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Phase 2 Mine > Revision List GI/Liver > Flashcards

Revision List GI/Liver Flashcards

1
Q

What is iron haemochromatosis?

A

Inherited disorder of iron metabolism leading to increased intestinal absorption so increased iron deposition in joints, liver, heart, pancreas, pituitary –> eventual fibrosis and organ failure.
AR

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2
Q

Cause of iron haemochromatosis?

A
  1. HFE gene mutation on chromosome 6 - AR
  2. High intake of iron/ chelating agents
  3. Alcoholics may have iron overload
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3
Q

What is hepicidin?

A

Regulates iron absorption - decreased in HFE mutation

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4
Q

Clinical presentation of haemochromatosis?

A
  1. Fatigue
  2. Joint pain
  3. Slate grey skin pigmentation, white flat nails
  4. Koilonychia
  5. Hepatomegaly, cirrhosis,
  6. Osteoporosis
  7. DM
  8. Skin dryness, melanoderma
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5
Q

Diagnosis of haematochromatosis?

A

Homozygous e.g. HFE genotyping
- increased serum ferritin, transferrin saturation, iron,
Liver biopsy for confirmation

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6
Q

Treatment of haematochromatosis?

A

Venesection - regular removal of blood - may regress fibrosis

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7
Q

Which part of the bowel tract does UC affect?

A

Only Colon

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8
Q

Which part of the bowel tract layer does UC affect?

A

Only mucosal inflammation

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9
Q

Which IBD is smoking protective in?

A

Ulcerative colitis

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10
Q

Risk factors for UC and Crohn’s?

A
  1. Fhx
  2. NSAIDs
  3. Chronic depression
  4. Stress
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11
Q

Clinical presentation of UC?

A
  1. Diarrhoea - often bloody and mucus
  2. Colicky LLQ pain
  3. Tenesmus
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12
Q

Pathophysiology of UC?

A
  1. Continuous mucosal inflammation spread from rectum to ileocaecal valve
  2. No granulomata
  3. Goblet cell decrease, crypt abscess increase
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13
Q

Clinical presentation of Crohn’s?

A

Colon: bloody mucus diarrhoea
Ileum - RIF
Small bowel - weight loss, abdominal pain
Extra GI symptoms: anorexia, tender abdomen, joint eye problems, oral ulcerations

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14
Q

Pathophysiology of Crohn’s?

A
  1. Transmural granulomatous inflammation –> epitheloid macrophages surrounded by lymphocytes
  2. Skip lesions
  3. Cobblestone mucosa
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15
Q

Diagnostic tests for IBD?

A
  1. Raised ESR, CRP, WCC and platelets
  2. Iron deficiency anaemia in UC
  3. Stool: exclude: campylobacter, c.diff, salmonella, shigella, E.coli
  4. Colonoscopy/ Sigmoidoscopy/ Rectal Biopsy:
    - -> UC: inflammatory infilitrate, decreased goblet cells, mucosal ulcers
    - -> Crohn’s spot lesion, granulomatous transmural inflammation
  5. Faecal calprotein
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16
Q

Treatment for UC?

A
  1. Topical 5 aminosalicyclate - mesalazine
  2. Oral 5ASA - if remission not achieved
  3. Topical/ oral corticosteroid - prednisolone
  4. Calcineurin inhibitors
  5. Immunosuppresive - thioprine, methotrexate, TNF a inhibitor
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17
Q

Surgery for UC?

A

Colectomy - ileoanal anastomoses

Panproctocolectomy with ileostomy

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18
Q

Treatment for Crohn’s?

A
  1. Smoking stop
  2. iron/b12/folate anaemia - replacement therapy
  3. Monotherapy: conventional glucocorticoids ve.g. prednisolone, hydrocortisone
  4. Thiopurines: azathioprine add SE: bone marrow suppression, acute pancreatitis
  5. Anti-TNF Ab - immunosuppressive drug - influximab, adalimumab
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19
Q

Complications of Crohn’s?

A

Malabsorption –> small bowel obstruction
Anal skin tags, fissure, fistula
Systemic: colorectal cancer, amyloidosis, neoplasia

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20
Q

Irritable Bowel Syndrome

A

Relapsing functional disorder, change in bowel habits

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21
Q

Causes of IBS?

A
  1. Stress
  2. Eating disorders
  3. Depression
  4. GI infections
  5. Sexual/physical/verbal abuse
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22
Q

Clinical presentation of IBS?

A
  1. Abdominal symptoms: pain/discomfort - relieve by defecation linked to bowel frequency altered
    Others: urgency, incomplete evacuation, abdominal distension/bloating, mucous in stools, worsen by food.
    Non-intestinal: nocturia, back pain, joint hypermobility
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23
Q

Diagnosis of IBS?

A
  1. Bloods: anaemia, ESR, CRP raised
  2. Coeliac serology testing tissue transglutinase Ab
  3. Faecal calprotein - raised in IBD
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24
Q

Treatment of IBS?

A
  1. Mild IBS: education, reassurance, dietary modifications - frequent small meals, avoid alcohol
  2. Moderate IBS: pharmacotherapy, psychology Tx
    - antispasmodic - mebeverine
    Constipation: laxative e.g. mavicol; linaclotide, 5 HT4 receptor agonist
    - Diarrhoea - anti-motility agents - loperamide
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25
Q

What are the 5 Fs? What do they indicate?

A

Someone presenting with RUQ –> fat/female/fair/fertile/forty = could be cholelithiases

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26
Q

What is peptic ulcer disease?

A

Break in epithelial lining of stomach/ duodenum –> penetrate muscularis mucosa

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27
Q

Where are gastric ulcers the most common?

A

Lesser curve of stomach

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28
Q

Where are duodenal ulcers most common?

A

Duodenal cap

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29
Q

What are the causes of peptic ulcer disease?

A
  1. Helicobacter pylori
  2. NSAIDs - steroids and SSRI too
  3. Excess acid secretion
  4. Delayed gastric emptying
  5. Smoking
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30
Q

How does mucosal ischaemia lead to ulcers?

A
  1. Atherosclerosis or decreased BP
  2. Decreased mucin production
  3. Damage –> ulcer
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31
Q

How do NSAIDs cause ulcers?

A
  1. NSAIDs are COX1/COX2 inhibitors and thus inhibit prostaglandin synthesis.
  2. Decreased mucus secretion
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32
Q

How does H. Pylori cause ulcer

A
  1. H. pylori inhibits mucus layer
  2. Decreased duodenal bicarbonate and increased acidiity
  3. Secretes urease to convert urea to ammonia + carbon dioxide.
  4. NH3 reacts with H+ to form ammonium which is toxic to the gastric mucosa
  5. Also secretes protease, phospholipase and vacuolating toxin A –> attack gastric epithelum –> decreased mucosal production
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33
Q

Clinical presentation of peptic ulcer disease?

A
  1. Recurrent burning epigastric pain - worse when hungry/night
  2. Nausea
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34
Q

Complications of PUD?

A
  1. Haemorrhage
  2. Peritonitis
  3. Pancreatitis
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35
Q

Lifestyle changes of PUD?

A
  1. Stop smoking
  2. Avoid stress
  3. Avoid irritating foods - caffeine/ spicy
  4. Stop NSAIDs
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36
Q

Helicobacter pylori Tx?

A
  1. 2 ABx + PPI

2. Clarithyromycin, metronidazole and omeprazole

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37
Q

What are the upper GI tumours you can get and which part of the tract do they affect?

A
  1. Oesophageal tumours
    - Squamous cell carcinoma - middle and upper 1/3rd of oesophagus
    - Adenocarcinoma - lower 1/3rd of oesophagus and cardia
  2. Gastric tumours
    - Adenocarcinoma
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38
Q

Investigations of PUD?

A
  1. Serology - detect IgG Ab
  2. C-urea breath test - measure CO2 in breath after ingesting urea
  3. Stool antigen test
  4. Endoscopy if - iron deficiency anaemia, weight decrease, persistent vomiting, epigastric mass
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39
Q

Aetiology of squamous cell carcinoma oesophageal tumours?

A
  1. High level of alcohol consumption
  2. Obesity –> increase reflux
  3. Decrease fruit and veg
  4. Smoking
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40
Q

What decreases the risk of oesophageal squamous cell carcinoma?

A
  1. Diet rich in fibres
  2. Carotene
  3. Folate
  4. Vitamin C
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41
Q

Aetiology/Causes of adenocarcinoma (oesophageal)?

A
  1. Smoking/tobacco
  2. GORD
  3. Obesity
  4. Barrett’s oesophagus
  5. Alcohol
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42
Q

How does oesophageal epithelium becomes neoplastic?

A
  1. Normal oesophageal squamous epithelium
  2. Metaplastic oesophageal glandular epithelium
  3. Dysplastic oesophageal glandular epithelium
  4. Neoplastic oesophageal glandular epithelium
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43
Q

Clinical presentation of adenocarcinoma of oesophageal epithelium?

A
  1. Progressive dysphagia - hoarse, cough
  2. Weight loss
  3. Lymphadenopathy
  4. Anorexia/ oesophageal obstruction
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44
Q

Diagnosis of oesophageal adenocarcinoma?

A
  1. Oesophagoscopy with biopsy
  2. Barium swallow
  3. CT/MRI/PET
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45
Q

Treatment of oesophageal adenocarcinoma?

A
  1. Surgical resection +/- chemo/radio

2. Treatment of dysphagia: endoscopy insertion of expanding metal stent

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46
Q

Main causes of gastric adenocarcinoma?

A
  1. Smoking
  2. H. pylori
  3. Decrease p53/APC gene
  4. Pernicious anaemia
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47
Q

Two major types of gastric tumours?

A
  1. Type 1: intestinal

2. Type 2: Difffuse

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48
Q

What is the Type 1: intestinal tumour?

A

Intestinal metaplasia in mucosa surrounding tumour - polypoid/ulcerating lesions
–> more likely to involve distal stomach.

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49
Q

Type 2: diffuse tumour?

A

Poorly cohesive undifferentiated cells –> infiltrate gastric wall –> can affect any part of cardia –> worse prognosis

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50
Q

Clinical presentation of gastric tumours?

A
  1. Epigastric pain - indistinguishable from PUD, pain = constant and severe
  2. Nausea/vomiting
  3. Anorexia/Weight loss
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51
Q

Diagnosis of gastric cancer?

A
  1. Gastroscopy and biopsy
  2. Endoscopic US
  3. CT/MRI for staging
  4. PET scan
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52
Q

Treatment of gastric tumours?

A
  1. Nutrition support
  2. Surgical resection + combination chemo
    +post op radiotherapy
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53
Q

Combination chemo used for gastric tumour?

A
  1. Epirubicin
  2. Cisplatin
  3. 5-fluoro-uracil
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54
Q

What are the common small intestine tumours?

A
  1. Adenocarcinoma - 50%

2. Lymphoma

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55
Q

Clinical presentation of small intestine tumours?

A
  1. Pain, diarrhoea, anorexia, weight loss, anaemia, palpable mass
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56
Q

Diagnosis of small intestinal tumours?

A
  1. US
  2. Endoscopic biopsy
  3. CT scan
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57
Q

Treatment of small intestinal tumours?

A
  1. Surgical resection

2. Radiotherapy

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58
Q

What are colonic polyps?

A

Abnormal growth of tissue projects from colonic mucosa

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59
Q

What are adenomas?

A

Precursor lesions in most cases of colon cancer

Benign dysplastic tumour of columnar cells of glandular tissue.

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60
Q

What are two genetic linked colonic tumours?

A
  1. Familial adenomatous polyposis

2. Hereditary non-polyposis colon cancer

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61
Q

What is FAP?

A

AD mutation in APC gene where cysts form over teen years and can lead to cancer in 40s

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62
Q

What is HNPCC?

A

AD inheritance of hmSH1/hmSH2 mismatch repair gene mutations –> instability of DNA –> rapidly progressing colorectal carcinoma.

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63
Q

What is colorectal carcinoma?

A

Most commonly an adenocarcinoma

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64
Q

Risk factors of colorectal carcinoma?

A
  1. Smoking + alcohol
  2. Increase age
  3. Low fibre diet
  4. Animal fat and red meat consumption
  5. Sugar consumption
  6. Colorectal polyps
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65
Q

How to diagnose colorectal carcinoma?

A
  1. Faecal Occult Blood Test
  2. Tumour markers e.g. CEA
  3. Colonoscopy: allow biopsy, remove polyps
  4. Double contrast barium enema
  5. DRE
  6. CT colonoscopy
  7. MRI
66
Q

Treatment of colorectal carcinoma?

A
  1. Surgery
  2. Endoscopic stenting - malignant obstruction, decreased need for colostomy
  3. Radiotherapy
  4. Chemo - Dukes C chemo post decreases mortality risk.
67
Q

Classification of Duke’s criteria?

A
  1. A = limited to muscularis mucosa
  2. B = extend to muscularis mucosa
  3. C = involve regional lymph nodes
  4. D = distant metastases
68
Q

What is coeliac disease?

A
  1. Inflammation of duodenum/ small bowel obstruction

2. Gluten sensitive enteropathy

69
Q

Epidemiology of coeliac disease?

A
  1. Infancy and 50s

2. Strong association with HLA DQ2 and DQ8

70
Q

Pathophysiology of coeliac disease?

A
  1. Alpha gliadin is resistant to proteases chymotrypsin and pepsin and so pass through epithelium.
  2. Deaminated by tissue transglutaminases –> interacts with APC with CD4 T cells in lamina propria via HLA class DQ2/DQ8
  3. Release of pro-inflammatory cytokines and inflammatory cascade
  4. Villous atrophy and crypt hyperplasia and intraepithelial lymphocytes.
71
Q

Risk factors for coeliac disease?

A
  1. Other autoimmune disease: T1DM, thyroid disease, Sjorgren
72
Q

Clinical presentation of coeliac disease?

A
  1. 1/3 asymptomatic –> increased MCV
  2. Stinking stool/ fatty stool
  3. Diarrhoea, abdominal pain, bloating, nausea, vomiting
    Systemically: prolonged fatigue, unexplained weight loss, iron/b12/folate deficiency
73
Q

Diagnosing coeliac disease?

A
  1. Serology IgA Ab: tissue transglutaminase Ab, endomysial Ab
  2. FBC: decrease Hb, B12, ferritin
  3. Duodenal biopsy at endoscopy - histological changes
74
Q

Treatment of coeliac disease?

A
  1. Gluten free diet
  2. Nutrient replacement = correct vitD and mineral deficiency
  3. DEXA - osteoporosis risk
75
Q

Complications of coeliac disease?

A
  1. Anaemia
  2. Secondary lactose intolerance
  3. Osteoporosis
76
Q

Presentation of acute liver injury

A
  1. Malaise, nausea, anorexia
  2. Jaundice
  3. Abdominal pain
  4. Confusion, bleeding, hypoglycaemia
77
Q

Presentation of chronic liver injury?

A
  1. Ascites/oedema
  2. Haematemesis
  3. Malaise/anorexia
  4. Easy bruising, itching
  5. Hepatomegaly

Rare jaundice

78
Q

What are the causes of unconjugated jaundice

A

Haemolysis

Gilbert’s - deficiency in UDP glucoronyl transferases –> usually harmless, no specific treatment

79
Q

What causes of hepatic jaundice?

A
  1. Hepatitis
  2. Ischaemia
  3. Neoplasm
  4. Congestion
80
Q

Causes of post-hepatic jaundice?

A

Obstruction due to
Stones
Strictures - malignancy, ischaemic inflammatory

81
Q

Symptoms of jaundice?

A

Rigor
Billiary pain
Weight loss
Abdominal swelling

82
Q

What are black pigment gallstones?

A

Calcium bilirubinate and network of mucin glycoproteins

Seen in haemolysis, spherocytosis, sickle cell and thalassaemia

83
Q

What are brown pigment gallstones?

A

Calcium salts e.g. calcium bicarb
Almost always in presence of bile stasis and/or biliary infection
Commonly recurs

84
Q

What are 3 things gall stones are not associated with?

A

Fat intolerance
Indigestion
Bowel Upset

85
Q

How does biliary colic present?

A

Epigastrium pain first then RUQ

Radiation to right shoulder

86
Q

How does gall stones lead to acute cholecystis?

A
  1. Gall bladder obstruction leads to increase gall bladder secretion which leads to progressive distension –> may compromise supply to gall bladder.
  2. Inflammatory response = secondary to bile retention within gall bladder
87
Q

RUQ pain, fever, jaundice in biliary colic?

A

Only RUQ pain

88
Q

RUQ pain, fever, jaundice in acute cholecystitis?

A

RUQ pain

Fever

89
Q

RUQ pain, fever, jaundice in cholangitis?

A

YES all three - CHARCOT’s triad

90
Q

Describe the pathway of paracetamol overdose?

A

Acetaminophen –> Phase I (CYP2E1) —> NAPQI (toxic metabolite) –> oxidative stress –> hepatocyte damage

91
Q

Early symptoms of paracetamol overdose?

A

Initially asymptomatic/ nausea/ vomiting +/- RUQ pain

92
Q

Late symptoms of paracetamol overdose?

A

Jaundice + encephalopathy +/- AKI

93
Q

Mechanism of DILI?

A
  1. Disruption of intracellular Ca2+ homeostasis
  2. Disruption of bile cannalicular transport
  3. Induction apoptosis
  4. Inhibited mitochondrial function –> prevent FA metabolism, accumulation of ROS and lactate
94
Q

Histological changes seen in alcoholic hepatitis?

A
  1. Infiltration by polymorphonuclear leukocytes - hepatocyte ballooning
  2. Dense cytoplasmic inclusions - sometimes seen in hepatocytes
  3. Progress to cirrhosis
95
Q

Clinical presentation of fatty liver?

A
  1. Often asymptomatic
  2. Vague abdominal symptoms
  3. Hepatomegaly
96
Q

Clinical presentation of alcoholic hepatitis/cirrhosis?

A
  1. Few symptoms - mild to moderate
  2. Mild jaundice - signs of CLD
    - ascites, bruising, clubbing, Dupuytren’s contracture
  3. Severe - jaundice, ascites, high fever etc
97
Q

Alpha 1 anti-trypsin deficiency commonly presents with

A
  1. Emphysema
  2. Cirrhosis
  3. Hepatocellular carcinoma
98
Q

Treatment for chronic Hep B?

A
  1. Pegylated interferon alpha - SC injection, long term control
  2. Oral nucleotide analogue e.g. tenofavir - inhibit HBV DNA polymerase - viral replication
99
Q

Treatment of HepC?

A

NS5a, NS5b, NS3/4a protease inhibitors

Lifestyle modifications

100
Q

Pre-hepatic causes of portal HTN?

A

Thrombus in splenic vein/ portal vein

101
Q

Intra-hepatic causes of portal HTN?

A
  1. Cirrhosis
  2. Congenital hepatic fibrosis
  3. Schistosomiasis
  4. Sarcoidosis
102
Q

Post-hepatic causes of portal HTN?

A
  1. Budd Chiari syndrome
  2. RHF
  3. Constrictive pericarditis
103
Q

What can obstruct lumen of appendix in appendicitis?

A
  1. Faecolith
  2. Normal stool
  3. Lymphoid hyperplasia
  4. Infective agents
104
Q

Pathophysiology of appendicitis?

A
  1. Distal to obstruction, mucous filled –> distension –> intraluminal and intramural pressure.
  2. Resident bacteria multiply E.Coli
  3. Pressure increase and exceed venous pressure –> small vessels thrombosed –> enlargement/cognestion of appendix –> RLQ when hits parietal peritoneum
105
Q

Symptoms of appendicitis?

A
  1. Periumbilical pain migrate to right iliac fossa with parietal peritoneum involvement
  2. Mc BURNEY POINT
  3. Anorexia, rare vomiting
106
Q

Signs of appendicitis?

A
  1. Abdomen tender
  2. Guarding - abdominal wall tender - local peritonitis
  3. Rebound and percussion tenderness
107
Q

Appendicitis differential diagnosis?

A

UTI, Crohn’s. ectopic pregnancy, PUD

108
Q

Examining acute appendicitis?

A
  1. Rovsing’s sign: RIF>LIF - when LIF pressed
  2. Psoas sign: extending hip if retrocaecal appendix
  3. Obturator’s sign: pain on flexion and internal rotation on hip
  4. Decrease bowel sounds on Right
109
Q

Investigation of acute appendicitis?

A
  1. Blood tests - increase leukocytes, neutrophil count
  2. ESR and CRP
  3. US, CT
110
Q

How to treat appendicitis?

A
  1. Laparoscopic appendicectomy
  2. IV Abx - metronidazole and cefuroxime
  3. Decrease risk of wound infections
111
Q

Complications of appendicitis?

A

Perforation
Appendix mass
Appendix abscess

112
Q

What drugs can causes C. diff?

A

Clindamycin
Cephalosporins
Ciprofloxacin
Co-amoxiclav

113
Q

What causes mucosal damamge in C .diff infection?

A

Toxin A and B leading pseudomembranous colitis - yellow plaques from over damaged epithelium

114
Q

What is nosocomial diarrhoea?

A

Diarrhoea due to hospital cause

115
Q

Presentation of C .diff

A

Fever,
Diarrhoea
Crampy abdominal pain

116
Q

Treatment of C .diff?

A

Metronidazole
Vancomycin
Stool transplant

117
Q

Time frame of acute vs chronic diarrhoea infections?

A

2 weeks

118
Q

Clinical presentation of gastroenteric fever

A

Fever
RLQ pain
Bradycardia, headache, rose spots, constipation, diarrhoea

119
Q

Complications of gastroenteric fever?

A
  1. Myocarditis
  2. Peritonitis/ perforation
  3. GI bleed
  4. Abscess
120
Q

How to treat liver abscess

A

Albendazole + percutaneous aspiration injection repair

121
Q

The 4 ways in which intestinal obstruction can be classified?

A
  1. Site - large/small bowel/ gastric
  2. Mechanism - functional/ mechanical
  3. Extent of luminal obstruction - partial/complete
  4. Pathology - simple, closed loop, strangulation, intussusception
122
Q

What is a functional cause of intestinal obstruction?

A

Paralytic ileus - adynamic bowel due to absence of normal peristaltic contractions due to abdominal surgery/ acute pancreatitis
- No pain, constipation or vomiting

123
Q

What are some causes of intraluminal obstruction?

A
  1. Tumour
  2. Diaphragmatic disease
  3. Meconium ileus
  4. Gallstone ileus
124
Q

What are some diseases in the bowel wall which lead to acute obstruction?

A
  1. Inflammatory - crohn’s disease
  2. Diverticular disease
  3. Hirschsprung’s disease
125
Q

What is diverticular disease?

A

Herniation of mucosa through weakened walls where BV penetrate

126
Q

Causes of extraluminal obstruction

A
  1. Adhesions
  2. Volvulus
  3. Tumours
127
Q

Causes of SBO in children?

A
  1. Appendicitis
  2. Volvulus
  3. Intussusception
  4. Atresia
128
Q

Causes of SBO in adults?

A
  1. Adhesion
  2. Hernia
  3. Crohn’s
  4. Malignancy
129
Q

Dyspepsia is characterised by?

A
  1. Postprandial fullness
  2. Early satiation
  3. Epigastric pain or burning for >4 weeks
130
Q

Aetiology of malabsorption?

A
  1. Defective intraluminal digestion
  2. Defective epithelial transport
  3. Insufficient absorptive area
  4. Insufficient digestive enzymes
  5. Lymphatic obstruction
131
Q

Causes of defective intraluminal digestion

A
  1. Pancreatic insufficiency

2. Defective bile secretion - biliary obstruction/ileal resection

132
Q

Causes of insufficient absorptive area?

A
  1. Coeliac disease
  2. Crohn’s
  3. Giardia Lamblia - extensive surface parasitization of villi
  4. Surgery - small bowel resection
133
Q

Defective epithelial transport causes

A

Abetaliproteinaemia

Primary bile acid malabsorption

134
Q

Causes of insufficient digestive enzyme?

A
  1. Disaccharidase deficiency -lactose intolerance
135
Q

Causes of lymphatic obstruction

A
  1. Lymphoma

2. TB

136
Q

Causes of transudate ascites?

A
  1. Low protein conc - nephrotic syndrome, malnutrition, protein losing enteropathy
  2. Raised central venous pressure - congestive cardiac failure
  3. Portal hypertension - portal vein thrombosis/cirrhosis
137
Q

Causes of exudate ascites?

A
  1. Pancreatic ascites
  2. Peritoneal malignancy
  3. Budd Chiari syndrome
  4. Tubercular peritonitis
138
Q

Clinical presentation of ascites?

A
  1. Distended abdomen ~2L
  2. Full flanks/ shifting dullness
  3. Mild abdominal pain
  4. Constipation
  5. Itching due to jaundice?
139
Q

Diagnosis of ascites?

A
  1. Ascitic tap - ~20ml of fluid

- raised WCC, gram stain and culture, microscopy and cytology, amylase to exclude pancreatic ascites

140
Q

Treatment of ascites?

A
  1. Treat underlying cause
  2. Reduce Na intake and give aldosterone antagonist - spironolactone
  3. Paracentesis to drain 5L at a time
  4. Tranjugular intrahepatic portosystemic shunts
141
Q

What are secondary bile acids?

A

Bacterial metabolites of bile acids formed in the colon

142
Q

Cholestasis

A

Bile secretion obstruction

143
Q

Signs of cholestasis?

A
  1. Jaundice - cholestatic
  2. RUQ pain - intermittent/painless
  3. Itching
  4. Weight loss/Lethargy
144
Q

Tests of cholestasis?

A
  1. Obstructive blood test : alkphosphate raised, ALT raised, bilirubin raised
  2. Imaging:
    - a. US - dilated CBD - see stones, but not useful for obese patient
    b. MRCP - less radiation but complex images and claustrophobia
    c. CT - good for cancer, bad for stones, radiation
    d. Endoscopic US
    e. ERCP - diagnostic/not therapy!
145
Q

Risk factors for cholelithiases?

A
  1. Cholesterol
  2. Rapid weight loss
  3. Age
  4. OCP/Pregnancy
  5. Primary biliary cholangitis
    Crohn’s
146
Q

Presentation of cholelithiases

A
  1. Epigastric pain –> RUQ - biliary colic
  2. Radiation to shoulder/axilla
  3. Post prandial
  4. Nocturnal
    Most are ASYMPTOMATIC
147
Q

Treatment of cholelithiases?

A
  1. Laparoscopic cholecystectomy

2. Ursodeoxycholic acid: stone dissolution therapy

148
Q

Clinical presentation of AC?

A
  1. Biliary pain - progressive
  2. Sepsis signs
  3. Murphy’s signs
  4. Palpable GB
  5. Mirizzi syndrome
149
Q

Murphy’s signs?

A

Expiration hitches when hand on gall bladder due to pain

150
Q

How to test for AC?

A
  1. WBC/CRP
  2. Bilirubin, Alk Phos
  3. USS - thick walled GB with stones
  4. CBD dilatation - MRI
151
Q

Differential diagnosis for acute cholecystitis?

A
  1. Pancreatitis –> serum amylase
  2. Appendicitis –> localising pain
  3. PUD –> endoscopy
  4. Liver abscess –> ultrasound
  5. Pneumonia –> CXR
  6. MI –> ECG
  7. Perforated bowel –> CXR
152
Q

Complication of acute cholecystitis?

A
  1. Gangrene - perforation/abscess
  2. Empyema
  3. Chronic cholecystits
  4. Cholangitis
  5. Hydrops
  6. Porcelain gall bladder
153
Q

What is choledocolithiases

A

Common bile duct stone

154
Q

What is ERCP? Complications?

A
  1. Endoscopic retrograde cholangiopancreaticography

Complications: pancreatitis, bleeding, failure

155
Q

What are the functions of the peritoneum?

A
  1. Visceral lubrication
  2. Fluid and particulate absorption
  3. Pain perception
  4. Inflammatory and immune response
  5. Fibrinolytic activity
156
Q

Main causes of peritonitis?

A
  1. Bacterial - E.Coli, Klebsiella, staphylococci
  2. Chemical: bile, old clotted blood - leakage of intestinal contents, ruptured ectopic pregnancy
  3. Traumatic
  4. Ischaemia
  5. Miscellaenous
    Fx mediterannean fever
157
Q

Clinical features of localised peritonitis?

A
  1. Symptoms and signs of underlying conditions - abdominal pain, nausea, anorexia, vomiting
  2. Fever and worse abdominal pain, tachycardia
  3. Localised guarding, rebound tenderness, shoulder tip pain (subphrenic)
158
Q

Clinical features of diffuse early peritonitis?

A
  1. Abdominal pain
  2. Tenderness/ generalised guarding
  3. Infrequent bowel sounds
  4. Fever, tachycardia
159
Q

Clinical features of diffuse late peritonitis?

A
  1. No resolution/ localisation - rigid abdomen
  2. Distension due to paralytic ileus
  3. Absent bowel sounds
  4. Circulatory failure - cold clammy dry tongue
  5. Loss of consciousness
160
Q

Diagnose peritonitis?

A
  1. Urinary dipstick
  2. Blood test
  3. Serum amylase
  4. hCG/ ECG
  5. erect CXR
  6. Abdominal X ray
  7. CT abdomen
161
Q

Treatment of peritonitis?

A
  1. ABC
  2. Treat underlying cause.
  3. IV fluid
  4. Cefuroxime and metronidazole
  5. Urinary catheterisation +/- GI depression
  6. Specific treatment of cause:
    - extension of perforated region +/- drainage
162
Q

Complications of peritonitis?

A
  1. Delayed treament: toxaemia, septicaemia
  2. Local abscess formation
  3. Kidney failure
  4. Common pelvic/subphrenic - CT/US
  5. Paralytic ileus - obstruction of intestine due to paralysis of intestinal

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