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Conditions + definitions > GI 3 > Flashcards

GI 3 Flashcards

1
Q

What are the investigations into stools?

A

FOB testing
Stool culture
Faecal calprotectin
Faecal elastase – investigation of pancreatic insufficiency/malabsorption

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2
Q

How do you screen the liver?

A 
hep B/C serology
autoantibodies (ANA, AMA), 
immunoglobulin
Ferritin
Alpha 1 antitrypsin
Caeuloplasmin, copper
Alpha fetoprotine
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3
Q

What is coeliac serology?

A

Tissue transglutaminase
Endomysial antibody
Check IgA levels

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4
Q

How do you manage a patient with low risk features with rectal bleeding?

A

Wait and watch for 6 weeks

Then review + refer if deteriorated or persistent

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5
Q

How do you manage a patient with high risk features with rectal bleeding?

A

Refer

Investigate

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6
Q

How do you investigate bleeding?

A 
Endoscopy (+ biopsy if suspicious)
Contrast imaging
CT
MRI
>Whatever is most appropriate
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7
Q

What is important for success in bowel anastomosis?

A 
Tension free
Well perfused
Well oxygenated
Clean surgical site
Acceptable systemic state
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8
Q

What are the complications of bowel surgery?

A 
Anaesthetic related
Bleeding
Sepsis
VTE
Anastomotic breakdown
Small bowel obstruction
Wound hernia
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9
Q

What is the acute abdomen?

A

A combination of symptoms and signs, including abdominal pain,
>which results in a patient being referred for an urgent general surgical opinion

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10
Q

What are the most common causes for acute abdomen?

A 
Non-specific pain
Acute appendicitis
Acute cholecystitis
Peptic ulcer perforation
Urinary retention
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11
Q

What are the routes of infection of the peritoneum? (causing peritonitis)

A

Perforation of GI/ biliary tract
Female genital tract
Penetration of abdominal wall
Haematogenous spread

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12
Q

When does generalised peritonitis occur?

A

It means localisation has failed and occurs when:

Contamination too rapid
Contamination persists
Abscess ruptures

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13
Q

What are the symptoms of intestinal obstruction?

A 
Pain
Vomiting
Distension
Constipation
Borborygmi
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14
Q

What are the types of abdominal pain? (character)

A

Visceral
Somatic
Referred

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15
Q

If pain comes and goes, what should you consider?

A

Peritonitic pain
Colic
Body wall pain

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16
Q

What are the aims of resus in regards to acute abdomen?

A 
Restore circulating volume
Ensure tissue is perfused
Enhance tissue oxygenation
Treat sepsis
Decompress gut
Ensure adequate pain relief
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17
Q

What are the types of viral hepatitis?

A

A and E (self limiting)

B, C and D are parenteral (cause chronic disease)

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18
Q

How is Hep A transmissible?

A

Transmission through fecal-oral route, sexual, or blood bourne

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19
Q

What are the features of Hep A?

A

5-14 commonenst (children affected for shorter, but more common)
Sporadic infection of epidemic
Diagnosed acutely with IgM antibodies

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20
Q

Who is advised to get the Hep A vaccine?

A 
Travellers
Patients with chronic liver disease (HBV or HCV especially!)
Haemophiliacs
Occupational exposure
Men who have sex with men
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21
Q

What is the structure of HBV?

A

Has a surface antigen coat
Inner coat with DNA polymerase
Inside with the core antigen

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22
Q

How does HBV avoid the immune system?

A

Creates a host of empty cells of surface antigens to confuse body (no inner core)
Sits in liver, but sends decoy antigen into blood (E antigen – HbeAg)
Difference between E antigen and core antigen is the lack of Pre C in code, what allows it to travel into the blood

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23
Q 
What do the different HBV antigens indicate?
Surface antigen
E antigen
Core antigen
HBV DNA
A

Surface antigen – presence of virus
Presence of E antigen in blood indicates acute infection (active replication)
Core antigen – active replication (not detectable in blood)
HBV DNA (active replication)

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24
Q 
What do the different HBV antibodies indicate?
Anti-HBs
IgM anti HBc 
IgG anti HBc 
Anti HBe
A

Anti-HBs - protection
IgM anti HBc – acute infection
IgG anti HBc – chronic infection/exposure
Anti HBe – inactive virus

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25
Q

What is the approach to HBV infection?

A

If HBsAG negative – no active infection, vaccinate
Positive – check if clinical evidence of acute infection
If no evidence, of no IgM anti-HBc then chronic infection
If clinical evidence and IgM anti HBc – acute infection
As acute infection clears in 90% of patients in 6 months, no treatment
Chronic – evaluate for ongoing monitoring and treatment
(Not all patients have chronic disease)

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26
Q

How do you treat chronic HBV?

A

If the HBV DNA IU/mL >2000, treatment indicated
Normally Tenofovir used, as low rates of resilience, works in HIV co-infected, high potency, category B in pregnancy. However, renal toxicity

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27
Q

What are the other potential agents used for HBV infection?

A

Other agents – Telbivudine
Entecavir
Adefovir
Lamivudine

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28
Q

What is the natural history of HCV?

A 
Rarely causes acute liver failure
Most asymptomatic until chirrotic
May have normal LFTs
10% report acute jaundice
An RNA virus – so uses DNA-RNA transcriptase which mutates rapidly (deliberately)
HIV/alcohol speed up disease
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29
Q

What are the drugs available for HCV?

A

sofosbuvir + ledipasvir

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30
Q

What is HDV?

A

A small RNA virus that doess not code for own protein coat, enveloped by HBsAg
Co infection or superinfection with HBV (same transmission)
Very resistant to treatment
Parasite of HBV

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31
Q

What is HEV?

A

Commonest cause of acute hepatitis in Grampian
Self-limiting
No specific treatment
No vaccine
Tropical Zoonotic virus (transmitted by animals, E - via pigs)

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32
Q

What does non-alcoholic liver disease encompass?

A

Simple steatosis
Non alcoholic steatohepatitis
Fibrosis and cirrhosis

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33
Q

What is NAFLD associated with?

A 
Diabetes mellitus
Obesity
Hypertriglyceridemia
Hypertension
Age
Ethnicity (Hispanics)
Genetics (PNPLA3 gene)
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34
Q

What is the progression of NAFLD?

A

Normal

  • -> steatosis
  • -> NASH +/- fibrosis
  • -> cirrhosis
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35
Q

How do you diagnose NAFLD?

A 
AST/A:T ratio
USS
Fibroscan
Liver biopsy
NAFLD tool on website
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36
Q

How do you treat NAFLD?

A

Diet and weight reduction (+/- surgery)
Exercise
Insulin sensitisers
Glucagon-like peptide 1 (GLP1) analogues (Liraglutide)
Farnesoid X nuclear receptor ligand (obeticholic acid)
Vitamin E

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37
Q

What are the autoimmune diseases of the liver/biliary tract?

A 
Autoimmune hepatitis
Primary biliary cholangitis (PBC)
Primary sclerosing cholangitis (PSC)
Overlap syndromes
Autoimmune cholangiopathy
IgG 4 disease
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38
Q

What is autoimmune hepatitis?

A 
Female predominant
Elevated IgG
Diagnosed by liver biopsy
Responds well to steroids
Long term azathioprine
3 types of antibodies; Type 1 – ANA, SMA. Type 2: LKM1. Type 3 SLA
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39
Q

Who is eligible for a liver transplant?

A

Chronic liver diseases with poor predictive survival or poor quality of life
Hepatocellular carcinoma
Acute liver failure
Genetic diseases – primary oxaluria, tyrosemia

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40
Q

What are the contraindications for liver transplant?

A

Active extrahepatic malignancy
Hepatic malignancy with macrovascular or diffuse tumour invasion
Active and uncontrolled infection outside of hepatobiliary system
Active substance or alcohol abuse
Severe cardiopulmonary or other comorbid conditions
Psychosocial factors that would preclude recovery
Technical/anatomical barriers
Brain death

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41
Q

How is liver transplant prioritised in cirrhosis?

A

Child’s Pugh scoring A, B, C
MELD score (Bilirubin, Creatinine and INR)
UKELD( Bilirubin, Sodium, Creatinine and INR)

42
Q

What is the post op treatment for a liver transplant?

A

Post operative ICU care
Multidisciplinary care
Prophylactic antibiotics and anti-fungal drugs
Anti-rejection drugs: Steroids, Azathioprine, Tacrolimus/Cyclosporine

43
Q

What can cause acute liver injury?

A

Hepatitis

Bile duct obstruction

44
Q

What is the pathophysiology of jaundice?

A

Increased circulation of bilirubin
Caused by altered metabolism on bilirubin
Pathway can be pre hepatic, hepatic, or post hepatic

45
Q

What is prehepatic metabolism (bilirubin pathway)?

A

Breakdown of haemoglobin in spleen to form haem and globin
Haem converted to bilirubin
Release of bilirubin into circulation

46
Q

What is hepatic metabolism of bilirubin?

A

Uptake of bilirubin by hepatocytes
Conjugation of bilirubin hepatocytes
Excretion of conjugated bilirubin into biliary system

47
Q

What is post hepatic metabolism of bilirubin?

A

Transport of conjugated bilirubin in biliary system
Breakdown of bilirubin conjugate in intestine
Re-absorption bilirubin – entero-hepatic circulation of bilirubin

48
Q

What causes prehepatic jaundice?

A

increased release of haemoglobin from red cells – haemolysis

49
Q

What causes hepatic jaundice?

A

cholestasis (accumulation of bile within hepatocytes or bile canaliculi)
Intra-hepatic bile duct obstruction

50
Q

What causes post-hepatic jaundice?

A

cholelithiasis
Disease of gall bladder
Extra hepatic duct obstruction
What are the causes of cholestasis

51
Q

What are the causes of cholestasis?

A

Viral hepatitis
Alcoholic hepatitis
Liver failure
Drugs – therapeutic/recreational predictable v unpredictable (dose vs other factors)

52
Q

What are the causes of intra-hepatic bile duct obstruction?

A

Primary biliary cholangitis
Primary sclerosing cholangitis
Tumours of liver – hepatocellular carcinoma, tumours of intra-hepatic bile ducts and metastatic tumours

53
Q

What is primary biliary cholangitis?

A

Organ specific auto immune disease (mainly females)
Anti-mitochondrial antibodies in serum
Raised serum alkaline phosphates
Granulomatous inflammation involving bile ducts
Loss of intra-hepatic bile ducts
Progression to cirrhosis

54
Q

What is primary sclerosing cholangitis?

A 
Chronic inflammation and fibrous obliteration of bile ducts
Loss of intra-hepatic bile ducts
Assoc. w/ inflammatory bowel disease
Progression to cirrhosis
Increased risk of developing cholangiocatcinoma
Male predominant
Recurrant cholangitis, Jaundice
Liver Tx, Biliary stents to treat
55
Q

What are the causes of cirrhosis?

A 
Alcohol
Hepatitis B, C
Immune mediated liver disease
>Auto-immune hepatitis
>Primary biliary cholangitis
Metabolic disorders (excess iron -  primary haemochromatosis
>Excess copper – wilsons disease
Obesity – diabetes mellitus
56
Q

What is the pathology of cirrhosis?

A

Involves whole liver – loss of normal liver structure

Replaced by nodules of hepatocytes and fibrous tissue

57
Q

What complications can arise from cirrhosis?

A

altered liver function so failure
Abnormal blood flow – portal hypertension
Increased risk of hepatocellular carcinoma

58
Q

What are the risk factors for gallstones?

A 
obesity, 
diabetes, 
female
Cholesterol
Parity + OCP
Bile infection
59
Q

What is the pathology of gallstones?

A

Caused by inflammation (acute/chronic cholecystitis)
Acute – empyema (perforation of gall bladder, biliary peritonitis)
May lead to chronic – causes fibrosis as well as inflammation

60
Q

What leads to bileduct obstruction?

A

Gallstones
Bile duct tumours
Benign stricture
External compression – tumours

61
Q

What are teh effects of bilestone obstruction?

A

Jaundice
No bile in duodenum
Infection of bile proximal to obstruction (ascending cholangitis)
Secondary biliary cirrhosis if obstruction prolonged)

62
Q

What is the presentation of gallstones?

A 
Majority asymptomatic
Dyspeptic symptoms
Biliary colic
Acute cholecytitis
Empyema
Perforation
Jaundice
Gallstone ileus
63
Q

What is choledocho-iliasis, what can it lead to?

A

Blockage of bile duct
Can lead to obstructive jaundice (painful)
Can lead to acute pancreatitis
Can lead to ascending cholangitis

64
Q

How do you investigate suspected gallstones?

A 
Blood tests – amylase, lipase, WCC, LFTs: AST/ALT,ALP
USS, EUS
Oral cholecystography
CT scan, radio-isotope scan
IV cholangiography
MRCP/ERCP
PTC
65
Q

How do you manage gallstones?

A

Asymptomatic – do nothing
Non-operative treatment – dissolution, lithotripsy
Operative
>Cholecystectomy - remove gallbladder, laproscopic gold standard

66
Q

What are the causes of benign biliary tract disease?

A

Congenital:
>biliary atresia
>Choledochal cysts

Benign biliary stricture

67
Q

What tumours can cause jaundice?

A

Cholangiocarcinoma (intra or extrahepatic, gallbladder, ampullary)
Cancer of head of pancreas

68
Q

What are the tisks of cholangiocarcinoma?

A 
(Bileduct cancer)
PSC (strong association)
Congenital cystic disease
Biliary-enteric drainage
Thorotrast (contrast)
Hepatolithiasis
Carcinigens: aflatoxins, etc.
69
Q

What is the presentation of cholangiocarcinoma?

A

Obstructive jaundice
Itching
Non-specific symptoms

70
Q

What are the three types oc cholangiocarcinoma?

A

Mass forming (blockage)
Peri-ductal (both sides)
Intra-ductal (one side)

71
Q

How do you manage cholagiocarcinoma?

A

Surgical – only potential cure

Palliative – 
surgical bypass
Stenting
Radiotherapy
Chemo
PDT
72
Q

How do you treat an ampullary tumour?

A 
Depends if adenoma or adenocarcinoma
Treatment:
Endoscopic excision
Trans-duodenal excision
Pancreatico-duodenectomy
73
Q

What are the liver function tests?

A 
Bilirubin
Aminotransferases 
Alkaline phosphatase 
Gamma GT 
Albumin 
Prothombin time 
Creatine 
Platelet count
74
Q

What are aminotransferases?

A

enzymes in hepatocytes –
>ALT more specific than AST.
>AST/ALT ratio points towards ALD
>suggests parenchymal involvement)

75
Q

What is alkaline phosphatase (ALP)?

A

enzyme in bile ducts,
elevated with obstruction or liver infiltration.
>Also present in bone, placenta and intestines

76
Q

What is Gamma GT?

A

A non specific liver test
Elevated in alcohol, however
>Useful to confirm ALP result

77
Q

What does low albumin indicate?

A

suggest chronic liver disease,

>can be low in kidney disorders and malnutrition

78
Q

Why is prothrombin time important?

A

Tells extent of liver damage

79
Q

Why is creatine important as a liver test?

A

It is essentially kidney function

>Used to determine survival from liver disease

80
Q

Why is platlet count a liver test? What do low levels indicate?

A

liver produces thromboprotein
>cirrhosis in splenomegaly
Platelets low in cirrhotic patients (hypersplenism) >Indirect marker of portal hypertension

81
Q

What are the symptoms of liver failure?

A

Jaundice,
ascites,
variceal bleeding,
hepatic encephalopathy

82
Q

What are the clues for pre-hepatic jaundice?

A

Clinical:
Pallor
Splenomegaly

History:
anaemia (fatigue, dyspnoea, chest pain), acholuric jaundice

83
Q

What are the clues for hepatic jaundice?

A 
Clinical:
Ascities, 
asterixis, 
stigmata of CLD 
>(spider naevi, gynaecomastia)
History:
risk factors for liver disease 
>(IVDU, drug intake), 
decompensation 
>(ascities, variceal bleed, encephalopathy)
84
Q

What are the clues for post-hepatic jaundice?

A

Clinical:
palpable gall bladder (courvoisier’s sign)

History:
abdominal pain,
cholestasis
>(puritus, pale stools, con. Urine)

85
Q

What can therapeutic ERCP be used for?

A

Dilated biliary tree (w/ or w/o visible stones/tumour)
Acute gallstone pancreatits
Stenting of biliary tract obstruction
Post-op biliary complications

86
Q

What complications can arise from ERCP?

A 
Sedation related
Procedure related
>pancreatitis, 
>cholangitis, 
>sphincterotomy -  
>bleed/ perforation
87
Q

What is chronic liver disease?

A 
Liver disease lasting more than 6 months:
Chronic hepatitis
Chronic cholestasis
Fibrosis and cirrhosis
Others – steatosis
Liver tumours
88
Q

How does compensated chronic liver disease present?

A

Routinely detected on screening tests

Abnormality of liver function tests

89
Q

How does decompensated liver disease present?

A

Ascites
Variceal bleeding
Hepatic encephalopathy

90
Q

What are the clinical features of ascites?

A 
Physical exam reveals dullness in flanks and shifting dullness
Can be confirmed by U/S
Corroborating evidence
>JVP elevation
>Spiders, 
>palmar erythema, 
>abdominal veins, 
>fetor hepaticus
>Unbilical nodule
>Flank haematoma
91
Q

How do you confirm ascites?

A

Protein and albumin concentration
Cell count and differential
Routine – cell count, protein, albumin

92
Q

What does a SAAG score of >1.1 mean?

A

SAAG (serum ascites albumin gradient) >1.1g/dl portal HTN related

93
Q

What does a SAAG score of <1.1 mean?

A

<1.1g/dl nonportal HTN causes (both 97% acc)

94
Q

What are the causes of a SAAG score >1.1g/Dl

A 
Portal hypertension
 CHF
 Constrictive pericarditis
 Budd Chiarri
 Myxedema
Massive liver metastases
95
Q

What are the causes of a SAAG score <1.1g/Dl

A 
Malignancy
 Tuberculosis
 Chylous ascites
 Pancreatic
Biliary ascites
Nephrotic syndrome
 Serositis
96
Q

How do you treat ascites?

A 
Diuretics
Large volume paracentesis
TIPS
Aquaretics
Liver transplant
97
Q

What is variceal haemorrhage?

A 
When an acites bleeds due to portal hypertension.
	Occur at porto-systemic anastomoses
Skin – caput medusa
Oesophageal and gastric
Rectal
Posterior abdominal wall
Stomal
A medical emergency!
98
Q

How do you treat variceal haemorrhage?

A 
Resuscitate patient
Good IV access
Blood transfusion as required
Emergency endoscopy
-	Band ligation
Add terlipressin for control
Sengstaken-blakemore tube for uncontrolledbleeding
TIPSS for rebleeding after banding
99
Q

What is hpatic encephalopathy?

A

Confusion due to liver disease

Graded 1-4: confusion to coma

100
Q

How does hepatocellular carcinoma present?

A 
Decompensation of liver disease
Abdominal mass
Abdominal pain
Weight loss
Bleeding from tumour
101
Q

How do you diagnose hepatocellular carcinoma?

A

Tumour markers – AFP
Radiological tests – U/S, CT, MRI
Liver biopsy rarely

102
Q

How do you treat hepatocellular carcinoma?

A 
Hepatic resection
Liver transplant
Chemo – locally delivered or systemic
Locally ablative treatmetns – alcohol injection, radiofrequency ablation
Sorafenib (tyrosinase kinase inhibitor)
Hormonal therapy – tamoxifen

Conditions + definitions (68 decks)

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