of IBS

A
  • Diagnosed based on history
  • Determine effect on daily functioning, look for features of alternative diagnosis
  • Check weight, BMI, palpate abdomen for massess or tenderness
  • Rectal exam
  • FBC, inflammatory markers ESR and CRP, coeliac serology
  • Diagnosis of exclusion

Rome III criteria - at least 3 months with onset at least 6 months previously of recurrent abdo pain or discomfort associated with 2 or more of:

  • Improvement with defecation and/or
  • Onset associated with a change in frequency of stool and/or
  • Onset associated with a change in appearance of stool
187
Q

Describe management of IBS

A
  • Lifestyle advice (eat regular fibrous meals, healthy diet, avoid caffine, lactose, fructose)
  • If diarrhoea or bloating reduce insoluble fibre and reduce foods which exacerbate symptoms
  • If constipation advise to try soluble fibre supplements, increase fibre intake gradually, and laxatives if necessary
  • Anti-diarrhoeals
  • Increase fluid intake
  • Identify stress/anxiety/depression (TCA medications)
  • Increase physical activity
  • Treat pain with antiplasmotics
188
Q

List complications of IBS

A
  • Mood disorder

- Poor quality of life

189
Q

List complications of functional dyspepsia

A

If associated with H pylori:

  • Reduced QOL
  • Increased risk of peptic ulcer disease
190
Q

Describe prognosis of IBS

A
  • Symptoms fluctuate over years
  • Symptoms resolve spontaneously in 50% of patients with post-infectious IBS within 6-8 years
  • Poorer prognosis associated with comorbid anxiety and depression, longer symptom duration and higher somatic scores
191
Q

Describe prognosis of functional dyspepsia

A
  • 70% untreated persistent symptoms
  • Recurrence 50%
  • H pylori positive 36% spontaneously improve, 7% eradication therapy improves symptoms
  • Persists over 3-12 months in 57%
192
Q

Describe classification of internal haemorrhoids

A
  • First degree (Grade 1) — haemorrhoids project into the lumen of the anal canal but do not prolapse.
  • Second degree (Grade 2) — haemorrhoids protrude beyond the anal canal on straining but spontaneously reduce when straining is stopped.
  • Third degree (Grade 3) — haemorrhoids protrude outside the anal canal and reduce fully on manual pressure.
  • Fourth degree (Grade 4) — haemorrhoids protrude outside the anal canal and cannot be reduced.
193
Q

Describe epidemiology of haemorrhoids

A
  • 13-16% population UK
  • US 4.4%
  • Peak prevalence between 45-65 years
  • White people and those of higher socioeconomic status more affected
194
Q

List risks for haemorrhoids

A
  • Constipation.
  • Straining while trying to pass stools.
  • Ageing (weakening of the support structures makes haemorrhoids more likely to prolapse).
  • Conditions that cause raised intra-abdominal pressure (such as pregnancy, childbirth, ascites, or a pelvic mass).
  • Chronic cough.
  • Heavy lifting.
  • Exercising.
  • Hereditary factors (possibly due to a congenital weakness of the venous walls).
  • A low fibre diet.
195
Q

List symptoms of haemorrhoids

A
  • Bright red painless rectal bleeding, typically occuring with defecation seen as streaks on the toilet paper or outside the stool
  • Anal itching or irritation
  • Feeling of rectal fullness, discomfort, incomplete evacuation
  • Soiling
  • Pain (external painless unless thrombosis, internal painless unless strangulated)
196
Q

List signs of haemorrhoids

A
  • Perinium may appear normal if non-prolapsed internal
  • Macerated perineum from chronic mucus discharge
  • Bluish soft building vessels covered by mucosa if internal prolapsed
  • External bluish building of blood vessel
  • Thrombosed external haemorrhoid purplish, oedematous, tense, tender, subcutaneous perianal mass
197
Q

describe investigations of haemorrhoids

A
  • History and examination
  • Check for skin tags or other anal pathology
  • DRE
  • Protoscopy
  • Full blood count if signs of anaemia
198
Q

Describe management of haemorrhoids

A
  • Admit people who have lots of pain, or prolapsed internal haemorrhoids, or perianal sepsis
  • Refer using cancer pathway if cancer suspected
  • Refer for non-urgent management if 4th or 3rd degree, perianal haematoma, combined internal and external, thrombolised or large skin tags
  • Ensure stools are soft and easy to pass. Advise adequate dietary fibre and fluid intake
  • Advise to keep dry and clean
  • Advise against straining or stool withholding
  • Offer simple analgesia - avoid NSAIDS and opoids due to constipation, topical steroids (grade 1)
  • Advise to keep up dietary changes
  • Secondary care may involve rubber band ligation (grade 2 or 3), injection sclerotherapy, infrared coagulation/photocoagulation, bipolar diathermy, haemorrhoidectomy, stapled haemorrhoidectomy, haemorrhoidal artery ligation
  • Haemorrhoidectomy for grade 4
199
Q

List complications of haemorrhoids

A
  • Perianal thrombosis.
  • Incarceration of prolapsing haemorrhoidal tissue — the tissue is unable to be reduced into the anal canal, causing severe pain.
  • Ulceration — from thrombosis of external haemorrhoids.
  • Skin tags — from repeated episodes of haemorrhoid dilatation and thrombosis. This causes enlargement of the overlying skin, problems with hygiene, and secondary irritation.
  • Maceration of the perianal skin — due to mucus discharge.
  • Ischaemia, thrombosis, or gangrene in fourth degree internal haemorrhoids — progressive venous engorgement and incarceration of the acutely inflamed haemorrhoid lead to thrombosis, infarction, and severe pain.
  • Anal stenosis.
  • Perianal or pelvic sepsis (rare).
  • Anaemia from continuous or excessive bleeding (rare).
200
Q

Describe prognosis of haemorrhoids

A
  • Many symptomatic episodes settle with conservative measures, with low rates of recurrence
  • Residual or recurrent symptoms are more likely in people with continuing predisposing factors, such as constipation and straining while trying to pass stool
  • About 10% of people will require surgery to alleviate their symptoms
201
Q

Define diverticular disease, diverticulitis and diverticulosis

A
  • Diverticula are sac-like protrusions of mucosa through the muscular wall of the colon. They are usually multiple, 5–10 mm in diameter, and occur in the sigmoid colon in about 85% of people.
  • Diverticulosis is a condition where diverticula are present without symptoms.
  • Diverticular disease is a condition where diverticula cause symptoms, such as intermittent lower abdominal pain, without inflammation and infection.
  • Diverticulitis is a condition where diverticula become inflamed and infected, typically causing severe lower abdominal pain, fever, general malaise, and occasionally rectal bleeding. (complicated associated with complications)
202
Q

List risk factors for diverticular disease

A
  • Genetic
  • Low fibre diet
  • Smoking
  • Obesity
  • Drugs (NSAIDs, opiods, corticosteroids)
  • Age 50-70
203
Q

Describe prevalence of diverticular disease

A
  • Exact prevalence is unknown as most people are asymptomatic
  • Increasing in developed countries
  • 75% of people asymptomatic diverticulosis, 25% diverticular disease
  • Rare before age of 40. 5-10% people age 45+, 80% of people age 85+
  • Lifetime risk of acute diverticulitis is 4-25%
  • 5% complicated disease
204
Q

List symptoms of diverticular disease

A
  • Intermittent abdominal pain in the left lower quadrant. Triggered by eating and relieved by passage of stool
  • Constipation, diarrhoes, large rectal bleeds
  • Bloating and passage of mucus rectally
205
Q

List signs of diverticular disease

A
  • Tenderness in left lower quadrant on abdo exam
  • Guarding, rigitdity, rebound tenderness
  • If acute, laying still, tachycardia, low–grade pyrexia
206
Q

List symptoms of diverticulitis

A
  • Constant abdominal pain, usually severe staring in hypogastrium before localising in left lower quadrant
  • Fever
  • Change in bowel habit with possible rectal bleeding
  • Nausea, vomiting, dysuria and urinary frequency
207
Q

List signs of diverticulitis

A
  • Tenderness in left lower quadrant

- Palpable abdominal mass or distention on abdominal examination

208
Q

Describe management of diverticular disease

A
  • Urgent admission if significant rectal bleeding. Diverticulosis high fibre diet + primary anastamosis. If diverteiculitis antibiotics, fluids, hartmanns
  • First presentation of diverticulitis oral abx as outpatient, if elderly/leukocytosis/ immunocompromosed bowel rest and IV ABX and fluids are used
  • Provide info and support
  • Reccommend healthy, balance diet containing whole grains, fruits and veg. Gradually increase fibre intake
  • High fluid intake
  • Consider bulk forming laxatives if high fibre diet is insufficient
  • Advise on alagesia (avoid NSAIDS and opiods due to increased risk of perforation)
  • Review
  • Barium enema
209
Q

List complications of diverticular disease

A

Diverticulitis can occur with risk of…

  • Diverticular haemorrhage 15% of people - 1/3 bleeds require transfusion and 70-80% stops spontaneously
  • Intra abdominal abscess formation
  • Perforation and peritonitis
  • Stricture and fistulae formation (to the bladder commonly)
  • Intestinal obstruction (from fibrosis and stricture formation)
  • Abscesses
210
Q

Describe prognosis of diverticular disease

A
  • 10-25% of people with diverticular disease develop diverticulitis
  • 13.3% of people have a recurance of diverticulitis
  • 5% of people have complications when followed for 20-30 years
  • Risk of complications worse during first episode
  • People who are immunocompromised have a 5 fold increased risk of recurrence
  • Surgery doesnt eliminate recurrence risk
211
Q

Define anal fissure and its classification

A
  • An anal fissure is a tear or ulcer in the lining of the anal canal, immediately within the anal margin. It is classified as:
  • Acute — if present for less than 6 weeks.
  • Chronic — if present for 6 weeks or longer.
  • Primary — if there is no clear underlying cause.
  • Secondary — if there is a clear underlying cause.
212
Q

List causes of primary anal fissure

A
  • Ischaemic ulcers associated with spasm of internal anal sphincter resulting in increased anal tone
  • May occur in response to pain from trauma such as passing hard stools, resulting in reduced blood flow and increased risk of tearing
  • May be local lack of nitric oxide synthase, a group of enzymes needed for production of nitric oxide
213
Q

List causes of secondary anal fissures

A
  • Constipation (tears of anal mucosa)
  • IBD
  • STI (HIV, syphilis, HSV)
  • Colorectal cancer
  • Psoriasis and pruritis ani
  • Anal trauma (previous surgery or anal sex)
  • Drugs (opiods, nicorandil and chemo)
  • Pregnancy and childbirth (increased pressure on perineum)
214
Q

Describe epidemiology of anal fissures

A
  • 1 in 350 people
  • Most common age 15-40, occur at any age
  • Common in pregnant and post partum women (2nd most common GI complication of pregnancy after haemorrhoids)
  • Primary uncommon in elderly
  • Acute significantly more common than chronic
215
Q

List symptoms of anal fissures

A
  • Pain always with defication, severe and sharp on passing stool with deep burning pain afterwards
  • Bleeding with defication (bright red on stool or paper)
  • Anal spasm and tearing sensation
216
Q

List signs of anal fissure

A
  • Acute are superficial with well demarcated edges
  • Chronic are wider and deeper with muscle fibres visible in the base
  • Primary singular in posterior midline
  • Secondary irregular outline, multiple, occur laterally
  • Pain with gentle pressure on anal margin
217
Q

Describe diagnosis of anal fissure

A
  • Take a history + ask about duration of symptoms
  • Ask about underlying cause (dietary habits, trauma, associated symptoms, family history)
  • Identify any risks (eg. constipation, cancer, STI, IBD)
  • Suspect sexual abuse in children
  • DRE not recommended, may be done under anaesthesia if unclear diagnosis
218
Q

Describe management of anal fissures

A
  • Suspected cancer referral pathway if renal cancer suspected
  • Or other specialist if other causes suspected
  • Elderly people refered to surgeon
  • Manage underlying cause
  • Ensure stools soft and easy to pass (adequate dietary fibre intake, increase gradually, adequate fluid intake, laxatives)
  • Manage pain (simple analgesia not opiods due to constipation)
  • Sitting in shallow warm bath may relieve pain
  • Topical anaesthetic if extreme pain for use before passing stool
  • 1 week without improvement prescribe GTN ointment, 2 times a day for 6-8 weeks, or topical diltiazem
  • Advise against stool withholding and anal hygiene
  • Butolium toxin injection or surgical sphincterectomy if persistant
219
Q

Describe prognosis of anal fissure

A
  • Primary acute resolve in 6-8 weeks, chronic require intensive treatments eg.surgery
  • Recurrence common following non-surgical treatment, especially if lifestyle advice not adhered to
  • Secondary anal fissures dependent on prognosis of underlying cause
220
Q

List complications of anal fissures

A
  • Failure to heal/chronic fissure.
  • Recurrent fissure.
  • Anorectal fistula.
  • Infection and/or abscess.
  • Faecal impaction (avoidance of defecation to avoid anal pain may worsen constipation and lead to faecal impaction).
  • Reduced quality of life (especially in people with chronic or recurrent anal fissure).
221
Q

Define gastroenteritis

A
  • Gastroenteritis is a transient disorder due to enteric infection with viruses, bacteria, or parasites.
  • It is characterized by the sudden onset of diarrhoea, with or without vomiting
  • Similarly, it can be defined as acute diarrhoeal disease of rapid onset, with or without nausea, vomiting, fever, or abdominal pain
  • Dysentry is bloody diarhhoea
  • Persistant diarrhoea is acute onset diarrhoea that lasts 14 days
222
Q

List causes of gastroenteritis

A
  • Feco-oral, foodborne, environmental, airborne
  • Food poisoning caused by enterotoxins produced by the microorganism
  • Clostridium perfrigens (inadequate storage and insufficient reheating of contaminated meat dishes or cooked meats)
  • Bacillus cereus (contaminated cooked foods with inadequate post cooking temperature control)
  • Staphylococcus aureus (cooked meats and cream)
  • 40-70% travellers diarrhoea no specific causative agent identified
  • Norovirus, rotovirus, salmonella, campylobacter, e.coli, yersinia enterolitica, giardia, trichinella
223
Q

List symptoms of gastroenteritis

A
  • Sudden-onset diarrhoea (change of stool consistency to loose or watery stools, usually at least three times in 24 hours); blood or mucus in the stool; faecal urgency.
  • Nausea or sudden onset of vomiting.
  • Fever or general malaise.
  • Abdominal pain or cramps.
  • Associated headache, myalgia, bloating, flatulence, weight loss, and malabsorption, depending on the underlying cause of infection.
224
Q

Describe diagnosis of gastroenteritis

A
  • Symptoms
  • Onset, frequency and duration
  • Severity
  • Complications
  • Co-morbid conditions
  • Occupation
  • Recent food intake
  • Exposure to contaminated water
  • Contact with other infected individuals
  • Recent foreign travel
  • PPI/ antibiotic use/ hospital admission - c.difficile
  • Drugs (diuretic, ACE inhibitors, efficacy affected)
  • Stool culture and sensitivity testing
225
Q

List signs of gastroenteritis

A
  • Dehydration (general appearance, temp, pulse, BP, breating)
  • Assess for sepsis
  • Examine abdomen (tenderness, distention, masses, bowel sounds)
  • Weight and malnutrition
226
Q

List complications of gastroenteritis

A
  • Dehydration, electrolyte disturbance, kidney injury
  • Haemorrhagic collitis (E.coli)
  • Haemolytic uraemic syndrome (children under 5 - AKI, thrombocytopenia, microangiopathic haemolytic anaemia)
  • Thrombotic thrombocytopaenic purpura
  • Reactive arthritis and Reiters syndrome
  • Aortitis, osteomyelitis
  • Sepsis
  • Toxic megacolon
  • Pancreatitis, liver sclerosis, sclerosing cholangitis
  • Faltering growth
  • Chronic diarrhoea
  • IBS
  • IBD
  • Lactose intolerance
  • Guillian barre
  • Meningitis
  • Invasive entamoeba infection
227
Q

Describe management of gastroenteritis

A
  • Emergency hospital admission if systemically unwell/ severe dehydration/ complication
  • Hospital assessment if at risk or unable to manage at home
  • Liaise with microbiologist if uncertainty about admission or management in travel diarrhoea
  • Encourage regular fluid intake, oral rehydration salt if at increased risk
  • Gradually increase usual diet
  • Not reccomended to use antidiarrhoeal drugs
  • No antibiotics
  • Advise on methods to prevent transmission
  • Stay at home for 48 hours after last episode of vomiting
228
Q

Describe prognosis of gastroenteritis

A

Symptoms usually resolve within 2 weeks, severe cases several weeks. Self limiting

229
Q

Describe epidemiology of gastroenteritis

A
  • 17 million cases in the UK each year

- Particularly common in summer with outbreaks of zoonotic infections

230
Q

Describe epidemiology of colorectal and anal tumours

A

Colorectal cancer:

  • Around 40,000 new colorectal cancers are diagnosed each year in the UK, up to a quarter of these following screening. 3rd most common cancer and 2nd most common cause of cancer death
  • A full time GP is likely to diagnose approximately one person with colorectal cancer every year.

Anal cancer:

  • Just over 1000 new anal cancers are diagnosed each year in the UK, meaning that a full time GP is likely to diagnose approximately 1–2 people with anal cancer during their career.
  • Anal cancer occurs in both sexes, though nearly two-thirds occur in women.
231
Q

Define colorectal tumour

A

A carcinoma of the large intestine or rectum

232
Q

List symptoms of colorectal cancer

A
  • Appetite loss (unexplained)
  • Deep vein thrombosis
  • Weight loss (unexplained)
  • Anal mass or anal ulceration (unexplained)
  • Anaemia (iron deficiency)
  • Abdominal pain
  • Rectal bleeding
  • Change in bowel habit
  • Occult blood in faeces
  • Tenesmus
  • Fecal incontinence

Left sided - tenesmus, bleeding in stools, altered bowel habit, mass PR, obstruction

Right sided - iron deficiency anaemia, weight loss, abdo pain

233
Q

List risk factors for colorectal cancer

A
  • Family history
  • Age
  • Diet rich in fat and meat, and low in fibre – associated with a Western Lifestyle
  • IBD – due to high cell trunover
  • Diabetes
  • Atherosclerotic disease
  • Age and family history are the two best predictors for colorectal cancer
  • Polyps
234
Q

List signs of colorectal cancer

A
  • Cachexia
  • Abdominal mass
  • Signs of anaemia (conjunctival pallor /peripheral cyanosis)
  • Palpable rectal mass
  • Ascites
235
Q

List investigations for colorectal cancer

A
  • Faecal Occult blood
  • Guaiac test – for Hb breakdown products. 98% specific, but only 40-80% sensitive
  • Antibody test – uses antibodies that bind to human blood to test for the presence of blood.
  • Routine biochemisty – U+E’s, FBC, LFT’s, CRP, ESR
  • Colonoscopy
  • Barium enema – in cases where colonoscopy cannot be performed
  • USS/CT – can asses bowel wall thickness as well as looking for metastatic spread
236
Q

List risk factors for coeliac disease

A
  • Genetic (HLA-DQ2/ more rarely DQ8)
  • Immune mediated - other autoimmune conditions increase risk
  • Gluten exposure
  • GI infections and changes in the gut microbiome
  • IgA deficiency
  • T1DM
237
Q

Describe epidemiology of coeliac disease

A
  • Increasing in incidence
  • 13.8 per 100000 or 1 in 100-300
  • Prevalence higher in females than males (1.5:1-2:1)
  • Peaks in childhood and age 50-60
  • Relative risk in first degree relatives 6 times higher
238
Q

List signs of coeliac disease

A
  • Peripheral neuropathy or ataxia
  • Recurrent miscarriage or subfertility
  • Enamel defects
  • Osteomalacia, osteopenia, osteoporosis fragility fractures
  • Dermatitis herpetiformis
  • Apthous ulcers
  • Angular stomatitis
  • Failure to thrive
239
Q

Describe diagnosis of coeliac

A
  • Blood test while person on coeliac diet (reduced Hb, increased RBCDW, low B12 and ferritin)
  • Check IgA anti- transglutaminase (MAIN), and total IgA in case of deficiency in IgA production
  • Check IgA endomysial antibody
  • Check IgG endomysial, deamidated gliadin peptide or transglutaminase if evidence of IgA deficiency
  • Duodenal biopsy and look at histology (intraepithelial lymphocytosis, crypt hyperplasia, villous atrophy, chronic inflammatory cell infiltrate at lamina propria)
  • If doubt remains, HLA DQ2/ DQ8
  • Bone scan
240
Q

Describe management of coeliac disease

A
  • Gluten free diet (rice, maize, soya, potatoes ok, limited oats in some patients)
  • Give info
  • Asess for recurrent symptoms
  • Assess for nutritional deficiencies
  • Assess osteoporosis, depression or anxiety
  • Monitor growth in children
  • Annual blood monitoring
  • Dietician, prescription gluten free food
  • Screen first degree relatives
241
Q

List complications of coeliac disease

A
  • Reduced QOL
  • Depression, anxiety, eating disorders
  • Faltering growth and delayed puberty in children
  • Nutritional deficiencies
  • Anaemia
  • Reduced bone density
  • Hyposplenism or asplenism
  • Malignancy (lymphoma, gastric, oesophageal, colorectal)
  • Refractory coeliac disease (persistant symptoms despite diet adherence)
  • Dermatitis herpetiformis
242
Q

List causes of high bilirubin

A
  • Haemolysis (prehepatic look at FBC and film)
  • Liver cirrhosis (Hepatic disease - viral hepatitis, alcoholic hepatitis, cirrhosis)
  • Gallstones (obstructive jaundice, pancreatic cancer)
  • Gilberts syndrome
243
Q

Describe arrangement of the liver

A
  • Lobules
  • Central vein
  • At each corner of the hexagon, there is a triad of bile duct, hepatic portal vein and hepatic artery
  • Blood goes to the central vein via sinusoids
244
Q

Describe features of gilberts disease

A
  • Recessively inherited
  • 50% carry the gene
  • UDP glucuronyl transferase activity reduced, therefore higher level of bilirubin
  • Elevated bilirubin, higher on fasting, other blood tests normal
  • Do not do a biopsy
  • Phenobarb lowers levels
245
Q

How is liver function best tested?

A
  • Prothrombin time most representative, rapidly increases.
  • Albumin can also be used, but does not change as fast.
  • Bilirubin
  • ALT, AST, alkaline phosphatase are the enzymes that leak out
  • High alkaline phosphatase indicates blockage of bile ducts
246
Q

List test results for liver enzymes and what they indicate

A
  • ALT and AST go up when hepatocytes are damaged.

- Alkaline phosphatase high in obstructive jaundice, ALT and AST normal

247
Q

Describe diagnosis of alcoholic hepatitis

A

Biopsy shows liver cell damage

  • Inflammation
  • Fibrosis
  • Fatty change (mallorys hyaline, balloon cells, steatosis)
  • Megamitochondria
  • Non alcoholic appears the same
  • High ALT, AST, bilirubin, high MCV.
  • Check for autoimmune (antibodies), viral hepatitis, lipids+HbA1c fo non-alcoholic
248
Q

List causes of non-alcoholic steatohepatitis

A
  • T2DM

- Obesity

249
Q

Describe treatment of alcoholic hepatitis

A
  • Alcohol cessation
  • Vitamin B1, thiamine, Vitamin D
  • 40mg prednisolone for 4 weeks (lille and maddrey score - maddrey score determines whether steroids are needed, lille looks at how well steroids are working). Beforehand check for infection due to risk of sepsis, check diagnosis is correct
250
Q

What is caused by thiamine deficiency?

A

Beri Beri

251
Q

List signs of portal hypertension

A
  • Splenomegaly
  • Ascites
  • Caput medusae (visible veins)
  • Spontaneous bacterieal peritonitis
  • Encephalopathy
252
Q

List features of cirrhosis on histology

A
  • Whole liver involved
  • Nodules of regenerating hepatocytes
  • Fibrosis
  • Shunting of blood
253
Q

List causes of cirrhosis

A
  • Fatty liver disease (micronodular)
  • Hepatitis B and C (macronodular)

Others:

  • Haemochromatosis
  • Wilsons disease
  • Primary biliary cholangitis
  • Primary sclerosing cholangitis
254
Q

What is the additional sign in liver failure not present in cirrhosis?

A

Flap

255
Q

List sites of porta-systemic anastomoses

A
  • Oesophagus
  • Lower rectum
  • Umbilicus
  • Retro-peritoneum
256
Q

List signs on examination of post hepatic jaundice

A
  • Scratch marks, due to bile salts not entering the gut. Specific to obstructive jaundice
  • Enlarged gallbladder in pancreatic cancer
257
Q

What is courvoisiers law?

A
  • Palpable gallbladder in a jaundiced patient the cause is a pancreatic cancer.
  • If gallstones for a long time you have a small and fibrotic gallbladder incapable of being large
258
Q

List signs on examination of autoimmune hepatitis

A
  • Hepatomegaly
  • Jaundice
  • Splenomegaly
  • Spider angioma (chronic liver disease)
  • Ascites
  • Encephalopathy
  • Liver flap
  • Palmar erythema
259
Q

Describe epidemiology of viral hepatitis

A
  • B and C in particular lead to chronic disease
  • 325 million people worldwide have hep B and/or C
  • Hep A uncommon (452 cases UK anually)
  • Hep B 0.3% of the population chronic infection
  • Hep C 185 mill hep C
  • 143000 people with chronic hepatitis. Most common in UK
260
Q

Describe management of viral hepatitis

A
  • 15-45% clear hep C without treatment
  • Direct acting antivirals
  • NSAID, opiod, anti-emetic, cream for itch
  • Hep A admit to hospital
  • Hep B peginterferon alpha or tenofovir/entefovir
  • Hep C sofosbuvir, ledipasvir, grazoprevir (directly acting antivirals)
  • Hep D most need transplant in the end
  • Hep E ribovarin
261
Q

List complications of viral hepatitis

A
  • Hepatocellular carcinoma (alpha fetoprotein monitoring, though will raise in pregnancy and teratoma)
  • Hepatic failure
  • Cirrhosis (fibroscan monitoring)
  • Chronic hepatitis
  • Chronic active hepatisis
  • Hepatic necrosis
262
Q

Describe prognosis of hepatitis

A
  • Hep B usually fully recover, infected children tend to develop long term infection. Never fully clear the virus therefore can reactivate eg. if on chemotherapy, can also get Hep D
  • Hep A usually passes, can be severe or life threatening
  • Hep C 1 in 4 people fight off virus, 3 in 4 chronic
263
Q

Define alcoholic hepatitis

A

Excessive alcohol intake resulting in liver disease, including fatty changes ie. steatosis of the liver

264
Q

Describe epidemiology of alcoholic hepatitis

A
  • 10-30% heavy drinkers develop cirrhosis
  • 50% fatty liver
  • 60% of all liver disease
265
Q

List risk factors for alcoholic hepatitis

A
  • Women have higher risk
  • Obesity
  • Genetic factors
  • Race and ethnicity (blacks and hispanics at higher risk)
  • Binge drinking
266
Q

List symptoms of alcoholic hepatitis

A
  • Weight loss
  • Loss of body hair
  • Tremor
  • Memory loss
  • Epilepsy
  • Loss of appetite
  • Nausea and vomiting
  • Pruritis
  • Melena/haematemesis if oesophageal varices
267
Q

List signs of alcoholic hepatitis

A
  • Spider naevi (chronic)
  • Abdominal distention/ caput medusae
  • Dupuytrens contracture
  • Tremor
  • Gynaecomastia
  • Testicular atophy
  • Malnutrition
  • Ascites
  • Jaundice
  • Varices
  • Liver flap
  • Tender hepatomegaly
268
Q

List complications of alcoholic hepatitis

A
  • Hepatic encephalopathy (slurred speech, coma)
  • Oesophageal varices (which can burst and lead to vomiting up blood)
  • Cirrhosis and liver failure
  • Kidney failure
  • Carcinoma
269
Q

Describe prognosis of alcoholic hepatitis

A
  • 30 day mortality when hospitalised is 15%
  • When hospitalised with severe liver disease, 50%
  • Mortality rate at 6 months 40%
  • Most common cause of death is infection leading to sepsis, with 50-90% mortality
270
Q

What is the difference between epigastric pain worse on eating and better on eating?

A
  • Gastric ulcer worse on eating

- Duodenal ulcer better on eating

271
Q

List causes of RUQ pain

A
  • Gall stones
  • Acute cholecystitis
  • Ascending cholangitis
  • Liver hepatitis
  • Liver abscess

Neighbouring

  • Basal pneumona
  • Appendicitis (retrocaecal appendix/pregnancy)
  • Peptic ulcer
  • Pancreatitis
  • Pyelonephritis
272
Q

List causes of epigastric pain

A
  • Peptic ulcer
  • GORD
  • Pancreatitis (chronic or acute)
  • Gastritis
  • Malignancy

Neighbouring

  • MI
  • AAA
  • Cholecystitis or hepatitis
273
Q

List causes of flank pain

A
  • Renal stones
  • Pyelonephritis
  • Polycystic kidney disease
274
Q

List causes of periumbilical pain

A
  • Appendicitis
  • Umbilical hernia
  • AAA
275
Q

List causes of right iliac fossa pain

A
  • Appendicitis
  • Crohns
  • Inguinal/femoral hernia (incarcerated)
  • Mesenteric adenitis
  • Infectious colitis
  • Ectopic pregnancy
  • Ovarian cyst accident
  • Pelvic inflammatory disease
  • Testicular torsion
276
Q

List causes of left iliac fossa pain

A
  • Inguinal/femoral hernia (incarcerated)
  • Infectious colitis
  • Ectopic pregnancy
  • Ovarian cyst accident
  • Pelvic inflammatory disease
  • Testicular torsion
  • Diverticulitis
  • Ulcerative colitis
277
Q

List causes of suprapubic pain

A
  • UTI
  • Bladder stones
  • Urinary retention
  • STI
  • Endometriosis
  • Painful periods
278
Q

List causes of diffuse abdominal pain

A
  • Obstruction
  • Peritonitis
  • Ischaemic colitis
  • Gastroenteritis
  • IBS/D
  • DKA
  • Hypercalcaemia
  • Addisons disease
  • Porphyria
  • Lead poisoning
279
Q

Compare presentation of Ulcerative Colitis and Crohns

A
  • PR bleeding UC
  • Weight loss crohns
  • Oral ulcers crohns
  • RIF pain crohns
  • Rectal pain UC
280
Q

Compare presentation of diverticulitis and diverticular disease

A
  • PR bleeding diverticular disease
  • LIF pain diverticulitis
  • Fever diverticulitis
281
Q

List the three factors that exacerbate jaundice in Gilberts

A
  • Fasting
  • Exercise
  • Stress
282
Q

Compare causes dysphagia in different presentations

A

Dysphagia
- Oesophageal cancer solids then liquids
- Achalasia both solids and liquids
- Dysphagia, diarrhoea, FHx autoimmune caused by graves disease
- Dysphagia and heartburn
caused by GORD (may cause strictures)
- Food stuck in mouth and pmhx AF caused by stroke (can’t coordinate swallowing)
- Odynophagia and weight loss caused by oesophageal cancer

283
Q

Define non-alcoholic steatohepatitis (nash)

A

A clinico-histopathological entity that includes a spectrum of conditions characterised histologically by macrovesicular hepatic steatosis in those who do not consume alcohol in amounts generally considered harmful to the liver.

284
Q

List risk factors for NASH

A
  • Obesity
  • Insulin resistance or diabetes
  • Dyslipidaemia
  • Hypertension
  • Metabolic syndrome
  • Rapid weight loss
  • Hepatotoxic medications
  • TPN
  • Weakly asssociated with wilsons, chronic hepatitis, alpha-1 antitrypsin deficiency
285
Q

Describe epidemiology of NASH

A

NAFLD

  • 24-40% of the western world
  • Majority of cases age 40-60
  • Affects both sexes equally
  • NASH 3% of individuals from developed countries
286
Q

List symptoms of NASH

A
  • Fatigue and malaise
  • RUQ pain
  • Pruritis
  • Rarely haematemesis and melaena
287
Q

List signs of NASH

A
  • Obesity
  • Hepatosplenomegaly
  • Jaundice
  • Spider angioma (chronic liver disease)
  • Palmar erythema
  • Nail changes
  • Dupuytrens contracture
  • Bruising
  • Petechiae
  • Excoriations
  • Gynaecomastia
  • Parotid gland enlargement
  • Testicular atrophy
  • Alopecia
  • Caput medusae
  • Murmur (venous hum in epigastric region)
  • Peripheral oedema
  • Ascites
  • Hypotension
  • Encephalopathy
  • Asterixes
  • Fetor hepaticus (odour of breath)
288
Q

Describe investigations used to diagnose NASH

A
  • AST and ALT mildly elevated. Ratio AST:ALT < 1
  • Raised bilirubin
  • Raised alk phos, gamma glutamyl transferase
  • FBC anaemia of thrombocytopenia
  • Mild hyponatraemia, elevated creatinine, urea and glucose
  • Elevated cholesterol
  • Increased PT
  • Low albumin
  • Liver ultrasound (hyperechoic echotexture, attenuation, vascular blurring)
  • CT, MRI showing increased liver fat content
289
Q

Describe treatment of NASH

A
  • Weight loss
  • Treat insulin resistance and diabetes (thiazolinediones)
  • Treat dyslipidaemia
  • Vitamin E
  • Transjugular intrahepatic portosystemic shunt for treating end stage liver failure
  • Liver transplantation
290
Q

List complications of NASH

A
  • Ascites
  • Variceal haemorrhage
  • Portosystemic encephalopathy
  • Hepatocellular carcinoma
  • Hepatorenal syndrome
  • Hepatopolmonary syndrome
  • Death
291
Q

Describe prognosis of NASH

A
  • Considered to be good
  • Progress to cirrhosis 9-20% of the time
  • 1/3 of patients with cirrhosis will die from liver complications
  • Can reoccur after transplant
292
Q

Describe treatment of hepatic encephalopathy

A
  • Treat predisposing factors and supporting care plus lactulose (first line)
  • Second line add rifamixin
  • Phosphate enemas
  • Avoid sedation
  • Treat infections and exclude GI bleed
293
Q

Describe epidemiology of appendicitis

A
  • The overall lifetime risk of developing acute appendicitis is 8.6% for males and 6.7% for females; lifetime risk of appendicectomy is around 12% in males and 23% in females.
  • The rate of appendicectomy is around 10 per 10,000 cases per year in the US.
  • Most commonly seen in patients aged between early teens and late 40s.
  • There is a slight male to female predominance
294
Q

List risk factors for appendicitis

A
  • Low fibre diet
  • Improved personal hygiene (imbalanced GI microbial flora)
  • Smoking
295
Q

List symptoms of appendicitis

A
  • Abdominal pain (begins in the umbilical region, moves to the RIF. Constant with intermittent cramps, worse on movement and coughing)
  • Anorexia
  • ## Nausea and vomiting
296
Q

List signs of appendicitis

A
  • Right lower quadrant tenderness. Mcburneys sign is tenderness at mcburneys point
  • Tense, rigid abdomen (perforated appendix)
  • Hypotension and tachycardia (shock or sepsis)
  • Palpable mass (peri-appendiceal abscess)
  • Low grade pyrexia
  • Flushed face and fetor
  • Reduced bowel sounds (perforated)
  • Loose stool/constipation
  • Illiopsoas sign - pain on passive extension of the thigh
  • Obturator test/copes - flex knee and hip, pain on rotation of the leg
  • Rosvings sign - pain in left lower quadrant after pressing in right lower quadrant
297
Q

Describe investigations used for appendicitis

A
  • FBC (Leucocytosis with neutrophilia)
  • CRP (elevated usually)
  • Abdominal ultrasound (rule out appendicitis if normal appendix, alternative causes of abdominal pain. Diameter over 6mm in appendicitis)
  • Contrast enhanced abdominal CT (if ultrasound inconclusive, or malignancy or appendicular mass suspected - shows appendix over 6mm, or calcified appendicolith very good)
  • Exclude UTI with urine dip
  • Prengnancy test
  • Group and save
  • Alvarado score (scoring system for diagnosing appendicitis)
298
Q

Describe treatment of appendicitis

A
  • Nil by mouth for surgery
  • Paracetamol or opiod
  • Appendicetomy
  • Antibiotics if surgery not wanted (amoxicillin + metronidazole)
  • If complicated, post operative antibiotics
  • If abscess or phlegmon supportive treatment, appendicectomy and antibiotics. Alternatively can be interval appendicectomy.
299
Q

Describe complications of appendicitis

A
  • Perforation (sepsis/shock)
  • Peritonitis (exploratory laparotomy)
  • Appendicular mass
  • Appendicular abscess (IV antibiotics and CT guided drainage of abscess)
  • Surgical wound infection
300
Q

Describe prognosis of appendicitis

A
  • Good if treated quickly

- Laproscopic appendicetomy has decreased incidence of overall complications

301
Q

What are the sepsis 6?

A
  • High flow oxygen (aim for sats over 96%. Start with 15ml)
  • Take blood cultures
  • Give broad spectrum antibiotics (within 1 hour of recognising the problem)
  • IV fluid challenges (give fluid bolus aiming to decrease HR and BP)
  • Measure serum lactate and haemoglobin (venous blood glass, raised lactate indicates ischaemia and therefore severity)
  • Measure accurate hourly urine output (decreasing output one of the earliest signs of acute renal injury)
302
Q

List characteristics of spider angiomas

A
  • Stable chronic liver disease
  • Distribution of the SVC
  • Above the nipple line
303
Q

List hand signs of chronic liver disease

A
  • Asterixis
  • Bruising
  • Clubbing
  • Duputryns contracture
  • Erythema
304
Q

Describe dukes classifications of colorectal cancer

A
  • Dukes A: tumour is not spread into the muscularis propria
  • Dukes B: tumour is invading beyond the muscularis propria
  • Dukes C: Tumour is spread to lymoh nodes
  • Dukes D: Tumour mets to other organs
305
Q

Describe glasgow criteria for pancreatis

A
  • PaO2 <8kPa
  • Age over 55
  • Neutrophilia
  • Calcium <2mmol/L
  • Renal function (urea over 16mmol/L)
  • Enzymes (LDH and AST high)
  • Albumin <32g/L serum
  • Sugar (blood glucose over 10mmol?l)
306
Q

Define intestinal ischaemia

A
  • Ischaemic bowel disease encompasses a heterogeneous group of disorders caused by acute or chronic processes, arising from occlusive or non-occlusive aetiologies, which result in decreased blood flow to the gastrointestinal tract.
  • 3 main types: acute mesenteric ischaemia, chronic mesenteric ischaemia and colonic ischaemia (large bowel)
307
Q

Describe epidemiology of bowel ischaemia

A
  • Colonic frequently affects older people with co-morbidities. 4.5-44 cases per 100000 person-years
  • Acute mesenteric 0.1% of hospital admissions, 1% of patients with acute abdomen
  • Non-occlusive 20-30% of acute mesenteric, more common over age 80
308
Q

Describe aetiology of bowel ischaemia

A

Acute mesenteric ischaemia

  • Small bowel
  • Superior mesenteric artery thrmbosis (35%) or embolism (35%)
  • Mesenteric vein thrombosis (5%, youger patients with hypercoagulable state)
  • Non occlusive disease (20%, poor cardiac output, recent cardiac surgery or renal failure)
  • Trauma, vasculitis, radiopathy, strangulation

Chronic mesenteric ischaemia

  • Low flow state + atheroma
  • 95% diffuse atherosclerotic disease in all 3 mesenteric arteries

Chronic colonic ischaemia
- Low flow in inferior mesenteric artery

309
Q

List risk factors for bowel ischaemia

A
  • Old age
  • History of smoking
  • Hypercoagulable states
  • Atrial fibrillation
  • Myocardial infarction
  • Structural heart defects
  • History of vasculitis
  • Recent cardiovascular surgery
  • Shock
  • Congestive heart failure
  • Atherosclerosis
  • Previous ileostomy
  • Irritable bowel syndrome
  • Colonic carcinoma
  • Constipation
  • Long-term laxative use
  • Use of vasopressors, digitalis, cocaine
310
Q

List signs and symptoms of acute mesenteric ischaemia

A
  • Acute severe abdominal pain (central, constant or RIF)
  • No/minimal abdominal signs (degree of illness out of proportion to clinical signs)
  • Rapid hypovolaemia leading to shock
311
Q

List signs and symptoms of chronic mesenteric ischaemia

A
  • Severe, colicky post-prandial abdominal pain (claudication)
  • Weight loss
  • Upper abdo bruit
  • May be nausea and vomiting, PR bleeding and mal-absorption
312
Q

List signs and symptoms of ischaemic colitis

A
  • Lower left sided abdominal pain

- With or without PR bleeding

313
Q

List investigations for intestinal ischaemia

A

1st AXR, 2nd CT abdo

  • FBC (leukocytosis, anaemia)
  • Chemistry panel including serum lactate (acidosis, uraemia, elevated creatinine and amylasaemia)
  • Coagulation panel (in case of underlying coagulopathy)
  • Arterial blood gas/lactate level (acidosis + elevated lactate)
  • ECG (may demonstrate arrythmia/infarction as a cause)
  • Erect CXR (for perforation)
  • Abdominal x-rays (air-fluid level, bowel dilation, bowel wall thickening, pneumatosis)
  • CT scan with contrast/CT angiogram (occlusion in vasculature, thumb printing sign of oedema/haemorrhage - best test for mesenteric ischaemia)
  • Sigmoidoscopy or colonoscopy (BEST TEST for ischaemic collitis- mucosal sloughing or friability, petechiae, haemorrhagic nodules, necrosis, gangrene)
  • Mesenteric angiography
  • Mesenteric duplex ultrasound
  • Magnetic resonance angiography- best test for mesenteric ischaemia
314
Q

What is haematochezia?

A

Bright red blood in stools

315
Q

What is gallstone ileus?

A
  • An uncommon cause of a mechanical small bowel obstruction.
  • It is a rare complication of chronic cholecystitis and occurs when a gallstone passes through a fistula between the gallbladder and small bowel before becoming impacted at the ileocaecal valve.
316
Q

List investigations and management of booerhaves oesophagus

A

Investigations

  • G+S
  • Contrast oedophagography
  • CT
  • OGD

Management

  • NBM
  • PPI
  • ABx
  • Surgery/ endoscopy

Year 3 - Diseases (27 decks)

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