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GI Flashcards

1
Q

Achalasia

Pathophysiology

A
  • Failure of oesophageal peristalsis
  • Failure of relaxation of lower oesophageal sphincter (LOS)
  • Degenerative loss of ganglia from Auerbach’s plexus
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2
Q

Achalasia

Likely population

A
  • Equally common in men and women

- Typically presents in middle-age

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3
Q

Achalasia

Features

A
  • Dysphagia of BOTH liquids and solids
  • Typically variation in severity of symptoms
  • Heartburn
  • Regurgitation of food: cough, aspiration pneumonia
  • Malignant change in small number
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4
Q

Achalasia

Investigations

A
  • Oeseophageal manometry: excessive LOS tone which doesn’t relax on swallowing
  • Barium swallow: shows grossly expanded oesophageal, fluid level. BIRDS BEAK APPEARANCE
  • CXR: wide mediastinum, fluid level
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5
Q

Achalasia

Tx

A
  • First-line = pneumatic (balloon) dilation
  • Surgical intervention -> heller cardiomyotomy (if recurrent or persistent symptoms)
  • Intra-sphincteric botulinum toxin if high surgical risk
  • Meds: Nitrates, CCBs - limited by side effects
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6
Q

Alcoholic ketoacidosis

Pathophysiology

A
  • Non-diabetic euglycaemic ketacidosis

- Alcoholic + not eating + vomiting leads to starvation and malnutrition, leading to body breaking down fat

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7
Q

Alcoholic ketoacidosis

Features

A
  • Metabolic acidosis
  • Elevated anion gap
  • Elevated serum ketones
  • Normal or low glucose
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8
Q

Alcoholic ketoacidosis

Management

A
  • Infusion of saline and thiamine

To avoid WE or Korsakoff

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9
Q

Appendicitis

Pathophysiology

A
  • Lymphoid hyperplasia causes obstruction of appendiceal lumen. Gut organisms invading the appendix wall leading to oedema, ischaemia +/- perforation.
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10
Q

Appendicitis

Presentation

A
  • Peri-umbilical abdominal pain, radiating to right iliac fossa
  • Worse on coughing or speed bumps
  • Children typically can’t hop on their right leg
  • Mild pyrexia (37.5 - 38)
  • Hunger
  • Nausea and vomit once or twice
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11
Q

Comparing appendicitis and mesenteric adentitis

A
  • Appendicitis causes a mild pyrexia, where as mesenteric adenitis is more likely to cause higher temperatures
  • Mesenteric adenitis is more common in children
  • Mesenteric adenitis often follows a recent viral infection and needs no treatment
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12
Q

Appendicitis

Examination findings

A
  • PR may cause right-sided tenderness
  • Rebound and percussion tenderness, guarding and rigidity (if perforation)
  • Rosving’s sign (palpation in LIF causes pain in RIF)
  • Psoas sign (pain on extending hip if retrocaecal appendix)
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13
Q

Appendicitis

Diagnosis

A
  • Raised inflammatory markers coupled with compatible history and examination
  • Neutrophil-predominant leucocytosis
  • Exclude pregnancy in women, renal colic and UTI
  • USS can help if see free fluid
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14
Q

Appendicitis

Management

A
  • Appendicectomy (open or laparoscopic)
  • Prophylactic IV Abx`- Cef and Met
  • Perforation requires copious abdominal lavage
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15
Q

Pernicious anaemia

Pathophysiology

A
  • Autoimmune disorder affecting the gastric mucosa, resulting in vitamin B12 deficiency
  • Antibodies to intrinsic factor +/- gastric parietal cells
  • No intrinsic factor produced
  • Blocks vitamin B binding sites
  • Therefore, reduced intrinsic factor leads to reduced B12 absorption
  • Not enough RBCs due to B12 deficiency
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16
Q

Pernicious anaemia

Risk factors

A
  • Female
  • Middle to older age
  • Autoimmune disorders: T1DM, RA, Thyroid, Addison’s, Vitiligo
  • Blood group A
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17
Q

Pernicious anaemia

Features

A

SLOW ONSET

  • Lethargy, pallor, dyspnoea
  • Lemon tinge to the skin (pallor and jaundice - unconjugated hyperbilirubinemia)
  • Sore tongue (glossitis)
  • PERIPHERAL NEUROPATHY
  • Weakness, ataxia, paraesthesia’s
  • Neuropsych: confusion, poor concentration, memory loss, depression
  • Can have a fever
  • Angular cheilitis
  • Brittle nails
  • Early grey hair
  • Tachycardia
  • Hypo/HTN
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18
Q

Pernicious anaemia

Blood film

A
  • Macrocytic anaemia
  • Normochromic
  • Hyper-segmented polymorphs
  • Low WCC and platelets
  • Megaloblasts
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19
Q

Pernicious anaemia

B12 levels

A

Normal is >= 200 nh

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20
Q

Pernicious anaemia

Investigations

A
  • FBC
  • B12 and folate serum levels (low)
  • Antibodies: anti-intrinsic factor and anti-gastric parietal cell
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21
Q

Pernicious anaemia

Sensitivity/specificity of tests

A
  • Anti intrinsic factor antibodies - low sensitivity but high specificity
  • Anti gastric parietal cell antibodies - low specificity, not often used clinically
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22
Q

Pernicious anaemia

Management

A

Vit B12 replacement (hydroxocobalamin)

  • Usually IM
  • No neurological features then 3 injections a week for 2 weeks, then 3 monthly
  • More frequent doses if neurological symptoms

Folic acid supplementation may also be required but NOT in B12 deficiency -> fulminant neuro deficit

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23
Q

Pernicious anaemia

Complications

A
  • Increased risk of gastric cancer
  • Subacute combined degeneration of the spinal cord
  • Delayed puberty and growth
  • Congestive heart failure
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24
Q

Iron-deficiency anaemia

Causes

A
  • Excessive blood loss (menorrhagia in pre-menopausal women, gastric bleeding in post-menopausal women and men - think colon cancer!!)
  • Inadequate dietary intake
  • Poor intestinal absorption (small intestine, e.g. coeliac)
  • Parasitic worms (Hook)
  • Increased iron requirements (pregnancy and children)
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25
Q

Iron-deficiency anaemia

Features

A
  • Fatigue, SOBOE, palpitations, pallor
  • Nail changes (koilonychia - spoon-shaped)
  • Hair loss
  • Atrophic glossitis
  • Post cricoid web
  • Angular stomatitis/cheilitis
  • Pale mucus membranes
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26
Q

Iron-deficiency anaemia

Investigations

A
  • FBC: hypochromic microcytic anaemia
  • Blood film: RBCs of different shapes and sized, target cells, pencil cells
  • de
  • LOW serum ferritin
  • Endoscopy to rule out malignancy
  • Low ferritin (but high would not rule out)
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27
Q

Iron-deficiency anaemia

Management

A
  • Identify and manage underlying cause
  • Exclude malignancy
  • Iron-rich diet: dark-green leafy veg, meat, iron-fortified bread

Oral ferrous sulfate

  • Continue taking for 3 months after anaemia corrected
  • SEs: nausea, abdo pain, constipation, diarrhoea
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28
Q

Iron-deficiency anaemia

Epidemiology

A
  • Most common anaemia worldwide

- Highest incidence is in preschool children

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29
Q

Coeliac disease

Pathophysiology

A
  • Autoimmune condition caused by sensitivity to gluten
  • Repeated exposure leads to villous atrophy which in turn leads to malabsorption
  • Villous atrophy and immunology normally reverses on a gluten-free diet
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30
Q

Coeliac disease

Common place

A

Jejenum

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31
Q

Coeliac disease

Associations

A

HLA-DQ2 and HLA-DQ8

  • Primary biliary cirrhosis
  • Primary sclerosing cholangitis
  • Autoimmune hepatitis
  • Dermatitis herpetiformis (vesicular, priuritis skin eruption)
  • T1DM - test all new cases of T1DM
  • IBS
  • Autoimmune thyroid disease
  • First-degree relatives with coeliac disease
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32
Q

Coeliac disease

Presentation

A
  • Diarrhoea
  • Persistent or unexplained GI symptoms including nausea and vomiting
  • Recurrent abdominal pain, cramping or distension
  • Prolonged fatigue
  • Weight loss
  • Iron-deficiency anaemia or other anaemia
  • Mouth ulcers
  • Children: failure to thrive of faltering growth
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33
Q

Coeliac disease

Who should be tested?

A
  • Dermatitis herpetiformis (vesicular, priuritis skin eruption)
  • T1DM - test all new cases of T1DM
  • IBS
  • Autoimmune thyroid disease
  • First-degree relatives with coeliac disease
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34
Q

Coeliac disease

Investigations

A

SEROLOGY

  • anti-TTG
  • anti-EMA

Endoscopic biopsy

  • Crypt hyperplasia
  • Villous atrophy
  • Increased intraepithelial lymphocytes
  • Lamina propria infiltration with lymphocytes
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35
Q

Coeliac disease

What do you need to consider when doing serological tests

x2 things

A

1) Some patients with coeliac have an IgA deficiency, so need to also test for total IgA because an IgA deficiency would produce a false negative coeliac test. You can also test for IgG versions of anti-TTG or anti-EMA or do a biopsy
2) If patients are already eating a gluten-free diet, they should reintroduce it for at least 6 weeks prior

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36
Q

Coeliac disease

Complications

A
  • Anaemia: iron, folate, vit B12
  • Hyposplenism
  • Osteoporosis/osteomalacia
  • Lactose intolerance
  • Enteropathy-associated T-cell lymphoma of small intestine (EATL)
  • Non-Hodgkin lymphoma (NHL)
  • Subfertility, unfavourable pregnancy outcomes
  • Rare: oesophageal cancer or other malignancies
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37
Q

Coeliac disease

Management

A
  • Lifelong gluten-free diet = essentially curative
  • Checking coeliac antibodies can be helpful in monitoring the disease
  • Patients with coeliac disease often have a degree offunctional hyposplenism
    • Therefore all coeliac patients are offered the pneumococcal vaccine and booster every 5 years
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38
Q

C. Diff

Pathophysiology

A
  • Gram positive rod
  • Develops when normal gut flora are supressed by broad spec Abx
  • Produces an exotoxin which causes intestinal damage, leading to pseudomembranous colitis
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39
Q

C. Diff

Causative Abx

A
  • Clindamycin
  • 2nd/3rd line cephalosporins
  • Quinolones
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40
Q

C. Diff

Features

A
  • Diarrhoea
  • Abdo pain
  • Raised WCC
  • Severe toxic megacolon
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41
Q

C. Diff

Classification

A

Mild: normal WCC

Moderate: WCC < 15 and 3-5 loose stools/day

Severe: WCC > 15 or raised creatinine (> 50% more) or temp >38.5 or severe colitis

Life-threatening: hypotension, partial or complete ileus, toxic megacolon, CT evidence of severe disease

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42
Q

C. Diff

Investigations

A
  • C. Diff toxin

- C. Diff antigen: glutamate dehydrogenase (GDH)

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43
Q

C. Diff

Management of first episode

A

First episode

  • Oral Vancomycin for 10 days
  • 2nd line fidaxomicin
  • 3rd line oral vanc +/- IV metronidazole
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44
Q

C. Diff

Management of recurrent episode

A
  • Within 12 weeks: Oral Fidaxomicin

- After 12 weeks: Oral Vancomycin OR Fidaxomicin

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45
Q

C. Diff

Management of life-threatening infection

A
  • Oral vancomycin AND IV metronidazole

- Specialist advice - surgery may be considered

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46
Q

H. pylori

Pathophysiology

A
  • Gram-negative bacteria

- Released bacterial cytotoxins causing disruption of gastric mucosa

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47
Q

H. pylori

Associations

A
  • Peptic ulcer disease
  • Gastric cancer
  • B cell lymphoma of MALT tissue
  • Atrophic gastritis
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48
Q

H. Pylori

Management

A

Eradication may be achieved with a 7-day course of

  • A proton pump inhibitor + amoxicillin + (clarithromycin OR metronidazole)
  • If penicillin-allergic: a proton pump inhibitor + metronidazole + clarithromycin
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49
Q

H. Pylori

Investigations

A

Urea breath test (13C)

  • Should not be performed within4 weeks of treatment with an antibacterial or within 2 weeks of an antisecretory drug (e.g. a proton pump inhibitor)
  • May be used to check for eradication

Others:

  • Rapid urease test
  • Serum antibody
  • Culture of gastric biopsy
  • Gastric biopsy
  • Stool antigen test
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50
Q

Ascites

Causes of high SAAG

A

Liver disorders = most common cause

  • Cirrhosis/alcoholic liver disease
  • Acute liver failure
  • Liver metastases

Cardiac

  • Right HF
  • Constrictive pericarditis

Other causes:

  • Budd-Chiari syndrome
  • Portal vein thrombosis
  • Veno-occlusive disease
  • Myxoedema
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51
Q

Ascites

Causes of low SAAG

A

Hypoalbuminemia

  • Nephrotic syndrome
  • Severe malnutrition

Malignancy

  • Peritoneal carcinomatosis

Infections

  • TB peritonitis

Other causes:

  • Pancreatitis
  • Bowel obstruction
  • Biliary ascites
  • Post-op lymphatic leak
  • Serositis in connect tissue diseases
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52
Q

Ascites

Management

A
  • Reduce dietary sodium
  • Fluid restriction is sometimes recommended if sodium < 125 mmol
  • Aldosterone antagonists, e.g. spironolactone
  • Drainage (large-volume paracentesis) if tense ascites, requires albumin cover
  • Prophylactic Abx to reduce risk of spontaneous bacterial peritonitis - Ciprofloxacin/norfloxacin
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53
Q

ERCP

Complications (4)

A
  • Excessive bleeding
  • Pancreatitis
  • Cholangitis
  • Duodenal perforation
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54
Q

Cholecystectomy

Complications (7)

A
  • Bleeding/infection/pain/scars
  • Damage to bile duct (leakage/strictures)
  • Stones left in bile duct
  • Damage to bowel, blood vessels, other organs
  • Anaesthetic risk
  • VTE
  • Post-cholecystectomy syndrome
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55
Q

Cholecystectomy

Post-cholecystectomy syndrome

A
  • Diarrhoea
  • Indigestion
  • Epigastric or right upper quadrant pain and discomfort
  • Nausea
  • Intolerance of fatty foods
  • Flatulence
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56
Q

Ascending cholangitis / Acute cholangitis

Pathophysiology

A

Infection and inflammation in the bile ducts

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57
Q

Ascending cholangitis / Acute cholangitis

The main causative organisms

A
  • Escherichia .coli
  • Klebsiella
  • Enterococcus
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58
Q

Ascending cholangitis / Acute cholangitis

Two main causes

A
  • Obstruction in the bile duct, e.g. gallstones

- Infection introduced by ERCP

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59
Q

Ascending cholangitis / Acute cholangitis

Features

A

CHARCOTS TRIAD

  • Fever
  • RUQ pain
  • Jaundice

+ Hypotension and Confusion (Reynold’s pentad)

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60
Q

Ascending cholangitis / Acute cholangitis

Investigations

A

Blood tests:

  • Raised inflammatory markers
  • Raised bilirubin

USS

  • Endoscopic = most sensitive
  • Abdo USS

Others

  • MRCP
  • CT scan
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61
Q

Ascending cholangitis / Acute cholangitis

Management

A
  • IV fluids, IV Abx, Cultures, NBM, involve seniors +/- HDU/ICU
  • ERCP within 1 week (ideally after 24-48 hrs)
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62
Q

Cholecystitis

Pathophysiology

A
  • Develops secondary to gallstones in 90% (calculous cholecystitis)
  • Other 10% = acalculous cholecystitis, caused by gallbladder stasis (ICU, severe illness, starvation), hypoperfusion or infection
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63
Q

Cholecystitis

Features

A
  • RUQ pain, may radiate to R shoulder
  • Fever
  • Murphy’s sign
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64
Q

Cholecystitis

Investigation

A
  • Raised inflammatory markers
  • LFTs typically normal
  • Abdo USS: thickened gallbladder wall, stones or sludge in gallbladder, fluid around gallbladder
  • MRCP or HIDA if more detail required
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65
Q

Cholecystitis

Management

A
  • IV fluids, IV Abx, NBM

- Laparoscopic cholecystectomy within 1 week, if not after 4+ weeks (after acute episode)

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66
Q

Gallstones

Risk factors

A

FOUR F’S

  • Fat
  • Fair
  • Female
  • Forty
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67
Q

Gallstones

Features

A
  • May be completely asymptomatic
  • If not, biliary colic
  • Worse after fatty foods
  • 30 mins - 8 hrs
  • Nausea and vomiting
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68
Q

Gallstones

Why fatty foods make it worse

A

Fat entering the digestive system causes cholecystokinin (CCK) secretion from the duodenum. CCK triggers contraction of the gallbladder, which leads to biliary colic. Patients with gallstones and biliary colic are advised to avoid fatty foods to prevent CCK release and gallbladder contraction.

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69
Q

Gallstones

Complications

A
  • Acute cholangitis
  • Acute cholecystitis
  • Pancreatitis
  • Obstructive jaundice
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70
Q

Gallstones

Investigations

A

LFTs:

  • Raised bilirubin - pale stools, dark urine
  • Raised ALP
  • May see slight raise in ALT and AST but if these are as raised/more raised than the ALP then you should consider a more hepatic picture

Imaging:

  • USS = first-line
  • MRCP if need to investigate further
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71
Q

Gallstones

Management

A

Asymptomatic gallstones located in the gallbladder = common and do not require treatment.

However, if stones are present in the common bile duct → in increased risk of complications such as cholangitis or pancreatitis → surgical management should be considered.

  • ERCP
  • Cholecystectomy
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72
Q

Primary sclerosing cholangitis

Pathophysiology

A
  • Inflammation, strictures and fibrosis of INTRA AND EXTRA-hepatic bile ducts
  • Causes obstruction to flow of bile
  • Sclerosis refers to the stiffening and hardening of the bile ducts
  • Cholangitis is inflammation of the bile ducts
  • May eventually lead to liver inflammation (hepatitis), fibrosis and cirrhosis
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73
Q

Primary sclerosing cholangitis

Risk factors

A
  • Male
  • Aged 30 - 40
  • Family history
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74
Q

Primary sclerosing cholangitis

Associations

A
  • UC (80% of those with PSC have UC)
  • Crohn’s
  • HIV
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75
Q

Primary sclerosing cholangitis

Features

A
  • Cholestasis -> jaundice, pruritus
  • RUQ pain
  • Fatigue
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76
Q

Primary sclerosing cholangitis

Investigations

A

LFTs:

  • Raised ALP
  • Raised bilirubin (later)

Immunology:

  • p-ANCA may be positive
  • Anti-ANA, Anti-aCL

Imaging:

  • MCRP: beaded appearance due to strictures
  • Liver biopsy: onion skin appearance
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77
Q

Primary sclerosing cholangitis

Management

A
  • Liver transplant can be curative, but about 80% survival at 5 years
  • Colestyramine - for pruiritis
  • Monitor for complications
  • ERCP
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78
Q

Primary biliary cholangitis/cirrhosis

Epidemiology

A

Middle-aged female

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79
Q

Primary biliary cholangitis/cirrhosis

Pathophysiology

A
    • Interlobular bile ducts become damaged by a chronic inflammatory process causing obstruction of outflow of bile → progressive cholestasis
  • Intralobar ducts are first to be damaged (Canals of Hering)
  • Back-pressure of bile obstruction may ultimately lead to fibrosis, cirrhosis and liver failure
  • Bile, bilirubin and cholesterol build up in the intestines, leading to the symptoms below
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80
Q

Primary biliary cholangitis/cirrhosis

Associations

A

Autoimmune conditions!

  • Sjogrens
  • RA
  • Systemic sclerosis
  • Thyroid disease
  • Coeliac disease
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81
Q

Primary biliary cholangitis/cirrhosis

Features

A
  • Bile: itching, RUQ pain
  • Bilirubin: jaundice, pale stools
  • Cholesterol: xanthelasma, increased risk of CVS disease
  • Hyperpigmentation
  • Stigmata of liver disease
  • Late - may progress to liver failure
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82
Q

Primary biliary cholangitis/cirrhosis

Investigations

A

LFTs:

  • Raised ALP
  • Other enzymes and bilirubin are raised in later disease

Immunology:

  • Anti-AMA !!!
  • ANA and SMA too

Bloods:

  • Raised IgG
  • Raised ESR

Imaging:
- MRCP or abdo USS

Liver biopsy:
- Diagnose and stage the disease

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83
Q

Primary biliary cholangitis/cirrhosis

Management

A
  • Ursodeoxycholic acid - slows disease progression and improves symptoms, reduces intestinal absorption of cholesterol
  • Cholestyramine - helps with pruiritis
  • Fat-soluble vitamin supplementation
  • Liver transplantation
    • E.g. if bilirubin > 100 (PBC is a major indication)
    • Recurrence in graft can occur but is not usually a problem
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84
Q

Primary biliary cholangitis/cirrhosis

Complications

A
  • Cirrhosis → portal hypertension → ascites, variceal haemorrhage
  • Osteomalaciaand osteoporosis
  • Significantly increased risk of hepatocellular carcinoma (20-fold increased risk)
  • Distal renal tubular acidosis
  • Hypothyroidism
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85
Q

Acute pancreatitis

Pathophysiology

A
  • Autodigestionof pancreatic tissue by the pancreatic enzymes, leading to necrosis
  • Gallstones: gallstones in ampulla of Vater blocks bile and pancreatic juice from flowing into duodenum → reflux of bile into pancreatic duct → prevention of pancreatic juices from being secreted → inflammation in pancreas
  • Alcohol: directly toxic to pancreatic cells → inflammation
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86
Q

Acute pancreatitis

All causes

A

I GET SMASHED

  • Idiopathic
  • Gallstones
  • Ethanol
  • Trauma
  • Steroids
  • Mumps (and other viruses)
  • Autoimmune
  • Scorpion poison
  • Hypercalcaemia, hypothermia, hypertriglyceridaemia, hyperchylomicronaemia
  • ERCP
  • Drugs (mesalazine, azathioprine, bendroflumethiazide, furosemide, pentamidine, steroids, sodium valproate)
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87
Q

Acute pancreatitis

Features

A
  • Severe epigastric pain
  • Radiating to back
  • Vomiting
  • Epigastric tenderness
  • Low-grade fever
  • Tachycardia

If haemorrhagic:

  • Grey-Turner’s sign (left flank bruising)
  • Cullens sign (periumbilical bruising)
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88
Q

Acute pancreatitis

Investigations

A

Can make clinical diagnosis if characteristic pain and SERUM AMYLASE/LIPASE (3x normal level)

  • USS for aetiology
  • Those needed for glasgow score - WBC, urea, transaminases, albumin, calcium, ABG for PaO2 and glucose
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89
Q

Acute pancreatitis

Glasgow scoring system

A

PANCREAS

  • PaO2 < 8kPa
  • Age > 55 yrs
  • Neutrophils (WBC > 15)
  • Calcium < 2
  • Renal - urea > 16
  • Enzymes (LDH > 600, AST/ALT > 200)
  • Albumin < 32
  • Sugar (glucose) > 10

0-1: Mild pancreatitis
2: Moderate pancreatitis
3+: Severe pancreatitis

90
Q

Acute pancreatitis

Management

A
  • ABCDE, fluids, analgesia (IV opioids)
  • Mod/severe to HDU/ICU
  • Enteral nutrition
  • Treat cause (gallstones - ERCP or cholecystectomy)
  • Offer Abx only if known infection
  • Necrosis: debridement, fine needle aspiration
  • Infected necrosis: radiological drainage, surgical necrosectomy
91
Q

Acute pancreatitis

Complications

A
  • Necrosis of the pancreas
  • Infection in a necrotic area
  • Abscess formation
  • Acute peripancreatic fluid collections
  • Pseudocysts (collections of pancreatic juice) can develop 4 weeks after acute pancreatitis
  • Chronic pancreatitis
  • Acute respiratory distress syndrome
92
Q

Autoimmune hepatitis

Types and epidemiology

A

Type I

  • Adults and children
  • Typically a middle-aged woman, after menopause with fatigue and liver disease stigmata

Type II

  • Children only
  • Typically teenage or early twenties present with acute hepatitis, high ALT/AST and jaundice
93
Q

Autoimmune hepatitis

Types and immunology

A

Type I

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

Type II

  • Anti-liver/kidney microsomal type 1 antibodies (LKM1)
  • Anti-liver cytosol antigen type 1 (anti-LC1)
94
Q

Autoimmune hepatitis

Associations

A
  • Other autoimmune conditions
  • Hypergammaglobulinemia
  • HLA B8 and HLA DR3
95
Q

Autoimmune hepatitis

Investigations

A
  • Raised AST and ALT (transaminases)
  • ANA/SMA/LKM1 antibodies
  • Raised IgG levels
  • Liver biopsy is diagnostic
96
Q

Autoimmune hepatitis

Features

A
  • Signs of chronic liver disease
  • Acute hepatitis: fever, jaundice (only 25% present like this)
  • Amenorrhoea - common
97
Q

Autoimmune hepatitis

Management

A
  • High dose steroids (Pred)
  • Other immunosuppressants, e.g. azathioprine
  • Liver transplantation
98
Q

Cirrhosis

Common causes

A
  • Alcoholic liver disease
  • NAFLD
  • Hep B and Hep C
99
Q

Cirrhosis

Other causes (7)

A
  • Autoimmune hepatitis
  • Primary biliary cirrhosis
  • Haemochromatosis
  • Wilsons disease
  • Alpha-1-antitrypsin deficiency
  • Cystic fibrosis
  • Drugs - amiodarone, methotrexate, sodium valproate
100
Q

Cirrhosis

Features

A
  • Jaundice
  • Hepatomegaly
  • Splenomegaly
  • Spider naevi
  • Palmar erythema
  • Gynaecomastia and testicular atrophy in males due to endocrine dysfunction
  • Bruising
  • Ascites
  • Caput medusae
  • Asterixis
101
Q

Cirrhosis

Investigations

A
  • LFTs can be normal, unless decompensated, where all markers become deranged (ALT, AST, ALP, bilirubin)
  • Albumin and PTT are useful markers of synthetic function of the liver
  • Hyponatraemia indicates fluid retention in severe liver disease
  • Every 6 months: USS and alpha-fetoprotein
  • Liver biopsy
  • Fibroscan (transient elastography)
  • If not NAFLD → enhanced liver fibrosis (ELF) blood test
  • Endoscopy: to look for varices
  • USS: nodularity of liver, corkscrew appearance of arteries, large portal vein with reduced flow
102
Q

Cirrhosis

Scoring systems and what for

A
  • Child-Pugh Score - measures severity and prognosis
  • MELD Score - measure mortality, may help in consideration of liver transplant

Both assess mortality

103
Q

Cirrhosis

Complications

A
  • Malnutrition - regular meals, low sodium, high protein and calorie, avoid alcohol
  • Portal Hypertension, Varices and Variceal Bleeding
  • Ascites and Spontaneous Bacterial Peritonitis (SBP)
  • Hepato-renal Syndrome
  • Hepatic Encephalopathy
  • Hepatocellular Carcinoma
104
Q

Crohn’s

Features

A
  • Non-specific features such as weight loss and lethargy
  • Abdo pain
  • Nausea and vomiting
  • Diarrhoea
  • Perianal disease, e.g. skin tags or ulcers
  • Extra-intestinal features, e.g. clubbing, skin, joint and eye problems
105
Q

Crohn’s

Investigations

A

Endoscopy w biopsy:

  • Granulomas
  • Transmural inflammation
  • Goblet cells
  • Skip lesions

Barium swallow:

  • Cobblestoning or terminal ileum
  • Rose thorn ulcers
  • Proximal bowel dilation
  • Kantor’s string sign
106
Q

Crohn’s

Where in bowel

A

Terminal ileum and proximal colon

But can be anywhere in GI tract

107
Q

Crohn’s

Management
Inducing remission

A
  • First-line = steroids (Pred)
  • 2nd line = Mesalazine

Others:

  • Azathioprine or Methotrexate (NOT as monotherapy)
  • Anti-TNF - e.g. Infliximab
  • NG tube feeding to improve growth
108
Q

Crohn’s

Management
Maintaining remission

A

1st line = Azathioprine or Mercaptopurine
Must assess thiopurine methyltransferase (TPMT) activity prior to commencing treatment

Alternatives:

  • Methotrexate
  • Infliximab
  • Adalimumab
109
Q

Crohn’s

Management
Surgery

A
  • When disease only affects distal ileum, is possible to resect this area to prevent further flares
  • Can have surgery to treat complications, e.g. strictures and fistulas
110
Q

Crohn’s

Complications

A
  • Small bowel cancer
  • Colorectal cancer
  • Osteoporosis - Vit D deficiency
111
Q

UC

Two peaks

A
  • 15-25 yrs

- 55-65 yrs

112
Q

UC

Where in bowel?

A
  • Always starts at the rectum (so most common place)
  • Never further than ileocaecal valve
  • Continuous and only superficial mucosa
113
Q

UC

Features

A
  • Rectal bleeding
  • Bloody diarrhoea
  • Colicky pain - LLQ
  • Urgency
  • Tenesmus
114
Q

UC

Risk factors for flares

A
  • Stress
  • Meds: NSAIDs/Abx
  • Cessation of smoking
115
Q

UC

Investigations

A

Endoscopy and biopsy:

  • Red, raw mucose that easily bleeds
  • Crypt hyperplasia/abscesses
  • Lymphocyte infiltration in lamina propria
  • Goblet cell depletion
  • Pseudopolyps
  • Glandular distortion
  • Widespread ulceration

Barium swallow:

  • Loss of haustrations
  • Superficial ulceration ( -> pseudopolyps)
  • Drainpipe/lead pipe colon
116
Q

UC

Classification of flares

A

The severity of UC is usually classified as being mild, moderate or severe:

  • Mild: < 4 stools/day, only a small amount of blood
  • Moderate: 4-6 stools/day, varying amounts of blood, no systemic upset
  • Severe: >6 bloody stools per day + features of systemic upset (pyrexia, tachycardia, anaemia, raised inflammatory markers)
117
Q

UC

Management
Inducing remission

A

Mild to moderate:

  • 1st line = Aminosalicylates, e.g. Sulfasalazine/Mesalazine
  • 2nd line = Corticosteroids

Severe:
Treat in hospital
- 1st line = IV corticosteroids
- 2nd line = IV ciclosporin

118
Q

UC

Management
Maintaining remission

A
  • Aminosalicylates - start with topical then change to PO if not improved after 4 weeks
  • Azathioprine or mercaptopurine

Methotrexate is not used in UC, unlike Crohn’s

119
Q

UC

Management
Surgery

A
  • Panproctocolectomy (removal of colon and rectum)

- Patient left with permanent ileostomy or ileo-anal anastomosis (J-pouch)

120
Q

Sideroblastic anaemia

Pathophysiology

A
  • RBCs fail to completely form haem, whose biosynthesis takes place partly in the mitochondrion
  • Iron can not be incorporated into Hb
  • Leads to deposits of iron in the mitochondria that form a ring around the nucleus called a ring sideroblast
  • May be congenital or acquired
121
Q

Sideroblastic anaemia

Causes

A

Acquired causes:

  • Myelodysplasia
  • Alcohol
  • Lead
  • Anti-TB medications

Congenital causes:

  • enzyme defect in haem synthesis
  • delta-aminolevulinate synthase-2 deficiency
122
Q

Sideroblastic anaemia

Features

A
  • Fatigue
  • Dizziness
  • Pallor
  • Hepatosplenomegaly
123
Q

Sideroblastic anaemia

Investigations

A
  • FBC: hypochromic microcytic anaemia
  • Iron studies: high serum ferritin, high serum iron, high transferrin saturation
  • Blood film: basophilic stippling of RBCs
  • Bone marrow biopsy/aspirate: Prussian blue staining will show ringed sideroblasts
124
Q

Sideroblastic anaemia

Management

A
  • Transfusion with desferrioxamine (chelating agent)
  • BM Tx
  • Pyridoxine
125
Q

Haemolytic anaemia

Pathophysiology

A

Anaemia due to the abnormal breakdown of RBC

126
Q

Haemolytic anaemia

Hereditary causes

A
  • Membrane: hereditary spherocytosis/elliptocytosis
  • Metabolism: G6PD deficiency, pyruvate kinase deficiency
  • Haemoglobinopathies: Sickle cell, thalassaemia
127
Q

Haemolytic anaemia

Acquired causes

A

Immune:

  • Warm-antibody: SLE, CLL, lymphoma
  • Cold-antibody: lymphoma, infectious mononucelosis
  • Transfusion reaction
  • Haemolytic disease of the newborn
  • Drugs:
    • Methyldopa
    • Penicillins and cephalosporins
    • Sulfonamides and sulfasalazine

Non-immune

  • Micrangipathic: TTP, HUS, DIC, malignancy, pre-eclampsia
  • Prosthetic heart valves
  • Hypersplenism
  • Paroxysmal nocturnal haemoglobulinuria (PNH) → dark urine in the MORNINGS
  • Infections: malaria
  • Drugs: Dapsone
128
Q

Haemolytic anaemia

Features

A
  • Fatigue
  • SOB
  • Children - FTT
  • Pallor
  • Jaundice
  • Dark urine (if restricted to morning → PNH)
129
Q

Haemolytic anaemia

Investigations

A
  • Increased bilirubin
  • Blood smear: schistocytes, spherocytes, bite cells
  • Coombs test +ve
  • LDH +ve
130
Q

Haemolytic anaemia

Management

A
  • Folate and/or iron supplements
  • If autoimmune → Prednisolone then Azathioprine
  • Splenectomy if spherocytosis
131
Q

What is Coombs Test?

A
  • Blood sample from a patient with an immune mediated haemolytic anaemia: identifies antibodies on RBC surface
  • Mixed with antihuman antibodies (Coombs reagent) which bind to human antibodies
  • Demonstrates an immune cause of the anaemia
132
Q

Which parts of the intestines are in the intraperitoneal space?

A

FIRST

F: First part of duodenum
I: Intestine - small
R: Rectum
S: Sigmoid colon
T: Transverse colon
133
Q

Which parts of the intestines are in the retroperitoneal space?

A

DADA

D: Distal duodenum
A: Ascending colon
D: Descending colon
A: Anal canal

134
Q

Four layers of intestinal wall

A

From out to in:

  • Serosa (if intraperitoneal) or adventitia (if retro)
  • Muscularis (contracts for peristalsis)
  • Submucosa (dense layer of tissue containing blood vessels, lymphatics and nerves)
  • Mucosa (surrounds lumen, direct contact with digested food - intestinal glands within)
135
Q

Most common type of colorectal cancer?

A

Adenocarcinoma

136
Q

Colorectal cancer

Predisposing factors

A
  • Sporadic mutations
  • Neoplastic polyps
  • Genetic predisposition - FAP and HNPCC
    • Familial adenomatous polyposis
    • Hereditary nonpolyposis colorectal Ca
  • IBD
  • Elderly
  • Male
  • Previous cancer
  • Alcohol excess
  • Smoking
  • Diet (low fibre, high red meat)
  • Obesity
137
Q

What is FAP?

A

Familial adenomatous polyposis

  • Autosomal dominant
  • Mutation in the adenomatous polyposis coli gene (APC) = a tumour suppressor gene
  • Normally identifies when a cell is undergoing a lot of mutations and targets the cell and causes it to undergo apoptosis (cell death)
  • If mutation - the mutating colon cells do not die, and divide uncontrollably and form polyps
  • Over time accumulate and may even lead to more mutations in other tumour suppressor genes (e.g. K-RAS, p53)
  • Can become a malignant adenomas and invade neighboring tissues
  • 100% lifetime risk of colorectal cancer
  • Patients have their entire large intestine removed prophylactically to prevent the development of bowel cancer (panproctocolectomy)
  • Also associated with gastric, duodenal polyps and abdominal desmoid tumours
138
Q

What is HNPCC / Lynch Syndrome

A
  • Hereditary nonpolyposis colorectal cancer
  • Also known as Lynch Syndrome
  • Autosomal dominant
  • Results from mutations in DNA mismatch repair (MMR) genes
  • Higher risk of a normal of cancers, but particularly colorectal
  • Increased risk of extracolonic malignancies (e.g. endometrial, gastric)
  • Unlike FAP, does not cause adenomas and tumours develop in isolation
  • Usually right-sided tumours
139
Q

Red flags for bowel cancer

A
  • Change in bowel habit (usually to more loose and frequent stools)
  • Unexplained weight loss
  • Rectal bleeding
  • Unexplained abdominal pain
  • Iron deficiency anaemia (microcytic anaemia with low ferritin)
  • Abdominal or rectal mass on examination
140
Q

Two week wait referral criteria for lower GI tract cancer

A
  • > 40 yrs with unexplained weight loss AND abdo pain
    OR
  • > 50 yrs with unexplained rectal bleeding
    OR
  • > 60 yrs with iron-deficiency anaemia OR changes in bowel habits (iron deficiency - colonoscopy AND gastroscopy)
    OR
  • Test shows blood in faeces (FIT)
141
Q

When might you consider a two-week wait referral for lower GI tract cancer?

A
  • Rectal or abdo mass
  • unexplained anal mass or anal ulceration
  • > 50 yrs with rectal bleeding AND one of:
    • abdo pain
    • change in bowel habit
    • weight loss
    • iron deficiency anaemia
142
Q

Screening for colon cancer

A
  • Screening every 2 yrs to all men and women 60 - 74 yrs

- FIT test in post (a type of faecal occult blood test)

143
Q

When might you do a FIT test?

A

In patients with new symptoms who do not meet the 2-week criteria

144
Q

Most common locations of colorectal cancer?

A
  1. Rectal
  2. Sigmoid colon
  3. Ascending and caecum
  4. Transverse colon
  5. Descending colon
145
Q

Colorectal cancer

Presentation of ascending

A

Typically grows beyond the mucosa, therefore can grow large before it is detected (late presentation)

  • Weight loss
  • Low Hb (microcytic anaemic)
  • Abdo pain
  • Obstruction = UNLIKELY
146
Q

Colorectal cancer

Presentation of descending

A

Tend to be infiltrating ring-shaped masses including the whole circumference of bowel wall - “napkin-ring constriction” of the lumen

  • Colicky abdo pain
  • Bleeding/mucus PR
  • Altered bowel habits
  • Tenesmus
  • PR mass
  • Obstruction = LIKELY
147
Q

Colorectal cancer

Investigations

A
  • FIT (a faecal occult test)
  • FBC - microcytic anaemia
  • Raised CEA (but not specific)
  • Barium enema: apple core sign if descending
  • Colonoscopy and biopsy
  • DNA test for FAP
  • Staging CT TAP
148
Q

Colorectal cancer

Management

A
  • Surgery (resection) = only cure
  • Different types of resection based on location of tumour
  • Adjuvant chemo
  • Radiotherapy used in palliative care
149
Q

Site, type of resection and type of anastomosis in colorectal cancers

A

Caecal, ascending, proximal transverse:

  • Right hemicolectomy
  • Ileo-colic anastomosis

Distal transverse and descending:

  • Left hemicolectomy
  • Colo-colon anastomosis

Sigmoid colon:

  • High anterior resection
  • Colo-rectal anastomosis

Rectum:

  • Anterior resection
  • Colo-rectal anastomosis (+/- defunctioning stoma is low rectum)

Anal verge:

  • Abdomino-perineal excision of rectum, suture over anus
  • Permanent colostomy
150
Q

Emergency management of perforated bowel in colorectal cancer?

A
  • Hartmann’s procedure
  • Removal of the rectosigmoid colon and creation of an colostomy
  • The rectal stump is sutured closed
  • The colostomy may be permanent or reversed at a later date
  • End colostomy instead as risk of perforation of an anastomosis
151
Q

Staging of colorectal cancer

A
  • CT of whole chest/abdo/pelvis
  • Whole colonoscopy or CT colonography
DUKE'S STAGING + prognosis
A: Limited to mucosa (95% 5yr)
B: Invading bowel wall (80% 5yr)
C: Lymph node mets (65% 5yr)
D: Distant mets (5% 5yr)
152
Q

Screening in FAP

A
  • Annual flexible sigmoidoscopy from 15 years

- If no polyps found then 5 yearly colonoscopy started at age 20

153
Q

Screening in HNPCC

A
  • Colonoscopy every 1-2 years from age 25
  • Consideration of prophylactic surgery
  • Extra colonic surveillance recommended
154
Q

Peptic ulcer disease

Investigations

A
  • 13C-urea test for H.pylori
  • ## Stool antigen test
155
Q

Colorectal cancer

Follow up after surgery

A

Every 3 years (for example):

  • Serum carcinoembryonic antigen (CEA)
  • CT thorax, abdomen and pelvis
156
Q

Peptic ulcer disease

Risk factors

A
  • Drugs: NSAIDs, steroids, SSRIs, bisphosphonates
  • H. pylori
  • Excess gastric acid (stress, alcohol, smoking, caffeine, spicy food)
  • Blood group O
  • Zollinger-Ellison syndrome
157
Q

Peptic ulcer disease

Presentation

A
  • Epigastric discomfort or pain
    • Worse when eating = gastric
    • Worse when hungry, relieved by eating = duodenal
  • Nausea and vomiting
  • Dyspepsia
  • Bleeding
  • Iron deficiency anaemia (usually incidental finding)
158
Q

Which is the most common peptic ulcer?

159
Q

Peptic ulcer disease

Investigations

A
  • 13-C urea breath test or stool antigen test for H.pylori
  • OGD, if do then can do rapid urease test for H. pylori
  • Biopsy during OGD to exclude malignancy - cancers can look similar to ulcers
160
Q

Peptic ulcer disease

Management

A

If H.pylori -ve:
- High dose PPIs

If H.pylori +ve:
- Metronidazole + Clarithromycin + Omeprazole

161
Q

Peptic ulcer disease

Complications

A
  • Bleeding from ulcer - common and potentially fatal
  • Perforation –> acute abdo (peritonitis) –> urgent surgical repair
  • Scarring and strictures –> may lead to narrowing of pylorus (pyloric stenosis) = upper abdo pain, reflux, distension, N+V, all worse after eating
162
Q

Oesophageal cancer

Types (Location and RFs)

A

Adenocarcinoma:

  • Lower third of oesophagus
  • RFs: GORD, Barretts, Smoking, Achalasia, Obesity

Squamous cell carcinoma:

  • Upper two thirds
  • RFs: smoking, alcohol, achalasia, plummer-vinson syndrome, diets rich in nitrosamines (FISH)
163
Q

Oesophageal cancer

Presentation

A
  • Dysphagia
  • Anorexia and weight loss
  • Vomiting
  • Odynophagia (painful swallowing)
  • Hoarseness (upper 3rd - SCC)
  • Melaena
  • Cough (upper 3rd, SCC)
164
Q

Oesophageal cancer

Investigations

A
  • Upper GI endoscopy
  • Endoscopic US - better for assessing mural invasion
  • CT TAP for staging
165
Q

Oesophageal cancer

Management

A
  • Surgical resection, most common = Ivor-Lewis type oesophagectomy
  • Adjuvant chemotherapy (cisplatin)
  • If surgery not indicated –> chemo > radio
  • Palliation aims to restore swallowing with chemo/radio, stenting, laser
166
Q

Anal fissure

Risk factors

A
  • Constipation
  • IBD
  • Sexually transmitted infection, HIV, syphilis, herpes
167
Q

Anal fissure

Features

A
  • Painful, bright red, rectal bleeding
  • 90% occur in posterior midline !!
  • If alternative location –> consider other underlying causes, eg. Crohn’s disease
168
Q

Anal fissure

Management of acute (< 1 week)

A
  • Soften stool: high fibre, high fluid intake
  • Bulk-forming laxatives are first line, lactulose if not tolerated
  • Lubricants, e.g. petroleum jelly prior to defecation
  • Topical anesthetics
  • Analgesia
169
Q

Anal fissure

Management of chronic

A
  • Above techniques continued
  • Topical GTN = first-line
  • If not effective after 8 weeks then 2ndry care referral to consider for sphincterotomy or botulinum toxin
170
Q

Diverticulum

Pathophysiology

A
  • In the large intestine wall, there is a layer of muscle called circular muscle
  • Where the blood vessels penetrate this are areas of weakness
  • Increased pressure in the lumen over time can cause a gap to form in these areas of circular muscle
  • The gap allows mucose to herniate through to form diverticula
  • Diverticula do not form in rectum because there is longitudinal muscle that completely surrounds the diameter
  • In the large bowel, there are three longitudinal muscles forming strips called teniae coli, so between these are vulnerable to diverticula
171
Q

Diverticulum

Define diverticula

A

Outpouching of the gut wall, usually at sites of penetrating arteries

172
Q

Diverticulum

Define diverticulosis

A

The presence of diverticula, but asynmptomatic

173
Q

Diverticulum

Define diverticular disease

A

When the diverticular become symptomatic, but no inflammation

174
Q

Diverticulum

Define diverticulitis

A

When the diverticula become inflamed, usually when faeces obstruct the neck

175
Q

Diverticulosis

Risk Factors

A
  • Low fibre diets = MOST COMMON
    • High intraluminal pressure forces the mucosa to herniate out
  • Increasing age
  • Obesity
  • NSAID use
  • Smoking
176
Q

Diverticular disease

Symptoms

A
  • Altered bowel habits
  • Rectal bleeding
  • Left-sided colic, relieved by defication
  • Nausea
  • Flatulence
177
Q

Diverticular disease

Diagnosis

A
  • Colonoscopy
  • CT cologram
  • Barium enema
178
Q

Diverticular disease

Management

A

No management needed if asymptomatic (diverticulosis)

  • Increase fibre intake - first-line
  • Bulk-forming laxatives
  • AVOID stimulant laxatives
179
Q

Diverticular disease

Complications

A
  • Diverticulitis
  • Haemorrhage
  • Development of fistula
  • Perforation and faecal peritonitis
  • Perforation and development of abscess
  • Development of diverticular phlegmon
180
Q

Diverticulitis

Presentation

A

Same as diverticular disease PLUS:

  • Pyrexia
  • High WCC and CRP
  • Tender colon
  • Peritonitis
  • LEFT LOWER QUADRANT pain
  • Nausea and vomiting
  • Constipation
  • Urinary frequency/urgency/dysuria (due to irritation of bladder by inflamed bowel)
  • PR bleeding
181
Q

Diverticulitis

Diagnosis

A
  • FBC (raised WCC)
  • Raised CRP
  • Erect CXR: pneumoperitoneum in perforation
  • AXR: dilated bowel loops, obstruction, abscesses
  • CT = best modality for suspected abscesses
  • Colonoscopy - AVOID due to risk of perforation
182
Q

Diverticulitis

Management if mild

A
  • Oral Co-Amoxiclav for 5 days at least
  • Analgesia - avoid NSAIDs and opioids if poss
  • Clear liquids diet until symptoms improve
  • Follow-up within 2 days
  • If not better within 72 hrs –> admit
183
Q

Diverticulitis

Management if severe

A
  • NBM, clear fluid only
  • IV Abx
  • IV fluids
  • Analgesia
  • Urgent CT
  • Urgent surgery if complications
184
Q

Diverticulitis

Complications

A
  • Perforation
  • Peritonitis
  • Peridiverticular abscess
  • Large haemorrhage requiring tranfusion
  • Fistula (between colon and bladder/vagina)
  • Ileus/obstruction
185
Q

Which artery is most likely to be damaged by duodenal ulcer?

A

gastroduodenal artery

186
Q

3 layers of gastric mucosa?

A

Epithelial layers:
- Absorbs/secretes mucus and digestive enzymes

Lamina propria:

  • Blood
  • Lymph vessels
  • MALT (lymphocytes that eliminate pathogens)

Muscularis mucosa:
- Contrast and helps to breakdown food

187
Q

Role or parietal cells?

A

Secrete hydrochloric acid to maintain pH of stomach

188
Q

Role of chief cells?

A

Secrete pepsinogen

189
Q

Role of G-cells?

A

Secrete gastrin

- Stimulate parietal cells to secrete HCl

190
Q

Gastric cancer

Risk factors

A
  • Smoking
  • H.Pylori
  • Blood group A
  • Increasing age
  • Male
  • Nitrosamine rich diet
  • Diet: high salt, high pickles, low Vit C, high nitrates
  • Fx
  • Pernicious anaemia
191
Q

Gastric cancer

Types

A
  • Adenocarcinoma (gland cells)
    • Intestinal (well-differentiated)
    • Diffuse (undifferentiated) - CDH1 mutation, more likely to metastasize
  • Lymphoma (leukocytes)
  • Carcinoid tumour (G-cells)
  • Leiomyosarcoma (smooth muscle)
192
Q

Where is gastric cancer most likely to be?

193
Q

Gastric cancer

Presentations

A
  • Can be asymptomatic
  • Starts with vague malaise, poor appetite, epigastric pain
  • Weight loss, anorexia
  • Nausea and vomiting
  • Dysphagia (if cancer arises in proximal stomach)
  • Anaemia
  • Dyspepsia
  • Acanthosis nigrans

If to lymph nodes:

  • VIRCHOWS NODE (troisiers signs) = left supraclavicular node
  • SISTER MARY JOSEPH NODE (periumbilical)
194
Q

Gastric cancer

Investigations

A
  • Gastroscopy and biopsy (at multiple points on ulcer)
    • WIll see SIGNET RING CELLS
    • The more, the worst the prognosis
  • Staging = CT TAP
195
Q

Gastric cancer

Management

A
  • Surgery, depends on extent:
    • Endoscopic mucosal resection
    • Partial gastrectomy
    • Total gastrectomy
  • Chemotherapy
196
Q

What is MALT lymphoma?

A
  • Lymphoma associated with H. pylori infection in 95% of cases
  • Good prognosis
  • If low grade then 80% respond to H. pylori eradication
  • paraproteinaemia may be present
197
Q

Vit A deficiency sign

A

Night blindness

198
Q

Vit D deficiency sign

A

Hypocalcaemia

199
Q

Vit E deficiency sign

A

Neurological deficits and ataxia

200
Q

Vit K deficiency sign

A

Prolonged PT/APTT

201
Q

Haemochromatosis

Genetics

A
  • Autosomal recessive

- Mutation in HFE gene on SHORT arm of chromosome 6

202
Q

Haemochromatosis

What is it

A

Iron overload

203
Q

Haemochromatosis

Features

A

Usually presents > 40 yrs as takes a while for iron to build up so high that it causes symptoms. Can be older for women due to menstruation regularly removing iron from the body.

  • Fatigue
  • Joint pain
  • Bronze skin colour
  • Cognitive issues - memory and mood
  • Hair loss
  • Amenorrhoea
  • Erectile dysfunction
204
Q

Haemochromatosis

Diagnosis

A
  • Serum ferritin - high (though is an acute phase reactant in inflammation so not reliable)
  • Transferrin saturation - high (more accurate, only raised in iron overload)
  • If both positive, can confirm with gene testing (HFE)
  • Previously did liver biopsy and Perl’s stain –> prussian blue, shows iron in liver
  • MRI for heart and liver deposits
  • CT abdo: increased attenuation in liver
205
Q

Haemochromatosis

Management

A
  • Venesection - each week to remove blood (+ iron)

- If intolerant: desferrioxamine (binds iron to aluminium to remove it)

206
Q

Haemochromatosis

Complications

A
  • T1DM
  • Liver cirrhosis –> hepatocellular carcinoma
  • Chondrocalcinosis –> arthritis
  • Hypogonadism –> erectile dysfunction/amenorrhoea
  • Cardiomyopathy
  • Hypothyroidism
207
Q

Wilson’s Disease

Genetics

A
  • ATP7B gene on chromosome 13

- Autosomal recessive

208
Q

Wilson’s Disease

Presentation

A
  • Grey skin
  • Blue nails
  • Kayser Fleischer rings in eyes
    Accumulation in:
  • Liver –> cirrhosis and liver failure
  • Brain –> psychosis and psychiatric problems
  • Basal ganglia –> symmetrical parkinsons, ataxia, chorea
  • Kidney –> renal tubular acidosis
209
Q

Wilson’s Disease

Investigations

A
  • Slit lamp examination for Kayser Fleischer rings
  • Serum caeruloplasmin - high
  • Serum copper - decreased
  • 24 hr urine copper
  • Definitive = liver biopsy for copper deposits
  • MRI brain - basal ganglia deposits
  • Genetic testing
210
Q

Wilson’s Disease

Management

A
  • Copper chelation:
    • Penicillamine or Trientine
  • Avoid copper-rich foods
211
Q

Gilbert’s Syndrome

What is it

A

Gilbert’s syndrome is an autosomal recessive* condition of defective bilirubin conjugation due to a deficiency of UDP glucuronosyltransferase

212
Q

Gilbert’s Syndrome

Features

A
  • unconjugated hyperbilirubinaemia (i.e. not in urine)

- jaundice may only be seen during an intercurrent illness, exercise or fasting

213
Q

Gilbert’s Syndrome

Investigations

A

Rise in bilirubin following prolonged fasting or IV nicotinic acid

214
Q

Gilbert’s Syndrome

Management

A

No treatment required

215
Q

Alpha-1-antitrypsin disorder

Patho

A
  • Elastase is secreted by neutrophils
  • This enzyme digests connective tissues
  • Alpha-1-antitrypsin (A1AT) is produced mainly in liver, travels around body, and offers protection by inhibiting neutrophil elastase enzyme
  • If deficiency –> liver and lungs are affected
216
Q

Alpha-1-antitrypsin disorder

Genetics

A
  • Autosomal recessive
  • Defect in chromosome 14
  • Normal = PiMM
  • Mutation = PiMZ or PiZZ (PiZZ is symptomatic)
217
Q

Alpha-1-antitrypsin disorder

Liver problems

A
  • Normally A1AT is created in liver
  • An abnormal mutant version is produced in A1AT deficiency
  • This gets trapped in liver, builds up and causes damage
  • Over time can lead to cirrhosis and hepatocellular carcinoma
218
Q

Alpha-1-antitrypsin disorder

Lung problems

A
  • Lack of normal functioning A1AT leads to an excess of PROTEASE enzymes that attack the connective tissue in th elungs
  • Leads to bronchiectasis and emphysema
  • Most marked in LOWER lobes
219
Q

Alpha-1-antitrypsin disorder

Investigations

A
  • A1AT concentrations = LOW (screening test of choice)
  • Liver biopsy = acid-Schiff-positive staining globules
  • Genotyping
  • High-resolution CT thorax
  • Spirometry = obstructive picture
220
Q

Alpha-1-antitrypsin disorder

Management

A
  • Stop smoking (drastically accelerate emphysema)
  • Symtomatic management
  • NICE advice against replacement of A1AT
  • Organ transplant for end-stage liver or lung disease
  • Monitor for complications, e.g. hepatocellular carcinoma
  • Lung volume reduction surgery

Finals (21 decks)

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