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Medicine Year 3 > GI > Flashcards

GI Flashcards

1
Q

Liver Abscess or cyst

A

Liver infection resulting in a walled off collection of pus or cyst fluid

Pyogenic cause: E. Coli, Klebsiella, etc.

  • > 60% caused by biliary tract disease (gallstones)
  • > 60 yrs age, most common liver abscess in industrialised area

Amoebic cause: Entamoeba histolytica (most common worldwide)

Hydatid cyst cause: Tapeworm
(sheep rearing countries)

Other: TB

History: Fever, malaise, nausea, anorexia, night sweats, weight loss, RUQ or epigastric pain, jaundice, PUO, foreign travel

Exam: Fever, jaundice, tender hepatomegaly

Investigation:

Blood: FBC (mild anaemia, leukocytosis, increased eosinophils due to hydatid disease), LFTs (increased ALP and bilirubin), increased ESR, increased CRP

Stool MCS: For tapeworm

Ultrasound to detect mass

Aspiration and culture of abscess material

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2
Q

Liver Failure

A

Severe liver dysfunction leading to jaundice, encephalopathy, and coagulopathy

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3
Q

Liver Failure causes

A
  • Viral (hepatitis a,b,d,e)
  • Drugs (paracetamol overdose)
  • Less common: Autoimmune hepatitis, budd-chiari syndrome, haemachromatosis, wilson’s disease
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4
Q

Liver failure: Pathogenesis of manifestations

A

Jaundice: Decreased secretion of conjugated bilirubin

Encephalopathy: Increased delivery of gut-derived products into the systemic circulation and brain due to decrease in extraction of nitrogenous products by liver and portal systemic shunting
Ammonia may play a part

Coagulopathy: Decreased synthesis of clotting factors, decreased platelets (hypersplenism if chronic portal hypertension)

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5
Q

Liver failure Epidemiology

A

Paracetamol overdose accounts for 50% of acute liver failure in the UK

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6
Q

Liver failure symptoms

A

May be asymptomatic. Fever, nausea, jaundice.

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7
Q

Liver failure examination

A

Jaundice
Encephalopathy
Liver asterixis
Fetor hepaticus (in portal hypertension where portosystemic shunting allows thiols to pass directly into the lungs -> sweet smelling breath)
Ascites and splenomegaly
Bruising
Look for secondary causes (kaiser Fleischer rings)

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8
Q

Liver failure Investigation

A

Identify cause: Viral serology, paracetamol levels, autoantibodies (ASM, LKM), ferritin, caeruplasmin and urinary copper (decreased and increased respectively in Wilson’s disease)

Blood: FBC (Hb decreased in GI bleed, WCC increased in infection), U&E (may show hepatorenal failure), glucose, LFTs, ESR/CRP, coagulation screen, group and save, ABG

Ultra sound and CT scan liver

Ascitic fluid: MCS, check for spontaneous bacterial peritonitis

Doppler scan of hepatic or portal veins: to exclude budd- chiari syndrome

Electroencephalogram: to monitor encephalopathy

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9
Q

Liver failure management

A

Resuscitation (according to airway, breathing, and circulation) ITU care

Treat the cause if possible: n-acetylcysteine for paracetamol overdose

Treatment/Prevention of complications:

  • Invasive ventilatory and cardiovascular support often required
  • Monitor: Vital signs, pH, creatinine, urine output, and encephalopathy
  • Manage encephalopathy: Lactulose and phosphate enemas
  • Antibiotic and anti-fungal prophylaxis
  • Hypoglycaemia treatment
  • Coagulopathy treatment: IV vitamin K, FFP

Renal failure: Haemofiltration and nutritional support

Surgical: transplantation

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10
Q

Complications of liver failure

A

infection, coagulopathy , hypoglaecaemia,

hepatorenal syndrome, cerebral oedema

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11
Q

Prognosis of liver failure

A

Childs Pugh score

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12
Q

Mallory Weiss tear

A

Persistent vomiting/retching causes hematemesis via an oesophageal mucosal tear.

Vomiting ALWAYS precedes bleeding

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13
Q

Mallory Weiss epidemiology

A

Account for around 10% of cases presenting with upper GI bleed

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14
Q

Mallory Weiss Aetiology

A

Most occur after a sudden rise in intra-abdominal pressure or transmural pressure gradient across the gastro-esophageal junction. This induces a tear and subsequent GI bleeding.

Risk factors:
Alcohol
Hiatal hernia
Retching, vomiting, straining

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15
Q

Mallory Weiss history and examination

A

Commonly presents with hematemesis after an episode of forceful or long-term vomiting, retching, coughing, or straining.

melena
light-headedness
syncope
abdominal pain

Examination is usually unremarkable (May have postural drop due to blood loss)

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16
Q

Mallory Weiss Investigations

A

Blood:

  • FBC (to evaluate the extent of blood loss)
  • U&Es (to evaluate the degree of volume loss)
  • Clotting screen if coagulopathy suspected
  • Pregnancy test
  • Endoscopy is diagnostic and can be therapeutic (shows linear laceration at the gastro-esophageal junction, perform within 24h to maximise diagnostic efficiency)
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17
Q

Mallory Weiss Management

A

In 80-90% of patients, haemorrhage stops spontaneously and re-bleeding is rare.

Monitor intravascular volume and stabilize if significant hypovolaemia.

Correct coagulopathy if present.

Uncontrolled haemorrhage usually responds to endoscopic injection clipping, and electrocoagulation.

Surgery is rarely required in the case of a bleeding artery at the base of the tear.

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18
Q

Nasogastric tube insertion

A

Tube that is passed through the nose and down through the nasopharynx and esophagus into the stomach.

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19
Q

NG tube indications

A
  • Aspiration of gastric contents for diagnostic (GI haemorrhage) or therapeutic purposes (Bowel obstruction, ileus, sepsis)
  • Intra or postoperatively where ileus may be expected to occur, or to facilitate surgery in laparoscopic procedures where a decompressed stomach is needed
  • Preoperatively to decompress the stomach to reduce risk of aspiration
  • Administration of drugs, enteral feeding
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20
Q

Ileus

A

Lack of movement somewhere in the intestine that leads to a build up and potential blockage of food material

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21
Q

NG tube insertion complications

A 
Trauma
Bleeding
Infection 
Vomiting
Misplacement of tube 
Blockage of tube
Aspiration of gastric contents risk
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22
Q

Non-alcoholic Fatty Liver Disease (NAFLD)

A

Results from fat deposition in the liver.

The hepatic manifestation of the metabolic syndrome ->3 out 5 of obesity, hypertension, diabetes, hypertryglyceridemia, hyperlipidemia

Spectrum of disease ranging from: Steatosis (fatty liver), steatohepatitis,
Fibrosis, and Cirrhosis.

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23
Q

NASH Epidemiology

A

Very common and increasing in incidence due to rising obesity rates.

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24
Q

Aetiology of NASH

A

-Associations: Obesity and diabetes, parenteral nutrition, short bowel syndrome, hyperlipidemia, drugs (amiodarone, tamoxifen)

Insulin resistance plays a key role and is linked to obesity.
Insulin resistance causes the accumulation of fat and hepatocyte injury. Inflammation of the hepatocytes leads to fibrosis and eventually, cirrhosis in some individuals.

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25
Q

NASH history

A

Most cases are asymptomatic and discovered because of abnormal liver function tests

Occasionally cases present with complications related to cirrhosis

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26
Q

Cirrhosis History

A

Early non-specific symptoms: anorexia, nausea, fatigue, weakness, weight loss

Symptoms caused by decreased synthetic function of liver: easy bruising, abdominal swelling, ankle oedema, leukonychia

Symptoms caused by decreased metabolic (detoxification) function of liver: Jaundice, confusion, amenorrhea

Portal hypertension: abdominal swelling, haematemesis, PR bleeding or malaena

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27
Q

NASH Examination

A 
Stigmata of chronic liver disease:
Asterixis (liver flap)
Bruises
Clubbing
Dupuytren's contracture
Erythema

Hepatomegaly

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28
Q

NASH Investigation

A

LFT:
Increase in liver enzymes

Generally in NASH:
Increase in ALT and sometimes AST

Generally in Alcoholic fatty liver disease:
Increased AST and AST:ALT >2

Imaging studies: USS, CT, MRI to look for fatty infiltrates

Biopsy: To diagnose and assess the severity of the disease (Liver with more than 5% fat content is abnormal)

Histopathologic changes: Mallory Denk bodies

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29
Q

NASH Prognosis

A

Steatosis has a very low risk of progression to chronic liver disease.

NASH progresses to cirrhosis in 10-15% of cases over 8 years.

Patients with cirrhosis due to NAFLD generally have a better survival rate than patients with cirrhosis due to alcoholic liver disease.

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30
Q

NASH Management

A

Aim of management is to reduce progression of NAFLD and to reduce risks of cardiac and liver related mortality.

  • Reverse factors that contribute to insulin resistance: Healthy diet, active lifestyle, medication that controls blood glucose
  • Advise on limiting alcohol intake
  • currently no specific drug licensed for treatment
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31
Q

NASH complications

A

Portal hypertension with ascites

Encephalopathy

Variceal haemorrhage

Hepatocellular carcinoma

Hepatorenal syndrome

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32
Q

Acute Pancreatitis

A

Acute inflammatory process of the pancreas.

Mild- minimal organ dysfunction and uneventful recovery

Severe- Organ failure and complications such as necrosis, abscess or pseudocyst

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33
Q

Acute pancreatitis aetiology

A

Insult results in activation of pancreatic proenzymes within the duct/acini resulting in tissue damage and inflammation.

Causes: I GET SMASHED

Idiopathic
Gallstones
Ethanol
Steroids
Mumps virus
Autoimmune diseases
Scorpion bites
Hypertryglyceridemia and hypercalcaemia 
ERCP
Drugs (azathioprine, valproate, thiazide, steroids)
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34
Q

Pancreatic acinar cells

A

Functional unit of the exocrine pancreas. Synthesizes, stores, and secretes digestive enzymes.

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35
Q

Acute pancreatitis history

A

Severe epigastric or abdominal pain (radiating to back, relieved by sitting forward, aggravated by movement)

Anorexia, nausea, vomiting

May be history of gallstones or alcohol intake.

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36
Q

Acute pancreatitis epidemiology

A

Common
peak age 60
Males: alcohol
Females: Gallstones (fat, female, fertile, forty)

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37
Q

Acute Pancreatitis Examination

A 
Epigastric tenderness
fever
shock 
tachycardia
tachypnoea
Decreased bowel sounds due to ileus

If severe and hemorrhagic -> Turners sign and Cullen’s sign

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38
Q

Acute Pancreatitis

Investigation

A 
BLOODS
Increased amylase 
FBC (increased WCC)
Hypocalcaemia
LFT

USS: gallstones or biliary dilatation

AXR: Exclude other causes. Psoas shadow may be lost

CT scan: inflammation, necrosis, pseudocyst

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39
Q

Acute Pancreatitis Management

A

Medical:

  • fluid and electrolyte resuscitation
  • urinary catheter
  • NG tube if vomiting
  • analgesia and blood sugar control
  • early HDU or intensive care support
  • enteral feeding over parenteral
  • antibiotics if infective pancreatic necrosis develops

ERCP and sphincterotomy:
For gallstone pancreatitis, cholangitis, jaundice, or dilated common bile duct, ideally within 72 hours

Early detection and treatment of complications

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40
Q

Acute Pancreatitis complications

A

Local: Pancreatic necrosis, pseudocyst, abscess

Systemic: Sepsis, ARDS, DIC

Long term: Chronic pancreatitis

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41
Q

Acute Pancreatitis

Prognosis

A

80% run milder course (5% mortality)

20% run fulminating course with high mortality

(Infected pancreatic necrosis associated with 70% mortality)

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42
Q

Chronic Pancreatitis

A

Chronic inflammatory disease of the pancreas characterised by irreversible changes to structure (atrophy, fibrosis, calcification) leading to impaired endocrine and exocrine function.

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43
Q

Chronic pancreatitis aetiology

A

Alcohol 70%
Idiopathic 20%

Rare: Recurrent acute pancreatitis, cystic fibrosis

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44
Q

Chronic pancreatitis epidemiology

A

Mean age 40-50 in alcohol abuse

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45
Q

Chronic pancreatitis history and exam

A
  • Recurrent severe epigastric pain
  • radiating to back
  • relieved by sitting forward
  • can be exacerbated by drinking alcohol or eating
  • weight loss, bloating, pale smelly stool (steatorrhea) due to pancreatic insufficiency (trouble absorbing food and fat)

Tenderness in epigastric region
weight loss
malnutrition (deficiency in fat soluble vitamins A,D,E,K)

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46
Q

Chronic pancreatitis Invesitgations

A

Bloods:

  • increased glucose may indicate endocrine dysfunction
  • amylase and lipase are usually normal

ERCP or MRCP:
Early changes-> main ductal dilatation and stumping of branches
Late changes-> chain of lake appearance

AXR: pancreatic calcification may be visible

CT: pancreatic cysts

Faecal elastase

47
Q

Chronic pancreatitis management

A

General:
Treatment is symptomatic and supportive - dietary advice, abstinence from alcohol and smoking, treatment of diabetes, oral pancreatic enzyme replacement (creon),
Chronic pain management

Endoscopic therapy: sphincterotomy, stone extraction, etc. (remove stones)

Surgical: Optional if medical treatment fails

48
Q

Chronic pancreatitis complications

A

Local: pseudocyst, biliary duct stricture, pancreatic ascites, pancreatic carcinoma

Systemic: Diabetes, steatorrhea, reduced QOL, chronic pain syndromes, dependence on strong analgesics

49
Q

Chronic pancreatitis prognosis

A

Difficult to predict as pain may improve, stabilise, or worsen

Surgery may improve symptoms in 60-70%

Life expectancy can be reduced by 10-20 years

50
Q

Peptic ulcer disease

A

Ulceration of areas of the GI tract caused by exposure to gastric acid and pepsin.

51
Q

Peptic ulcer disease aetiology

A

Imbalance between damaging action of acid and pepsin and mucosal protective mechanism.

Very strong association with H. pylori infection and NSAID use

Rare: Zollinger-Ellison syndrome (tumours form which secrete gastrin and lead to increase in acid)

52
Q

Peptic ulcer disease epi.

A

Common

more common in males

53
Q

Peptic ulcer disease history and exam

A

Epigastric pain relieved by antacids

If worse soon after eating food, gastric

If worse several hours after eating food, duodenal

May present with haematemesis and malaena

May be no physical findings
Epigastric tenderness
Anaemia

54
Q

Peptic ulcer disease Investigations

A

Bloods: FBC (anaemia), amylase (to exclude pancreatitis), cross match if actively bleeding

Secretin test (in patients suspected of Zollinger- Ellison syndrome: IV secretin causes a rise in serum gastrin in ZE patient but not controls)

Endoscopy:
-4 quadrant gastric ulcer biopsy to rule out malignancy (duodenal ulcer do not need biopsy)

Rockall scoring for severity after GI bleed (less than 3 has good prognosis, greater than 8 have a high mortality)

Testing for H. pylori:
C-Urea breath test
Stool antigen test
Serology

55
Q

Peptic ulcer disease Management

A

Acute:
Resuscitation if perforated or bleeding (IV colloids/crystalloids), vital sign monitoring, endoscopic/surgical treatment

Endoscopy:
Haemostasis by injection sclerotherapy, laser, or electrocoagulation

Surgery:
If bleeding cannot be controlled

H. Pylori eradication

If not associated with H. pylori: PPi or H-2 antagonists + stop NSAID use

56
Q

Patients with acute upper GI bleeding

A

Should be treated with IV PPI (omeprazole) at presentation until the cause of the bleeding is confirmed.
Patients with actively bleeding ulcers or ulcers with high-risk stigmata should continue IV PPI.
Switch to oral PPI if there is no rebleeding within 24 hours.

57
Q

H. Pylori eradication

A

triple therapy for 1-2 weeks

One PPI (omeprazole)
2 antibiotics (clarithromycin and amoxicillin)
58
Q

Peptic ulcer disease

Complications and Prognosis

A

Rate of complication is 1% per year (haemorrhage, perforation, obstruction/pyloric stenosis)

Overall lifetime risk is 10%
generally good prognosis

59
Q

Gastritis

A

Irritation and inflammation of the stomach lining

Most common causes: H. Pylori, NSAIDs, alcohol, stress, autoimmune

Investigation: Gastritis is suspected when people complain of pain and discomfort in the upper part of the abdomen. Biopsy and endoscopy.

Treatment depends on aetiology:

  • H-pylori eradication therapy
  • reduction in NSAIDs or alcohol exposure
  • symptomatic therapy with h2 antagonists and PPIs

If untreated progression to gastric carcinoma and lymphoma

60
Q

Features of upper GI malignancy that require urgent endoscopy

A 
GI bleeding
anaemia
early satiety
unexplained weight loss
progressive dysphagia (difficulty)
odynophagia (pain)
persistent vomiting
61
Q

Perianal abscess

A

Thought to arise due to obstruction and infection within an anal gland and subsequent spread of infection into the adjacent tissue space. (E. coli and enterococci are common)

History: severe, perianal pain, worse sitting, lying supine, or bowel motions
Sometimes perianal pus discharge

Examination: tachycardia may be present, exam of anus reveals tender, fluctuant swelling in the perianal region with redness of overlying skin, DRE is not possible cause of pain

Investigation: Inflammatory markers

Treatment: Surgical drainage

62
Q

Perianal fistula

A

Most anal fistulae present initially as anorectal abscesses.

It is an abnormal tract or cavity communicating between the skin and the rectum or anus.

Surgical treatment, obliterate internal fistulous opening

63
Q

Peritonitis

A

Inflammation of the peritoneum, the membrane that lines the abdominal cavity and its organs.

  1. Primary
  2. Secondary
64
Q

Primary Peritonitis: Spontaneous bacterial peritonitis

A

Occurs in patients with ascites and is thought to be caused by bacterial translocation into the peritoneal cavity in the setting of:

  1. immune system dysfunction
  2. altered portal circulation
  3. abnormal gut motility
  • Patients are commonly minimally symptomatic but may present with abdominal pain, fever, vomiting, altered mental status, GI bleeding
  • Investigation: Paracentesis, peritoneal lavage, abdominal imaging
  • defined as ascitic fluid absolute neutrophil count >250 cells/mm^3
  • treatment: antobiotics and albumin
  • complication: renal dysfunction
65
Q

Secondary Peritonitis

A

A clear site of origin is identified (perforated viscus, external penetrating injury, presence of foreign body)

66
Q

Most frequent encountered bacterial infection in patients with cirrhosis

A

Spontaneous bacterial peritonitis

67
Q

Pilonidal sinus

A

Small hole or tunnel in the skin, usually at the top of the cleft between the buttocks.

Most commonly occur in young adults, more men than women, and people with a lot of body hair and overweight

May be asymptomatic or may become infected. This will cause pain and swelling and abscess full of pus to develop.

Treatment:
Minimal disease-> hygiene, keep area hair free
Abscess-> drained
Surgery: Wide excision or excision and primary closure

68
Q

Portal hypertension

A

Increased PB within the portal venous system and defined as an increase in the pressure gradient between the portal veins and the the hepatic veins (>5mmHg)

69
Q

Portal Hypertension Pathophysiology

A

Portal pressure depends on portal blood flow and vascular resistance.

A rise in portal pressure leads to the development of collaterals to carry blood from the portal system to the systemic circulation.

Collaterals occur at specific sites:

  1. Oesophagus (varices)
  2. Anal canal (varices)
  3. Falciform (umbilical varices)
  4. Abdominal wall and retroperitoneum

Leads to dilated cutaneous veins, varices, splenomegaly, ascites, small intestine mucosal oedema (malabsorption)

70
Q

Portal hypertension aetiology

A

Prehepatic cause: Portal vein occlusion

Intrahepatic: commonest cause -> cirrhosis from chronic liver disease

Posthepatic: Hepatic vein occlusion (budd-chiari)

71
Q

Portal Hypertension Investigation

A

Bloods
FBC (anaemia, low platelets in hypersplenism)

Abdominal USS: splenomegaly, collateral veins

MRI: liver lesions

GI endoscopy: Varices

Liver biobsy

72
Q

Management of portal hypertension

A

Emergency management of bleeding varices
-> variceal banding (endoscopic ligation technique)
Surgical portosystemic shunting
Liver transplantation

Primary prophylaxis: Beta blockers (splanchnic vasoconstriction and reduction of cardiac output)

73
Q

Primary biliary cirrhosis

A

A chronic inflammatory liver disease involving progressive destruction of intra-hepatic bile ducts, leading to cholestasis and, ultimately, cirrhosis.

74
Q

Cholestasis

A

Reduction or stoppage of bile flow

75
Q

Primary biliary cirrhosis aetiology and epi.

A

unknown
autoimmune is likely

1-2 in 10,000
more women than men (9:1)

76
Q

PBC history and exam

A

Incidental finding on blood test (increased alkphos & cholesterol)

Insidious onset
Fatigue, weight loss, pruritus
discomfort in RUQ

May present with complication of liver decompensation (jaundice, ascites, variceal bleeding)

Early: no signs
Late: Jaundice, sctrach marks, xanthomas, hepatomegaly, ascites, palmar eythema, clubbing, spider naevi

77
Q

Associated conditions of PBS

A

Sjogrens syndrome (dry eyes and mouth)

athritis

raynaud phenomenon

autoimmune thyroid disease

78
Q

PBC Investigations

A

Blood: LFT (+AlkPhos, +GGT, +AMA, +IgM, +cholesterol)

USS: Exclude extra-hepatic biliary obstruction

Liver biopsy: Chronic inflammatory cells and granulomas around intra-hepatic bile ducts, destruction of bile ducts, fibrosis, and regenerating nodules of hepatocytes.

79
Q

Primary sclerosing cholangitis

A

Chronic cholestatic liver disease characterised by progressive inflammatory fibrosis and obliteration of intra-hepatic and extra-hepatic bile ducts.

80
Q

Primary scleosing cholangitis aetiology and epi.

A

Unknown.

Close association with IBD, especially UC

2-7 in 100,000
Presents between 25-40

81
Q

PSC History and exam

A

Asymptomatic
Diagnosed with persistently raised alkphos
Intermittent jaundice, RUQ pain, puritus, weight loss, fatigue
May have acute cholangitis: fever, rigors

No signs or evidence of jaundice, hepatospenomegaly ,etc.

82
Q

PSC Investigations

A

Blood
LFT: (+alkPhos, +GGT)
Serology: Immunoglobulin levels (pANCA present in 70%)

ERCP: Stricturing and interspersed dilatation of intrahepatic and extrahepatic bile ducts

MRCP: non invasive

Liver biopsy: Confirms diagnosis and allows staging of disease

83
Q

Rectal prolapse

A

Prolapse of the rectum through the anus.

Most often occurs in elderly females.

Presentation: Recurrent rectal prolapse on staining that this time fils to reduce spontaneously

Exam: Non-tender, oedematous, circumferential, full thickness rectal tissue protrudes through the anal canal

Unlike prolapsed piles, a rectal prolapse looks like a complete ring with a central orifice

May present with minor bleeding

Management: reduce rectal prolapse, stool softener, will probably happen again, avoid straining, operative repair

84
Q

Ulcerative colitis

A

Relapsing and remitting inflammatory disorder of the large bowel.

Classification: Location
Mild, Moderate, Severe

Presents at age 15-30

85
Q

Ulcerative Colitis

A 
Mucosa and submucosa
Starts distally (rectum) and spreads proximally
Continuous inflammation 
Pseudopolyps
BLOODY DIARRHOEA always present 
Tenesmus
Pain diffuse/Lower abdominal pain
Relapse/remitting (well between attacks)
P-anca positive 
Increased risk of PSC, CRC, cholangiocarcinoma -> surveillance colonoscopy
86
Q

EXTRA GI features of IBD

A 
Aphthous mouth ulceration
Erythema nodusum
Pyoderma gangrenosum
Episcleritis/scleritis/anterior uveitis
Arthritis
87
Q

Crohns disease

A

Non-caseating granulomas
Transmural
Any part of the GI tract, esp. terminal ileum and AC
Skip lesions
Ulcers, strictures, perianal abscesses, fistulae
Diarrhoea (Not blood usually)
Pain diffuse/RLQ
Weight loss/ systemically unwell more likely
p-anca negative

88
Q

Diagnosis of UC and Crohns

A

Stool sample
(Infectious? Faecal calprotectin - IBS?)

Bloods: FBC, iron studies, folate, B12, LFT, U and E, CRP, ESR, Auto-antibodies

Imaging: AXR, Ct abdomen, MRI abdo/pelvis, double contrast barium enema

Flexible sigmoidoscopy/colonoscopy and biopsy

89
Q

Wilson’s disease (hepatolenticular degeneration)

A

Autosomal recessive disorder characterized by decreased biliary excretion of copper and accumulation in liver and brain, especially basal ganglia.

90
Q

Wilson’s disease

Aeti. and epi.

A

Mutation in gene coding for a copper transporting ATPase in hepatocytes.

Excess copper damages hepatocyte mitochondria, causing cell death and release of free copper into plasma, which is then deposited in other tissues.

prevalence 1 in 30,000
carrier 1 in 100
liver disease presents in kids >5 yrs

Neurology in adults

91
Q

Wilson’s disease

History and exam

A

Liver: Hepatitis, liver failure or cirrhosis, jaundice, easy bruising

Neuro: Dyskinesia, rigidity, tremor, dystonia, dysarthria, dysphagia, ataxia

Psychiatry: Personality change, conduct disorder, psychosis

Liver: Jaundice, ascites, gynaecomestia

Neuro: as above

Eyes: Kayser- Fleischer ring and sunflower cataract

92
Q

Wilson’s Investigation

A

Blood
LFT (+AST, ALT, ALKPHOS)
Serum caeruloplasmin and copper (low, but may provide false negative as it is an acute phase protein)

24 Hour urinary copper level increased

Liver biopsy: Increased copper content

Genetic analysis: difficult

93
Q

UC management

A

Acute Exacerbation:
IV rehydration, IV corticosteroids, antibiotics, bowel rest, parenteral feeding may be necessary, and DVT prophylaxis. Monitor vital signs and fluid balance.

Mild disease: Oral or rectal 5-aminosalicylic acid derivates

Moderate disease: Oral steroids and oral 5-asa. Immunosuppression with azathioprine, cyclosporine, inlfiximab, 5-mercaptopurine

Advice: Patient education and support. Treatment of complications. Regular colonoscopic surveillance.

Surgical: Indicated for failure of medical treatment, presence of complications , or to prevent cancer.
Proctocolectomy with ileostomy or an ileo-anal pouch formation.

94
Q

UC Investigation

A

Bloods: FBC (-Hb, +WCC)
Increased CRP and ESR

Stool: Culture as infectious colitis is differential diagnosis.

AXR: Rule out toxic megacolon

Flexible sigmoidoscopy or colonoscopy: determines severity, histological confirmation , detection of dysplasia

Barium enema: Pseudocyst, colon has leadpipe appearance

95
Q

UC Aetiology

A

Positive family history of IBD (15%)

Associated with increase in serum pANCA and PSC

96
Q

Viral Hepatitis

A

3 main symptoms apply to all hepatitis:
Fever
Jaundice
Raised ALT and AST

97
Q

Hepatitis A

A 
Fecal oral transmission
Travelers
Acute
vaccination 
Management: Supportive and avoid alcohol
98
Q

Hepatitis E

A

Faecal oral
epidemics
Very bad for pregnant women (fulminant hepatitis)
Supportive management

99
Q

Hepatitis B

A

sexual contact, blood, vertical transmission

Prodrome: flu-like, rash, lymphadenopathy

Acute: Nausea, RUQ pain, anorexia, jaundice

Outcome: 90% completely recover 10% develop chronic infection

Management: Acute (symptom supportive) and chronic (peginterferon alpha and tonofovir)

100
Q

Risk factor for hepatocellular carcinoma

A

Hepatitis B and C

101
Q

Hep C

A

Parenteral route transmission
(sex and vertical transmission uncommon)

acute and chronic (80% develop chronic)

Acute management: supportive

Chronic management: Interferon and ribavarin

102
Q

Hep D

A

Can only happen if infected with hep b

103
Q

Volvulus

A

Twisting of the small or large bowel around its mesenteric axis.

104
Q

Volvulus aetiology

A

Risk factors: chronic constipation and high fiber diet

Most common location: Sigmoid and Caecum (most mobile segments)

Can lead to obstruction and
torsion and occlusion of mesenteric vessels resulting in ischaemia and necrosis (emergency)

105
Q

Sigmoid and caecal volvulus

A

Sudden onset abdominal pain, constipation, nausea, and vomiting

Pain is continuous with overlying colicky pain during peristalsis

Abdomen distended, tympanic, tender to palpation.

may have fever, tachycardia, hypotension

106
Q

Sigmoid volvulus

A

Coffee bean sign

107
Q

Caecal Volvulus

A

Presents with features of bowel obstruction.

Colicky abdominal pain, vomiting, and abdominal distension.

Looks like embryo

108
Q

Sigmoid volvulus

A

No ischaemia -> endoscopic reduction -> if fails surgery

Usually occurs in institutionalised elderly

109
Q

caecal volvulus

A

young population

surgical

110
Q

Bowel obstruction

A

Mechanical or functional obstruction of the intestines which prevents the normal movement of products of digestion.

111
Q

Bowel obstruction symptoms

A 
abdominal pain
distension
nausea
vomiting
fever

Complete obstruction or strangulation is a surgical emergency

Can present atypically in elderly

112
Q

Bowel obstruction investigations

A

Blood count and lactate
Ct abdomen
Mri

113
Q

Bowel obstruction management

A 
IV fluids
Drip and suck
catheter
enemas
stents
surgery

Medicine Year 3 (13 decks)

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