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Adult health 1 > Learning Objectives GI > Flashcards

Learning Objectives GI Flashcards

1
Q

Learning objectives AH1 Rotation outline:

A
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2
Q

What are the causes of acute upper GI bleed? List 6 (3 marks)

What are the clinical features of UGIB? (2 marks)

What needs to be covered on history: Think: Symptoms/ALARMS symptoms, Pmhx, medications:

Exam: DRSABCDE, Goals of assessment, VS, peripheral stigmata of disease, abdo, DRE, underlying comorbidites

Investigations: Labs, Imaging (4 marks) important!

A
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3
Q

What are common causes of upper GI bleeds (2.5 marks)

What is the risk assessment tool associated with UGIB bleeds called? What is the rockall score and its use?

A

Risk assessment score

    • Glasglow Blatchford Score (GBS)
  • Use - calculated in ED for risk stratification for further investigation
  • Interpretation: 1+ = high risk bleed requires intervention

Rockall score

  • Use calculate risk of recurrent risk after endoscopy
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4
Q

Outline management of acute UGIB:

Resus (ABCDE), Medical (different if varices), Upper endoscopy, preventing reoccurence.

A
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5
Q

Differential diagnosis for Melaena: Upper GI vs Lower GI.

Outline brief assessment for Melaena:

Investigations for patient with melaena?

A
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6
Q

Lower GI bleed:

Eitology: List 4- (2 marks)

Clinical features:

Management: (emergency, definitive management: Unstable vs stable) Give examples.

A
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7
Q

Upper GI Bleed: Toronto notes:

Definition:

Eitology: Above GE, Stomach, duodenum

Clinical features:

Treatment:

Prognosis:

A
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8
Q

What is an esophageal varice?

Eitology:

Clinical features:

Investigations:

Management. Acute, long term.

A
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9
Q

What is a Mallory-weiss tear?

Definition?

Eitology:

Clinical features:

Management:

A
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10
Q

What is the function of the pancreas?

Where is it located?

What is the main fuct of the pancreas? What are the two major cell types of the pancreas?

A
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11
Q

What is the function of the exocrine component of the pancreas? What are the 3 major pancreatic enzymes? Functions?

What are the three endocrine hormones of the pancreas?

What are important pancreatic markers? (lipase and amylase explain)

A
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12
Q

What are the three diagnostic criteria for acute pancreatitis?

What are the causes of acute pancreatitis? (IGETSMASHED)

What are the most common causes?

Pathophysiology: read !

What can acute pancreatitis lead to?

A
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13
Q

What are the gross and microscopic features of pancreatitis?

Clinical features: List 4 (symptoms), Signs (list 4)

What is your differential diagnosis for patient with severe epigastric pain radiating to back? (4 marks) GI/CV?Obsgyn/uro

A
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14
Q

What are complications of pancreatitis? Think: local and systemic: (2 marks for each)

A

Local

  • Pseudocyst (delayed) - encapsulated fluid collection; mass effect can cause biliary or gastric outlet obstruction; prone to infection, rupture & haemorrhage; treat by aspiration
  • Pancreatic fat necrosis
  • Infection & pancreatic sepsis
  • Haemorrhage - retroperitoneal haemorrhage, portal vein thrombosis (portal vein sits just posterior to pancreas)

Systemic

  • Hypovolemic shock & multi-organ failure : 3rd space loss (capillary leak) + SIRS (systemic cytokine release) + GI loss (vomiting, ↓intake) + retroperitoneal haematoma
  • AKI - hypovolemia; ↑intra-abdominal pressure –> abdominal compartment syndrome with occlusion of renal veins
  • Metabolic derangement - HAGMA, ↓Ca2+
  • Respiratory failure - (systemic cytokine release), pleural effusion, APO (cytokines + IVFs)
  • Diabetes mellitus
  • DIC
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15
Q

Investigations:

Bedside?

Labs? Bloods and findings? (2 marks) What is diagnostic?

Imaging and findings?

A

Investigation:

Bedside

  • VBG - HAGMA, hypocalcaemia
  • ↑BSL - necrosis of endocrine part of pancreas
  • ECG
  • BHCG

Labs Bloods

  • FBC (neutrophils↑)
  • Lipase (3x upper limit) - NOW THE DIAGNOSTIC TEST OF CHOICE
  • UECs, LFTs, CRP
  • G&H and cross-match
  • Coagulation

LFTs

  • ↑AST & ALT - very high suggests gallstone pancreatitis due to CBD obstruction (but also may be mildly elevated from surrounding inflammation)
  • ↑bilirubin/GGT - very high suggests gallstones as cause
  • ↓albumin (<32 used for severity)

UECs

  • Hypocalcaemia - enzyme release –> mesenteric fat necrosis –> free fatty acid release –> Ca2+ binds to fatty acids causing soap precipitation in abdomen
  • ↑urea & creatinine (AKI)
  • CRP >200 suggests necrotizing pancreatitis (used in severity)

Imaging

  • Erect CXR - perforation, complications (ARDS, APO, effusion)
  • USS abdomen (1st line imaging) - gallstones, biliary obstruction
  • CT abdomen with IV contrast - complications (haemorrhage, pseudocyst, necrosis), necrotic tissue has no enhancement
  • ERCP - identify and remove stones; if gallstone cause or diagnosis is uncertain
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16
Q

Imaging of pancreatitis?

USS findings? What to rule out as cause?

CT with contrast findings? List 4 features:

A
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17
Q

What is the Glasgow criteria for acute pancreatitis severity?

Whats it uses?

What is the Ranson criteria? Whats its use? Criteria? Interpretation?

A

Grading severity Glasgow criteria

  • Use - assess severity <48 hours of admission

Criteria = PANCREAS

  • Pa02 <60mmHg
  • Age >55y
  • Neutrophils - WCC >15
  • Ca2+ <2mmol/L
  • Renal function - urea >16 (or >1.8)
  • Enzymes - LDH >600,
  • Albumin < 32
  • Sugar - BSL >10

Interpretation

  • ≥3 in <48hrs = severe pancreatitis –> needs transfer to ICU

Ranson criteria

  • Use - estimate mortality after >48 hours of investigation
  • Criteria - similar criteria to Glasgow but uses both initial values & values after 48 hours of admission

Interpretation

  • 0-2: 2% mortality
  • 3-4: 15% mortality
  • 5-6: 40% mortality
  • 7-8: 100% mortality
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18
Q

Outline management for acute pancreatitis:

Think, Resus, supportive (mainstay), Specific (underlying causes, medical, surgical) Monitoring, communication, referral, monitor and follow up.

What is ERCP? What are complications of it?

A

ManagementResus

  • DRS
  • A - intubate if ↓LOC or ARDS
  • B - protective ventilation, high flow O2 15L non-rebreather
  • C - 2x IV access, aggressive IVFs (pancreatitis are IV depleted but fluid overloaded due to 3rd spacing & SIRS response), replace electrolytes

Supportive care (mainstay of pancreatitis)

  • U/O & IDC - monitor fluid balance with fluid chart

Nutrition

  • NBM initially then enteral feeding via nasojejunal tube (bypass pancreas to ↓stimulation)
  • IVFs & correct electrolytes
  • Analgesia - opioids
  • VTE - TED stockings, assess risk but enoxaparin often not used immediately as may require surgery

Specific management

  • Treat underlying causes: Biliary obstruction - treat gallstones (cholecystectomy etc.)
  • Cease alcohol

Medical

  • Alcoholic pancreatitis - put on AWS + thiamine + diazepam
  • Abx - ONLY for confirmed necrotising pancreatitis or evidence of infection only (done by aspirating necrotic area); use meropenem

Surgical

  • Gallstone pancreatitis (as for choledocholithiasis)
  • ERCP - remove CBD stone
  • Laparoscopic cholecystectomy - done on same admission due to high recurrence rate

Other surgical procedures (rare)

  • Debridement of infected necrotising pancreatitis - only other surgical indication
  • Drainage of pancreatic cyst

Monitoring

  • Vitals - hourly
  • Communication, referral, monitor and follow up

Referral - general surgeon review, ATODs etc.

  • Follow-up CT for complications

ERCP complications (must rule out if present)

  • Bleeding
  • Cholangitis (introduce organisms into tract)
  • Pancreatitis
  • Perforation
  • Strictures
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19
Q

What is chronic pancreatitis? What is it characterized by?

What are the causes (eitology)? Common? Others?

Pathophysiology? Read: What does it result it?

Clinical features (2.5 marks) (signs)

Differentials for malabsorption syndromes? (most common causes- 5 cs) 2.5 marks!

A

Definition: Irreversible pancreatic damage characterised by

  • Fibrosis
  • Necrosis
  • Inflammation

Etiology

Common

  • Chronic alcoholic (>90%)
  • Cystic fibrosis (2nd most common cause)

Others

  • Pancreatic duct obstruction - chronic gallstones, other CBD obstruction (malignancy, divisum)
  • Autoimmune pancreatitis
  • Tropical pancreatitis
  • Idiopathic

Pathophysiology

  • Alcohol - see mechanisms above
  • Recurrent acute pancreatitis results in: (similar to liver cirrhosis)
  • Fibrosis
  • Exocrine atrophy (destruction of exocrine pancreas)Cystic dilated ducts
  • Results in loss of pancreatic function causing clinical features
  1. Steatorrhea - fatty, pale stools
  2. Malabsorption –> weight loss, decreased albumin
  3. Fat intolerance

Late stage endocrine pancreas also lost

  1. Hyperglycaemia

Clinical features

  1. Recurrent attacks of severe epigastric pain radiating to back
  2. May be poorly localised upper abdominal and back pain

Pancreatic insufficiency

  • Malabsorption syndrome - steatorrhea, bloating/indigestion, weight loss, nutritional deficiencies (B12, folate etc.), anemia
  • DM
  • Repeated episodes of jaundice
  • If gallstone induced biliary obstruction (gallstone causing the pancreatitis)

DDx malabsorption

Most common causes (5Cs)

  1. Chronic pancreatitis
  2. Celiac disease
  3. Crohn disease
  4. CF
  5. Chronic infection - giardiasis, tropical sprue, Whipple’s
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20
Q

Investigations in chronic pancreatitis? (think:malabsorption steatorrhoea, DM)

Blood? Stool? Imaging?

Complications of Chronic pancreatitis? (list 4) 2 marks

A

Bloods

  • HbA1c
  • FBC - anemia
  • Lipase (usually normal)
  • UEC CMP - deficiencies
  • LFTs - ↑ALP/GGT if obstruction, hypoalbuminemia
  • Nutrients - iron, B12, folate, vitamin A D E K
  • Coagulation - vit K
  • Coeliac serology

Stool

  • OCP & MCS
  • Faecal elastase
  • 72h faecal fat test (measures exocrine function)

Imaging

  • AXR - pancreatic calcifications
  • Abdominal CT or USS - calcifications, dilated ducts, pseudocyst
  • Endoscopic USS (EUS)* (most sensitive) - dilated ducts, abnormal parenchyma
  • ERCP - abnormalities of ducts
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21
Q

Pathology of Chronic fibrosing pancreatitis: (x ray, ct macro, micro findings)

Management: Resus, active, supportive?

A
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22
Q

What is “pancreatic divisum”? What is the cause of it? how does it present?

Autoimmune pancreatitis? Clinical features? Ix? Rx?

Pancreatic neoplasm: Most common type? Clinical features (list 4) 2 marks?

A
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23
Q
  • Complications of :
  • Acute pancreatitis?
  • Chronic pancreatitis?
A
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24
Q

What is your differential for pancreatic cyst? (2 marks)

What are the types of pancreatic neoplasms?

What are the risk factors for pancreatic ductal adenocarcinoma? Mutations associated with it?

Patho: Gross:

A

Pancreatic masses

Pancreatic cyst differential

  • Simple pancreatic cysts
  • Pseudocyst
  • Cystadenoma
  • Syndromes - ADPKD, VHL disorder
  • Ductal adenocarcinoma with cystic degeneration
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25
Q

What are clinical feature of Head of pancreas tumour (70%)? Tail of pancreas?

What is your Differential diagnosis for Painless jaundice? (obstructive, hepatic, pre-hepatic)

What investigations are needed for head of pancreas tumour?

Why is the K10 screening tool for depression important in pancreatic cancer?

A

Head of pancreas tumour (70%)

  • Present earlier due to obstruction of CBD
  • Non-specific - weight loss, fatigue, nausea

Specific

  • Painless obstructive jaundice with pruritus (characteristic)
  • Courvoisier’s sign = palpable gall bladder (due to obstruction) + obstructive jaundice
  • Malabsorption syndrome- steatorrhea due to obstruction of pancreatic ductMay have vague constant epigastric pain

Body or tail of pancreas (30%)

  • Vague epigastric pain radiating to the back
  • Non-specific - weight loss, fatigue

Others

  • Depression
  • Significantly higher incidence in PaCa patients
  • Depression and anxiety may even precede symptoms or knowledge of the diagnosis
  • Migratory thrombophlebitis (Trousseau’s sign) - inflammation of veins in the lower leg
  • Type 1 DM - B-cell destruction
  • Hepatomegaly - biliary obstruction

DDx painless jaundice

Obstructive

  • Head of pancreas tumour - until proven otherwise
  • Cholangiocarcinoma

Hepatic

  • Chronic viral hepatitis, ALD, NAFLD, drugs, liver Ca, PBC, autoimmune, PBC, PSC

Pre-hepatic

  • Haemolytic anemia, gilbert’s syndrome
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26
Q

Management principles of pancreatic cancer?

What are the different types of endocrine tumors of the pancreas?

A
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27
Q

What are important tests for liver function? list

What does PT/INR test determine? whats its clinical use?

What role does serum albumin have?

Serum direct Bilirubin?

A
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28
Q

What are the diagnositic blood tests for:

Autoimmune hepatitis?

Hepatitis A, B, C?

Haemochromatosis?

Wilsons disease?

NASH?

Drug induced liver injury?

DDx for hepatomegaly?

A
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29
Q

Tests for liver injury:

Hepatocellular injury?

Cholestatic injury?

What is the liver picture in hepatitis? Alcoholic liver disease?

A
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30
Q

What are risk factors for viral hepatitis?

What is the eitology? Infective acute hepatitis? Other viruses? What viruses have a risk of becoming chronic?

What are non-viral causes of hepatitis?

A

Risk factors

  • Migrants or traveller from a high risk area - most hep B in Australia is in migrants
  • IVDU
  • Tattoos
  • Sexual - MSM, unprotected, overseas, with paid workers etc.
  • Blood products before 1990s
  • ATSI
  • Imprisonment
  • Occupational exposure
  • Body building - steroids
  • Sharing razor & personal hygiene equipment with someone with hepatitis

Etiology

Viral causesInfective acute hepatitis

  • Hepatitis viruses A,B,C,D,E

Other non-specific viral causes

  • CMV - immunocompromised or newborn
  • EBV - mild hepatitis common in the acute phase
  • Herpes simplex - rarely may cause hepatitis in newborn or immunosuppressed → may lead to necrosis
  • Yellow fever - major cause in tropical regions → hepatic apoptosis can be severe and extensive

Risk of chronic hepatitis

  • HBV - 5% progress to chronic hepatitis
  • HCV - 85% progress to chronic hepatitis

Non-viral causes

  • Bacterial - leptospirosis, brucellosis, Q feve
31
Q

Which of the viral hepatitis are blood born? How can they be transmited?

Hepatitis C? B?

Water born?

Which is most likely to become chronic?

A
32
Q

Clinical features Acute hepatitis vs Chronic Hepatitis?

Lab features of both acute and chronic?

A

Clinical features

Acute viral hepatitis Pre-icteric prodrome

  • Fever, weight loss, malaise, N&V, myalgia & arthralgia, diarrhoea, urticaria

Icteric phase

  • RUQ tenderness
  • Jaundice (mixed hyperbilirubinemia)
  • Dark urine and pale stool (obstruction due to swelling)
  • Splenomegaly and cervical lymphadenopathy - minority of cases

Chronic (HBV,HCV,HDV only)

  • Fatigue, malaise, loss of appetite, bouts of jaundice, hepatic tenderness
  • Asymptomatic carriers - HBV
33
Q

Outline Workup for Acute hepatitis:

Causes? List 4- Viral, bacterial, ischemic, autoimmune, drug.

DDX for acute hepatitis?

Investigations? Bloods?

WHat is needed in acute hepatitis panel?

A

Work-up of acute viral hepatitis

Causes of acute hepatitis

Infective

  • Viral - HAV, HBC, HCV
  • Bacterial - leptospirosis, Q fever
  • Acute alcoholic hepatitis
  • Drug induced - paracetamol overdose
  • Ischemic hepatitis
  • Autoimmune hepatitis - anti-smooth muscle antibodies (PBC & PSC present chronic)

DDx acute hepatitis

  • GB - cholecystitis, cholangitis
  • RSHF
  • Pancreatitis
  • PUD

Investigating acute hepatitis

Bloods

FBC

  • Leukocytosis, aplastic anemia (rare complication)

LFTs

  • ALT/AST very high (>1000) - DDx = viral, drug induced, autoimmune, ischemic
  • GGT/ALP mildly elevated

Coagulation

  • Raised INR

UECs

  • Urea & creatinine reduced

Acute hepatitis panel

  • Anti-HAV Ab IgM
  • HBV serology - HBsAg, HBsAb, HBcAb
  • HCV - Hep C antibodies, HCV-RNA
  • EBV & CMV serology
  • If RFs present - HIV serology, syphilis
  • Lipase

Other causes to consider (depending on presentation)

  • Paracetamol levels
  • Autoimmune hepatitis - anti-smooth muscle antibodies
34
Q

Management Principles of Acute viral hepatitis:

Indications for hospitilization?

Specific medical?

Supportive: (mainstay)?

Follow up?

Closing?

Pregnancy and chronic hepatitis?

Complications of hepatitis?

A

Management of acute viral hepatitisIndications for hospitalisation

  • Coagulopathy
  • Hypoglycaemia
  • Encephalopathy
  • Severe vomiting

Specific medical

  • Refer to gastroenterology - should be reviewed by gastroenterologist
  • Not usually required acutely (for chronic infections)

Supportive (mainstay)

  • Nutrition - maintain
  • Fluids - hydrate
  • Analgesia
  • Anti-emetics

Follow-up viral serology in 6 months to determine if developed chronic infection

  • Hep B - if Hep B Ag positive = chronic
  • Hep C - likely

Closing

  • Give information
  • Referral - gastroenterologist, GP
  • Safety-net

Follow-up - GP for treatment

Pregnancy and chronic hepatitis

  • There is a risk of vertical transmission to baby if they have acute or chronic infection in pregnancy
  • Risk with HBV>HCV
  • During lifespan they have a high risk of cirrhosis and hepatocellular carcinoma

Preventing

  • 3rd trimester anti-viral
  • At birth give HBV vaccination PLUS shot of HBV Ig

Advice

  • Not yet pregnant - pregnancy should not be advised until >6 months after cessation of anti-viral therapy due to teratogenicity
  • Already pregnant - does not affect route of pregnancy, breastfeeding still encouraged

Complications

  • Acute fulminant hepatitis
  • Cirrhosis and its complications
  • Hepatocellular carcinoma
  • Aplastic anemia - rare
  • Membranous glomerulonephritis - immune complex formation
  • Polyarteritis nodosa - immune complex formation
35
Q

Hepatitis A:

Transmission:

Epidemiology:

Clinical?

Investigations/Diagnosis?

Prevention?

Management:?

A

Hepatitis A

Epidemiology

  • Very common WW in developing countries with poor hygiene
  • Main differential in acute hepatitis of returning traveller

Clinical

  • N&V, diarrhoea, fatigue, arthralgia (common), jaundice, fever, RUQ pain, dark urine
  • Acute liver failure <1%
  • 2-3 week course with no chronic state

Diagnosis

  • LFTs
  • Anti-HAV IgM positive

Prevention

  • HAV vaccine available for travellers - inactivated

Hand hygiene

  • Safe travelling practices - bottled water, avoid washed fruit/veges, avoid undercooked meat

Management

  • Supportive
36
Q

Viral Hepatitis: Clinical features: General Management principles: Toronto Notes:

A
37
Q

What is hepatitis B?

How is it transmitted? How infective is it?

What investigations? (what are diagnostic for HBV serology) What are patterns of serological testing for hepatitis B?

A
38
Q

What is the serological state in hep B of the following:

Anti-HBc positive? (but rest negative)

Acute state?

Chronic hep b?

Immune tolerance?

Immune clearance?

Immune control?

Immune Escape?

A

Hepatitis B

à DNA virus

  • Parenteral spread: Blood products, IVDU, sexual, direct contact

Risk factors

  • IVDU
  • Sexual partners/carers of IVDU
  • People receiving blood transfusions eg haemophiliacs
  • Haemodialysis and ESRF
  • Babies of HBsAg +ve mothers
  • Immigrants from HBV endemic countries (eg Vietnam, East Timor, Africa)

Clinical features

Prodrome before jaundice:

  • Flu-like symptoms = N+V, anorexia, headaches, fatigue, myalgia, low-grade fever
  • Arthralgia, urticaria

Clinical jaundice (only some progress this far)

  • Pale stools and dark urine preceding jaundice
  • Hepatomegaly, RUQ pain
  • Splenomegaly, cervical lymphadenopathy

Diagnosis

  • HBV serology
    • HbsAg: active infection (acute or chronic)
    • HBeAg: present in acute infection
    • HBcAg: Positive for life after infection
    • Anti HBs: immunity (infection or vaccination)
    • HBeAb: no replication is occurring
    • AntiHBc IgM: recent acute infection
    • AntiHBc IgG: marker of past infection
  • HBV PCR for monitoring response to Tx

Investigation

  • Bloods: FBC, LFTs, coag profile, AFP
  • Imaging: Liver USS

Natural progression of chronic HBV infection

Four phases of chronic HBV infection over the patient’s lifetime:

  1. Immune tolerance = 15-30 years, normal transaminases, high HBV DNA
  2. Immune clearance = Deranged transaminases, if prolonged there is worse prognosis.
    - Risk of progression to cirrhosis and HCC
  3. Immune control = Normal transaminases, low or undetectable HBV DNA
  4. Immune escape = Deranged transaminases,
    - Risk of progression to cirrhosis and HCC
39
Q

Management principles of Hepatitis B?

Risk factors for contracting hepatitis B?

Clinical features? (toronto)

A

Treatment

Acute

  • Supportive
    • Simple analgaesia, IVF

Chronic

  • Education and harm minimisation
    • Transmission prevention (body fluids, sexual contact, IVDU, tattoos)
    • Avoid EtOH
    • Weight management (prevent NAFLD)
    • Vaccinate against HepA
    • Vaccinate sexual contacts against HepB
  • Treatment should be considered in chronic infection (immune clearance and immune escape phases).
    • Antiviral medications or pegylated interferon (at least 12-months)
      • Entecavir PO OR Tenofovir PO OR Pegylated IFN
  • Monitor for HCC
    • If evidence of chronic infection (↑AST/ALT and HBsAg +ve for >6 months = chronic hepatitis) OR HBsAg in a risk group (Asian men >40, Asian women >50, cirrhosis, HCC FHx), do HCC surveillance:
    • Liver USS every 6-months

Prognosis

  • Cirrhosis: 20-50%
  • HCC: ↑Risk with duration of infection (eg if infected as a child, higher risk of HCC in later life)
40
Q

What is hepatitis C?

Risk factors?

Clinical features?

Diagnosis?

Investigations?

Treatment?

A

Hepatitis C

  • RNA virus.
  • ↑↑Develop into chronic infection (85%).
  • Blood-borne spread: IVDU, needle-stick injuries

Risk factors

  • IVDU: Main RF
  • Blood transfusion before 1992
  • Tattoos

Clinical features

  • Clinical manifestations develop 6-8 weeks after exposure
  • Mild and non-specific features (fatigue, malaise, nausea)
  • Most people are asymptomatic

Diagnosis

  • Suspected on basis of elevated ALT/AST and positive serum anti-HCV
  • Diagnosis: Serum PCR (HCV RNA)

Investigation

  • Bloods: FBC, LFTs, coag profile, AFP, HCV serology, HCV genotype (has implications for response to Tx)
  • Imaging: Liver USS

Treatment

  • Supportive
    • Simple analgaesia, IVF
  • Observe for spontaneous resolution of HCV infection
  • Tx with IFN
    • Significant SEs
  • +/- Pegylated interferon started within 12-wks of hepatitis onset for 24-wks of Tx
41
Q

What are the three Cs of Hepatitis C?

Transmission?

Clinical? (acute phase, chronic phase, recovery)

Diagnosis (HCV serology)? What are the tests

What bloods should be done? What imaging?

What are the management principles of hepatitis C? (non pharm, lifestyle, new interferon free) how long to reassess?

A

Further work-up after chronic hepatitis C diagnosed

To be done before referral for treatment

Bloods

  • HCV genotype
  • FBC - anemia, thrombocytopenia
  • LFTs - hypoalbuminemia, raised AST/ALT
  • Coagulation
  • Screen for other disease - HBV, HIV, syphilis

Imaging (chronic)

  • USS & FibroScan - determine cirrhosis

Management of chronic infection

  • Non-pharmacologicalCounsel
  • Now curable; requires treatment to prevent cirrhosis and HCC
  • Cure rates >90%

Lifestyle

  • Avoid alcohol
  • Vaccination - HAV, HBV
  • Avoid transmission - safe sex, no syringe sharing, don’t share personal equipment

Refer ALL CHRONIC HEP C to specialist for anti-viral treatment New interferon-free regimens have revolutionised hep C (many drugs)

  • Became available in 2016
  • >90% success rate without significant side effects

Cannot be used in pregnancy unlike Hep B

Duration = 12 weeks then reassess Serology

HCV RNA –> if undetectable = cured

HCV antibodies - do NOT mean they are immune (can be reinfected)

42
Q

What investigations should be done in chronic hepatitis?

Bloods? Imaging? Biospy?

Hepatitis E? What are the 3es of hepatitis E?

Clinical features? Diagnosis?

A
43
Q

Charateristic of differen viral hepatitdes:

Hep A-E, CMV, EBV, Yellow fever

A
44
Q

What is Autoimmune Hepatitis? What are associated extrahepatic manifestations?

Drug induced Liver disease? Common causes? Clinical features? Investigations?

Treatment of paracetomol poisoning?

A

Autoimmune Hepatitis

  • Diagnosis of exclusion: rule out viruses, drugs, metabolic or genetic causes
  • Can be severe: 40% 6 month mortality without treatment
  • Extrahepatic manifestations
    • Sicca, Raynaud’s, thyroiditis
    • Hypergammaglobulinemia

Drug-Induced Liver disease

Causes

  • Acetaminophen: active ingredient in many over the counter medications e.g. paracetamol
    • Direct hepatotoxin
    • 10-15g in healthy adult, less in EtOH abuse
    • Saturates glucoronidase enzyme → reactive metabolites build up and not eliminated → damage to hepatocyte membrane
    • Blood levels of acetaminophen proportionate to severity of liver damage
  • Methotrexate
  • Amiodarone
  • Chlorpromazine, Isoniazid
  • Statins, phenytoin, PTU, sulfonamides, tetracyclines

Clinical features

  • Acetaminophen: Fulminant liver failure (AST, ALT >1000 then jaundice and encephalopathy)
  • Methotrexate: Cirrhosis
  • Amiodarone: Similar picture to alcoholic hepatitis
  • Chlorpromazine: Cholestasis, fever, rash, jaundice, pruritus, eosinophilia
  • Isoniazid: ↑AST, ALT

Investigation

Bloods: Serum paracetamol level, LFTs

Treatment

Paracetamol poisoning

  • Oral activated charcoal if <1h after ingestion
  • Gastric lavage / emesis if <2h after ingestion
  • N-acetylcysteine (NAC) PO or IV (best within 8-10h of ingestion) to promote hepatic glutathione regeneration
45
Q

What is haemochromatosis?

Epidemiology?

Aetiology?

Clinical features? (early, late, endocrinopathies)

Investigations?

Treatment? (diet, venesection)

A

Haemochromatosis

à Inherited disorder of Fe metabolism causing excessive Fe storage → multiorgan dysfunction (liver, pancreas, heart, joints, pituitary, adrenals, skin).

Epidemiology

  • Northern European descent
  • Tends to present in middle-age
  • Men are more frequently and severely affected than women
    • Women tend to present with the disease 10yrs later than men (menstruations)

Aetiology

  • Primary (hereditary) hemochromatosis
    • Hepcidin deficiency results in ongoing gut absorption of iron despite adequate iron stores
      • HFE gene found on chromosome 6 is the most common mutation. Incomplete penetrance.
    • Results in ongoing gut absorption of iron despite adequate iron stores 

  • Secondary hemochromatosis
    • Parenteral iron overload (e.g. transfusions)
    • Chronic haemolytic anaemia: thalassemia, pyruvate kinase deficiency
    • Excessive iron intake 


Clinical features

à Usually presents with trivial ↑ transaminases

Early

  • Asymptomatic
  • Tiredness, arthralgia (2nd and 3rd MCP joints, knee)
  • Erectile dysfunction

Late

  • Slate-grey skin (melanin)
  • Chronic liver disease (cirrhosis, HCC)
  • Dilated cardiomyopathy
  • Osteoporosis

Endocrinopathies

  • DM (bronze diabetes), hypogonadism (pituitary)

Investigations

  • Bloods: ↑LFTs, FBC, AFP (6-monthly HCC screening if cirrhosis)
    • Fe studies - transferrin saturation >45%, ↑ferritin
  • HFE gene testing
  • Imaging: Liver USS (6-monthly HCC screening if cirrhosis)
  • Liver biopsy in late stage to define degree of Fe overload and detect cirrhosis

Treatment

  • Venesection
    • Once every 1-3 weeks returns life expectancy to normal if no permanent organ damage done. Continue for life.
  • Diet
    • Well balanced low-iron diet. Tea and coffee with meals to ↓Fe absorption. Limit vit C with meals as it ↑Fe absorption.
  • Screening
    • Monitor pt with LFTs, BSLs, HbA1cs
    • Genetic testing for 1st degree relatives for haemochromatosis
  • Pharmgological: Desferrioxamine (Fe chelator) if intolerant of venesection or contraindicated
46
Q

What is alcoholic liver disease? (what does it encompass - e.g fatty liver, alcoholic hepatitis, cirrhosis)

Pathophysiology?

Clinical features? (liver, other organ systems- CVS, CNS, GIT, blood)

Investigations? (blood, imaging, Tap- MCS)

Treatment: Non pharmacological, pharmacological?

A

Alcoholic Liver disease

  • Fatty liver (all alcoholics): reversible if EtOH stopped.
  • Alcoholic hepatitis (35%): usually reversible if EtOH stopped.
  • Cirrhosis (10%): potentially irreversible

Pathophysiology

  • Ethanol oxidation → acetalaldehyde
    • Impaired lipolysis
    • FAs and TGs accumulate in the liver
  • Necrosis and hepatic vein sclerosis
  • Immune reaction to acetaldehyde and by extension, hepatocytes

Clinical features

Liver

  • Fatty liver
    • Mildly tender hepatomegaly, jaundice rare
    • Mildly ↑transminases
  • Alcoholic hepatitis
    • Variable severity, mild to fatal
    • Jaundice, low grade fever, RUQ discomfort, ascites, ↑WCC
  • Cirrhosis (see below)

Other organs

  • CVS: Arrhythmias, HTN, cardiomyopathy
  • CNS: Self-neglect, ↓memory/cognition, cortical atrophy, ataxia, neuropathy, Wernicke’s encephalopathy, Korsakoff’s dementia
  • GIT: Obesity, D+V, gastritis and gastric erosions, peptic ulcers, varices, pancreatitis, cancer, Mallory-Weiss tears, oesophageal rupture (Boerhaave’s syn.)
  • Blood: Macrocytic anaemia

Investigations

  • Bloods: FBC, U&Es, LFTs, coag profile
    • LFTs: AST > ALT (2:1), ↑GGT
    • FBC: ↑MCV
  • Imaging: Liver USS
  • MCS: Ascitic tap

Treatment

Non-pharmacological

  • EtOH cessation
    • Alcoholics Anonymous, disulfiram (↑acetaldehyde if drink), naltrexone, acamprosate (↓ cravings)
  • Optimise nutrition, high-protein diet
  • Daily weight, LFTs, U&Es, INR

Pharmacological

  • Thiamine PO/IM/IV and multivitamins
    • 100mg PO tds +/-
    • 200mg IM/IV for 3 days
  • Benzodiazepines (loading dose then maintenance) for EtOH withdrawal
  • Prednisolone 40mg daily for 4 wks if hepatic encephalopathy or severe liver disease
  • Lactulose PO to ↓ risk of hepatic encephalopathy
47
Q

What is non-alcoholic fatty liver disease?

What are risk factors for it?

Clinical features?

Investigations: Blood, imaging, biopsy?

Treatment? Prognosis?

A

Non-Alcoholic Fatty Liver Disease (NAFLD)

à ↑ Fat deposition in hepatocytes (steatosis) +/- inflammation (steatohepatitis).

à Spectrum of disorders characterized by macrovesicular hepatic steatosis 


Risk factors

  • DM, dyslipidaemia, metabolic syndrome
  • Drugs (eg amiodarone, MTX, tetracycline)
  • Rapid weight loss/gain

Clinical features

  • Often asymptomatic
  • Fatigue, malaise, vague RUQ discomfort
  • Mildly ↑transaminases (typically ALT>AST)
  • Insulin resistance
  • ↑TGs, ↑cholesterol

Investigations

  • Bloods: LFTs, lipids, coag profile, BSL/HbA1c
  • Imaging: Liver USS (echogenic texture)
  • Liver biopsy (rarely performed unless severe): diagnostic

Treatment

  • Gradual weight loss is the best Tx
  • Modify risk factors (eg BSL, HTN, lipids etc)

Prognosis

  • Most die from CVS or cerebrovascular disease
  • Risk of progression to cirrhosis <25% , but ↑ if steatohepatitis
48
Q

Define Acute liver failure: + Acute on chronic (most common)

What are causes list 5 (2.5 marks)

Clinical features? (Prodrome, clinical jaundice (icterus), hepatic encephalopathy, +/- CLD features)

Investigations: Bloods - think liver specific, Imaging? MCS?

Treatment: non pharmacological+ Pharmacological: Specifics (e.g Ascites, bleeding, encephalopathy)

A

Acute Liver Failure

à Liver failure either sudden onset (acute hepatic failure) or more often, decompensation of chronic liver disease (acute on chronic hepatic failure)

  • Fulminant hepatic failure is a clinical syndrome resulting from massive necrosis of hepatocytes → severe impairment of liver function.

Causes

  • Infections
    • Viral hepatitis - Hep B, Hep C, CMV
    • Yellow fever, leptospirosis
  • Neoplasm
  • Vascular: Budd-Chiari syndrome
  • Drugs: Paracetamol overdose, isoniazid, EtOH
  • Metabolic
    • Haemochromatosis, a1-antitrypsin deficiency, Wilson’s disease
    • Fatty liver of pregnancy, HELLP syndrome (haemolysis, elevated liver enzymes, low plts)

Clinical features

  • Flu-like prodrome may precede jaundice by 1-2 weeks
    • N/V, anorexia, taste/smell disturbance, headaches, fatigue, myalgia, low-grade fever
    • Arthralgia and urticaria (especially HBV)

  • Only some progress to icteric (clinical jaundice) phase, lasting days to weeks
    • Pale stools and dark urine 1-5 d prior to icteric phase
    • Hepatomegaly and RUQ pain
    • Splenomegaly and cervical lymphadenopathy (10-20% of cases)
  • Hepatic encephalopathy, hepatic asterixis, constructional apraxia (cannot copy a 5-pointed star)
  • +/- Signs of CLD (suggests acute-on-chronic hepatic failure)

Investigations

  • Bloods: FBC, U&E, LFTs, coag profile, BGL
    • Paracetamol level
    • Serology - hepatitis, CMV, EBV
    • Fe studies, caeruloplasmin, a1-antitrypsin
    • Autoantibodies (ANA, AMA, SMA)
  • Imaging: Abdo USS, Doppler flow studies of portal vein, CXR
  • MCS: Blood cultures, urine, ascitic tap

Treatment

à Risk of sepsis, hypoglycaemia, GI bleeds/varices, encephalopathy

Non-pharmacological

  • Transfer to ICU, intubation, NG tube
  • IDC for fluid monitoring
  • Regular observations, daily weights
  • Optimise nutrition

Pharmacological

  • Treat cause (eg GI bleed, sepsis, paracetamol toxicity)
  • Thiamine PO/IM/IV and multivitamins
    • 100mg PO tds +/-
    • 200mg IM/IV for 3 days
  • Lorazepam (seizures)
  • Ascites
    • Restrict fluid, low salt diet
    • Diuretics: Spironolactone 100mg PO daily +/- frusemide PO
  • Bleeding
    • Vit K and platelets
    • FFP
    • +/- Endoscopy (varices)
  • Encephalopathy
    • Lactulose 30-50mL TDS aiming for 2-4 soft stools/day
49
Q

What is cirrhosis?

What is the aetiology of cirrophosis- List 4 (2 marks)

Clinical features: List 5 think GI exam!

Complications of cirrohosis?

A

Cirrhosis

  • Liver damage characterised by diffuse distortion of the basic architecture and replacement with scar tissue and nodular regeneration.
  • Stage 1 = cirrhosis is compensated and asymptomatic. Can last for 10-20yrs with almost normal life expectancy.
  • Stage 2 = cirrhosis is the onset of first decompensation, typically development of ascites, variceal bleeding, encephalopathy.

Aetiology

  • Most often chronic EtOH abuse, HBV or HCV.
  • Other causes:
    • Metabolic - haemochromatosis, a1-antitrypsin def, Wilson’s disease, NAFLD
    • Autoimmune - primary biliary cirrhosis, primary sclerosing cholangitis
    • Drugs - amiodarone, methotrexate

Clinical features

  • May be asymptomatic with ↑LFTs
  • Leuconychia, half-and-half nails (Terry’s nails), clubbing, palmar erythema
  • Dupuytren’s contracture, parotid enlargement, xanthelasma
  • Spider naevi, gynaecomastia, testicular atrophy, loss of body hair
  • Hepatomegaly or small liver in late disease

Complications

à VARICES

  • Varices
  • Anaemia, pancytopenia
  • Renal failure, hepatopulmonary syndrome
  • Infection
  • Coagulopathy
  • Encephalopathy
  • Sepsis
50
Q

Investigations in patient with cirrhosis? (and potential findings)

Diagnosis? Scoring system? (child pugh- what is the scoring based upon)

What is the MELD score? what is it based upon?

What are the treatment options for patients with cirrhosis? Symptomatic? Ascites? Screening? Transplant? Varices? Managing complications (total management) + Hepatic encephalopathy? General measures?

A

Investigations

  • Bloods: LFTs (may be ↑ or normal in late stage), coag profile, FBC (↓WCC, ↓plts from hypersplenism)
    • Look for cause - Fe studies, antibody studies (ANA, AMA, SMA), AFP, caeruloplasmin, a1-antitrypsin deficiency
  • Imaging: Liver USS +/- Doppler flow studies
    • MCS: Ascitic tap (spontaneous bacterial peritonitis)
  • Liver biopsy: Gold standard, but not generally performed for diagnosis alone

Diagnosis

Child-Pugh

à Used to assess the prognosis of chronic liver disease, mainly cirrhosis

  • Used to determine the prognosis as well as required strength of treatment and the necessity of liver transplantation
  • Scoring based on
    • Bilirubin
    • Albumin
    • Prothrombin time/INR
    • Ascites
    • Hepatic encephalopathy

à Each measure given a score of 1 to 3

Interpretation

Points

Class

One year survival

Two year survival

5-6

A

100%

85%

7-9

B

81%

57%

10-15

C

45%

35%

MELD score – Model for End Stage Liver Disease

à Scoring system for assessing the severity of chronic liver disease

  • Useful in determining pronogis and prioritizing for receipt of liver transplant
  • Score based on
    • Serum bilirubin
    • Serum creatinine
    • INR

Interpretation

à Score required for possible transplantation: 15-30

à 3 month mortality

  • 40 or more — 71.3% mortality
  • 30–39 — 52.6% mortality
  • 20–29 — 19.6% mortality
  • 10–19 — 6.0% mortality
  • <9 — 1.9% mortality

Treatment

  • Symptomatic treatment
    • Cholestyramine for pruritus
  • Ascites: Fluid restriction, low-salt diet, spironolactone 100mg PO daily +/- frusemide PO
  • Prevent further complications
    • Hepatic encephalopathy: Lactulose 30-50mL PO tds aiming for 2-4 loose stools/day
  • Screen for HCC 6-monthly (AFP, liver USS)
  • Liver transplant is the definitive Tx

Treatment of varices

  • Propranolol
  • Octreotide
  • Vasopressin
  • PPI
  • Surgery: banding + sclerotherapy

Managing complications of liver failure

  • Seizures: Lorazepam
  • Bleeding: vitamin K, FFP +/- transfusion
  • Ascites
    • Mild: Spironolactone
    • Mod: add furusemide
    • Severe: paracentesis + albumin IV
    • Refractory: repeated paracetesis/TIPDS/transplant
  • Infection: ceftriaxone
  • Bleeding varices
    • Primary prevention: propranolol
    • Initial management of bleeding: octreatide (somatostatin anolouge – decreased sphlancnic blood flow + partial pressure)
      • IV resuscitation – IVF + PRBC’s
      • prophylactic antbiotiocs
    • Emergency endoscopy +/- banding/sclerotherapy
    • If this fails à Balloon tamponade
    • If ongoing, consider emergency TIPS
  • Hepatic encephalopathy
    • Recognise + treat: infection, constipation, reanl impairment, non-adherence, electrolyte disturbances, drugs
    • First line: lactulose
    • Consider empirical treatment of infection
    • Monitor for 2-4 stools/day
  • Cerebral oedema: mannitol

General meatures

  • ICU and elevate head of bed
  • Protect the airway with intubation
  • NGT, IDC
  • Salt + water restriction
  • Determine Child’s Pugh score (A, B, C) – albumin, bilirubin, INR, encephalopathy, ascites
51
Q

Cirrhosis:

Symptoms: List 4

Examinations findings: General etc, 1 for each part of exam+Others

Investigations? Bedside? Bloods? Imaging?

What are Some expected hamatological abnormalities associated with cirrhosis?

Complications?

A

Clinical

Symptoms

  • Non-specific early symptoms - N&V, weight loss, anorexia, weakness, abdominal distention, jaundice
  • Often presents acutely with complications

Exam

  • General - orientation (encephalopathy), jaundice, ascites, weight loss/wasting, SOB (pulmonary edema), if very sick consider spontaneous bacterial peritonitis
  • Vitals - tachypnoea, tachycardia, febrile (chronic)
  • Hands - clubbing (mostly biliary cirrhosis), koilonychia, leukonychia (white nails), muehrcke’s lines (white lines parallel to lunula), dupyutren’s contracture, tremor, palmer erythema, hepatic flap
  • Arms - bruising, scratch marks
  • Face - scleral icterus, conjunctival pallor, enlarged parotids, fetor hepaticus
  • Chest - spider naevi (>3 is abnormal), gynaecomastia
  • Abdomen - distended ascites, caput medusa, palpate liver + percuss span, splenomegaly, percuss/shifting dullness, auscultate, DRE (haemorrhoids)
  • Legs - pedal edema, bruising
  • Others - CV (AF, alcoholic DCM), resp (pulmonary edema), neuro (peripheral neuropathy, Korsakoff’s/Wernicke’s)

Ix

Bedside

  • VBG - respiratory alkalosis, metabolic acidosis

Bloods

  • Glucose - hypoglycaemia
  • FBC (anemia, thrombocytopenia, leukopenia)
  • Smear (target cells)
  • UECs (↓urea, hyponatremia, hepatorenal)
  • LFTs - AST/ALT may be normal, hyperbilirubinaemia, low albumin
  • Coagulation studies (↑INR)
  • Viral serology - HBV, HCV, HIV

Imaging

  • Liver USS & FibroScan - shrunken, nodular (only good for advanced cirrhosis)
  • CT abdomen - varices, nodular liver, splenomegaly, ascites
  • Upper GI endoscopy * - all cirrhosis for varices

Haematological abnormalities

  • Macrocytic anemia - alcohol BM toxic, hypersplenism, bleeding, dietary folate deficiency
  • Thrombocytopenia - ↓thrombopoietin, hypersplenism
  • Leukopenia - hypersplenism, alcohol
  • ↑INR - relationship to bleeding is controversial as it doesn’t measure altered fibrinolysis/prothrombotic factors also affected –> therefor may not have bleeding diathesis
  • Hyponatremia - diuretics, renal impairment, water retention

Cirrhosis complications = VARICES

  • Varices
  • Anemia/ascites (& SBT)
  • Renal failure (hepatorenal syndrome)
  • Infection & sepsis
  • Coagulopathy/Cancer (HCC)
  • Encephalopathy
  • Spleen (hypersplenism)
52
Q

Cirrhosis Severity scoring:

Use:

Mnemonic: ABCDE: Interpretation? A, B, C

What is the MELD score?

A
53
Q

What is Primary Sclerosing Cholangitis? (PSC)

What is Primary biliary cirrhosis?

How are each diagnosed?

What are features of each?

A

Primary Biliary Cirrhosis

à Chronic inflammation and fibrous obliteration of intrahepatic bile ductules

  • Likely an autoimmune cause

Clinical features

  • Often asymptomatic

  • Initial symptoms: pruritus, fatigue

  • Chronic: jaundice and melanosis (darkening skin) and other signs of cholestasis
  • End-stage: hepatocellular failure, portal HTN, ascites

  • High incidence of osteoporosis 


Investigations

  • Bloods
    • LFT: elevated ALP, GGT
    • Antibodies: anti-microbial antibodies (AMA)
    • Serum cholesterol: Mild decrease in LDL and large increase in HDL
  • Liver biopsy: confirms diagnosis and stages severity
  • MRCP: normal bile duct

Treatment

  • Ursodiol +/- cochicine, methotrexate
  • Cholestyramine: pruritis, hypercholesterolaemia
  • Calcium and vitamin D for low bone density: bisphosphonates if osteoporosis severe
  • Monitor for thyroid disease
  • Liver transplant if disease severe, progressive

Primary Sclerosing Cholangitis

à Inflammation of the biliary tree (intra and/or extrahepatic bile ducts) → scarring and strictures.

Aetiology

  • Primary = idiopathic
    • Associated with IBD (UC)
  • Secondary causes:
    • Long-term choledocholithiasis
    • Cholangiocarcinoma
    • Surgical/traumatic injury
    • Contiguous inflammatory process
    • Post-ERCP
    • Associated wit HIV/AIDS

Clinical features

  • Fatigue and pruritus
  • Advanced disease: ascending cholangitis (biliary obstruction), cirrhosis, liver failure

Complications

  • Repeated bouts of cholangitis may lead to complete biliary obstruction with resultant secondary biliary cirrhosis and hepatic failure
  • Increased incidence of Cholangiocarcinoma

Diagnosis

  • ERCP shows narrowing & dilatations of bile ducts (“beading”), both intra- and extra-hepatic bile ducts

Investigation

  • Bloods
    • LFTs: ↑ALP, mildly ↑AST
    • Autoantibodies: ↑ ANCA typical, elevated IgM
  • Imaging: ERCP, MRCP

Treatment

  • Cholestyramine: Bile acid sequestrant
  • Abx for cholangitis
  • Surgery
    • Sphincterotomy, stenting
  • Liver transplant is definitive treatment
54
Q

Portal HTN:

Causes? Pre -hepatic, hepatic, post hepatic:

Investigations? (think ascites)

Complications?

Treatment:

A

Portal hypertension

à Pressure gradient between hepatic vein pressure and wedged hepatic vein pressure (corrected sinusoidal pressure) >5 mmHg

Causes of portal HTN

  • Pre-hepatic*
  • Thrombosis (portal or splenic vein)
  • Hepatic*
  • Cirrhosis (most common in developed countries), schistosomiasis (most common worldwide), sarcoid, myeloproliferative diseases
  • Post-hepatic*
  • Budd-Chiari syn, RVF, constrictive pericarditis

Investigations

SAAG – Serum ascites albumin gradient

  • Calculation used to determine cause of ascites
  • SAAG = Serum albumin – ascetic fluid albumin
  • High gradient (>11g/L) indicates ascites is due to portal hypertension
    • This is due to increased hydrostatic pressure within the blood vessels of the hepatic portal system
  • Low gradient (<11g/L) indicates causes of ascites are not associated with increased portal pressure
    • E.g. TB, pancreatitis, infections, serositis or nephritic syndrome

Complications

  • GI bleeding from varices in oesophagus, less commonly in stomach, even less frequently from portal hypertensive gastropathy
  • ascites 

  • hepatic encephalopathy 

  • thrombocytopenia 

  • renal dysfunction 

  • sepsis 

  • arterial hypoxemia 


Treatment

  • Control bleeding
    • Vasopressin
    • Octreotide
    • Flexible viewing tube: endoscope
  • Portosystemic shunting
    • If bleeding continues
  • Liver transplantation
55
Q

Managmenet cirrhosis/ Acute liver failure:

non-pharm?

Medical?

Transplantation:

Monitor for complications: HCC, Ascites (SBP), Variceal bleed, renl failure, bleeding, hepatic encephalopathy

A
56
Q

What is Diverticular disease?

What is a False diverticular? (diverticulosis)

What is a true diverticular?

Epidemiology?

Risk factors?

Pathogenesis?

A
57
Q

Pathology of Diverticulosis:

Clinical Features: Diverticulosis if usually asymptomatic:

Symptoms? Exam findings?

DDx for LLQ pain in elderly?

What are complications of diverticulosis:

A
58
Q

Investigations in acute diverticulititis?

Bedside? Labs? Imaging? (erect CX, CT abdo findings with contrast) TVUS?

What is the Hinchey staging for diverticulitis?

Management of Diverticulosis? Diverticulitis?

A

Management

Diverticulosis

  • Education
  • Lifestyle
  • Nutrition - high fibre diet + 2L water a day + Metamucil
  • Physical activity

Diverticulitis DRSABCDE

  • DRS - gen surg
  • C - IVF replacement

Admit if any 1 of:

  • Hx - severe pain or diffuse peritonitis, sepsis, significant comorbidities or immunocompromised, unable to tolerate PO intake
  • Workup - complicated diverticulitis on CT, high fever or leukocytosis

Supportive

  • UO
  • NBM - clear fluids only until improve due to chance of surgery
  • IVFs
  • Analgesia
  • VTE prophylaxis

Management depends on imaging

  • Diverticulitis with no complications is managed conservatively:
  • Consider none if systemically well
  • Antibiotics PO - gentamicin + amoxycillin + metronidazole
  • Cover - usual GIT flora (Gram -ve & anaerobic cover); particularly E.coli & Bacteroides

Complicated diverticulitis

  • What - generalised peritonitis, abscess, fistula etc.
  • IV antibiotics - IV gentamicin + metronidazole + amoxycillin (triple therapy)

Procedures

  • Abscess or fistula - percutaneous drainage or surgery to resect with anastomosis
  • Peritonitis (ruptured) - peritoneal washout + Hartmann procedure (bowel resection with colostomy –> later re-anastomosis)
59
Q

How are the following managed in Liver failure/ end stage chronic liver disease/cirrhosis etc.

Ascites?

Spontaneous bacterial peritonitis?

Hepatic encephalopathy?

A

Ascites

à Accumulation of excess fluid in the peritoneal cavity

  • Key factor: increased sodium (and water) retention by the kidney for reasons not fully understood
  • Types*
  • Refractory ascites: Ascites which cannot be mobilized by low sodium and maximal diuretics
    • Occurs in 5% of cirrhotic patients
    • Poor prognosis
  • Non-refractory ascites: Responds to low sodium and diuretics

Diagnosis

  • Abdominal ultrasound
  • Physical exam
    • Bulging flanks, shifting dullness, fluid wave test positive
    • Most sensitive symptom: ankle swelling
  • Diagnostic paracentesis
    • Cell count
    • Chemistry
    • MCS, gram stain
    • Cytology

Treatment

  • Non-refractory ascites
    • Na+ restriction
    • Diuretics: spironolactone, furosemide
  • Refractory ascites: Ascites which cannot be mobilized by low sodium and maximal diuretics
    • Therapeutic paracentesis with IV albumin

Spontaneous Bacterial Peritonitis

à Infection of ascitic fluid that cannot be attributed to any intra-abdominal, ongoing inflammatory, or surgically correctable condition

à Defined by an ascitic fluid absolute neutrophil count >250 cells/mm^3, whether or not there is culture growth.

  • One of the most frequently encountered bacterial infections in patients with cirrhosis, and most commonly seen in patients with end-stage liver disease.
  • Complicates ascites, but does not cause it
    • High risk in patients with GI bleed

Aetiology

  • Infection of the ascetic fluid
  • Most common pathogens
    • E coli
    • S aureus
    • S pneumonia

Clinical features

  • Patients are commonly minimally symptomatic, and may even be asymptomatic.
    • 1/3 of patients are asymptomatic
  • Fever, chills, abdominal pain, ileus, hypotension, worsening encephalopathy, acute kidney injury
  • Abdominal pain
  • Fever, vomiting
  • Altered mental status
  • GI bleeding
  • Diarrhoea
  • Hypothermia, hypotension, tachycardia

Investigations

  • FBC: leukocytosis, anaemia
  • Ascitic fluid laboratory tests should include cell count and culture
    • Including an absolute neutrophil count (ANC) and gram stain
  • Bedside leukocyte esterase reagent strip testing can more rapidly rule in spontaneous bacterial peritonitis (SBP) but cannot rule it out.
  • Blood cultures
  • LFTs
  • INR

Diagnosis

  • Absolute neutrophil count in peritoneal fluid >0.25x109 cells/L
  • Gram stain in only 10-50% of patients
  • Culture positive in <80% of patients

Treatment

  • Empiric antibiotic regimens that have been found to be equally efficacious include cefotaxime, ceftriaxone, fluoroquinolones, and ampicillin/sulbactam.
  • Albumin is indicated in the treatment of patients with renal dysfunction.
  • Continuous oral fluoroquinolone prophylaxis is indicated in patients with an ascitic fluid protein concentration

Hepatic Encephalopathy

à Potentially reversible neuropsychiatric syndrome secondary to liver disease.

Pathophysiology

  • ↑ Systemic toxins due to portosystsemic shunting and reduced hepatocyte function. Especially ammonia from the gut, mercaptans, amino acids. These are believed to affect the brain.

Clinical features

Stages I to IV:

  1. Altered mood/behaviour, sleep pattern disturbance, dyspraxia (5-point star drawing)
  2. Drowsiness, confusion, slurred speech, personality change and inappropriate behaviour
  3. Incoherent, restless, hepatic flap, stupor (rousable), hyperactive reflexes
  4. Coma

Investigations

à Need to rule out other causes of acute confusion and behavioural changes

  • Bloods: FBC, U&Es, LFTs, coag profile, BSL
  • Imaging: CXR, CT head, EEG findings
  • MCS: Blood cultures, ascitic tap, urine
  • Clinical diagnosis: supported by laboratory findings and exclusion of other neuropsychiatric diseases

Treatment

  • Treat precipitating factors
    • Renal impairment, GI bleeding, infections, medications (sedatives, opioids)
  • Lactulose 30mg PO
    • Hourly to 2 hourly initially
    • 3-4 times daily
    • Traps and binds ammonia in colon
  • Empirical Abx for infection until septic workup back
    • Ceftriaxone IV OR Cefotaxime IV OR Pip-taz IV

Severe encephalopathy and coma

  • Endotracheal intubation
  • Respiratory support
  • Enteral nutrition
60
Q

Liver Malignancy:

Clinical features?

Investigations? (important specific ones)

Management?

A

Liver tumours

Clinical features

  • Hepatomegaly: smooth, hard, irregular
  • Look for signs of chronic liver disease: Abdominal mass, bruit
  • Evidence of decompensation: ascites, jaundice, hepatic encephalopathy, HRS, HPS

Investigations

  • Blood: FBC, LFT, coags, U&E, ESR, alpha fetoprotein, hepatitis, serology
  • Imaging

o USS/CT

o MRI

  • Pathology: liver biopsy

o Biopsy not required for diagnosis

Management

  • HCC: resect solitary tumours <3 cm: high recurrent rate

o Liver transplant

  • Cholangiocarcinoma: very poor prognosis

o Major hepectomy + Extrahepatic bile duct excision _ caudate lobe resection

§ Lots of post op complications

o Stenting can provide temporary relief

  • Hemangiomas common: anabolic steroids, OCP, pregnancy

o Only treat if symptomatic of >5cm

  • Others: cysts
61
Q

What is the IBD spectrum?

Epidemiology?

Eithopathogenesis? Hygeine hypothesis:

Risk factors?

Pathogenesis:

Crohns vs UC? Major features?

Crohns: Define: What and where is its characteristic lesions?

Epidemiology? Clinical features?

Complications?

Diagnosis:

A

Inflammatory bowel disease (IBD)

à Crohn’s disease (CD) and ulcerative colitis (UC)

Pathophysiology

  • Unknown.
  • Genetic susceptibility + abnormally high immune responsiveness (lack of down-regulation) →
  • Sustained autoimmune response
    • Lack of appropriate down-regulation of immune responsiveness

Crohn’s Disease

Ulcerative Colitis

Location

Any part of GIT: skip lesions

Colon and rectum: Continuous

Macroscopic

Thin, deep fissures ‘cobblestone’

Narrowing and proximal dilation of normal tissue, broad oedematous pseudopolyps

Wide, shallow fissures with psuedopolyps

Chronic inflammation à atrophy: smooth flat mucosa

Microscopic

Deep crypt abscess with lymphocytes and granuloma

Shallow crypt abscess with lymphocytes but no granuloma

Rectal bleeding

Uncommon

Very common

Diarrhoea

Occasional

Frequent small stools

Abdominal pain

Colicky

Less common

Fever

Common

Uncommon

Palpable mass

Frequent: RLQ

Rare

Dermatologic manifestations

Erythema nodosum

Pyoderma gangrenosum

Psoriasis

Crohn’s plaques

Perianal skin tags

Mucosal ulcers

Erythema nodosum

Pyoderma gangrenosum

Psoriasis

Radiologic features

Cobblestone mucosa

Frequent strictures and fistualae

AXR: bowel wall thickening ‘string sign’

Lack of haustra

Rheumatology

Arthritis more common

Ankylosis spondylitis

Sarcoilitis

Arthritis less common

Sacroilitis

Hepatobiliary

Cholelithiasis

Fatty liver

Primary sclerosing cholangitis

Cholelithiasis

Fatty liver

Urology

Calculi: Most Common

Fistula: due to deep penetrating ulcer

Calculi

Ocular

Uveitis :More common

Uveitis

Complications

Fistula, Anorectal disease

Toxic megacolon

Strictures, adhesions, perforation, peritonism, abscess, malabsorption, anaemia

Colon cancer

Risk increased if >30% bowel involved

Risk increased

Crohn’s disease

à Chronic inflammatory GI disease characterised by transmural granulomatous inflammation affecting any part of the gut from mouth to anus

  • Terminal ileum and proximal colon most commonly affected. Skip lesions (unaffected bowel) between areas of active disease

Epidemiology

  • F > M
  • Presentation mostly 20-40yrs
  • Associated with smoking (↑risk)

Clinical features

  • Usually presents with recurrent episodes of abdominal cramps, diarrhoea and weight loss
  • Diarrhoea/urgency
  • ↓Weight / FTT (children)
  • Fever, malaise, anorexia
  • Ileitis can mimic acute appendicitis
    • Presents with post-prandial pain, vomiting and RLQ mass
  • Perianal skin tags and fissures, fistulae, abscesses
  • Extra-intestinal manifestations of IBD more common

Complications

  • Bowel obstruction, perforation
    • Deep fissures with risk of perforation into contiguous viscera
  • Abscesses: Perianal, abdominal, pelvic
  • Fistulae: Colovesical, colovaginal, perianal
    • Enteric fistulae may communicate with skin, bladder, vagina, bowel
  • Rectal bleeding, colon cancer

Diagnosis

Diagnosed if typical features are seen in a combination of endoscopic, histological and radiological investigations.

Investigation

  • Bloods: FBC, U&Es, LFTs, ESR/CRP, Fe studies, vitamin B12, folate, coag profile, bacterial cultures
    • CRP elevated in most new cases, useful to monitor treatment response
  • Colonoscopy, endoscopy (less frequent)
  • Stool: MCS (rule out C. difficile, Campylobacter, E. coli)
  • Imaging: AXR, MRI (fistulae, abscesses, strictures)

Treatment

  • Aims of drug therapy are to induce remission in active disease, maintain corticosteroid-free remission and prevent relapse
  • The severity of disease and the site(s) of affected bowel determine which drugs and route of administration may be used

Acute

  • Admission if severe exacerbation
    • NBM
    • IVF
  • Induce remission
    • Mild to moderate CD
      • High dose oral steroids: Prednisone 40-50mg PO daily until response
        • Wean down steroids over 8-12 wks
      • +/- Metronidazole or Ciprofloxacin
    • Severe CD
      • IV steroids: Hydrocortisone 100mg IV QID
        • Generally given for 3-7 days
      • Surgery
      • Metronidazole or Ciprofloxacin
      • +/- Infliximab IV or Adalimumab SC (anti-TNF)
      • Antibiotics do not have a role unless transmural complications (e.g. abscess)

Chronic

Non-pharmacological

  • Smoking cessation
  • Diet change
    • During exacerbation low fibre may help control diarrhoea and pain related to food intake
    • 2˚ lactose intolerance
    • Correct micronutrient deficiencies with appropriate supplements
      • Iron, zinc, vitamin B12, calcium, magnesium, folic acid, Vitamin D

Pharmocological

  • Maintain remission
    • Azathioprine PO (immunosuppressant)
    • Methotrexate plus Folic acid IV 8-weekly (immunosuppressant)
      • If Azathioprine not tolerated
    • Infliximab IV (anti-TNF alpha)
    • Steroids should not be used as maintenance therapy
  • Perianal and fistulising disease
    • Metronidazole or Ciprofloxacin PO bd
    • Azathioprine
    • Infliximab IV or Adalimumab SC

Ulcerative colitis

à Inflammatory disease affecting the colonic mucosa anywhere from the rectum (always involved) to the caecum

  • It ‘never’ spreads proximal to the ileocaecal valve (except for backwash ileitis).
  • Pseudopolyps (oedematous intact mucosa) on colonoscopy.

Epidemiology

  • More common than CD.
  • Presentation mostly 15-30yrs.
  • More common in non-smokers.

Clinical features

  • Rectal bleeding
  • Episodic or chronic diarrhoea +/- blood, mucus
  • Crampy abdominal pain
  • Tenesmus, urgency, incontinence
  • Fever, malaise, anorexia
  • ↓ Weight
  • Extraintestinal manifestations less common in UC

Complications

  • Perforation
  • Haemorrhage
  • Toxic megacolon (colonic diameter >6cm)
  • Colon cancer

Investigation

  • Bloods: FBC, U&Es, LFTs, ESR/CRP
  • Stool: MCS
    • Rule out C. difficile, Campylobacter, E. coli, Salmonella, Shigella
  • Imaging: AXR (dilated colon from toxic megacolon), erect CXR (perforation)
  • Sigmoidoscopy or colonoscopy with biopsy plus exclusion of infectious causes: diagnostic

Treatment

Acute

  • Active proctitis/distal colitis
    • Mesalazine/5-aminosalicyclic acid (5-ASA) suppository
    • Hydrocortisone or prednisolone
      • If 5-Aminosalicylates are ineffective
  • Surgery
    • Needed in ~20% of UC patients, higher mortality if performed as an emergency
    • Procoto-colectomy, terminal ileostomy

Chronic

  • Maintain remission
    • Mesalazine/5-aminosalicyclic acid (5-ASA)
      • Active form of sulfasalazine and contains sulfapyridine and mesalazine
    • Immunomodulators
      • Azathioprine PO or Mercaptopurine PO or Methotrexate + Folate
      • Infliximab
  • Surveillance colonoscopy for bowel cancer
    • Every 2-4 yrs
62
Q

What are complications of Crohns and UC?

What is faecal calprotectin? What do the scores indicate?

What is a Toxic megacolon? What is the diagnositic criteria for it?

What is your DDX for toxic megacolon? Management?

A
63
Q

Management of Ulcerative Colitis:

Resus, flare ups, non-pharm, medical, maintenance, surgical (indications)

A
64
Q

Crohns managment:

Non-pharmacological:

Medical: Surgical?

Ongoing investigations?

Closing - Info, refer, safety net, follow up (Same for everything)

A
65
Q

Gallbladder: What is ascending cholangitis?

Clinical features? What is charcots triad?

What is reynolds pentad?

Investigations?

Treatment:

A

Gallbladder

Ascending Cholangitis

à Infection of the biliary tree

  • Stasis in the biliary tract due to obstruction or stricture
  • Infection originates in the duodenum or spreads haematogenously from the portal vein
  • Bacteria
    • E coli, Klebsiella, enterobacter, enterococcus
    • Co-infection with bacteroides and clostridia

Clinical features

  • Charcot’s triad: fever, RUQ pain, jaundice
    • 50-70% of patients
  • Reynolds pentad: Charcot’s triad, hypotension, altered mental status

Investigations

  • Bloods
    • Increased WBC
    • Increased ALP, ALT, bilirubin
    • Blood culture
  • Imaging: abdominal US - CBD dilation, stones

Treatment

  • Drainage via ERCP
    • If not possible: percutaneous biliary or surgical routes
  • Antibiotic therapy: broad spectrum to cover gram-negatives, enterococcus, anaerobes
    • Pip-taz, ampicillin, sulbactam
66
Q

What are important pancreatic enzymes?

What are causes of increased serum amylase?

Increased serum lipase?

Acute pancreatitis? Aetiology (IGETSMASHED)

Pathophysiology?

Clinical features? Think examination

Investigations: Bloods, Imaging

Treatment: Severe Pancreatitis:

Chronic pancreatitis? Causes?

Clinical features:

Complications?

Investigations? think complications (DM)

Treatment: Non-pharm, Pharmacological

A

Pancreas

Pancreatic Enzyme Abnormalities

Increased serum amylase

  • Pancreatic disease
    • Pancreatitis, pancreatic duct obstruction, pseudocyst, abscess, ascites, trauma, cancer
  • Non-pancreatic abdominal disease
    • Biliary tract disease, bowel obstruction, perforated or penetrating ulcer, ruptured ectopic pregnancy, aneurysm, chronic liver disease, peritonitis
  • Non-abdominal disease
    • Cancer, salivary gland lesions
    • Macroamylasemia

Increased serum lipase

  • Pancreatic disease
  • Non-pancreatic abdominal disease
  • Non-abdominal disease: macrolipasemia, renal failure

Acute pancreatitis

Aetiology à I GET SMASHED

  • Idiopathic
  • Gallstones
  • Ethanol
  • Tumours
  • Scorpion stings
  • Microbiological
    • Bacterial: mycoplasma, campylobacter, TB, legionella, leptospirosis
    • Viral: mumps, rubella, varicella, viral hepatitis, CMV, EBV, HIV, Coxsackie virus
    • Parasites
  • Autoimmune: SLE, polyarteritis nodosa, Crohn’s disease
  • Surgery/trauma
  • Hyperlipidemia, hypercalcaemia, hypothermia
  • Emboli or ischaemia
  • Drugs/toxins

Pathophysiology

  • Activation of proteolytic enzymes within pancreatic cells, starting with trypsin, leading to local and systemic inflammatory response 

  • In gallstone pancreatitis, this is due to mechanical obstruction of the pancreatic duct by stones 

  • In ethanol-related pancreatitis, pathogenesis is unknown 

  • In rare genetic diseases, mutations prevent the physiological breakdown of trypsin required 
normally to stop proteolysis (e.g. mutant trypsin in hereditary pancreatitis or mutation in SPINK 1 gene which normally inhibits activated trypsin); may be model for ethanol-related pancreatitis 


Clinical features

  • Pain: epigastric, constant
    • Can radiate to back
  • Jaundice: compression or obstruction of bile
  • May improve when leaning forward (Inglefinger’s sign)
  • Tender rigid abdomen; guarding

  • N/V

  • Abdominal distention from paralytic ileus
  • Fever: chemical, not due to infection
  • Cullen’s/Grey-Turner’s signs

  • Tetany: transient hypocalcemia

  • Hypovolemic shock: can lead to renal failure
  • Acute respiratory distress syndrome

  • Coma

Investigations

  • Bloods
    • Increased WBC, glucose
    • Decreased Ca2+
    • Increased serum pancreatic enzymes: amylase, lipase
    • LFT: ALT
  • Imaging
    • X-ray: sentinel loop/dilated proximal jejunum
    • US: useful for evaluating biliary tree
    • CT scan with IV contrast
    • ERCP or MRCP

Treatment

  • IV fluids
  • Analgesia: Morphine, fentanyl

Severe pancreatitis

  • Nasogastric tube
  • Early enteral nutrition
  • Treatment of hyperglycaemia
  • Treatment of symptomatic hypocalcaemia
  • Imaging of the biliary tree with MRCP to confirm biliary obstruction and guide ongoing management

Chronic pancreatitis

à Irreversible damage to pancreas characterised by pancreatic cell necrosis, inflammation and fibrosis.

Causes

  • EtOH (most common)
  • CF
  • Severe protein-calorie malnutrition
  • Idiopathic

Clinical features

  • Recurrent attacks of severe abdo pain (upper abdo and back)
  • May be chronic painless pancreatitis
  • Malabsorption syndrome → steatorrhoea
  • Diabetes
  • Weigth loss

Complications

  • Pseudocyst
  • Diabetes
  • Biliary obstruction
  • Gastric varices
  • Pancreatic cancer

Investigations

  • Bloods: Glucose, LFTs, lipase and amylase
  • Imaging: AXR (pancreatic calcifications), USS or CT abdo (calcification, pseudocysts)
  • Other: 72h faecal fat test, faecal elastase

Treatment

Chronic

Non-pharmacological

  • Lifestyle modification
    • Abstain from EtOH
    • Low fat diet, high in protein
  • Vit ADEK supplementation

Pharmacological

  • Analgaesia
    • Coeliac-plexus blocks
  • Insulin
  • Pancreatic enzyme replacement
    • Creon
  • Surgery
    • Resistant pain
    • Opiate abuse
    • Blocked pancreatic duct
67
Q

What is IBS?

What are the causes?

What are the clinical features? (ROME III criteria) NEED TO KNOW for IBS

What are clinical features that support IBS diagnosis?

When is diagnosis less likely (think red flags)

Investigations: Bloods, Stool, Imaging, Colonscopy

Treatment: Chronic

A

Irritable bowel syndrome (IBS)

à Functional bowel disease. Usually a diagnosis of exclusion.

Cause

  • Unknown.
  • Altered bowel motility, visceral hypersensitivity and psychosocial factors.

Clinical features

Rome III criteria for IBS

  • ≥12 wks in the past 12 months of abdominal discomfort that is either:
    • Relieved by defecation OR
    • Associated with change in frequency or consistency of stool

Suggestive features:

  • Abnormal stool frequency, consistency
  • Mucus
  • Bloating
  • Abnormal stool passage (straining, urgency, feeling of incomplete emptying)

Diagnosis less likely in presence of red flag features

  • Weight loss
  • Fever
  • Nocturnal defecation
  • Anaemia
  • Blood or pus in stool
  • Abnormal gross findings on flexible sigmoidoscopy

Investigation

  • Bloods: FBC, TFT, LFTs, CRP/ESR, tTG serology (coeliac)
  • Stool MCS, O&P (ova and parasite)
    • Faecal calprotectin: rule out IBD
  • Imaging: +/- Sigmoidoscopy
  • Colonoscopy

Treatment

Chronic

  • Reassurance, education
    • Tx has low success rate so aim to make symptoms more tolerable, no drugs are very effective
  • Symptomatic treatment
    • ↑ Fibre (but can also worsen bloating/flatulence)
    • +/- Anti-diarrhoeal medications (eg Loperamide)
  • +/- Laxatives
68
Q

Management: IBD

GESA guideline: Outline key points:

A
69
Q

Appendicitis:

Clinical features? List 6

Investigations: Bedside: Bloods: Imaging:

Management: 2 marks

A

Appendicitis

Clinical features

  • Lying still, dehydrated, shallow breaths
  • Tachycardia, hypotensive, fever
  • Furred tongue, fetor, flushing
  • Guarding, rigidity, rebound and percussion tenderness
  • Rovsing’s, Psoas, Obturator sign
  • PR painful on right side

Investigations

  • Bedside: glucose, ABG, urinalysis, pregnancy test
  • Bloods: FBC, CRP elevated, LFT, ESR, lipase
  • Imaging: USS, CT

Management

  • Admit to general surgery for prompt appendectomy
  • Antibiotics: metronidazole 500mg/8hour + cefuroxime
  • Emperical antibiotics: gentamycin, amoxicillin, metronidazole
  • Rehydrate
  • Pain relief
70
Q

Lower GIT Bleeding:

Bleeding distal to the Ligament of treitz:

Aetiology: (CHAND) Colitis,

Clinical features?

What is a carcinoid tumour? What are the common sites? Clinical features? Diagnosis (think VMA), Treatment?

What is a carcinoid crisis?

A

Lower GIT Bleeding

à Bleed distal to the ligament of Treitz

Aetiology à CHAND

  • Colitis: Radiation, infectious, ischemic, IBD (UC > CD)
  • Haemorrhoids/fissure

  • Angiodysplasia

  • Neoplastic

  • Diverticular disease

Clinical features

  • Haematochezia
  • Anaemia

  • Occult blood in stool

  • Rarely melena

Carcinoid tumours

à Tumours of neural crest origin (enterochromaffin cells) that produce serotonin (5HT)

  • Can be part of MEN-1 syndrome

Common sites

  • Appendix, ileum, rectum
  • Less commonly anywhere along the GIT, ovary, testes, bronchi.

Clinical features

  • Initially few symptoms
  • GI tumour: Appendicitis, intussusception, obstruction
  • Hepatic metastases: RUQ pain
  • Carcinoid syndrome (5%)
    • Bronchoconstriction
    • Paroxysmal flushing
    • Tachycardia
    • Diarrhoea
    • CHF (pulmonary stenosis → pulmonary HTN → tricuspid regurgitation)

Diagnosis

  • CXR + CT chest/abdo/pelvis to locate primary tumours
  • 24h urine 5HIAA (5HT metabolite)

Treatment

  • Octreotide (somatostatin analogue) blocks release of tumour mediators
  • Surgery: Gold standard - only cure
  • +/- Loperamide for diarrhoea

Carcinoid crisis

  • When a tumour outgrows it blood supply mediators escape
  • Results in life-threatening vasodiltation, hypotension, tachycardia, bronchoconstriction and hyperglycaemia
  • Treated with high dose octreotide
71
Q

List 6 causes of hepatomegaly?

List 6 causes of Splenomegaly?

Outline a complete GI examination:

Special tests for

1) Appendicitis?
2) Cholecystitis

A

Gastrointestinal Examination

Introduction, Vital Signs

General inspection

Consider: stool charges, medications, if patient is in isolation bay

Body habitus

Cachexia

Malignancy

Malabsorption

Cirrhosis

Obesity

Fatty liver: non-alcoholic steatohepatitis

Colour

Jaundice

Hyperbilirubinemia: Pre-hepatic, hepatic or hepatic

Pallor

Abnormal skin pigmentation

Haemochromatosis

Excess iron à Haemosiderin stimulates melanocytes to produce melanin

Slate grey discolouration of the skin

Malabsorption

Sunkissed pigmentation

Mostly of nipples, palmar creases, pressure areas and mouth

Confused/drowsy

Hepatic encephalopathy due to decompensated advanced cirrhosis

Features depend on aetiology and precipitating factors

Patients eventually become stuporous and comatose

Caused by the combination of hepatocellular damage and porto-systemic shunting

Fulminant hepatitis (acute liver failure)

Pain/anxiety

Patient lying very still

Parietal irritation

Patient can’t get comfortable

Visceral irritation

Nephrolithiasis

Hands/Arms

Nails

Clubbing: Not very common

Chronic liver disease, cirrhosis

Inflammatory bowel disease

Coeliac disease

Capillary refill

Leuconychia: white in nails (may cover all but near end of nail)

Hypoalbuminemia due to chronic liver disease

Muehrcke’s lines: transverse white lines

Koilonychia: Spoon nails

Iron deficiency

Palms

Sweaty/dry

Erythema of the palmar creases

à Affects the thenar and hypothenar eminences

Chronic liver disease

Thyrotoxicosis

Rheumatoid arthritis

Polycythaemia: excess Hb in blood

Can be a normal finding, particularly in pregnancy

Pallor of the palmar creases

Anaemia

Dupuytren’s contracture: tendon-like appearance at base of finger – often ring finger and bilateral

Alcoholism

Manual workers – often familial

Arms

Hepatic flap/Asterixis

à Arms stretched out in front with fingers separated and wrists extended for 15 seconds

à Positive if jerk, irregular flexion extension movement at the wrist and metacarpophalangeal joints, often accompanied by lateral movements of the fingers, usually bilateral

Hepatic encephalopathy

Cirrhosis

Wilson’s disease

Opiate overdose

Bruising/petichiae

Large bruises (echymoses): clotting abnormalities

Hepatocellular damage

Obstructive jaundice

Petichiae: chronic excessive alcohol consumption, splenomegaly

Scratch marks

Cholestatic jaundice: causes itchiness

Primary biliary cirrhosis

Spider naevi

à Central arteriole from which radiate numerous small vessels, vary in size, occasionally bleed profusely, blanching

à Number can vary depending on stage in underlying condition

à Only occur in the upper part of the body

Alcohol

Cirrhosis

Pregnancy

Acanthosis nigricans in axilla: Black to brown velvety elevations of the epidermis due to confluent papillomas

Skin marker of GIT malignancy

Face

Eyes

Xanthelasma

Primary biliary cirrhosis

Scleral jaundice

Bitot’s spots: yellow keratinised areas of the sclera

Severe vitamin A deficiency

Conjunctival pallor

  • Liver disease
  • Wilson’s disease

Kayser-Fleischer ring: Brown ring on edge of iris

  • Wilson’s disease

Iritis: red eyes

Inflammatory bowel disease

Cheeks

Parotid gland enlargement

à Ask patient to clench jaw: gland felt behind masseter and in front of ear

Alcoholism

  • Due to fatty infiltration, perhaps secondary to alcohol toxicity +/- malnutrition

Mouth

Angular stomatitis

Deficiency of iron, folate and B12

Brown-black lesions around mouth

Peutz-jeghers syndrome

  • Lesions associated with hamartomas of the small bowel and colon
  • Can be present with bleeding or intussusception (inversion of a portion of the intestine)
  • Increases risk of GIT adenocarcinoma

Telangiectasia around mouth

Hereditary haemorrhagic telangiectasia

  • Multiple small telangiectasias occur
  • Often present on lips and tongue but may be found anywhere on the skin

Fetor hepaticus: Sweet smell of breath

Portal hypertension

Late sign of liver failure/hepatocellular disease

Mucosal petichiae and ulcers

Crohn’s disease

Coeliac disease

Tongue

Leukoplakia

Premalignancy

Causes

  • Smoking
  • Spirits
  • Sepsis
  • Syphilis

Glossitis: inflammation of tongue

à causes a smooth appearance and may be erythematous

Deficiency of iron, folate and B12

Hydration

Neck and chest

Supraclavicular lymph nodes

Virchow’s node: Enlarged left supraclavicular node

  • Secondary to gastric malignancy

When enlarged and palpable: named Trosier’s sign

Gynaecomastia in males

Chronic liver disease

Medication: E.g. Digoxin, cimetidine

Spider naevi

>5 = abnormal: Cirrhosis

Abdomen

à Remember to watch patients face whilst palpating

à During palpation palmar surfaces of the fingers are used but during palpation of the edge of organs the lateral surface of the index finger is used

To decrease voluntary guarding: draw patients knees up, encourage deep breathing, engage patient in conversation

Inspection

Scarring

Previous surgery or trauma

Skin lesions

  • Herpes zoster: radicular pattern, localised to one side of the abdomen
  • Striae: Stretching of abdominal wall, results in pink linear marks with a wrinkled appearance. Caused by ascites, pregnancy, recent weight gain or Cushing’s syndrome

Stomata

  • Colostomy, ileostomy, ileal conduit

Prominent veins

Caput medusa: Around umbilicus with blood flowing away towards legs (very rare)

  • Portal hypertension

IVC obstruction: Blood flows towards head

Due to a tumour, thrombosis or tense ascites

Pulsations

  • AAA

Visible peristalsis

Intestinal obstruction

  • Pyloric obstruction: peptic ulceration or tumour

Normal in very thin people

Generalised distension

Causes:

  • Fat: Gross obesity
  • Fluid: Ascites
  • Foetus
  • Flatus: Gaseous distension due to bowel obstruction
  • Faeces

Tumour: ovarian tumour, hydatid cyst

Discolouration

Cullen’s sign: around umbilicus

  • Faintly bluish hue
  • In cases of extensive haemoperitoneum or acute pancreatitis
  • Rare

Grey-turner’s sign: in flanks

  • Acute pancreatitis
  • Rare

Visible masses

à Look at abdomen squatting down and watch for any asymmetrical movement

  • Enlargement of one of the abdominal/pelvic organs
  • Hernia
  • Congenital abdominal wall defect
  • Chronically increased intrabdominal pressure

Palpation

Light palpation: 9 quadrants

Feel for any tenderness or lumps

Deep palpation: 9 quadrants

Detect deeper masses and characterise masses already found

Guarding: tending of abdominal wall muscles

Voluntary, involuntary

Rigidity: constant involuntary contraction of abdominal muscles

Peritoneal irritation

Rebound tenderness/Blumberg’s sign

If patient winces = rebound test positive

Peritoneal irritation

Liver palpation

If edge is felt note:

  • Regular/irregular
  • Consistency
  • Tender/non-tender
  • Pulsatile/non-pulsatile

Gallbladder palpitation

Felt as a bulbus, focal, rounded mass which moves downwards on inspiration

Spleen palpation

Splenomegaly

Wilson’s disease

Kidney palpation/blotting

Occasionally the kidney can be felt

  • The lower pole of the right kidney may be palpable in thin, healthy people

Aorta

  • Pulsation from the abdominal aorta may be present, usually in the epigastrium, in thin healthy people
  • Aortic aneurysm: pulsation is expansile, enlarges more in systole, large than 5cm

Percussion

Liver

* Do if liver was palpated

Normally liver border begins at 6th rib

Liver is usually 8-13cm

Ascites

Presence of fluid in abdomen

  • When ascites is gross, the abdomen distends, the flanks bulge, umbilical eversion occurs and dullness is detectable closer to the midline

Shifting dullness à If ascites is present

If there is shifting dullness = ascites

  • Shifting dullness is present if the area of dullness has changed to become resonant, this is because the peritoneal fluid moves under the influence of gravity to the right side of the abdomen when this is the lowermost point

Fluid thrill à If ascites is present

  • Occurs mostly with massive ascites
  • May also occur if there is a massive ovarian cyst or pregnancy with hydroaminos

Auscultation

Bowel sounds

à Place diaphragm of stethoscope below the umbilicus

Present/absent

  • Absent for >4 minutes: Paralytic ileus, obstruction
  • Tinkling: obstruction
  • Hypoactive: gastroenteritis, diarrhoea, peritonitis, ileus
  • Hyperactive: obstruction, diarrhoea, increased peristalsis, malabsorption

Liver friction rub

  • Indicate an abnormality of the parietal and visceral peritoneum due to inflammation
  • Rough, creaking or grating noise is heard as the patient breathes

Carcinoma

Liver infarct, abscess, recent biopsy

Chlamydial perihepatitis

Spleen friction rub

Infarct

Bruit

Renal, liver, spleen

  • Liver: high pitched than a venous hum, it not continuous and is well localised
  • Liver: Hepatocellular cancer, alcoholic hepatitis, post-liver biopsy
  • Renal: renal artery stenosis,

Venous hums:

à Heard between xiphisternum and umbilicus

Portal hypertension

  • Continuous, low pitched soft murmur that may become louder with inspiration and diminish when more pressure is applied
  • Caused by large volumes of blood flowing in the umbilical or paraumbilical veins in the falciform ligament are responsible

Special tests

Appendicitis

Rovsing’s test

à Press fingers in LIQ and quickly withdraw

Pain in right iliac fossa during left side pressure = positive Rovsing’s sign

Psoas sign

à Place your hand above the patients right need and ask patient to raise thigh against your hand

Increase pain = positive psoas sign

Obturator sign

à Flex patient’s right thigh at the hip and the knee bent, then internally rotate the leg at the hip

Right hypogastric pain = positive obturator sign

MacBurney’s sign:

MacBurney’s point is 4-5cm along a line from the anterior superior iliac spine to the umbilicus

Deep tenderness here is a sign of acute appendicitis

Cholecystitis

Murphy’s sign

à Place right hand in right costal margin just lateral to lateral border of the rectus abdominis muscle

On taking a deep breath the patient catches his breath when an inflamed gall bladder presses on the patients hand

Renal tenderness

Murphy’s punch

à Tap on costovertebral angle

Tenderness = positive

Legs

  • Check of bruising, oedema and changes noted in the arms

* A hernia, rectal, vaginal and external genitalia examination is essential to a GIT examination

* Note: CVS, RS and CNS examinations may be helpful in patients with hepatomegaly

72
Q

What are functional GI disorders?

What does these class of disorders encompass?

What is Irritable bowel syndrome: What is the epidemiology?

What is the Rome IV critera?

What are red flags for IBS? 3 marks

Clinical findings: Exam IBS?

Investigations? 1st line for IBS (what things do you need to rule out) + Imahing? (when is it indicated)

A

Clinical

  • Intermittent abdominal pain related to defecation
  • Bowel dysfunction - constipation & diarrhoea
  • Change in stool consistency
  • NO BLOOD IN STOOL IN IBS

Exam

  • Systems exam
  • In the absence of gynaecological or perianal symptoms, neither pelvic examination nor rectal examination would be routinely indicated on initial investigation

InvestigationsLabs (1st line for IBS)

  • FBC - anemia a red flag
  • IgA TTG Ab - rule out Coeliac
  • CRP - investigate for IBD

Imaging

  • Not indicated in the absence of red flags
  • Any red flags –> ?CT or USS depending on provisional diagnosis

Assessment

Red flags

  • Anemia
  • Loss of weight
  • Age >50 at onset
  • Radiates to back
  • Melaena or haematochezia
  • Nocturnal with waking at night
  • Family history of CRC or IBD
73
Q

List 6 different causes/catergories of disease that can cause a Transaminitis?

What is the classification of acute liver failure?

Outline a workup for acute liver failure with unknown cause? Bloods/imaging/biopsy

A

Adult health 1 (24 decks)

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