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Phase 2 > GI and Liver > Flashcards

GI and Liver Flashcards

1
Q

What are the upper GI tract red flags (5)

A
  • Anaemia
  • Loss of weight
  • Anorexia
  • Recent onset/progressive
  • M (haemetamesis)
  • Swallowing difficulty
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2
Q

What is the epidemiology of GORD (2)

A
  • Common

- Prolonged reflux can cause stricture/Barretts (squamous - columnar)

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3
Q

What can cause/are risk factors for GORD (8)

A
  • Hiatus hernia (sliding or rolling)
  • Smoking
  • Alcohol
  • Obesity
  • Loss of peristalsis/sphincter function loss
  • Overeating
  • Pregnancy
  • Increased acid secretion
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4
Q

How might GORD present (6)

A
  • Heartburn (worse on alcohol/hot drinks, stooping/bending, relieved by antacids)
  • Belching
  • Acid/food brash (reflux of acid and food into mouth)
  • Water brash (excess salivation)
  • Pain on swallowing
  • Cough
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5
Q

How do you diagnose GORD (3)

A
  • Clinical unless ALARMS or over 55
  • Endoscopy
  • Barium swallow
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6
Q

How do you treat GORD (6)

A
  • Lifestyle change
  • Antacids (Mg trisilicate)
  • Gaviscon
  • PPI (lansoprazole)
  • H2 receptor antagonists (cimetidine)
  • Fundoplication
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7
Q

What is a peptic ulcer

A
  • A break in the superficial epithelial lining penetrating down to muscularis mucosa of stomach or duodenum. Have a fibrous base and increased inflammatory cells
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8
Q

What is the epidemiology of peptic ulcer disease (4)

A
  • Increases with age
  • Most commonly caused by H.pylori or NSAIDs
  • Duodenal ulcers more common than gastric
  • Duodenal cap and Lesser curvature of stomach are most common areas
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9
Q

What is the pathophysiology of peptic ulcer disease

A
  • NSAIDs or H.pylori disrupt the mucosal layer covering the gastric mucosa
  • This leads to acid destroying the epithelial layer and infiltrating to the muscularis mucosa layer
  • This leads to ulceration and also gastritis
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10
Q

How might peptic ulcer disease present (4)

A
  • Very localised burning epigastric pain
  • Weight loss
  • Nausea
  • Ulcers can get deeper until they cause haemorrhage or peritonitis
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11
Q

How do you diagnose peptic ulcer disease (3)

A
  • Stool antigen test
  • C-urea breath test (for H.pylori)
  • Endoscopy (ALARMS/over 55)
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12
Q

How do you treat peptic ulcer disease (3)

A
  • PPI/H2 receptor antagonist (cimetidine)
  • Stop NSAIDs
  • H.pylori (clarithromycin + amoxicillin)
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13
Q

What is a varice

A
  • A dilated vein at risk of bleeding
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14
Q

What is the epidemiology of oesophago-gastric varices (2)

A
  • 90% with cirrhosis will develop varices

- Usually develop in the lower oesophagus/gastric cardia

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15
Q

What are the causes of oesophago-gastric varices (3)

A
  • Pre-hepatic portal hypertension (thrombus)
  • Intra-hepatic portal hypertension (cirrhosis)
  • Post-hepatic portal hypertension (heart failure/budd chiari syndrome)
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16
Q

How might oesophago-gastric varices present (5)

A
  • Rupture
  • Abdominal pain
  • Haematemesis
  • Pallor
  • Tachycardia/hypotension
  • Shock
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17
Q

How do you diagnose oesophago-gastric varices

A
  • Endoscopy
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18
Q

How do you treat oesophago-gastric varices (4)

A
  • Acute (rupture)
  • Blood transfusion
  • Variceal banding
  • iv terlipressin (vasoconstriction)
  • Prevention
  • Beta-blockers
  • Variceal banding
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19
Q

What is gastritis

A
  • Stomach inflammation associated with mucosal damage
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20
Q

What can cause gastritis (5)

A
  • NSAIDs
  • H.pylori
  • Ischaemia
  • Increased acid secretion
  • Autoimmune gastritis
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21
Q

How might gastritis present (5)

A
  • Epigastric pain
  • Abdominal swelling
  • Vomiting/haemetamesis
  • Indigestion
  • Nausea/stomach upset
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22
Q

How do you diagnose gastritis (2)

A
  • Endoscopy/biopsy

- H.pylori stool antigen/C urea breath test

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23
Q

How do you treat gastritis (3)

A
  • Stop NSAIDs
  • PPI/H2 receptor agonists (cimeditine)
  • H.pylori (clarithromycin + amoxicillin)
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24
Q

What are the main causes of malabsorption (4)

A
  • Pancreatic insufficiency
  • Decreased bile secretion
  • Decreased absorptive surface area (coeliac/crohns/surgery)
  • Non-pancreatic enzyme insufficiency (lactose intolerance)
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25
Q

What is coeliac disease

A
  • A T-cell mediated autoimmune disorder leading to small bowel inflammation, damage and malabsorption in response to prolamin
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26
Q

What is the epidemiology of coeliac (3)

A
  • 1% population affected
  • Associated with family
  • Peaks in infancy and 50-60
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27
Q

Describe the pathophysiology of coeliac

A
  • Gluten sensitive T-cells cause inflammatory response to prolamin
  • This causes villous atrophy, crypt hyperplasia and wc in the epithelium
  • Affects proximal small bowel most leading to Fe, vitamin D and folate deficiency (anaemia)
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28
Q

How might coeliac present (6)

A
  • Abdominal pain
  • Bloating
  • Nausea and vomiting
  • Weight loss
  • Diarrhoea
  • Anaemia
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29
Q

How do you diagnose coeliac (2)

A
  • Duodenal biopsy (villous atrophy etc.)

- Serum antigen testing (tissue transglutimase antibody)

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30
Q

How do you treat coeliac (2)

A
  • Gluten free diet

- Replace Vit. D, Fe and folate

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31
Q

What is the epidemiology of ulcerative colitis (UC) (3)

A
  • More common than Crohns
  • More common in non-smokers
  • Usually presents at 15-30
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32
Q

Describe the pathophysiology of UC

A
  • Non-granulatomous inflammation of superficial mucosal layer
  • Starts at rectum spreads out to ileocaecal valve
  • No skip lesions (continous)
  • 50% rectum, 30% rectum and distal colon, 20% rectum and colon
  • Crypt abscesses and goblet cell depletion
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33
Q

How might UC present (6)

A
  • Remission/exacerbation (depression, stress, NSAIDs)
  • Diarrhoea (blood + mucus)
  • Left lower quadrant pain
  • Weight loss/malaise
  • Cramps
  • Oral ulcers/erythema nodosum
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34
Q

How do you diagnose UC (3)

A
  • Bloods (raised CRP/ESR/WCC)
  • Stool sample to exclude infection
  • Colonoscopy and biopsy
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35
Q

How do you treat UC (6)

A
  • Mild/moderate
  • Oral 5 aminosalicylic acid (sulfasalazine)
  • Oral prednisolone
  • Severe
  • iv hydrocortisone
  • Infliximab
  • Remission
  • Azathioprine
  • Surgery
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36
Q

What is the epidemiology of crohns (3)

A
  • More common in females
  • More common in smokers
  • Usually presents at 20-40
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37
Q

Describe the pathophysiology of crohns

A
  • Transmural granulatomous inflammation of mouth to gut
  • Skip lesions (non-continous)
  • Cobblestone appearance
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38
Q

How might crohns present (4)

A
  • Diarrhoea
  • Abdominal pain (less localised)
  • Anal tags
  • Weight loss/malaise
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39
Q

How do you diagnose crohns (3)

A
  • Bloods (raised ESR/CRP/WCC)
  • Stool sample to exclude infection
  • Colonsocopy with biopsy
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40
Q

How do you treat crohns (6)

A
  • Smoking cessation
  • Mild/moderate
  • Slow releasing steroid
  • Prednisolone
  • Severe
  • IV hydrocortisone
  • Infliximab
  • Remission
  • Azathioprine
  • Surgery
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41
Q

What is intestinal obstruction

A
  • Arrest/blockage of the forward propulsion of intestinal contents
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42
Q

What are the 3 types of intestinal obstruction

A
  • Obstruction of lumen
  • Disease of wall
  • Disease outside wall
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43
Q

What can cause obstruction of bowel lumen (2)

A
  • Tumour

- Bile stone (ileum)

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44
Q

What can cause Disease of bowel wall (4)

A
  • Tumour
  • Crohns
  • Diverticulitis
  • Neural
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45
Q

What can cause disease outside bowel wall (2)

A
  • Adhesion (most common cause)

- Volvulus

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46
Q

What are the main causes of small bowel obstruction (SBO) (4)

A
  • Adhesion (most common)
  • Tumour
  • Hernia
  • Crohns
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47
Q

Describe the pathophysiology of SBO

A
  • Obstruction leads to proximal dilation and distention of bowel
  • This causes malabsorption and ischaemia
  • Ischaemia can lead to necrosis and perforation
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48
Q

How might SBO present (5)

A
  • Abdominal pain (initially colicky)
  • Abdominal distension (less than LBO)
  • Vomiting
  • Late constipation
  • Increased bowel sounds
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49
Q

How do you diagnose SBO (3)

A
  • X-Ray (distended bowel)
  • FBC
  • CT (gold standard)
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50
Q

How do you treat SBO (4)

A
  • Fluids
  • Analgesia and anti-emetics
  • Bowel decompression
  • Surgery
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51
Q

What are the main causes of large bowel obstruction (LBO) (2)

A
  • Malignancy

- Volvulus

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52
Q

Describe the pathophysiology of LBO

A
  • Bowel proximal to obstruction dilates/distends
  • This leads to ischaemia, which causes mucosal oedema
  • This leads to necrosis and perforation
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53
Q

How might LBO present (5)

A
  • Abdominal pain (less colicky than SBO)
  • Abdominal distension (more than SBO)
  • Constipation
  • May be faecal vomiting
  • Palpable mass
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54
Q

How do you diagnose LBO (3)

A
  • X-Ray (bowel distension)
  • FBC
  • CT
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55
Q

How do you treat LBO (4)

A
  • Fluids
  • Analgesia and anti-emetics
  • Bowel decompression
  • Surgery
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56
Q

What is the epidemiology of acute mesenteric ischaemia (2)

A
  • Usually seen in older patients

- Nearly always affects small bowel

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57
Q

What are the causes of acute mesenteric ischaemia (4)

A
  • Superior mesenteric artery thrombosis (Most common)
  • SMA embolus (eg. in A.F)
  • Mesenteric vein thrombosis
  • Decreased flow/C.O
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58
Q

How might acute mesenteric ischaemia present (3)

A
  • Triad of
  • Acute severe abdominal pain
  • Absence of abdominal findings
  • Hypovolaemia (shock)
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59
Q

How do you diagnose acute mesenteric ischaemia (3)

A
  • X-Ray (to exclude other causes)
  • Laparotomy
  • CT/MRI angiography
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60
Q

How do you treat acute mesenteric ischaemia (4)

A
  • Fluids
  • IV gentamicin
  • IV heparin
  • Surgery to remove necrosed bowel
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61
Q

What is the epidemiology of ischaemic colitis (2)

A
  • More common in older

- Related to underlying CVS disease

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62
Q

What are the causes of ischaemic colitis (4)

A
  • Thrombus
  • Embolus
  • Low flow/C.O
  • Drugs
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63
Q

How might ischaemic colitis present (3)

A
  • Sudden onset LLQ abdominal pain
  • Bright red blood in stools +/- diarrhoea
  • May be hypovolaemic/shock
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64
Q

How do you diagnose ischaemic colitis (2)

A
  • Urgent CT to exclude perforation

- Colonoscopy and biopsy

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65
Q

How do you treat ischaemic colitis (3)

A
  • Antibiotics
  • Fluids
  • Gangrenous (peritonitis + shock)
  • Urgent surgery
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66
Q

What is irritable bowel syndrome (IBS)

A
  • A mixed group of abdominal symptom with no organic cause found
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67
Q

What is the epidemiology of IBS (3)

A
  • Onset before 40
  • Common
  • More common in females
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68
Q

What are the main causes of IBS (5)

A
  • Depression/anxiety
  • Stress
  • Abuse
  • GI infection
  • Eating disorders
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69
Q

What are the types of IBS (3)

A
  • IBS-D
  • IBS-C
  • IBS-M
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70
Q

How might IBS present (8)

A
  • ABC
  • Abdominal pain/discomfort
  • Bloating
  • Change in bowel habit
  • 2+ of:
  • Urgency
  • Incomplete emptying
  • Bloating
  • Mucus in stool
  • Symptoms worse after food
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71
Q

What is the epidemiology of acute pancreatitis

A
  • Inflammation of pancreatic gland initiated by any acute injury
  • Reoccurs if untreated
  • Can be difficult to distinguish from chronic
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72
Q

What are the causes of acute pancreatitis

A
  • IGETSMASHED
  • Idiopathic
  • Gallstones (most common)
  • Ethanol (alcohol)
  • Trauma
  • Steroids
  • Mumps
  • Autoimmune
  • Scorpion venom
  • Hyperlipidaemia
  • E
  • Drugs
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73
Q

Describe the pathophysiology of acute pancreatitis

A
  • Premature activation of pancreatic enzymes leads to autodigestion of the pancreas by its own enzymes
  • This leads to acute inflammation of the pancreas
  • Destruction of Beta cells on islets of langerhans leads to hyperglycaemia
  • Blood vessel damage leads to haemorrhage
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74
Q

How might acute pancreatitis present (6)

A
  • Sudden/subacute onset severe epigastric/middle abdominal pain, radiating to back (may be relieved by sitting forward)
  • Nausea and vomiting
  • Fever
  • Jaundice
  • Tachycardia/hypotension
  • Bruising on stomach/flank (greys/cullens signs)
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75
Q

How do you diagnose acute pancreatitis (4)

A
  • Bloods (raised serum amylase and lipase)
  • Erect CXR (exclude gastro-duodenal perforation)
  • MRI
  • Ultrasound (gallstones)
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76
Q

How do you treat acute pancreatitis (6)

A
  • Remove stones
  • Analgesia (morphine)
  • Nasogastric tube
  • Catheter
  • Drain build up
  • ANtibiotics
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77
Q

What is chronic pancreatitis

A
  • Debilitating continuous inflammation of the pancreas leading to progressive fibrosis of exocrine pancreatic tissue
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78
Q

What is the epidemiology of chronic pancreatitis (2)

A
  • More common in males

- Usually presents around 50

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79
Q

What are the causes of chronic pancreatitis (5)

A
  • Alcohol (most common)
  • Recurrent acute pancreatitis
  • Cystic fibrosis
  • CKD
  • Autoimmune pancreatitis
80
Q

How might chronic pancreatitis present (5)

A
  • Epigastric pain radiates to back, relived by sitting forward and worse on alcohol
  • Nausea and vomiting
  • Weight loss/decreased appetite
  • Diabetes
  • Diarrhoea
81
Q

How do you diagnose chronic pancreatitis (3)

A
  • Serum amylase and lipase
  • Enhanced contrast CT
  • Abdominal ultrasound
82
Q

How do you treat chronic pancreatitis (3)

A
  • Alcohol cessation
  • Pain relief (NSAIDs/opiates)
  • Duct drainage
83
Q

What is the epidemiology of appendicitis (3)

A
  • Most common surgical emergency
  • More common in males
  • Most common 10-20
84
Q

How might appendicitis present (5)

A
  • Right iliac fossa pain
  • Anorexia
  • Nausea and vomiting
  • Guarding/tenderness
  • Diarrhoea
85
Q

How do you diagnose appendicitis (3)

A
  • Bloods (raised WWC, ESR, CRP)
  • Ultrasound
  • CT
86
Q

How do you treat appendicitis (2)

A
  • Appendicectomy

- Post-op antibiotics

87
Q

Describe the process of bilirubin catabolism

A
  • Old/damaged erythrocytes broken down by the liver and spleen producing biliverdin
  • Biliverdin is then converted into unconjugated bilirubin
  • Unconjugated bilirubin travels to the liver bound to albumin where it is converted to conjugated bilirubin
  • This is then released into bile, where it enters the small intestine and is converted to urobilinogen
  • 10% of urobilinogen converted to urobilin whioch is excreted in urine
  • 90% of urobilinogen is converted to stercobilin where it is excreted in faeces
88
Q

What is jaundice

A
  • A yellow discolouration of the skin caused by raised serum bilirubin
89
Q

What are the two types of jaundice

A
  • Pre hepatic (raised unconjugated) (haemolysis and Gilberts)
  • Cholestatic (raised conjugated) (Liver and Biliary obstruction)
90
Q

What questions might you ask to distinguish between cholestatic and Pre-hepatic jaundice (3)

A
  • Itching? (Yes in cholestatic)
  • Stools? (pale in cholestatic)
  • Urine? (dark in cholestatic)
  • All normal in pre-hepatic
91
Q

What is biliary colic

A
  • Pain associated with temporary obstruction of the cystic/bile duct caused by a stone
92
Q

What is cholangitis

A
  • Inflammation of the bile duct
93
Q

What is cholecystits

A
  • Inflammation of the gallbaldder
94
Q

What is the epidemiology of gallstones (3)

A
  • More common in females
  • Increases with age
  • Most are formed in the gallbladder
95
Q

What are the risk factors for gallstones (5)

A
  • Obesity
  • Increasing age
  • Smoking
  • Diabetes
  • Female
96
Q

How might gallstones present (3)

A
  • Biliary colic (severe sudden onset epigastric/RUQ pain that radiates over shoulder, associated with nausea and vomiting)
  • Tenderness and guarding
  • Jaundice
97
Q

Where might gallstones get stuck

A
  • Bile duct (cholangitis)

- Cystic duct (cholecystitis)

98
Q

How do you diagnose Cholangitis (4)

A
  • Ultrasound
  • Abnormal Liver biochem. (raised AST, ALP, ALT)
  • Raised WCC, CRP, ESR
  • Raised serum bilirubin
99
Q

How do you diagnose Cholecystitis (3)

A
  • Ultrasound
  • Raised WCC, CRP, ESR
  • May be abnormal Liver biochem./raised bilirubin
100
Q

How do you treat gallstones (6)

A
  • Iv fluids
  • Nasogastric tube
  • Opiates
  • IV antibiotics
  • Shockwave lithotripsy
  • Surgery eg. cholecystectomy
101
Q

How do you define acute and chronic hepatitis

A
  • Acute <6 months

- Chronic >6 months

102
Q

What can cause acute hepatitis (4)

A
  • Virus (hep. A to E and EBV)
  • Alcohol
  • Autoimmune
  • Drugs/toxins
103
Q

How might acute hepatitis present (6)

A
  • RUQ pain
  • Malaise and myalgia
  • Cholestatic jaundice
  • GI upset
  • Tender hepatomegaly
  • Raised serum ALP/AST and bilirubin
104
Q

What can cause chronic hepatitis (4)

A
  • Viral (hep. B, C, D)
  • Alcohol
  • Drugs
  • Autoimmune
105
Q

How might chronic hepatitis present (4)

A
  • Cholestatic jaundice
  • Ascites/oedema (albumin def.)
  • Bleeding/bruising (clotting factor def.)
  • Liver biochem and LFTs may be raised or normal
106
Q

What are the methods of blood borne transmission (5)

A
  • Needlestick
  • IV drug use
  • Tattoo
  • Sex
  • Blood products
107
Q

What is the major risk of chronic hepatitis

A
  • Chronic hepatitis leads to cirrhosis which leads to hepatocellular carcinoma
108
Q

What type of virus is hepatitis A and is it acute or chronic

A
  • RNA virus

- Acute

109
Q

How is hepatitis A spread

A
  • Faeco-oral transmission
110
Q

How do you treat hepatitis A (3)

A
  • Monitor liver function
  • Supportive treatment
  • Vaccinate + human normal immunoglobulin for close contacts
111
Q

What type of virus is hepatitis B and is it acute or chronic

A
  • DNA virus

- Acute and chronic

112
Q

How is hepatitis B spread

A
  • Blood-borne transmission
113
Q

How do you treat hepatitis B (3)

A
  • Acute
  • Monitor liver function + vaccinate close contacts
  • Follow up blood test after 6 months to see if antibody is still there
  • Chronic
  • Alpha interferon
114
Q

What type of virus is hepatitis C and is it acute or chronic

A
  • RNA virus

- Acute and chronic

115
Q

How is hepatitis B spread

A
  • Blood borne transmission
116
Q

How do you treat hepatitis C (3)

A
  • Acute
  • Monitor liver function + vaccinate close contacts
  • Follow up blood test after 6 months to see if antibody is still there
  • Chronic
  • Alpha interferon + Ribavirin
117
Q

What type of virus is hepatitis D and is it acute or chronic

A
  • RNA virus

- Acute and chronic

118
Q

How is hepatitis D spread

A
  • Blood borne transmission
119
Q

How do you treat hepatitis D (3)

A
  • Acute
  • Monitor liver function + vaccinate close contacts
  • Follow up blood test after 6 months to see if antibody is still there
  • Chronic
  • Alpha interferon
120
Q

What type of virus is hepatitis E and is it acute or chronic

A
  • RNA virus

- Acute

121
Q

How is hepatitis E spread

A
  • Faeco-oral transmission
122
Q

How do you treat hepatitis E (3)

A
  • Monitor liver function
  • Supportive treatment
  • Vaccinate + human normal immunoglobulin for close contacts
123
Q

What is Cirrhosis

A
  • End stage of all progressive liver diseases, which is irreversible and associated with portal hypertension and liver failure
124
Q

What are the main causes of cirrhosis (3)

A
  • Alcohol
  • Hepatitis B, C, D
  • Non alcoholic fatty liver disease
125
Q

What is the pathophysiology of cirrhosis

A
  • Chronic liver injury results in inflammation necrosis and hence progressive fibrosis of liver parenchyma
  • If cause of fibrosis is treated early then can be reversed
  • Later stage can improve/regress but will not reverse
126
Q

How might cirrhosis present (6)

A
  • Oedema/ascites
  • Hepatomegaly
  • Jaundice
  • Bleeding/bruising
  • Hair loss
  • White nails/clubbing
127
Q

How do you diagnose cirrhosis (4)

A
  • Liver biopsy (gold standard)
  • LFTs (low albumin/prothrombin time)
  • Liver biochem. (raised AST/ALT)
  • Imaging (ultrasound/CT)
128
Q

How do you treat cirrhosis (5)

A
  • Alcohol abstinence
  • Good nutrition
  • Transplant
  • Avoid NSAIDs
  • Hepatocellular carcinoma screening
129
Q

What are the causes of portal hypertension (3)

A
  • Pre-hepatic (portal vein thrombus)
  • Intra-hepatic (cirrhosis)
  • Post-hepatic (RH failure)
130
Q

What is the epidemiology of primary biliary cirrhosis (3)

A
  • More common in females
  • Usually presents around 50
  • Autoimmune, unknown cause
131
Q

What are the risk factors for primary biliary cirrhosis (4)

A
  • Smoking
  • Recurrent UTI
  • Family history
  • Other autoimmune disease
132
Q

Describe the pathophysiology of primary biliary cirrhosis

A
  • Autoimmune granulatomous inflammatory damage of interlobar bile ducts, leading to Liver fibrosis and cirrhosis
133
Q

How might primary biliary cirrhosis present (4)

A
  • Itching
  • Hepatomegaly
  • Jaundice
  • Lethargy/fatigue
134
Q

How do you diagnose primary biliary cirrhosis (4)

A
  • Liver biochem. (raised ALP)
  • LFTs (raised cholsterol/bilirubin)
  • Ultrasound
  • Liver biopsy
135
Q

What is the treatment for primary biliary cirrhosis (3)

A
  • Ursodeoxycholic acid (improves bilirubin levels)
  • Vitamin ADEK
  • Liver transplant
136
Q

Describe the pathophysiology of alcoholic liver disease

A
  • Fatty liver is caused by excess alcohol as fat is produced by livers metabolism of alcohol
  • Hepatitis/cirrhosis occurs due to lymphocytic infiltration and fat deposition
137
Q

How might alcoholic liver disease present (6)

A
  • Hepatomegaly
  • Jaundice
  • Bleeding/bruising
  • Ascites/oedema
  • Malaise/fever
  • Clubbing/white nail discolourations
138
Q

How do you diagnose alcoholic liver disease (4)

A
  • Liver biochem. (raised AST/ALT)
  • LFTs (raised bilirubin/prothrombin time)
  • Liver biopsy (fatty liver/cirrhosis)
  • Ultrasound/CT
139
Q

How do you treat alcoholic liver disease (4)

A
  • Alcohol cessation
  • Iv thiamine (avoid wernicke-korsakoff encelopathy which is caused by alcohol withdrawal)
  • Avoid NSAIDs/good diet
  • Liver transplant
140
Q

What is liver failure

A
  • Liver loses the ability to repair/regenerate leading to decompensation
141
Q

What are the two types of liver failure

A
  • Acute liver failure - When acute liver injury leads to hepatic encephalopathy and coagulation issues in a patient with a previously healthy liver
  • Acute on chronic - When liver fails as a result of decompensation of chronic liver disease
142
Q

What are the main causes of liver failure (3)

A
  • Viral (hepatitis and EBV)
  • Drugs (most commonly paracetamol)
  • Hepatocellular carcinoma
143
Q

How might liver failure present (5)

A
  • Jaundice
  • Nausea/vomiting/fever
  • Hepatic encephalopathy (confusion, dec. consciousness)
  • Fetor hepaticus (smell like pear drops)
  • If acute on chronic signs of chronic liver disease (Clubbing/oedema/ascites/bleeding/bruising)
144
Q

How do you diagnose liver failure (4)

A
  • Liver biochem. (raised AST/ALT)
  • LFTs (raised bilirubin/prothrombin time)
  • CT/Ultrasound
  • Raised NH3
145
Q

How do you treat liver failure (4)

A
  • Iv mannitol if raised ICP
  • Iv glucose if hypoglycaemia
  • Platelets and electrolytes
  • Liver transplant
146
Q

What may cause a raised ALT

A
  • Specific to liver injury
147
Q

What may cause a raised ALP

A
  • Liver injury or cholestatic disease (not just liver specific)
148
Q

What is ascites

A
  • Accumulation of free fluid in the peritoneal cavity
149
Q

What is the epidemiology of ascites (2)

A
  • Poor prognosis (20% 5 year survival)

- Common post-op and in cirrhosis

150
Q

What are the main causes of ascites (3)

A
  • Low albumin
  • Low flow (portal hypertension - cirrhosis and HF)
  • Local inflammation (peritonitis)
151
Q

How might ascites present (4)

A
  • Abdominal swelling/distention
  • Dull shifting
  • Discomfort/mild pain - Severe suggests peritonitis
  • May be peripheral oedema
152
Q

How do you diagnose ascites (2)

A
  • Dull shifting

- Ascitic tap (protein - transudate or exudate)

153
Q

How do you treat ascites (3)

A
  • Treat underlying cause
  • Diuretics/sodium restriction
  • Fluid drain/shunt
154
Q

What are the causes of peritonitis (2)

A
  • Bacterial - primary (perforation)

- Chemical - secondary (bile)

155
Q

How might peritonitis present (6)

A
  • Sudden onset severe abdominal pain
  • Initially diffuse and then localises
  • Shock and collapse
  • Fever/sweats
  • Patient wants to lie still
  • Pain relieved by resting hands on abdomen
156
Q

How do you diagnose peritonitis (2)

A
  • Bloods (raised WCC/ESR/CRP)

- Erect CXR to look for bowel perforation

157
Q

How do you treat peritonitis (4)

A
  • Iv fluids
  • Iv antibiotics
  • Nasogastric tube
  • Surgery
158
Q

What is the epidemiology of oesophageal cancer (3)

A
  • More common in males
  • Upper 2/3 = SSC, lower 1/3 = Adenocarcinoma
  • 6th most common cancer
159
Q

What are the risk factors for oesophageal cancer (5)

A
  • Smoking
  • Alcohol
  • Obesity
  • GORD/barretts
  • Achalasia (dysmotility)
160
Q

How might oesophageal cancer present (4)

A
  • Usually late and advanced
  • Progressive dysphagia (initially solids then liquids)
  • Weight loss/malaise
  • Cough/hoarseness
161
Q

How do you diagnose oesophageal cancer (3)

A
  • Endoscopy and biopsy
  • Barium swallow
  • PET/MRI/CT (staging)
162
Q

How do you treat oesophageal cancer (2)

A
  • Surgical excision + chemo. +/- radiotherapy

- Palliative stent/laser treatment for dysphagia

163
Q

What is the epidemiology of gastric cancer (4)

A
  • 4th most common cancer
  • More common in males
  • Increases with age
  • Adenocarcinoma
164
Q

What are the risk factors for gastric cancer (4)

A
  • Smoking
  • Family history
  • H.pylori
  • Diet
165
Q

What are the two types gastric cancer

A
  • Intestinal (type 1)
  • Well formed, differentiated
  • Better prognosis
  • Diffuse (type 2)
  • Poorly formed, undifferentiated
  • Poor prognosis
166
Q

How might gastric cancer present (5)

A
  • Severe, constant epigastric pain
  • Weight loss/malaise
  • Nausea and vomiting
  • Dysphagia if in fundus
  • Anaemia
167
Q

How do you diagnose gastric cancer (2)

A
  • Endoscopy and biopsy

- PET/MRI/CT

168
Q

How do you treat gastric cancer (2)

A
  • Surgery + combo. chemo. + radiotherapy

- Nutritional support

169
Q

What is the epidemiology of small intestine cancer (2)

A
  • Rare

- Mostly adenocarcinoma, some lymphomas

170
Q

How might small intestine cancer present (4)

A
  • Abdominal pain
  • Diarrhoea
  • Weight loss
  • Mass
171
Q

How do you diagnose small intestine cancer

A
  • Endoscopy and biopsy
172
Q

How do you treat small intestine cancer

A
  • Surgery and radio/chemotherapy
173
Q

What are colorectal polyps

A
  • An abnormal growth of tissue projecting from the colonic mucosa
174
Q

Why are colorectal polyps significant

A
  • They are adenomas, which are precursors for adenocarcinomas
  • So they are removed at colonoscopy
175
Q

What is the epidemiology of colorectal cancer (4)

A
  • 3rd most common cancer
  • More common in males
  • Usually in older people
  • Usually adenocarcinomas
176
Q

What are the risk factors for colorectal cancer (6)

A
  • Smoking
  • Polyps
  • Ulcerative colitis
  • Family history
  • Obesity
  • Alcohol
177
Q

How might right sided colorectal cancer present (4)

A
  • Mass
  • Abdominal pain
  • Anaemia
  • Weight loss
178
Q

How might left sided/sigmoid colorectal cancer present (3)

A
  • Change in stool habit
  • Blood and Mucus in stool
  • Weight loss/malaise
179
Q

How might rectal colorectal cancer present

A
  • Rectal bleeding/mucus
180
Q

How do you diagnose colorectal cancer (3)

A
  • Colonoscopy and biopsy (gold standard)
  • Double contrast barium enema
  • CT colonoscopy
181
Q

How do you treat colorectal cancer (3)

A
  • Surgery (colectomy)
  • Radiotherapy (palliative/rectal)
  • Chemotherapy (post-op)
182
Q

What is the epidemiology of hepatocellular carcinoma (3)

A
  • 5th most common cancer
  • 90% of liver tumours
  • More common in males
183
Q

What is the main risk factor for hepatocellular carcinoma

A
  • Cirrhosis (especially chronic hepatitis B and C)
184
Q

How might hepatocellular carcinoma present (6)

A
  • Jaundice
  • RUQ pain
  • Hepatomegaly
  • Bleeding/bruising
  • Ascites/oedema
  • Weight loss/malaise
185
Q

How do you diagnose hepatocellular carcinoma (2)

A
  • Liver biopsy

- Enhanced contrast CT

186
Q

What is the treatment for hepatocellular carcinoma (2)

A
  • Surgical resection

- Liver transplant

187
Q

What is the epidemiology of pancreatic cancer (4)

A
  • 99% in exocrine pancreas
  • More common in males
  • More common in older people
  • Most are adenocarcinomas
188
Q

What are the risk factors for pancreatic cancer (4)

A
  • Smoking
  • Diabetes
  • Chronic pancreatitis
  • Family history
189
Q

How might pancreatic cancer present (5)

A
  • Diabetes
  • Weight loss
  • Acute pancreatitis
  • Head - painless obstructive jaundice
  • Tail - epigastric pain radiates to back
190
Q

How do you diagnose pancreatic cancer

A
  • Ultrasound guided biopsy
191
Q

How do you treat pancreatic cancer (2)

A
  • 5 year survival 3%
  • Surgery + post-op chemo.
  • Palliative care
192
Q

What is the definition of diarrhoea

A
  • Abnormal passage of loose or liquid stools more than 3 times a day
  • Chronic >2 weeks, acute <2 weeks
193
Q

What factors suggest infective diarrhoea

A
  • Sudden onset associated with crampy abdominal pains
194
Q

What factor suggests bacterial infection

A
  • Blood in the stools
195
Q

What are the risk factors for infective diarrhoea (4)

A
  • Foreign travel
  • Crowding
  • Poor hygiene
  • PPI and H2 antagonists
196
Q

What are the causes of infective diarrhoea (5)

A
  • Mostly caused by virus
  • Rotavirus (children)
  • Norovirus (adults)
  • Campylobacter (adults)
  • E. coli, shigella, salmonella (children)
  • C. diff
197
Q

How do you treat infective diarrhoea (4)

A
  • Anti-emetics
  • Anti-motility agents
  • Fluids/k+
  • Antibiotics

Phase 2 (10 decks)

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