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Gastrointestinal Flashcards

1
Q

What is Wilson’s disease

A

It is an autosomal recessive disorder characterised by a reduced biliary excretion of copper and thus, accumulation of copper in the liver and brain. ATP7B Mutations

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2
Q

Who is usually affected by Wilson’s disease

A

Liver disease usually presents in children

Neurological disease usually presents in young adults

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3
Q

What are the signs and symptoms of Wilson’s disease

A

Liver

  • Jaundice
  • Easy bruising
  • Variceal bleeding
  • Encephalopathy
  • Hepatosplenomegaly
  • Ascites/Oedema
  • Gynaecomastia

Neurological (6Ds)

  • Drooling
  • Dementia
  • Dystonia
  • Dysarthria
  • Dysphagia
  • Dyskinesis
  • Ataxia
  • Rigidity
  • Tremor

Psychiatric

  • Conduct disorder
  • Personality change
  • Psychosis

Eyes
- KF Rings

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4
Q

What are the appropriate investigations for Wilson’s disease

A

LFTs - Abnormal
Serum Copper - Elevated

24hr Urine Copper - Elevated
Liver biopsy - Increased copper content
Genetic analysis

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5
Q

What is a Volvulus

A

Rotation of a loop of small bowel around the axis of its mesentery causing bowel obstruction and potential ischaemia

65% Sigmoid
30% Caecum

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6
Q

What are risk factors for Volvulus

A

Long sigmoid
Long mesentery
Mobile caecum

Chronic constipation
Adhesions
Chagas disease
Parasitic infection

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7
Q

What are the signs and symptoms of Volvulus

A

Severe colicky pain & swelling & tenderness
Absolute constipation
Vomiting

Hx of transient attacks in which spontaneous reduction of the volvulus has occurred

Absent or tinkling bowel sounds
Fever
Tachycardia
Signs of dehydration

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8
Q

How is Volvulus investigated

A

AXR
Erect CXR - If perforation is suspected
Water soluble contrast enema - Shows site of obstruction

CT scan

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9
Q

What are the risk factors for Rectal prolapse

A

Straining
Abnormal rectal anatomy or physiology

Constipation
Cystic fibrosis
Previous trauma to the anus/perineum
Neurological conditions

Biphasic distribution

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10
Q

What are signs and symptoms of Rectal prolapse

A

Initially associated with defecation
Faecal incontinence
PR mucus or bleeding

Strangulating emergency
Reduced anal sphincter tone

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11
Q

What are the appropriate investigations in Rectal prolapse

A

Imaging: Proctosigmoidoscopy + Defacting proctogram or barium enema

Anal sphincter manometry
Pudendal nerve studies

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12
Q

Define the 4 main types of Viral Hepatitis

A

Hep A & E: Can only cause acute infection
Hep B & D: Can cause acute and chronic disease with D only being able to infect when B is present
Hep C: Can cause an acute course and in most cases progresses to a chronic course

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13
Q

Describe the causes and distribution of HAV and HEV

A

HAV is caused by picornavirus
HEV is caused by calicivirus

They are both transmitted faecal-orally

HAV is endemic in the developing world and infection often occurs sub-clinically - Acquired by travellers
HEV is endemic in Asia, africa and central America - Causes fulminant hepatitis in pregnancy

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14
Q

Describe the causes and distribution of HCV

A

This is an ss-RNA virus. Many genotypes

It is transmitted parenterally (Sexual transmission, Childbirth, IDUs, Exposure to needles)

Different genotypes have different geographical prevalences

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15
Q

Describe the causes and distribution of HBV and HDV

A

HBV is a ds-DNA virus
HDV is a ss-RNA virus

HBV is transmitted parenterally (Sexual transmission, Childbirth, IDUs, Exposure to needles)

Common in South east Asia, Africa and the mediterranean

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16
Q

What are the signs and symptoms of HAV and HEV

A

Incubation period of 2-6 weeks

Malaise
Fever
Anorexia
N&V

  • Dark Urine (High CB & UBG)
  • Acholic stools
  • Jaundice lasting 3 weeks
  • Pruritus
  • RUQ pain
  • Hepatosplenomegaly
  • Arthralgia and skin rash
  • No stigmata of chronic liver disease
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17
Q

What are investigative findings of HAV and HEV

A

Bloods
LFTs: High ALT, AST, ALP & Bilirubin + Low Albumin
FBC: High platelets

Serology
HAV:
- IgM - During acute illness (Present 3-4 weeks after exposure and Disappears after 3-6 months)
- IgG - Recovery phase and life-long persistence (Sign of previous infection or vaccination)
HEV:
- IgM - During acute illness (Present 1-4 weeks after exposure)
- IgG - Recovery phase and life-long persistence (Sign of previous infection)

Urinalysis
Bilirubin and UBG

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18
Q

How is HAV and HEV managed

A

No specific management it is just supportive.

Anti-pyretics, Anti-emetics, Cholestyramine (Foe pruritus)

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19
Q

What are complication of HAV and HEV

A
  • Cholestatic hepatitis - Pruritus, Diarrhoea, Weight loss, Malabsorption
  • Fulminant hepatitis
  • Relapsing HAV
  • Post-hepatitis syndrome
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20
Q

What are the signs and symptoms of HCV

A

90% of acute infections are asymptomatic

10% become jaundiced with

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21
Q

What are investigative findings of HCV

A

a

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22
Q

How is HCV managed

A

a

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23
Q

What are the complications of HCV

A

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24
Q

What are the signs and symptoms of HBV and HDV

A

a

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25
Q

What are investigative findings of HBV and HDV

A

a

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26
Q

How is HBV and HDV managed

A

a

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27
Q

What are the complications of HBV and HDV

A

a

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28
Q

What is a Pilonidal sinus

A

This is an epithelium-lined tract filled with hair that opens onto the skin surface - Commonly in the natal cleft

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29
Q

What causes the formation of a Pilonidal sinus

A

It caused by shed or sheared hairs penetrating the skin and inciting an inflammatory reaction

RFs include:

  • Hirsutism
  • Spending a long time siting down
  • Occupational
  • Diabetics
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30
Q

What are the signs and symptoms of Pilonidal sinuses

A

Painful natal cleft
Discharging swelling- Hair
Tender if infected

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31
Q

How is a Pilonidal sinus treated

A

Acute - Incision and drainage
Chronic - Excision under GA with exploration
Prevention - Good hygiene + Shaving

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32
Q

What is a Perineal abscess and fistula

A

Perineal abscess: A pus collection in the perineal region

Perineal fistula: An abnormal connection between the epithelial surface of the outer and inner anus

Fistula develop as a complication of an abscess

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33
Q

What are risk factors for Perineal abscess and fistulae

A

Crohn’s disease - Pepper pot perineum
IBD
DM
Malignancy

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34
Q

What are the signs and symptoms of Perineal abscess and fistulae

A
  • Constant throbbing pain in the perineum - Tender
  • Intermittent discharge (Mucus/feacal staining) near he anal region
  • FHx/Hx IBD
  • Small skin lesion near the opening of the anus

DRE - Thickened area over the abscess/fistula

Goodsall’s Law

  • Anterior <3cm will run directly into the anal canal
  • Posterior or >3cm will follow a curved path and open in the posterior midline
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35
Q

How would the Perineal abscess and fistulae be imaged without surgical exploration

A

CT/MRI

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36
Q

How are Perineal abscess and fistulae treated

A

Surgical treatment
Open drainage of abscess
Laying open of fistula
- Superficial fistula can be managed by Fistulotomy avoiding the anal sphincter or Placement of Seton
- Deep fistula only placement of a Seton is an option

Antibiotics are also given

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37
Q

What are Peptic ulcer disease and gastritis

A

Ulceration of areas of the GI tract. More commonly in the stomach or duodenum

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38
Q

What are the causes of Peptic ulcer disease and gastritis

A

Imbalance between the damaging action of acid and pepsin secretions and the protective mechanisms of mucosal secretion.

H. Pylori
NSAIDs
Rare: Zollinger-Ellison syndrome (a syndrome of gastric acid hypersecretion NET)

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39
Q

What are the signs and symptoms of Peptic ulcer disease and gastritis

A
  • Epigastric pain - Relieved by antacids
  • Worse after eating (Gastric sooner than duodenal)
  • Haematemesis
  • Malaena
  • Microcytic Anaemia
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40
Q

What are the investigative findings of Peptic ulcer disease and gastritis

A 
Serum amylase (Exclude pancreatitis)
Secretin test (IV secretin will cause a rise in serum gastrin in Zollinger-Ellison)

OGD (First test if >55) - Biopsy rule out malignancy (Duodenal no biopsy)

Rockall scoring:
Scores the severity after a GI bleed
Score <3 carries good prognosis
>8 carries high risk of mortality

Testing for H. Pylori (First test if <55)

  • C-13 Urea breath test: Radiolabelled urea taken mouth - C13 Detected in expelled air
  • Serology - IgG against H. Pylori confirms exposure but not eradication
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41
Q

How are Peptic ulcer disease and gastritis treated

A

H pylori negative:
1st - Treat underlying cause + PPI
2nd - H2 antagonist (Ranitidine) or sucralfate or misoprostol

H pylori positive:
1st - Eradication triple therapy (PPI + Clarithromycin + Amoxicillin/Metronidazole)
2nd - Try alternative regime
3rd - PPI

Active bleed
1st - Endoscopy (Injection sclerotherapy, Laser coagulation, Electrocoagulation) + Blood transfusion
+ PPI
2nd - Surgery or embolisation via interventional radiology

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42
Q

What is Crohn’s disease

A

This is chronic granulomatous inflammatory disease that can affect any part of the GI tract

Usually affects the ileum and colon or just the ileum

RF: Ashkenazi Jewish people

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43
Q

What are signs and symptoms of Crohn’s disease

A 
Crampy abdominal pain
Diarrhoea
Bloody/steatorrhoea stool
Fever, malaise, weight loss
RIF pain if ileum affected

Clubbing
Anaemia
Mouth ulcers
Perianal skin tags, fistulae and abscesses
Extra intestinal: Uveitis, Erythema nodosum, Pyoderma gangrenous

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44
Q

What are the investigative findings in Crohn’s disease

A

FBC - Anaemia, High platelets, High WCC
ESR - Raised

Stool MC - Exclude infective colitis

AXR - Assess severity

Contrast radiology - Strictures, Deep ulcers (Through the submucosa - Mucosa to serosa), Cobblestone mucosa

OGD/Colonscopy + Biopsy- Definitive
Shows mucosal oedema
Fistulae/Abscesses
Transmural inflammation

Faecal calprotectin - Elevated

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45
Q

What is the treatment for Crohn’s disease

A

Acute:

  • Fluid restrict
  • Corticosteroids
  • 5-ASA analgoues (Mesalazine)
  • Analgesia
  • Parenteral nutrition
  • Monitor markers of disease activity

Chronic:

  • Corticosteroids for episodes
  • 5-ASA analogues decreased relapse frequency (Useful for mild to moderate, better in UC)
  • Immunosuppression - Azathioprine, 6-Mercaptopurine, Methotrexate
  • Anti-TNF agents (Infliximab) - Very effective at inducing and maintaining remission

Surgery - Risk of reccurence due to skips

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46
Q

What are the complications of Crohn’s disease

A

GI:

  • Haemorrhage
  • Strictures
  • Perforation
  • Fistulae (between bowel, bladder, vagina)
  • Perianal fistulae and abscesses
  • GI cancer
  • Malabsorption

Extraintestinal Features:

  • Uveitis
  • Episcleritis
  • Gallstones
  • Kidney stones
  • Arthropathy
  • Sacroiliitis
  • Ankylosing spondylitis
  • Erythema nodosum
  • Pyoderma gangrenosum
  • Amyloidosis
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47
Q

What is Ulcerative colitis (UC)

A

Chronic relapsing and remitting inflammatory disease affecting the large bowel

Associated with pANCA and Primary sclerosing cholangitis
Ashkenazi jews

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48
Q

What are the signs and symptoms of UC

A
  • Bloody or mucous diarrhoea (Frequency coincides with severity)
  • Tenesmus and urgency
  • Crampy abdominal pain before passing stool
  • Weight loss
  • Fever
    Extra articular: Uveitis, scleritis, erythema nodosum and pyoderma gangrenosum
  • Anaemia
  • Dehydration
  • Clubbing
  • Abdominal tenderness
  • Tachycardia
  • DRE - Blood mucous
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49
Q

What are the investigative findings in UC

A

FBC - Anaemia, High WCC
ESR - High
Low albumin

Stool culture - Faecal calprotectin elevated. Eliminated infectious colitis

AXR

Colonoscopy + Biopsy - Diagnostic
Determines severity
Histological confirmation
Detection of dysplasia

Barium enema - Narrow colon, Ulcers - May be dangerous during exacerbation

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50
Q

How is UC treated

A

Acute

  • IV rehydration
  • Corticosteroids
  • Antibiotics
  • Parenteral feeding may be necessary
  • DVT prophylaxis

Mild
Oral or rectal 5-ASA (-Alazine) and/or rectal steroids

Severe 
Oral steroids
Oral 5-ASA
Immunosuppression - Azothioprine, 6-Mercaptopurine, Cyclosporine
Anti-TNF - Infliximab

Surgical - Resection

  • Ileostomy bag from protocolectomy
  • Ileo-anal pouch
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51
Q

What are the complication of UC

A

GI:

  • Haemorrhage
  • Toxic megacolon
  • Perforation
  • Colonic carcinoma
  • Gallstones
  • Primary sclerosing cholangitis

Extraintestinal Features:

  • Uveitis
  • Kidney stones
  • Arthropathy
  • Sacroiliitis
  • Ankylosing spondylitis
  • Erythema nodosum
  • Pyoderma gangrenosum
  • Amyloidosis
  • Osteoporosis
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52
Q

What is portal hypertension

A

This is abnormally high pressure in the hepatic portal vein

Hepatic venous pressure gradient >10mmHg

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53
Q

What are causes of portal hypertension

A

Pre-hepatic:

  • Congenital stenosis
  • Portal vein thrombosis
  • Splenic vein thrombosis
  • Extrinsic compression

Hepatic:

  • Cirrhosis
  • Chronic hepatitis
  • Schistosomiasis
  • Myeloproliferatice disease

Post-Hepatic

  • Budd-Chiari syndrome (Hepatic vein obstruction)
  • Constrictive pericarditis
  • RHF
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54
Q

What are signs and symptoms of Portal hypertension

A
  • Haematemesis or melaena
  • Lethargy, irritability, changes in sleep
  • Abdominal distension
  • Abdominal pain and fever
  • Pulmonary involvement
  • Caput medusa
  • Splenomegaly
  • Ascites
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55
Q

What are the investigative findings of Portal hypertension

A
  • Abdominal US check Liver and spleen size
  • Doppler US - Assess direction of blood flow in vessels
  • CT/MRI - If other imaging methods are inconclusive
  • OGD check for oesophageal varices
  • Measure hepatic venous pressure gradient
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56
Q

How is Portal hypertension treated

A

Difficult to treat portal hypertension specifically
Mainly treating underlying cause

BB or Terlipressin - Reduce portal venous pressure

Transjugular intrahepatic portosystemic shunt

Liver transplant

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57
Q

What are the complications of portal hypertension

A
  • Bleeding oesophageal varices
  • Ascites + Complications of ascites (Spontaneous bacterial peritonitis, hepatorenal syndrome, hepatic hydrothorax)
  • Pulmonary complication (Hepatopulmonary syndrome: Hepatic dysfunction, hypoxaemia, Extreme vasodilation)
  • Liver failure
  • Encephalopathy
  • Cirrhotic cardiomyopathy
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58
Q

What is Peritonitis

A

This is inflammation of the peritoneal lining or the abdominal cavity

Localised or generalised

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59
Q

What are the different examples and causes of Peritonitis

A

Localised:

  • Appendicitis
  • Cholecystitis
  • Diverticulitis
  • Salpingitis

Primary generalised:
- Bacterial infection of the peritoneal cavity without an obvious source (RFs: Ascites, Nephrotic syndrome) - Ascending UTI in adolescent females

Secondary generalised:

  • Caused by bacterial translocation from a localised focus
  • It could also be non-bacterial due to spillage of bowel contents
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60
Q

What are signs and symptoms of Peritonitis

A

Inflammation of the parietal peritoneum is usually continuous, sharp and localised, exacerbated by movement and coughing

Localised:

  • Tenderness
  • Guarding
  • Rebound tenderness

Generalised:

  • Very unwell
  • Systemic signs of toxaemia or sepsis
  • Patient lying still
  • Shallow breathing
  • Rigid abdomen
  • Generalised abdomen tenderness
  • Reduced bowel sounds
  • DRE may show anterior tenderness
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61
Q

What are the investigative finding in Peritonitis

A
  • FBC - Low Hb, High WCC
  • Ascitic tap - Hazy/Cloudy/Bloody, >250 Neutrophil count, Gram-stained bacteria, Growth in culture, Leukocyte esterase reagent strip testing of ascitic fluid -ve rules out SBP

Imaging - Erect CXR for pneumoperitoneum
AXR - Check for bowel obstruction

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62
Q

How is Peritonitis treated

A

Localised - Depends on cause. May be surgical may be antibiotics

Generalised:

  • IV fluids
  • IV antibiotics
  • Urinary catheter
  • NG tube
  • Central venous line (to monitor fluid balance)
  • Laparotomy - Remove the infected or necrotic tissue, treat cause, peritoneal lavage
  • Primary peritonitis - Antibiotics

SBP:
Quinolone antibiotics or cefuroxime + metronidazole

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63
Q

What are the complications of Peritonitis

A 
Septic shock
Respiratory failure
 Multiorgan failure
Paralytic ileum
Wound infection
Abscesses
Incisional hernia
Adhesions
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64
Q

What is Non-alcoholic steatohepatitis (NASH)

A

Build up of fat in the liver due to causes other than excessive alcohol consumption

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65
Q

What are causes of Non-alcoholic steatohepatitis (NASH)

A 
Obesity
T2DM
HTN
Hypercholesterolemia
Age >50
Smoking

(Cardiac risk factors)

NASH is the most common liver disorder in the developed world

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66
Q

What are the signs and symptoms of Non-alcoholic steatohepatitis (NASH)

A

In early stages no symptoms
Incidental finding

Possible:
RUQ aching pain
Fatigue
Weight loss
Weakness
Advanced = Signs of cirrhosis
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67
Q

What are the investigative findings in Non-alcoholic steatohepatitis (NASH)

A

LFTs = Raised AST, ALT, ALP, Bilirubin

Liver US = Steatosis

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68
Q

How is Non-alcoholic steatohepatitis (NASH) managed

A

All conservative to prevent or slow progression to cirrhosis

BP
DM
Cholesterol
Smoking cessation
Weight Loss
Exercise
Reduced alcohol consumption
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69
Q

What are the complications of Non-alcoholic steatohepatitis (NASH)

A

Cirrhosis

  • Ascites
  • Oesophageal varices
  • Hepatic encephalopathy
  • Hepatocellular carcinoma
  • End-stage liver failure
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70
Q

What is Mallory–Weiss tear

A

This is a tear in the lining of the oesophagus around the junction with stomach. Usually as a result of violent vomitting or straining of the oesophagus

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71
Q

What are risk factors of Mallory–Weiss tear

A

Chronic alcohol abuse
Bulimia
Trauma, intese coughing, gastritis

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72
Q

What are the signs and symptoms of Mallory–Weiss tear

A

Most cases do not cause any symptoms

Potential:
Abdominal pain
Severe vomiting prior
Haematemesis
Involuntary retching
Black tarry stools - Melaena
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73
Q

How is Mallory–Weiss tear investigated

A

OGD - Tear

Bloods - Anaemia?

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74
Q

How is Mallory–Weiss tear treated

A

Most of the time the bleeding will stop on its own

If not:
Surgery - Injection scleropathy, Coagulation therapy, Arteriography

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75
Q

What is a complication of Mallory–Weiss tear

A

Boerhaave’s perforation

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76
Q

What is Liver failure

A

This is sever liver dysfunction leading to:
Jaundice
Encephalopathy &
Coagulopathy

It is classified based on time interval between the onset of jaundice and the development of the hepatic encephalopathy
Hyperacute <1w, Acute 1-4w, Subacute >4w

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77
Q

What are causes of Liver failure

A

Viral: Hep ABCDE
Drugs: Paracetamol overdose (50% in UK), idiosyncratic drug reactions

Less common causes:

  • Autoimmune Hepatitis
  • Budd-Chiari syndrome
  • Pregnancy
  • Malignancy
  • Haemochromatosis
  • Mushroom poisoning
  • Wilson’s disease
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78
Q

What are the signs and symptoms of Liver failure

A

Fever, Nausea, Jaundice

Encephalopathy
Asterixis
Fetor hepaticus
Ascites and splenomegaly (Less common if acute or hyperacute)
Bruising or bleeding
Pyrexia
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79
Q

What are the investigative findings in Liver failure

A

Identify the cause:

  • Viral serology
  • Paracetamol levels
  • Autoantibodies (ASM, Anti-LKM)
  • Ferritin
  • Caeruloplasmin and urinary copper

LFTs: Elevated AST, ALT, ALP, Bilirubin, GGT. Low Albumin

Liver US/CT

Ascitic tap - MC&S + ANC >250/mm3 = SBP

Doppler scan of hepatic or portal vein

EEG - Monitors encephalopathy

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80
Q

How is Liver failure treated

A

Resuscitation
Treat cause if possible: N-acetylcysteine - Paracetamol overdose

  • Monitor
  • Manage encephalopathy - Lactulose and phosphate enemas
  • Antibiotic and anti fungal prophylaxis
  • Hypoglycaemia treatment
  • Coagulopathy treatment - IV vitamin K, FFP, Platelet infusions
  • Gastric mucosa protection - PPIs or sucralfate
  • Avoid sedatives or drugs metabolised by the liver
  • Cerebral oedema decreased ICP with mannitol

Surgical - Transplant

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81
Q

What are complications of Liver failure

A 
Infection
Cerebral oedema
Haemorrhage
AKI
Respiratory failure
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82
Q

What are the different classifications for Intestinal obstruction

A
  • Small or large bowel
  • Partial or complete obstruction
  • Simple or strangulated
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83
Q

What are the causes of Intestinal obstruction

A
  • Extramural - Hernia, Adhesions, Bands, Volvulus
  • Intramural - Tumours, Inflammatory strictures
  • Intraluminal - Pedunculated tumours, foreign body
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84
Q

What are the signs and symptoms of Intestinal obstruction

A
  • Severe colicky pain with periods of ease
  • Abdominal distension
  • Frequent vomiting
  • Absolute constipation
  • Generalised tenderness
  • Tinkling bowel sounds
  • Peritonitis
  • Hernias
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85
Q

What are the investigative findings in Intestinal obstruction

A

AXR

  • Large bowel - Peripheral, Presence of haustration
  • Small bowel - Central, Jejunum: Vulvulae conniventae, Ileum: may appear tubeless, No gas

Water soluble contrast enema
Barium follow through

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86
Q

How is Intestinal obstruction treated

A
  • Gastric aspiration via NG tube if the patient is vomiting
  • IV fluids
  • Electrolyte replacement
  • Monitor vital signs, fluid balance and urine output
  • Surgical - Emergency laparotomy in acute obstruction
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87
Q

What are the complication of Intestinal obstruction

A 
Dehydration
Bowel perforation
Peritonitis
Toxaemia
Gangrene of ischaemic bowel wall
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88
Q

What are the different types of Hiatus hernia

A
  • Congenital - Asymptomatic
  • Sliding
  • Paraoesophageal (Rolling)
  • Mixed - Sliding and paraoesophageal
  • Upside down stomach
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89
Q

What are risk factors for Hiatus hernias

A 
Obesity
Low-fibre
Chronic oesophagitis
Ascites
Pregnancy
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90
Q

What are the signs and symptoms of Hiatus hernias

A

Most are asymptomatic

Sliding hernias are more likely to cause symptoms

Symptoms of GORD - Heartburn and waterbrash

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91
Q

How are Hiatus hernias investigated

A

CXR - Gastric air bubble above diaphragm
Barium swallow
OGD

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92
Q

How are Hiatus hernias treated

A

Medical - Weight loss + PPI
Surgical - Nissen fundoplication (The fundus of the stomach is wrapped around the oesophagus 360)
- Belsey mark IV fundoplication - 270 degree wrap
- Hill repair - Gastric cardia is anchored to the posterior abdominal wall

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93
Q

What are the complications of Hiatus hernias

A

Oesophageal

  • Intermittent bleeding
  • Oesophagitis
  • Erosions
  • Barrett’s oesophagus
  • Oesophageal strictures

Non-oesophageal

  • Incarceration of hiatus hernia (Rolling hernia)
  • This can lead to strangulation and perforation
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94
Q

What are Haemorrhoids

A

This is when the anal vascular cushions become enlarged and engorged with tendency to protrude, bleed and prolapse in the anal canal

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95
Q

How are Haemorrhoids classified and graded

A

They can be internal or external

Internal: Arise from a superior haemorrhoids plexus above dentate line
External: Lie below dentate line

4 Degrees of severity:

1: Do not prolapse
2: Prolapse with defecation but reduce spontaneously
3: Prolapse and require manual reduction
4: Prolapse and irreducible

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96
Q

What are causes of Haemorrhoids

A

Exact cause is disputed

RFs: Constipation, Prolonged straining, derangement in internal anal sphincter, Pregnancy, Portal hypertension

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97
Q

What are the signs and symptoms of Haemorrhoids

A

Usually asymptomatic

  • Bleeding: Bright red on toilet paper and in pan - Not mixed in
  • Absence of red flag symptoms
  • Itching, Anal lumps, Prolapsing tissue
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98
Q

What are investigative findings of Haemorrhoids

A

DRE - Felt if thrombosed
Proctoscopy - Visualised
Rigid or flexible sigmoidoscopy - Important to exclude other causes of bleeds further upstream

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99
Q

How are Haemorrhoids treated?

A

Conservative

  • High fibre
  • Increased fluid intake
  • Bulk laxatives
  • Topical creams (Local anaesthetic)

Injection sclerotherapy

Banding - Higher cure rate than injection sclerotherapy but more painful

Surgery
- Reserved for symptomatic 3rd and 4th degree haemorrhoids

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100
Q

What are complications of Haemorrhoids

A

Bleeding
Prolapse
Thrombosis
Gangrene

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101
Q

What are causes of gastrointestinal perforation

A

Large bowel: Diverticulitis, Colorectal cancer, Appendicitis

Gastroduodenal: Ulcer, Gastric cancer

Small bowel (Rare): Trauma, Infection (TB), Crohn’s disease

Oesophageal: Boerhaave’s perforation - Forceful profuse vomiting

RFs: NSAIDs, Steroids, Bisphosphonates

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102
Q

What are the signs and symptoms of Gastrointestinal perforation

A

Large bowel:

  • Peritonitic abdominal pain
  • Important to rule out AAA

Gastroduodenal:

  • Sudden-onset severe epigastric pain - Worse on movement
  • Pain becomes generalised
  • Gastric malignancy may have accompanying weight loss

Oesophageal:

  • Severe pain following an episode of violent vomiting
  • Neck/chest pain and dysphagia develop soon afterwards
Very unwell patients
Signs of shock
Fever
Pallor
Dehydration
Signs of peritonitis (Gaurding, rigidity, rebound tenderness, absent bowel sounds)
Loss of liver dullness
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103
Q

What are the investigative findings in Gastrointestinal perforation

A

CXR - Pneumoperitoneum
AXR - Abnormal gas shadowing
Gastrograffin swallow - Suspected oesophageal perforations

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104
Q

How is Gastrointestinal perforation treated

A

Resuscitation: IV antibiotics + Correct electrolytes and fluids

Surgery
Pleural lavage + Somethings

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105
Q

What are the complications of Gastrointestinal perforation

A

Large and Small Bowel: Peritonitis

Oesophageal: Mediastinitis, shock, overwhelming sepsis and death

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106
Q

What is Gastro-oesophageal reflux disease (GORD)

A

This is inflammation of the oesophagus caused by reflux of gastric acid and/or bile

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107
Q

What are the causes of GORD

A

Disruption of mechanisms that prevent reflux:

  • Lower oesophageal sphincter
  • Acute angle of junction
  • Mucosal rosette
  • Intra-abdominal portion of oesophagus
  • Prolonged acid clearance - 50%

BMI
Alcohol
Smoking

108
Q

What are the symptoms of GORD

A
  • Heartburn - Burning discomfort (Lying down, Bending, Large meals, Alcohol)
  • Acid regurgitation
  • Dysphagia
  • Bloating
  • Aspiration - Hoarness, laryngitis, nocturnal cough

Relieved by antacids

Potential:
Wheeze and tenderness

109
Q

What are the appropriate investigations for GORD

A

Clinical diagnosis with further confirmation by PPI trial

  • OGD - Exclude malignancy, oesophagitis
  • Barium swallow - Hiatus hernia, Peptic stricture, extrinsic compression of the oesophagus
  • Ambulatory pH monitoring
110
Q

How is GORD treated

A

Conservative:

  • Weight loss
  • Elevating head of bed
  • Lower fat meals
  • Avoid large meals late in the evening

Medical:

  • Antacids
  • Alginates
  • H2 antagonists (Ranitidine)
  • PPIs

Annual endoscopic surveillance - Barrett’s

Refractory surgery/Nissen fundoplication

111
Q

What are the complications of GORD

A 
Barrett's
Adenocarcinoma
Oesophageal ulceration
Anaemia
Associated asthma and chronic laryngitis
112
Q

What is Biliary colic

A

This is pain resulting from obstruction of the gall bladder or CBD usually by a stone

113
Q

What are risk factors for Biliary colic

A

The pain is due to the contraction of the biliary tree against the stone

6Fs
Fair - White
Fat
Fertile - Pregnancy + Exogenous oestrogen
Forty - Increasing age
Female
FHx
114
Q

What are the signs and symptoms of Biliary colic

A

RUQ/Epigastric pain + tenderness
N&V
Postprandial pain

115
Q

What are the investigative findings in Biliary colic

A

LFTs - Elevated ALT, ALP, Bilirubin
Lipase and amylase - Elevated 3 times in acute pancreatitis
Abdominal US - Diagnostic
ERCP - High risk - Also diagnostic

116
Q

How is Biliary colic treated

A

Symptomatic:
Cholecystectomy

Choledocholithiasis
1. ERCP
A Lithotripsy, balloon dilation, stenting
2. Laproscopic CBD exploration

Asymptomatic:
Observational unless risk of cancer or complications

117
Q

What are complications of Biliary colic

A 
ERCP - Pancreatitis
Iatrogenic bile duct injury
Cholecystitis
Ascending cholangitis
Acute biliary pancreatitis
118
Q

What is Cholecystitis

A

This is gallbladder inflammation and is one of the major complications of cholelithiasis

10% of symptomatic gallstones

119
Q

What are the different types of gallstones

A

Mixed stones 80% - Cholesterol, Calcium bilirubinate, Phosphate, Protein

Pure cholesterol stones 10%

Pigment stones 10% - Black stones made from calcium bilirubinate - Increased Bilirubin

120
Q

What are risk factors for Cholecystitis

A 
Forty
Female
Fat + DM
Fertile - High oestrogen states + Octreotide
Fair - White
FHx

Pigment stones - Haemolytic disorders e.g. sickle cell anaemia

121
Q

What are the signs and symptoms of Cholecystitis

A

Systemically unwell
Fever
Prolonged abdominal pain (Referred to right shoulder)

Tachycardia
Fever
RUQ pain
Guarding or rebound tenderness
Murphy's sign +ve
122
Q

What are the appropriate investigations for Cholecystitis

A

FBC - Elevated WCC
CRP - Elevated
LFTs - Elevated ALT, ALP, GGT, Bilirubin

RUQ US - Pericholecystic fluid + Thickened and distended gallbladder
Murphy’s sign positive

123
Q

How is Cholecystitis treated

A

Supportive: IV fluids, NBM, NSAIDs
IV Antibiotics - Cefuroxime or ciprofloxacin and metronidazole

Early LC only by skilled surgeon

124
Q

What are complications of Cholecystitis

A 
Perforation
Suppurative Cholecystitis
Gangrenous Cholecystitis
BD injury
Gallstone ileus
125
Q

What is Acute cholangitis

A

This is infection of the biliary tree

126
Q

What are causes of Acute cholangitis

A

Cholelithiasis leading to choledocholithiasis leading to obstruction

Iatrogenic biliary injury during Cholecystectomy or ERCP

Benign stricture - Chronic pancreatitis, Radiation induced, Chemotherapy

Malignant stricture

Sclerosis Cholangitis - 2nd Leading cause

Parasitic infection of the bile duct (Ascariasis)

127
Q

Who is typically affected by Acute cholangitis

A

Age 50 - 60
1% of cholelithiasis
Latin Americans and American Indians

128
Q

What are signs and symptoms of Acute cholangitis

A

Charcots triad:
RUQ pain
Fever
Jaundice

Reynolds pentad (Severe):
Hypotension
Altered mental status

Acholic stools
Pruritus

129
Q

What are the investigative findings in Acute cholangitis

A 
FBC -  High WCC
U&amp;ES - High urea and creatinine
LFTs - High ALT, AST, ALP, Bilirubin
Coag panel
CRP - Elevated
Blood culture

Abdominal US
ERCP

130
Q

How is Acute cholangitis treated

A
  1. IV antibiotics - Cefepime & metronidazole
    + decompression - ERCP/PTC
    A - lithotripsy - Large stone
    A - Analgesia - Opiods
  2. Surgical decompression -
    IV antibiotics + Opiods
131
Q

What are the complications of Acute cholangitis

A

Acute pancreatitis
Hepatic Abscess
Inadequate drainage

132
Q

What are prognostic factors in Acute cholangitis

A

High bilirubin, Fever, WCC, Age

or Low Albumin

133
Q

What is Alcohol withdrawal and what causes it

A

Patients with alcohol dependance with sudden drop in consumption of alcohol.

Occurs 4-12hrs after stopping

Caused by over active SNS due to NMDA up regulation and GABA down regulation

134
Q

What are the signs and symptoms of Alcohol withdrawal

A

Mild:

  • HTN
  • N&V
  • Fine tremore

Moderate:

  • Agitation
  • Coarse tremor

Severe:

  • Delirium
  • Tonic-clonic seizures
  • Hallucinations
  • Hyperthermia
135
Q

What are the appropriate investigations in Alcohol withdrawal

A

U&Es - Metabolic acidosis +/- Hypokalaemia
LFTs - Potential additional diagnosis of alcoholic hepatitis
Ethanol - If ethanol levels are still high during withdrawal then there may be risk of severe AWS

CT head - Exclude IC causes
CXR - Exclude cardiopulmonary causes

136
Q

How is Alcohol withdrawal treated

A

1st Line: Benzodiazepine (Diazepam) or clomethiazole
+ Supportive
A - Phenobarbital - Severe
A - Vitamin supplementation - Thiamine, Folic acid, Mg sulphate

Severe + ICU:
A - Dexmedetomidine - Makes Benzos more effective

Benzo resistant + ICU:
A - Propofol

137
Q

What are complications of Alcohol withdrawal

A 
Over sedation
Delirium tremens 5%
AW seizures
Status epilepticus <3%
Mortality

Usually persistent insomnia for 6 months
50% remain abstinent for a year

138
Q

How does one get Alcoholic hepatitis

A

Drinking a lot!
Women 20-40g/day
Men 40-80g/day
For 10-12 years!

This leads to Alcoholic hepatitis or liver cirrhosis

The less severe form is Alcoholic fatty liver

Females + Obesity

139
Q

What is the CAGE questionnaire

A

The CAGE questionnaire is commonly used as an alcohol misuse screening tool because it is fast, easy, and effective:

C: Have you ever felt you needed to CUT down on your drinking?
A: Have people ANNOYED you by criticising your drinking?
G: Have you ever felt GUILTY about drinking?
E: Have you ever felt you needed a drink first thing in the morning (EYE-OPENER) to steady your nerves or get rid of a hangover?

140
Q

What are symptoms of Alcoholic hepatitis

A

Fatigue
N+V

Anorexia
Weight loss

Jaundice
Fever
RUQ discomfort

141
Q

What are signs of Alcoholic hepatitis

A

Face: Telangiectasia, Parotid enlargement
Hands: Palmar erythema, Dupuytren’s contracture, Clubbing
Hormonal: Gynaecomastia, testicular atrophy
Organomegaly: Hepatomegaly, Splenomegaly

General: Spider naevi, Easy bruising, Malnourished, Ascites, Encephalopathy, Jaundice, Fever

142
Q

What are appropriate investigations for Alcoholic hepatitis

A

FBC - Elevated WCC, Low Hb, Platelets, High MCV
LFTs - High AST, ALT, ALP, GGT, Bilirubin, Low Albumin
U&Es - Normal or low Na, K, Mg, Phosphate. Normal or high Urea, Creatinine
Coagulation profile - PT and INR Elevated

Hepatic US - Hepatomegaly, Fatty liver, Portal hypertension
OGD - Varices
Biopsy

143
Q

How is Alcoholic hepatitis treated

A
  1. Abstinence + withdrawal management
    + Weight reduction + smoking cessation
    + Nutritional supplementation + multivitamins
    + Immunisations
    A - Corticosteroids
    A - Sodium restriction
    A - Pentoxifylline - Prophylactic reduce risk of Hepatorenal syndrome
144
Q

What are complications of Alcoholic hepatitis

A 
Portal hypertension
Hepatic encephalopathy
Hepatorenal syndrome
Renal failure
Coagulopathy
GI bleeding
Sepsis
HCC
145
Q

What is an anal fissure

A

This is a split in the distal anal canal characterised by pain on defecation and PR bleeding

146
Q

What are causes of Anal fissures

A

Hard stool
Constipation (Opiates)
Ischaemia - Anterior/POsterior midline deficiency in NO

147
Q

What are signs and symptoms of Anal fissure

A

Pain of defecation
Burning after initial sharp pain
PR bleeding on wiping or fresh in bowel
Posterior midline cut

Anal ulcer - Crohns, TB, syphilis, HIV, Anal cancer

148
Q

How are Anal fissures treated

A

1st line: Conservative - High fibre, more water, sitz baths and topical analgesia. Stool softeners
A - Topical GTN - Promotes healing
A - Topical Diltiazem - No headache side effects

Recurrent

1st: Botulinum toxin
1st: Surgical sphincterotomy
2nd: Anal advancement flap

149
Q

What is the prognosis of Anal fissures

A

60% heal 6-8 weeks

20% after diltiazem

150
Q

What are the symptoms of Appendicitis

A 
Periumbilical pain that moves to the right iliac fossa
Anorexia
Vomiting
Constipation
Diarrhoea
151
Q

What are the signs of Appendicitis

A 
Tachycardia
Fever
Furred tongue
Lying still
Coughing hurts
Foetor with/without flushing
Shallow breaths

RIF:
PR Pain on right side
Guarding
Rebound and percussion tenderness

Special signs:
Rovsing’s - Palpation of LIF causes pain in RIF
Psoas - pain of hip extension - Retrocaecal appendix
Cope - Pain on flexion and internal rotation of hip - Close to obturator internus

Retrocaecal/peritoneal appendix can cause flank pain or RUQ pain

152
Q

What are the investigative findings in Appendicitis

A

Bloods - Elevated WCC & CRP
CT - High sensitivity
Pregnancy test - Not ectopic

153
Q

How is Appendicitis treated

A

Prompt appendicectomy

Antibiotics: Cefuroxime and metronidazole

154
Q

What are complications of Appendicitis

A

Perforation
Generalised peritonitis
Abscess

155
Q

What is Achalasia

A

Loss of LOS closer
Loss of coordinated peristalsis

Due to oesophageal smooth muscle fibres failing to relax

156
Q

What causes Achalasia

A

Progressive degeneration of the ganglion cells in myenteric plexus within the oesophageal wall (Smooth muscle).

Primary achalsia (Most common)
- No known underlying cause

Secondary achalasia

  • Oesophageal cancer
  • Chagas disease - Protozoan infection due to Trypanosoma Cruzi leads to loss of intramural ganglion cells and therefore incomplete LOS relaxation and aperistalsis (Central & South America)
157
Q

What are the signs and symptoms of Achalasia

A

Insidious onset and gradual progression

  • Dysphagia with solids and liquids
  • Reguritation
  • Heartburn - Unresponsive to PPIs
  • Chest pain - Retrosternal
  • Difficulty belching
  • Hiccups
  • Weight loss
  • Aspiration of food - Aspiration Pneumonia
158
Q

What are the investigative findings in Achalasia

A

Endoscopy

  • Excludes malignancy
  • May show retained food

Barium swallow x-ray and continuous fluroscopy

  • Dilated oesophagus (Double right heart border) which smoothly tapers down to sphincter (Bird-beak appearance)
  • Air-fluid margin over barium column due to lack of peristalsis. Abscence of normal gastric air buble.

Manometry - Diagnostic

  • Elevated resting LOS pressure (Greater than 45mmHg)
  • Incomplete LOS relaxation
  • Aperistalsis in the distal oesophagus

Maybe serology for antibodies against Trypanosoma Cruzi if Chagas disease is suggested

159
Q

What is Autoimmune hepatitis

A

This is chronic inflammatory disease of the liver

Characterised by:
Auto-antibodies
Hyperglobulinaemia
A favourable response to immunosuppressive treatment

160
Q

What are the causes of Autoimmune hepatitis

A

HLA-DR3/4 association

Complex interaction between:

  1. Genetic predisposition
  2. Environmental triggering agents
  3. Auto-antigens
  4. Dysfunction of immunoregulatory mechanisms

Classifications
Type 1: ANA, ASMA, pANCA, Anti-SLA

Type 2: Anti-LKM1, Anti-LC1

Type 1 occurs in all ages but mainly young women
Types 2 essentially only affects girls and young women

161
Q

What are the signs and symptoms of Autoimmune hepatitis

A 
Fatigue + Malaise + Lethargy
Anorexia
Nausea
Abdominal discomfort
Mild pruritus
Arthralgia of small joints

Rarely: Fever, oligomenorrhoea, encephalopathy, GI bleeding

Sign: Hepatomegaly, Jaundice, Splenomegaly, Spider Naevi

162
Q

How is Autoimmune hepatitis diagnosed

A

Bloods
LFTs - Raised AST, ALT, Bilirubin, GGT and ALP, Raised globulin, Low Albumin

Coagulation Profile - Prolonged PT

Imaging
Abdominal ultrasound - Diagnose hepatic biliary obstuction

Liver Biopsy but after treatment is being prescribed

Other
ANA
SMA
Alpha-1 antitrypsin
Loads of other antibodies
163
Q

What are Liver abscesses and cysts

A

Abscesses: Liver infection resulting in a walled off collection of pus
Cysts: Liver infection resulting in a walled off collection of cyst fluid

164
Q

What are causes of Liver abscesses and cysts

A 
Pyogenic - Pus - Most common in industrialised
- E. coli
- Klebisiella
- Enterococcus
- Bacteriodes
- Streptococci
- Staphylococci
60% are caused by biliary tract disease
15% have unknown causes

Amoebic abscess - Entamoeba histolytica - Most common worldwide

Hydatid cyst - Tapeworm - Common in sheep-rearing countries

165
Q

What are the symptoms of Liver abscesses and cysts

A 
Fever
Malaise
Nausea
Anorexia
Night sweats
Weight loss
RUQ/Epigastric pain - Tender
Jaundice
Diarrhoea

Ask foreign travel!!

Right side: Reactive Pleural Effusion

166
Q

How are Liver abscesses and cysts diagnosed

A

Bloods
FBCs - Leukocytosis, elevated neutrophil count, Anaemia
LFTs - Elevated ALP, Mildly ALT & AST & Bilirubin, Hypoalbuminaemia

Cultures - Pyogenic potentially

US - Variably echoic lesion
Contrast-enhanced CT - Hypodense liver lesion

Gram stain and culture of aspirated abscess fluid
Pyogenic potentially

Other
CXR
Serum antibody test

167
Q

What is Barrett’s oesophagus

A

Change in the normal squamous epithelium of the oesophagus to the specialised intestinal metaplasia (simple columnar epithelium, goblet cells - Usaully found in the lower GI tract)

This is a premalignant condition.

168
Q

What are causes of Barrett’s oesophagus

A

The primary aetological factor is gastro-oesophageal reflux (GORD). There is evidence that bile reflux is also involved.

Chronic acid exposure causes reflux esophagitis and therefore metaplastic change.

Squamous epithelium to Simple Columnar epithelium

Risk Factors
Acid/bile reflux/GORD
Age - Older more likely
White 
Male (2 times more likely)
Hiatus Hernia

Obesity
Family history
Smoking

169
Q

What the signs and symptoms of Barrett’s oesophagus

A

Symptoms of GORD are the key feature:

  • Heartburn
  • Regurgitation
  • Nausea
  • Water-brash

Many patients are asymptomatic

Atypical Symptoms

  • Chest Pain
  • Voice Changes
  • Respiratory symptoms (Dyspnoea or Wheezing)
  • Dysphagia
170
Q

How is Barrett’s oesophagus diagnosed

A

OGD with biopsy - Abnormal epithelium characteristic of Barrett’s Oesophagus. The Z line boundary is migrated proximally

Barium Oesophagogram - May be intial test if there is dysphagia
Identifies Hiatus Hernia and reflux

171
Q

How is Barrett’s oesophagus treated

A

Non-dysplatic
1 - PPI + Surveillance
A - Radiofrequency ablation if high risk of progression (Older white men)
2 - Anti reflux surgery + Surveillance

Low grade
1 - Radiofrequency ablation with or without endoscopic mucosal resection

High grade
1 - Radiofrequency ablation with or without endoscopic mucosal resection
+ PPI
2 - Oesophagectomy

172
Q

What is Liver cirrhosis

A

This is end stage chronic liver disease

  • Fibrosis
  • Normal liver architecture to structurally abnormal nodules known as regenerative nodules
173
Q

What are the causes of Liver cirrhosis

A

Cirrhosis can be derived from chronic liver disease - The primary event is hepatic fibrosis due to over activation of the hepatic stellate cells which are the major source of extracellular matrix

Alcoholic liver disease: Most common UK cause

Worldwide the most common causes are chronic hepatitis C followed by non-alcoholic fatty liver disease (steatohepatitis) and chronic hepatitis B

Drugs: Methotexate, Hepatotoxic drugs

Inherited: alpha 1-Antitrypsin deficiency, Haemochromatosis, Wilson’s disease, Galactosaemia, Cystic Fibrosis

Vascular: Budd-Chiari syndrome or hepatic venous congestion

Chronic biliary disease: PBC, PSC, biliary atresia

Cryptogenic is idopathic - 5-10%

Risk Factors

  • Alcohol misuse
  • IV drug use
  • Unprotected intercourse
  • Obesity
  • Blood transfusion
  • Tattooing
174
Q

What are the symptoms of Liver cirrhosis

A 
Symptoms:
Fatigue
Weakness
Anorexia + Weight loss
Nausea

Decreased liver synthetic function:

  • Easy bruising
  • Abnormal swelling
  • Ankle oedema

Reduced detoxification function:

  • Jaundice
  • Encephalopathy
  • Amenorrhoea
  • Galactorrhoea

Portal hypertension:

  • Abdominal swelling - Ascites
  • Haematemesis - Oesophageal Varices
  • PR bleeding or melaena

Decompensated if complicated by any of:

  • Ascites
  • Jaundice
  • Encephalopathy
  • GI bleed
175
Q

What are the signs of Liver cirrhosis

A

General - Jaundice

Hands and Nails - Leukonychia, Palmar erythema, Spider Naevi, Clubbing, Dupuytren’s contracture

Facial - Telangiectsia, Bruising, Rhinophyma, Parotid swelling, Paper-dollar skin, Seborrhoeic Dermatitis, Jaundiced sclerae, Xanthelasma

Chest - Gynaecomastia & Loss of secondary sexual hair in men, breast atrophy in women, Spider Naevi

Abdominal - Ascites, hepatomegaly, splenomegaly, Abdominal distension, Hepatic bruit, Loss of secondary sexual hair and testicular atrophy in men, Caput medusae
Lower extremity swelling

176
Q

How is Liver cirrhosis diagnosed

A

Bloods

  • LFTs - Deranged! Raised AST and ALT, Raised GGT, Normal or Raised Bilirubin, Reduced Albumin, Prolonged PT
  • FBC - Reduced Platelet count,
  • Electrolytes - Reduced Sodium
  • Viral Serology - Antibodies to Hep B/C may or may not be present

Other
- Iron studies - Raise total Iron, Reduced TIBC, Raised transferrin saturation and ferritin in haemochromatosis.

  • Anti-self antibodies (ANA, ASMA, AMA) - Autoimmune hep
  • Alpha 1 anti-trypsin
  • Ceruloplasmin - Wilson’s disease

Ascitic tap:
- MC&S - Signs of infection

Liver Biopsy - Most sensitive diagnostic

Abdominal US, CT, MRI - Ascites, splenomegaly, collateral circulation

OGD - Varices

Child-Pugh grading: 
- Class A is score 5-6
- Class B is score 7-9
- Class C is score 10-15
It is based on: 1s are as follows
- Albumin >35, 35-28, <28
- Bilirubin <2, 2-3, >3
- PT <4, 4-6, >6
- Ascites None, Mild, Moderate
- Encephalopathy None, Grade 1-2, Grade 3-4
177
Q

How is Liver cirrhosis treated

A

1st Line - Treatment of underlying cause of CLD and prevention of superimposed hepatic insult

+ Monitoring for complications

  • Portal HTN, Hepatorenal syndrome, HCC
  • Encepathopathy
  • SBP - Antibiotics: Cefuroxime and metronidazole. Prophylaxis against SBP with ciprofloxacin

A - Sodium restriction and diuretic therapy for ascites

  • Spironolactone and or Furosemide
  • Avoid alcohol and NSAID due to their hepatotoxicity

2nd Line - Liver transplant (Especially if decompensated)

178
Q

What is the most lethal complication of Liver cirrhosis

A

Gastro-oesophageal varices

20% mortality after 6 weeks

179
Q

What is Coeliac disease

A

This is a systemic autoimmune disease triggered by dietary gluten peptides causing chronic intestinal malabsorption

180
Q

What causes Coeliac disease

A

Sensitivity to Gliadin component of gluten
HLA-B8/DR3/DQW2

Rare in East Asia
FHx component

181
Q

What are the signs and symptoms of Coeliac disease

A

May be asymptomatic

Diarrhoea
Bloating
Abdominal pain
Fatigue
Weight loss
Intese itchy blisters - Dermatitis herpetiformis
Failure to thrive in children
Signs of anaemia
Signs of malnutrition:
- Short stature
- Abdominal distension
- Wasted buttocks in children
- Triceps skin fold thickness gives indication of fat stores
Signs of vitamin/mineral deficiencies:
- Osteomalacia
- Easy bruising
182
Q

How is Coeliac disease diagnosed

A

Bloods
FBC - Low Hb

Serology

  • Immunoglobulin A-tissue transglutaminase (IgA-tTG) - Titre above normal range for lab - 1st Line investigation
  • Endomysial Antibody (EMA) - Elevated titre
  • IgG DGP - Elevated titre
  • IgG-tTG - Elevated titre

Histology - Diagnostic test
Presence of intra-epithelial lymphocytes, villous atrophy and crypt hyperplasia - Gold standard diagnostic

Endoscopy
Atrophy, Scalloping of folds, Nodularity

Other
HLA typing - HLA-DQ2 or DQ8
Skin bipsy for dermatitis herpetiformis
Gluten challenge

183
Q

How is Coeliac disease treated

A

1st Line - Gluten-free diet
Plus - Calcium and Vitamin D supplementation +/- Iron

Refractory
1st Line - Gluten-free diet
Plus - Calcium and Vitamin D supplementation +/- Iron
Plus - Referral to dietician or gastroenterologist

Crisis
1st Line - Gluten-free diet
Plus - Calcium and Vitamin D supplementation +/- Iron
Plus - Rehydration + Correction of electrolyte abnormalities
Adjunct - Corticosteroid - Short course

184
Q

What are the complications of Coeliac disease

A 
Iron, B12, Folate deficiency
Osteomalacia
Ulcerative jejunoileitis
GI lymphoma (T-cell)
Bacterial Overgrowth
Cerebellar ataxia
185
Q

What are the different stages of Diverticular disease

A

Diverticulosis is the herniation/out-pouching of the mucosa and submocusa through the muscle layer of the colonic wall.

Diverticular disease is the presence of diverticulosis associated with symptoms. These include, haemorrhage, infection and fistulae

Diverticulitis is the acute inflammation and infection of the colonic diverticulae

Classifications

  • Asymptomatic diverticulosis
  • Symptomatic uncomplicated diverticular disease
  • Complicated diverticular disease

Hinchey’s Classification of Acute Diverticulitis
Stage I - Small/confined mesenteric abscess
Stage II - Large paracolic abscess
Stage III - Perforated diverticulitis with purulent peritonitis
Stage IV - Perforated diverticulitis with faecal peritonitis

186
Q

What are risk factors for Diverticular disease

A 
Low dietary fibre
Increasing age
Western diet
Obesity
NSAIDs

Ehler’s-Danlos syndrome/Herniosis - Saint’s triad (Hiatus hernia, Diverticulosis, Gallstones)

187
Q

What are the signs and symptoms of Diverticular disease

A

90% Asymptomatic

Reccurent LIF pain
Fever
Bloating
Constipation
Diarrhoea
PR bleeding
Diverticulitis - LIF and fever
Diverticular fistula - Pneumaturia, faecaluria and recurrent UTIs
Pelvic tenderness on DRE
Rebound tenderness and Guarding
188
Q

How is Diverticular disease diagnosed

A

Bloods

  • FBC - polymorphonuclear leukocytosis - Acute
  • CRP - Raised

Barium enema - Diagnostic but not in acute setting because there is a high risk of perforation

Flexible sigmoidoscopy - Diagnostic visualisation

In acute setting: CT AP may be used look for evidence of diverticular disease and complications

189
Q

How is Diverticular disease treated

A

GI bleed: PR bleeding is often managed conservatively with nil by mouth, IV
rehydration, antibiotics, blood transfusion if necessary.

Diverticulitis: Nil by mouth, IV antibiotics (cephalosporin and metronidazole)
and IV fluid rehydration.

Chronic: High-fibre diet with bulking agent (e.g. methylcellulose). Laxatives
may be required if constipation is severe. Encourage high fluid intake.

Surgery: May be necessary with recurrent attacks or when complications develop,
e.g. severe bleeding or infection.
Sigmoid colectomy, Hartmann’s procedure,
fistulectomy or drainage of pericolic abscesses are some operations performed.

190
Q

What is Primary biliary cirrhosis (PBC)

A

Chronic inflammation liver disease involving progressive destruction of intrahepatic bile ducts leading to cholestasis and ultimately cirrhosis

Autoimmune

191
Q

Who is affected by PBC

A

Middle-aged women 9:1

192
Q

What are signs and symptoms of PBC

A

Asymptomatic

Fatigue
Pruritus preceding jaundice
Xanthomas
Skin pigmentation
Hepatomegaly
Ascites
Signs of chronic liver disease

Other autoimmunity: Sjogren’s syndrome, RA, Raynaud’s

193
Q

How is PBC diagnosed

A

Bloods
LFTs: Increased ALT, AST, ALP, GGT, Bilirubin. Decreased Albumin. Prolonged PT
(Transaminases normal until later disease)

AMA (Anti-Mitochondrial Antibodies)
High IgM
High Cholesterol
ANA

US scan: Obstructive duct lesions must always be excluded radiologically before the diagnosis of PBC is made

Biopsy: Not usually needed anymore

194
Q

What is Primary sclerosing cholangitis (PSC)

A

Primary sclerosing cholangitis is inflammation and fibrosis of the intrahepatic and/or extra hepatic bile ducts resulting in diffuse, multi focal stricture formation

195
Q

Who is usually affected by PSC

A

Males with IBD
4% of people with UC have it
80% of people with PSC have UC

196
Q

What are the signs and symptoms of PSC

A 
RUQ pain
Pruritus
Fatigue
Fever
Jaundice
197
Q

How is PSC diagnosed

A

LFTs - first line - GGT elevated

MRCP - Diagnostic - Beading

AMA antibodies should be negative
ANCA - May be present

198
Q

What are risk factors for Pancreatic cancer

A 
Age
Smoking
DM
Chronic pancreatitis
Dietary (Low intake of fresh fruit and vegetables)
2x Male
199
Q

What are signs and symptoms of Pancreatic cancer

A

Initial nonspecific

Weight loss
Anorexia
Painless Jaundice and a palpable gallbladder (Courvoisier’s law)
Epigastric tenderness or mass
Met-Hepatomegaly
Trousseau’s sign of malignancy - Superficial thrombophlebitis

200
Q

How is Pancreatic cancer diagnosed

A

Bloods

  • CA19-9
  • CEA is also elevated
  • Obstructive jaundice - High bilirubin, ALP and deranged clotting

Imaging
US
CT +/- biopsy (Diagnostic)
ERCP = May allow biopsy

201
Q

What are the 2 types of Oesophageal cancer

A

Squamous cell carcinoma

Adenocarcinoma

202
Q

What causes each type of Oesophageal cancer

A

Squamous cell (Most common worldwide)

  • Alcohol
  • Achalasia
  • Scleroderma
  • Coeliac disease
  • Plummer-Vinson syndrome
  • Dietary toxins

Adenocarcinoma (Most common western)

  • GORD
  • Barrett’s oesophagus

3x Men

203
Q

What are the signs and symptoms of Oesophageal cancer

A
  • Progressive dysphagia (Initially worse with solids)
  • Odynophagia
  • Weight loss
  • Hoarseness
  • Hiccups

Mets - Liver and lungs

204
Q

How is Oesophageal cancer diagnosed

A

OGD with biopsy - Diagnostic

205
Q

What are causes of Intestinal ischaemia

A

Embolus (60%)
Thrombosis (40%)

Volvulus
Intussusception
Bowel strangulation
Failed surgical resection

RFs:
AF
Endocarditis can throw emboli
Arterial thrombosis: Hypercholesterolaemia, HTN, DM, smoking
Venous thrombosis: Portal HTN, splenectomy, septic thrombophlebitis, OCP, thrombophilia

206
Q

What are the signs and symptoms of Intestinal ischaemia

A
  • Severe colicky pain + Tenderness
  • Vomiting
  • Rectal bleeding
  • Hx of chronic mesenteric artery insufficiency - Gross weight loss + Post prandial abdominal pain
  • Hx heart or liver disease

Distension
Mass
Bowel sounds absent

207
Q

How is Intestinal ischaemia diagnosed

A

Diagnosis is based on clinical suspicion or after laparotomy

AXR - Thickening of the small bowel folds and signs of obstruction

ABG - Lactic acidosis

Mesenteric angio is stable

208
Q

What are associated risk factors for Hepatocellular carcinoma

A

Chronic liver disease: ALD, HEP C, Autoimmune Hep
Metabolic disease: Haemochromatosis
Aflatoxins: Cereals contaminated with fungi

209
Q

What are the signs and symptoms of Hepatocellular carcinoma

A

Malaise
Weight loss
Loss of appetite

Distension
Jaundice
Hepatomegaly
Ascites
Bruits over liver
Lymphadenopathy
210
Q

How is Hepatocellular carcinoma diagnosed

A

Bloods -
FBC - Microcytic anaemia and thrombocytopenia
LFTs - Elevated ALT, AST, ALP, Bilirubine, Low albumin
U&Es - Hyponatraemia and high urea
Alpha-fetoprotein - Elevated (60%)

Imaging
Abdominal US
CT - Gold standard staging

211
Q

What are the different types of Gastric cancer

A

Adenocarcinoma
Lymphoma
Leiomyoscarcoma
Stromal tumours

212
Q

What are risk factors for Gastric cancer

A 
Smoked and processed foods
Smoking
Alcohol
H. Pylori
Atrophic gastritis
Pernicious anaemia
Partial gastrectomy
Gastric polyps

Highest incidence in Japan

213
Q

What are the signs and symptoms of Gastric cancer

A 
Early satiety
Epigastric discomfort
Systemic symptoms: weight loss, anorexia
Dysphagia
Met - Liver
Anaemia

Virchows node
Sister Mary Joseph Nodule (Metastatic node on the umbilicus)
Krukenberg’s tumour (Ovarian metastases)

214
Q

How is Gastric cancer diagnosed

A

OGD
Endoscopic US (EUS) - After diagnosis - Assess depth of gastric invasion and lymph node involvement
CT - Aid with mets

215
Q

What is Haemochromatosis

A

This is a multisystem genetic disorder of dysregulated dietary iron absorption and increased iron release from macrophages - Autosomal recessive (HFE gene)

216
Q

Who is usually affected by Haemochromatosis

A

Middle aged
White
Men
FHx

217
Q

What are the signs and symptoms of Haemochromatosis

A

Asymptomatic until the last stage of the disease

Fatigue
Weakness
Lethargy
Arthalgias
Impotence
Loss of libido
Skin pigmentation
Hepatomegaly + Cirrhosis
Congestive heart failure
Porphyria cutanea tarda
Diabetes mellitus
218
Q

What are the investigative findings in Haemochromatosis

A

Serum ferritin

Bloods
Iron studies - Ferritin raised, Transferrin Low, Transferrin saturation raised, TIBC Low

CRP - Inflammation
LFTs - ALT raised in liver necrosis
Other liver tests

HFE mutation analysis

Liver biopsy

219
Q

What is Amyloidosis

A

This is heterogenous group of diseases characterized by extracellular deposition of amyloid fibrils

Any histological tissue specimen that binds the cotton wool dye, Congo red, and demonstrates green birefringence when viewed under polarised light is an amyloid deposit.

Deposition may be localised in tissue or part of a systemic process

220
Q

What are the different types of Amyloidosis

A

There are 3 types of Amyloidosis:

  • Primary amyloidosis (Immunoglobin light chain amyloidosis - AL)
  • Secondary amyloidosis (Non familial or familial periodic fever syndrome - AA)
  • Inherited forms (AF)
AL
Potential predisposing conditions: 
- Multiple myeloma, 
- Waldenstroms macroglobulinaemia
- B-cell lymphoma 
- MGUS

AA

  • Chronic inflammatory diseases (RA, Seronegative arthritides, Crohn’s disease, familial mediterranean fever)
  • Chronic infections (TB, bronchiectasis, osteomyelitis)
  • Malignancy (Hodgkin’s disease, renal cancer)

AF
Autosomal dominantly transmitted mutations in the gene for transthyretin

221
Q

What are risk factors for Amyloidosis

A
  • Monoclonal gammopathy of undetermined significance
  • Inflammatory polyarthropathy - Rheumatoid arthritis, juvenile arthritis, psoriatic arthritis, Ankylosing spondylitis
  • Chronic infections - Bronchiectasis, Subcutaneous injections of illicit drugs, decubitis ulcers, chronic UTIs and osteomyelitis
  • IBDs - Crohn’s
  • Familial periodic fever syndromes - Familial Mediterranean fever and TNF receptor associated
  • Castleman’s disease
222
Q

What are signs and symptoms of Amyloidosis

A

AL is associated with restrictive cardiomyopathy and peripheral neuropathy

AA is associated with nephrotic syndrome and hepatosplenomegaly

Symptoms:

  • Weight loss
  • Fatigue
  • Dyspnoea
  • Paraesthesias

Signs:

  • Lower extremity oedema
  • Elevated JVP
  • Periobital amyloid purpura
  • Eyelid petechiae
  • Macroglossia
  • Enlargement of submandibular salivary glands
  • Palpable hepatomegaly, splenomegaly
  • Shoulder pad sign
  • Diffuse muscle weakness
  • Amyloid peripheral neuropathy
223
Q

How is Amyloidosis diagnosed

A

Initial:

  • Serum Immunofixation - Prescence of monoclonal protein - 60% - AL
  • Urine Immunofixation - 80% -AL
  • Immunoglobulin free light chain assay - Extremely high sensitivity for AL
  • Bone marrow biopsy - AL

Diagnostic - Tissue biopsy to prove the tissue stains positive for Congo red. Apple-green birefringence is seen when Congo red stained material is viewed under polarised light

Immunohistological studies of amyloid deposits - To distinguish the type of Amyloidosis

224
Q

What are risk factors for Cholangiocarcinoma

A

Chronic liver disease due to hepatitis B or C leading to cirrhosis, alcoholic liver disease, non-specific cirrhosis, bile duct diseases, choledocholithiasis, cholecystolithiasis, UC and HIV. Primary sclerosing cholangitis

  • Age >50
  • Diabetes
  • Cigarrette smoking
  • Exposure to toxins/medicines - PCBs, isoniazid, oral contraceptives, chronic typhoid carriers
225
Q

What are the signs and symptoms of Cholangiocarcinoma

A 
Obstructive jaundice
Acholic stools
Dark urine
Pruritus
Abdominal pain or fullness
Systemic symptoms of malignancy: Weight loss, malaise, Anorexia

Palpable gallbladder - Courvoisier’s Law - Presence of a non-tender palpable gallbladder and jaundice is unlikely to be due to gallstones

Epigastric/RUQ
Hepatomegaly

226
Q

How is Cholangiocarcinoma diagnosed

A

LFTs - Elevated ALP, Bilirubin, GGT
PT Prolonged

Cancer markers: CA19-9, CEA
serum CA 19-9 + (40 times CEA) Equation used to calculate the likelihood of tumour progression. PPV of 100%, CA-125 Dectable in up to 65% of patients

Abdominal US - Malignancy vs Benign

ERCP - Tissue diagnosis and therapeutic

227
Q

What is the distribution of Colorectal carcinomas

A

60% - Rectum and sigmoid
30% - Descending colon
10% - Rest of colon

228
Q

What are risk factors for Colorectal carcinoma

A
  • Western diet (Red meat, alcohol)
  • Colorectal polyps
  • Previous colorectal cancer
  • FHx
  • IBD

Familial forms:

  • Familial adenomatous polyposis (FAP)
  • Hereditary nonpolyposis colorectal cancer (HNPCC)
229
Q

What are the signs and symptoms of Colorectal carcinoma

A

Left-sided colon:

  • Change in bowel habit
  • Rectal bleeding (blood or mucus mixed with the stools)
  • Tenesmus (due to a space-occupying tumour in the rectum)

Right-sided colon:

  • Presents later
  • Anaemia symptoms (lethargy)
  • Weight loss
  • Non-specific malaise
  • Lower abdominal pain (rare)

20% of the tumours present as an emergency with pain and distension due to:

  • Large bowel obstruction
  • Haemorrhage or peritonitis due to perforation

Abdominal mass
Met - Hepatomegaly + Ascites

Low-lying rectal tumours may be palpable on DRE

230
Q

How is Colorectal carcinoma diagnosed

A

FBC - Anaemia
LFT - Deranged with met
Renal function - Just in case pelvic tumour is compressing on ureter

Colonoscopy requires full bowel preparation with oral laxatives - Multiple biopsies required

Double contrast Barium Enema - May show ‘apple core’ strictures

Contrast CT - Duke’s staging

231
Q

What is Irritable bowel syndrome (IBS)

A

This is a chronic condition characterised by abdominal pain associated with bowel dysfunction. There are recurrent episodes of abdominal pain/discomfort for >6 months of the previous year, associated with 2 of the following:

  • Altered stool passage
  • Abdominal bloating
  • Symptoms made worse by eating
  • Passage of mucous
232
Q

What are risk factors of IBS

A 
Physical and sexual abuse
Age <50 years
Female sex
Previous enteric infection
Family and job stress
Food intolerance (Lactose)
233
Q

What are the signs and symptoms of IBS

A
  • Abdominal pain/discomfort
  • Altered bowel habits
  • Pain relieved by defecation
  • Abdominal bloating
  • Passage of mucus with stools
  • Sensation of incomplete evacuation following a bowel movement

Carnett test (Pain on tightening the abdomen = abdominal wall, Less pain on tightening = intraperitoneal pain)

234
Q

How is IBS investigated

A

Bloods
FBC - Normal though anaemia suggests non-IBS disease

Stool studies
Stools - Normal though WBCs in stools or parasites suggest non-IBS diseasea

Antibodies

  • Anti-endomysial antibodies - Negative though positive in coeliac disease
  • Anti-tTG antibodies - Negative though raised in coeliac disease

Imaging
- Plain abdominal x-ray - Normal, abnormal bowel position suggests obstruction

Endoscopy

  • Flexible sigmoidoscopy - Normal, abnormal mucosa suggests IBD
  • Colonscopy - Normal, Muscosal inflammation or ulceration suggests IBD

Other

  • Hydrogen breath test - Lactase deficiency
  • Faecal calprotectin - Lower than 40micrograms IBD unlikely
  • Serum CRP - Lower than 0.5mg/L IBD unlikely
235
Q

How is IBS treated

A

Advice: Dietary modification

Medical: Depends on the main symptoms affecting the patient

  • Antispasmodics (e.g. buscopan)
  • Prokinetic agents (e.g. domperidone, metaclopramide)
  • Anti-­‐diarrhoeals (e.g. loperamide)
  • Laxatives (e.g. Senna, movicol, lactulose)
  • Low-­‐dose tricyclic antidepressants (may reduce visceral awareness)

Psychological therapy:

  • CBT
  • Relaxation and psychotherapy
236
Q

What is Gastroenteritis/Infectious colitis

A

This is acute inflammation of the lining of the GI tract manifested by N+V, Diarrhoea and Abdominal discomfort

237
Q

What are causes of Gastroenteritis/Infectious colitis

A

Can be caused by viruses, bacteria, protozoa or toxins contained in contaminated food or water

(Incubation/Duration)

Viral:

  • Rotavirus (Young) (1d/7d),
  • Norovirus (Adults) (1d/4d),
  • Enteric adenovirus 40+41 (3-10d/9d)
Bacterial: 
- Camplyobacter Jejuni 
- E Coli (0157 - Enterohaemorrhagic)
- Salmonella
- Shigella
Vibrio cholerae
Listeria
Yersinia enterocolitica

Protozoal:

  • Entamoeba histolytica
  • Cryptosporidium parvum
  • Giardia lamblia
Toxins: 
Staphylococcus aureus
Clostridium botulinum
Clostridium perfringens
Bacillus cereus
Mushrooms
Heavy metals
Seafood

Commonly contaminated food: - Meat (S. aureus, C, Perfringens)

  • Old rice (B. cereus, S. aureus)
  • Eggs and poultry (Salmonella)
  • Milk and cheeses (Listeria, Campylobacter)
  • Canned food (Botulism)
  • Travel generally - E. coli causes traveller’s diarrhoea
  • Travel to Asia, Africa and South America - Rotavirus
  • Travel to Asia or Central America - Vibrio Cholera
  • Travel to developing countries - Giardia, Aeromonas, Cryptosporidium (Water)
  • Recent Antibiotics (C Dif)
  • Daycare - Rota
  • Homosexual men - Shigella, Campylobacter, Salmonella
238
Q

What are the signs and symptoms of Gastroenteritis/Infectious colitis

A

Sudden N+V and anorexia

  • Diarrhoea
  • Abdominal pain or discomfort
  • Increased bowel sounds
  • Dehydration

Fever and malaise

Time onset:
Toxins - Early within a day
Microorganism = 12hrs+

Botulinum = Paralysis
Mushrooms can cause fits renal or liver failure

239
Q

How is Gastroenteritis/Infectious colitis investigated

A

FBC/blood culture/U&Es/dehydration assessment

CXR/AXR: colitis ‘thumbprinting’ of submucosal swelling

Stool culture: Sortibtol MacConkey agar (E.coli O157:H7),

240
Q

How is Gastroenteritis/Infectious colitis treated

A
  • Bed rest
  • Fluid and electrolyte replacement with oral rehydration solution (contains glucose and salt)
  • IV rehydration may be necessary in those with severe vomiting
  • Most infections are self-limiting (so will go away with time)
  • Antibiotic treatment is only used if severe or if infective agent has been identified
  • NOTE: if botulism is present (due to Clostridium botulinum) treat with botulinum antitoxin (IM) and manage in ITU
  • NOTE: this is often a notifiable disease and is an important public health issue
241
Q

What are complications of Gastroenteritis/Infectious colitis

A 
Dehydration
Electrolyte imbalance
Sepsis and shock
]Haemolytic uraemia syndrome associated with toxins from E. coli O157
GBS weeks after campylobacter
Botulinum may cause paralysis
242
Q

What is a Hernia

A

The abnormal protrusion of peritoneal sac through a weakness of the abdominal wall in the inguinal region

243
Q

What are the main types of Hernias

A

Direct inguinal:

  • Protrusion of the hernial sac directly through a weakness in the transversals fascia and posterior wall of the inguinal canal
  • Arises medial to the the inferior epigastric vessels
  • Appear through Hesselbach’s triangle (Lateral border of rectus abdominal, inferior epigastric vessel, Inguinal ligament)

Indirect inguinal:
- Protrusion of the hernial sac through the deep inguinal ring, following the path of the inguinal canal

Femoral:
- Occur just below the inguinal ligament when abdominal contents pass though a naturally occurring weakness in the abdominal wall called the femoral canal

Umbilical: Women during and after pregnancy and overweight people

244
Q

What are causes of Hernias

A

Congenital: Abdominal contents enter the inguinal canal through a patent processes vaginalis

Acquires - Due to increased IAP along with muscles and transversals fascia weakness

RFs:
Male
Prematurity
Age
Obesity
Constipation
Bladder outflow obstruction
Intraperitoneal fluid
Heavy lifting

Female (Femoral)

245
Q

What are the signs and symptoms of Hernias

A

Asymptomatic

Lump in groin
May cause discomfort or pain
May be irreducible

Tender is strangulated
Auscultation there may be bowel sounds over the hernia
Cough impulse

246
Q

How are Hernias diagnosed

A

Clinical diagnosis

Diagnostic uncertainty: US
CT - Contrast: Very obese

247
Q

How are hernias treated

A

Surgical

  • Usually elective repair of uncomplicated hernia
  • Hernia reduced and a mesh is inserted to reinforce the defect in the transversals fascia

Emergency

  • If obstructed or strangulated
  • Laparotomy with bowel resection may be indicated if the bowel is gangrenous
248
Q

What are the complications of Hernias

A

Incarceration
Strangulation
Bowel obstruction

Maydl’s hernia - W loop
x

249
Q

What is Acute pancreatitis

A

Acute inflammation of the pancreas with variable involvement of other regional tissues

Mild: Minimal organ dysfunction and uneventful recovery
Severe: Organ failure and/or local complications such as necrosis, abscesses and pseudocysts

250
Q

What are causes of Acute pancreatitis

A

GET SMASHED

Gallstones
Ethanol
Trauma
Steroids
Mumps/HIV/Coxsackie
Autoimmune
Scorpion venom
Hypercalcaemia/Hypertryglceridaemia
ERCP
Drugs (Valproate, Steroids, thiazides, azathioprine)
251
Q

What are the signs and symptoms of Acute pancreatitis

A

Severe Epigastric pain and tenderness radiating to the back - Relieved by sitting forward and aggravated by movement
Fever
Shock
Decreased bowel sounds

Severe:

  • Cullen’s sign (Periumbilical bruising)
  • Grey-Turner signs (Flank bruising)
252
Q

How is Acute pancreatitis diagnosed

A

Serum amylase/lipase (3x upper limit)
FBC
LFTs

MRCP
US

Gold standard: CT scan with contrast

253
Q

What are the scoring systems used in Acute pancreatitis

A

Glasgow score, APACHE II score and ransom score used to assess severity

Poor prognosis:
Glasgow >3
APACHE >8
Ranson >8

Glasgow
PaO2 - <8kPa
Age - >55
Neutrophils, WCC - >15
Calcium - <2
Renal, Urea - >16
Enzymes, LDH >600 or AST >200
Albumin <32
Sugar, Glucose >10
254
Q

How is Acute pancreatitis treated

A

Medical:

  • Fluid and electrolyte resuscitation
  • Urinary catheter and NG tube if vomiting
  • Analgesia
  • Blood glucose control
  • HDU and ITU support if necessary
  • Prophylactic antibiotics may be useful in reducing mortality

ERCP and sphincterotomy:
Used for gallstones in the presence of cholangitis.
If there is gallstones with no cholangitis a cholecystectomy is preferred.

Surgical:
If there is a sterile pancreatic necrosis then catheter drainage or a necrosectomy can be performed

If it is infected then IV antibiotic should be given before drainage or necrosectomy

255
Q

What are complications of Acute pancreatitis

A 
Pancreatic necrosis
Pseudocyst
Abscess
Ascites
VT

Multiorgan failue
Sepsis
Renal failure
ARD
DIC
Hypocalcaemia
Diabetes
256
Q

What is Chronic Pancreatitis

A

Chronic inflammatory disease of the pancreas characterised by irreversible parenchymal atrophy and fibrosis leading to impaired endocrine and exocrine function and recurrent abdominal pain

257
Q

What are the causes of Chronic pancreatitis

A

Alcohol - 70%
Idiopathic - 20%

Rare: Recurrent acute pancreatitis, ductal obstruction, pancreas divisor, hereditary pancreatitis, tropical pancreatitis, autoimmune pancreatitis, hyperparathyroidism

258
Q

What are the signs and symptoms of Chronic pancreatitis

A

Recurrent severe epigastric pain and tenderness radiating to the back relieved by sitting forward
Aggravated by eating or drinking alcohol

Over year:
Weight loss
Bloating
Steatorrhoea

259
Q

How is Chronic pancreatitis diagnosed

A

Bloods:
High glucose

Faecal elastase-1 - Low

Abdo US

ERCP - Gold standard

260
Q

How is Chronic pancreatitis treated

A

General:

  • Treatment is mainly symptomatic and supportive (e.g. dietary advice, stop smoking/drinking, treat diabetes, oral pancreatic enzyme replacement, analgesia)
  • Chronic pain management may need specialist input

Endoscopy Therapy:

  • Sphincterotomy
  • Stone extraction
  • Dilatation and stenting of strictures
  • Extracorporial shock-wave lithotripsy (ESWL) is sometimes used to fragment larger pancreatic stones before removal

Surgical:

  • May be indicated if medical management fails
  • Lateral pancreaticojejunal drainage (modified Puestow procedure)
  • Pancreatic resection (pancreaticoduodenectomy or Whipple’s procedure)
  • Limited resection of pancreatic head (Beger procedure)
  • Combining opening of the pancreatic duct and excavation of the pancreatic head (Frey procedure)
261
Q

Outline Vitamin A deficiency

A

Fat soluble - Absorbed in the small intestine

Found in Liver, Milk and eggs (Protein generally)

Deficiency due to malnutrition, poor conversion from carotene to vitamin A or reduced absorption

S+S: Night blindness then as the diseases progresses, the cornea becomes hazy and can develop erosions which can lead to its destruction and eventually complete blindness.
Can also get drying, scaling and follicular thickening of the skin due to keratinisation of skin
Respiratory infections due to keratinisation of mucous membranes in respiratory tract.

T: Daily oral vitamin A supplements/Dietary intake

262
Q

Outline Vitamin B1 (Thiamine) deficiency

A

Absorbed in small intestine

Beri-beri and Werincke’s encephalopathy

Wet Beriberi - There is heart failure with general oedema

Dry Beriberi - Neuropathy

RFs:

  • Diets consisting of high levels of milled rice and raw freshwater fish
  • High consumption of tea, coffee and betel nuts
  • Alcoholic state
  • Starvation state
  • Prolonged vomiting
  • Gastric bypass surgery – due to limited caloric intake post surgery
  • Parental nutrition without adequate thiamine supplementation

S+S: Wet: palpitations, SOB, leg swelling, tachycardia
Dry: Numbness of peripheries, confusion, trouble moving legs, pain

T: Thiamine (Pabrinex) I, Oral supplementation to continue after IV

263
Q

Outline Vitamin B3 (Niacin) deficiency

A

Pellagra

Niacin found in beans, milk and eggs

Dementia
Diarrhoea
Dermatitis

S+S: 
Loss of appetite
Generalised weakness
Irritability and aggression
Abdominal pain
Vomiting
Stomatitis.
Bright red glossitis.
Vaginitis.
Oesophagitis.
Dermatitis - classically, a pigmented, scaly rash prominent in sun-exposed skin

T: Oral supplementation

264
Q

Outline Vitamin C deficiency

A

Scurvy

Important for wound healing

265
Q

Outline Vitamin E deficiency

A

Fat soluble

266
Q

Outline Vitamine K deficiency

A

Fat soluble

All conditions - Year 3 (16 decks)

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