Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Phase 2A revision > LIVER & FRIENDS > Flashcards

LIVER & FRIENDS Flashcards

1
Q

Give 4 functions of the liver

A
  1. Glucose and fat metabolism
  2. Detoxification and excretion
  3. Protein synthesis (e.g. albumin, clotting factos)
  4. Bile production
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Name 3 things that liver function tests measure

A
  1. Serum bilirubin
  2. Serum albumin
  3. Pro-thrombin time
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Name an enzyme that increases in the serum in cholestatic liver disease (duct and obstructive disease)

A

Alkaline phosphate (ALP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What enzymes increase in the serum in hepatocellular liver disease?

A

Transaminases - e.g. AST and ALT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What tests give no index of liver function and why?

A

Liver enzymes - alkaline phosphate, GGT, AST, ALT Released by damaged cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Define jaundice

A

Raised serum bilirubin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Name the 3 broad categories of jaundice

A
  1. Pre-hepatic (unconjugated)
  2. Hepatic (conjugated)
  3. Post-hepatic (conjugated)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Give 2 causes of pre-hepatic jaundice

A

Excess bilirubin production

  1. Haemolytic anaemia
  2. Gilberts disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Give 4 causes of hepatic jaundice

A
  1. Liver disease
  2. Hepatitis - viral, drug, immune, alcohol
  3. Ischaemia
  4. Neoplasm - HCC, mets
  5. Congestions - CCF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Give 3 causes of post-hepatic jaundice

A

Duct obstruction

  1. Gallstones
  2. Stricture - Malignancy, ischaemia, inflammatory
  3. Blocked stent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What colour is the urine and stools in pre-hepatic jaundice?

A

Both are normal

No itching and the LFTs are normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What colour is the urine and stools in someone with cholestatic jaundice (hepatic and post hepatic)?

A

Dark urine
Pale stools
Itching
LFTs are abnormal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What can cause raised unconjugated bilirubin?

A

A pre-hepatic problem (haemolysis, hypersplenism)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What can cause raised conjugated bilirubin?

A

Indicated cholestatic problem

[liver disease (hepatic) or bile duct obstruction (post hepatic)]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Give 3 symptoms of jaundice

A
  1. Biliary pain
  2. Rigors - indicate an obstructive cause
  3. Abdomen swelling
  4. Weight loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Why are liver patients vulnerable to infection?

A
  1. Impaired reticuloendothelial function
  2. Reduced opsonic activity
  3. Leucocyte function
  4. Permeable gut wall
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Give 3 causes of Gallstones

A
  1. Obesity and rapid weight loss
  2. DM
  3. Contraceptive pill
  4. Liver cirrhosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what are the risk factors for gallstones

A
  1. Female
  2. Fat
  3. Fertile
  4. Forty
  5. Family history
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Name 2 types of gallstones

A
  1. Cholesterol (70%)

2. Pigment (30%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Describe the pathophysiology of cholesterol gallstones

A

Excess cholesterol/lack of bile salts –> cholesterol crystals –> gallstone formation, precipitated by reduced gallbladder motility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Describe the pathophysiology of pigment gallstones

A

Excess bilirubin –> polymers and calcium bilirubinate –> stones
seen in haemolytic anaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Give 4 symptoms of gallstones

A

Most are asymptomatic

  1. Biliary colic (sudden RUQ pain radiating to the back and epigastrium +/- nausea/vomiting) - AFTER EATING FATTY MEALS
  2. Acute cholecystitis (gallbladder distension –> inflammation, necrosis, ischaemia)
  3. Obstructive jaundice
  4. Cholangitis
  5. Pancreatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How can gallstones be removed from the gallbladder?

A

Laparoscopic cholecystectomy
ERCP with removal or destruction (mechanical lithotripsy) or stent placement
Bile acid dissolution therapy (for people not suitable for surgery)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is liver failure?

A

When the liver has lost the ability to regenerate to repair, so that decompensation occurs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Name 3 types of liver failure

A
  1. Acute = sudden failure in previously healthy liver
  2. Chronic = liver failure on the background cirrhosis
  3. Fulminant = massive necrosis of liver cells –> severe liver function impairment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Give 5 causes of acute liver disease

A
  1. Viral hepatitis
  2. Drug induced hepatitis
  3. Alcohol induced hepatitis
  4. Vascular - Budd-Chiari
  5. Obstruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Give 2 possible outcomes of acute liver disease

A
  1. Recovery

2. Liver failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Give 5 causes of chronic liver disease

A
  1. Alcohol
  2. NAFLD
  3. Viral hepatitis (B,C,E)
  4. Autoimmune diseases
  5. Metabolic
  6. Vascular - Budd-Chairi
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Give 2 possible outcomes of chronic liver disease

A
  1. Cirrhosis

2. Liver failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Give 5 signs of acute liver failure

A
  1. Jaundice
  2. Fetor hepaticus (smells like pears)
  3. Coagulopathy
  4. Asterixis - liver flap
  5. Malaise
  6. Lethargy
  7. Encephalopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Give 5 signs of chronic liver disease

A
  1. Ascites
  2. Oedema
  3. Bruising
  4. Clubbing
  5. Depuytren’s contracture
  6. Palmar erythema
  7. Spider naevi
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What investigations are conducted on someone on with liver failure?

A

Blood tests - FBCs, U+Es, LFTs, clotting factors, glucose

Imaging - EEG, USS, CXR, doppler USS

Microbiology - blood and urine culture and ascitic tap

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What do the blood tests show in someone with liver failure?

A 
Raised bilirubin 
Low glucose 
High AST and ALT 
Low levels of coagulation factors 
Raised prothrombin time 
High ammonia levels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Describe the treatment for liver failure

A
  1. Nutrition
  2. Supplements
  3. Treat complications
    - Raised intracranial pressure = mannitol
    - PPI = reduce GI bleeds
    - bleeding = vitamin K
    - encephalopathy = lactulose
    - ascites = diuretics
    - sepsis = sepsis 6, antibiotics
  4. Liver transplant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Give 4 complications of of liver failure

A
  1. Hepatic encephalopathy
  2. Abnormal bleeding
  3. Jaundice
  4. Ascites
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What drugs should be avoided in liver failure?

A

Constipators
Oral hypoglycaemics
Warfarin has enhanced effects
Opiates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is cirrhosis?

A

Loss of normal hepatic architecture with fibrosis - liver injury causes necrosis and apoptosis- irreversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Give 3 causes of cirrhosis

A

common:

  • chronic alcohol abuse
  • non-alcoholic fatty liver disease
  • hepatitis

others

  • haemochromatosis
  • Wilson’s disease
  • alpha-antitrypsin deficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Give 4 signs of cirrhosis

A
  • ascites
  • clubbing
  • palmar erythema
  • xanthelasma
  • spider naevi
  • hepatomegaly
  • peripheral oedema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What investigations are done in someone with cirrhosis?

A
  • Bloods = low platelets, high INR, low albumin
  • US and CT - hepatomegaly
  • liver biopsy - diagnostic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is the treatment for liver cirrhosis?

A
  1. Good nutrition and alcohol abstinence
  2. Treat underlying cause
  3. Fluid and salt restriction for ascites –> spironolactone, furosemide, prophylactic ciprofloxacin
  4. liver transplant = definitive
  5. Screen for HCC - increased AFP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Give 4 complications of cirrhosis

A

Ascites
portal hypertension

  1. Decompensation
  2. SBP
  3. Increased risk of HCC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Approximately what percentage of blood flow to the liver is provided by the portal vein?

A

75%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Give 3 causes of portal hypertension

A
  1. Pre-hepatic = blockage of hepatic portal vein before the liver (portal vein thrombosis)
  2. Hepatic = distortion of liver architecture (cirrhosis, schistosomiasis, Budd Chiari syndrome)
  3. Post-hepatic = venous blockage outside the liver (RHF, IVC obstruction)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what is the clinical presentation of portal hypertension?

A
  • often asymptomatic
  • splenomegaly
  • spider naevi
  • GI bleeding
  • ascites
  • hepatic encephalopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Why can portal hypertension lead to varices?

A

Obstruction to portal blood flow

Blood is diverted into collaterals and so causes varices

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are the potential consequences of varices?

A

If they rupture –> haemorrhage

blood is then digested -> melaena

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is the primary treatment for varices?

A

Variceal banding – band put around varices using endoscope – after few days the banded varix degenerates and drops off leaving a scar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Describe the pathophysiology of hepatic encephalopathy

A

Ammonia accumulates and crosses the BBB causing cerebral oedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Name 4 conditions that can develop as a result of having hepatic encephalopathy

A

SAVE

  1. Splenomegaly
  2. Ascites
  3. Varices
  4. Encephalopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is ascites?

A

Chronic accumulation of fluid in the peritoneal cavity that leads to abdominal distension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Give 4 causes of ascites and an example for each

A
  1. Local inflammation - peritonitis
  2. Leaky vessels - imbalance between hydrostatic and oncotic pressures
  3. Low flow - cirrhosis, thrombosis, cardiac failure
  4. Low protein - hypoalbuminaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Describe the pathophysiology of ascites

A
  1. Increased intra-hepatic resistance leads to portal hypertension –> ascites
  2. Systemic vasodilation leads to secretion of RAAS, NAd and ADH –> fluid retention
  3. Low serum albumin also leads to ascites
    Transudate = blockage of venous drainage
    Exudate = inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Give 3 signs of ascites

A
  1. Distension
  2. Dyspnoea
  3. Shifting dullness on percussion
  4. Signs of liver failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What investigations might you do in someone who you suspect has ascites?

A
  1. USS

2. Ascitic tap

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Describe the treatment for ascites

A
  1. Restrict sodium and fluids
  2. Diuretics - spirolactone
  3. Paracentesis
  4. Albumin replacement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Describe the effects of alcoholic liver disease

A
  1. Fatty liver –> hepatitis –> cirrhosis and fibrosis
  2. GIT –> gastritis, varices, peptic ulcers, pancreatitis , carcinoma
  3. CNS –> Degreased memory and cognition, wernicke’s encephalopathy
  4. Folate deficiency –> anaemia
  5. Reproduction –> testicular atrophy, reduced testosterone/progesterone
  6. Heart –> dilated cardiomyoapthy, arrhythmias
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What might be seen histologically that indicates a diagnosis of alcoholic liver disease?

A

Neutrophils and fat accumulation within hepatocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What type of anaemia do you associate with alcoholic liver disease?

A

Macrocytic anaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What blood test might show that someone has alcoholic liver disease?

A

Serum GGT will be elevated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What distinctive feature is often seen on biopsy in people suffering form alcoholic liver disease?

A

Mallory bodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What are the CAGE questions?

A
  1. Cut down?
  2. Annoyed at criticism?
  3. Guilty about drinking?
  4. Eyeopener?
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

How do you treat alcoholic liver disease?

A

● Stop alcohol – treat delirium tremens with diazepam
● IV thiamine to prevent Wernicke-Korsakoff encephalopathy
● High vitamin and protein diet
● Fatty liver – if alcohol stopped fat disappears
● Hepatitis
o Nutrition maintained with enteral feeding and vitamin supplements
o Steroids show short term benefit – reduce inflammation
o Infections treated and prevented
● Cirrhosis
o Reduce salt intake, stop drinking for life
o Avoid aspirin and NSAIDS
o Liver transplant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

How does alcoholic hepatitis present?

A 
Jaundice
Anorexia
Nausea and vomiting
Fever
Encephalopathy 
Cirrhosis 
Hepatomegaly
Ascites, bruising, clubbing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

How long does hepatitis persist for to be deemed chronic?

A

6 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Give 4 types of hepatitis?

A
  1. Viral - A,B,C,D,E
  2. Drug induced
  3. Alcohol induced
  4. Autoimmune
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Give 3 infective causes of acute hepatitis

A
  1. Hepatitis A-E infections
  2. EBV
  3. CMV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Give 3 non-infective causes of acute and chronic hepatitis

A
  1. Alcohol
  2. Drugs
  3. Toxins
  4. Autoimmune
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Give 3 symptoms of acute hepatitis

A
  1. General malaise
  2. Myalgia
  3. GI upset
  4. Abdominal pain
  5. Raised AST, ALT
  6. +/- jaundice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What are the potential complications of chronic hepatitis?

A

Uncontrolled inflammation –> fibrosis –> cirrhosis –> HCC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

If HAV a RNA or DNA virus?

A

RNA virus - PicoRNAvirus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

How is HAV transmitted?

A

Faeco-oral transmission - contaminated food/water, shellfish

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Who could be at risk of HAV infection?

A

Travellers and food handlers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Is HAV acute or chronic?

A

Acute 100% immunity after infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

How might you diagnose someone with HAV infection?

A

bloods - ALT/AST raised

raised IgG and IgM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Describe the management of HAV infection

A
  1. Supportive
  2. Monitor liver function to ensure no fulminant hepatic failure
  3. Manage close contacts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What is the primary prevention of HAV?

A

Vaccination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Is HBV a RNA or DNA virus?

A

DNA virus Replicates in hepatocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

How is HBV transmitted?

A

Blood borne transmission - blood products and bodily fluids
IVDU, needle-stick, sexual, vertical
Highly infectious
Vertical transmission from mother to child during parturition is most common method of transmission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Describe the natural history of HBV in 4 phases

A
  1. Immune tolerance phase: unimpeded viral replication –> high HBV DNA levels.
  2. Immune clearance phase: the immune system ‘wakes up’ = liver inflammation and high ALT
  3. Inactive HBV carrier phase: HBV DNA levels are low = ALT levels are normal, no liver inflammation
  4. Reactivation phase: ALT and HBV DNA levels are intermittent and inflammation is seen on the liver –> fibrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What HBV protein triggers the initial immune response?

A

The core proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

How might you diagnose someone with HBV?

A

HBV assay- HBs-Ag - present 1-6 months after exposure. Presence for >6 months implies carrier status- anti-HBs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Describe the management of HBV infection

A 
vaccination
pegylated interferon alpha 2a
nucleotide analogue (tenofovir) - inhibits viral replications
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

How would you know if someone had acute or chronic HBV infection?

A

Follow up appointment at 6 months to see if HBsAg still present
still present = chronic hepatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What are the potential consequences of chronic HBV infection?

A
  1. Cirrhosis
  2. HCC
  3. Decompensated cirrhosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

How can HBV infection be prevented?

A

Vaccination - injecting a small amount of inactivated HbsAg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Give 3 side effects of alpha interferon treatment for HBV

A
  1. Myalgia
  2. Malaise
  3. Lethargy
  4. Thyroiditis
  5. Mental health problems
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Give 2 HBV specific symptoms

A

Arthralgia

Urticaria (hives)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

If HCV a RNA or DNA virus?

A

RNA virus - flavivirus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

How is HCV transmitted?

A

Blood borne

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Give 4 risk factors for developing HBV/HCV infection

A
  1. IVDU
  2. People who have required blood products - blood transfusion
  3. Needle stick injuries
  4. Unprotected sex
  5. Vertical transmission
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

How might you diagnose someone with current HCV infection?

A

HCV RNA - indicates current infection

Anti-HCV serology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Describe the treatment for HCV

A

Direct acting antivirals
NS5A inhibitor - Ritonavir
NS5B inhibitor - Sofosbuvir

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What percentage of people with acute HCV infection will progress onto chronic infection?

A

Approximately 70%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

What percentage of people with acute HBV infection will progress onto chronic infection?

A

Approximately 5%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

How can HCV infection be prevented?

A
  1. Screen blood products
  2. Lifestyle modification
  3. Needle exchange
    No vaccination, and previous infection doesn’t confer immunity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Is HDV a RNA or DNA virus?

A

Incomplete RNA virus Needs Hep B for assembly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

How is HDV transmitted?

A

Blood borne transmission - particularly IVDUit is transmitted in the same way as HBV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Is HEV a RNA or DNA virus?

A

Small RNA virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

How is HEV transmitted?

A

Faeco-oral transmission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Is HEV acute or chronic?

A

Usually acute but there is a risk of chronic disease in the immunocompromised

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

How might you diagnose someone with HEV infection?

A

HEV RNA - HEV IgM, IgGanti-HEV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Describe the primary prevention of HEV

A

Good food hygiene

Vaccine is in development

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

What types of viral hepatitis are capable of causing choric infection?

A

Hepatitis B (+/- D), C and E in the immunosuppressed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

What is non alcoholic steatoheptitis (NASH)?

A

An advanced form of non-alcoholic fatty liver disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Give 3 causes of non-alcoholic fatty liver disease

A
  1. T2DM
  2. Obesity
  3. Hypertension
  4. Hyperlipidaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

How do you manage NAFLD?

A

Lose weight
Control HTN,
DM and lipids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

What is Budd-Chiari syndrome?

A

Hepatic vein occlusion –> ischaemia and hepatocyte damage –> liver failure or insidious cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

Name 3 metabolic disorders that can cause liver disease

A
  1. Haemochromatosis - iron overload
  2. Alpha 1 anti-trypsin deficiency
  3. Wilson’s disease - disorder of copper metabolism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

90% of people with haemochromatosis have a mutation in which gene?

A

HFE - chromosome 6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Haemochromatosis is a genetic disorder, how is it inherited?

A

Autosomal recessive inheritance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

Describe the pathophysiology of haemochromatosis

A

Uncontrolled intestinal iron absorption –> deposition of iron in liver, heart, pancreas, joins, skin –> fibrosis and functional organ failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

Give 4 signs of haemochromatosis

A
  • Fatigue, arthralgia, weakness
  • Hypogonadism – eg erectile dysfunction
  • SLATE-GREY SKIN (brownish/bronze)
  • Chronic liver disease, heart failure, arrythmias
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

How might you diagnose someone with haemochromatosis?

A
  1. bloods - Raised ferritin, LFTs
  2. HFE genotyping - C282Y
  3. Liver biopsy - gold standard
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

What is the treatment for haemochromatosis?

A
  1. Iron removal - venesection
  2. Monitor DM
  3. Low iron diet
  4. Screening for HFE
  5. iron-chelating drugs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

Give 2 complications of haemochromatosis?

A

Liver cirrhosis –> failure/cancer

DM due to pancreatic depositions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

How is alpha 1 anti-trypsin deficiency inherited?

A

Autosomal recessive mutation in serine protease inhibitor gene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

How does Alpha 1 anti-trypsin deficiency present?

A

Liver disease in the young - cirrhosis, jaundice Lung disease in the old (smokers) - emphysema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

What is the treatment for Alpha 1 anti-trypsin deficiency?

A

Smoking cessation

Liver/lung transplant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

What is Wilson’s disease?

A

An autosomal recessive disorder of copper metabolism

Excess deposition of copper in the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

Describe the pathophysiology of Wilson’s disease

A

Impaired incorporation of Cu into caeruloplasmin –> Cu accumulation in liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

How does Wilson’s disease present?

A

Children = liver disease - hepatitis, cirrhosis, fulminant liver failure

Adults = CNS problems, mood changes, and Kayser-Fleischer rings

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

What are Kayser-Fleischer rings?

A

Cu in iris and cornea –> bronze ring

124
Q

What CNS changes are seen in a patient with Wilson’s disease?

A 
Tremor
Dysarthria 
Dyskinesia 
Ataxia
Parkinsonism 
Dementia 
Depression
125
Q

What is the treatment for Wilson’s disease?

A

Lifetime treatment with penicillamine (chelating agent)
Low Cu diet - no liver, nuts, chocolate, mushrooms, shellfish
Liver transplant

126
Q

Describe the pathophysiology of autoimmune hepatitis

A

Abnormal T cell function and autoantibodies vs hepatocyte surface antigens

127
Q

What people are more likely to present with autoimmune hepatitis?

A

Young (10-30) and middle aged (>40) women

128
Q

How does autoimmune hepatitis present?

A 
Fatigue, fever, malaise 
Hepatitis 
Hepatosplenomegaly
Amenorrhoea 
Polyarthritis 
Pleurisy 
Lung infiltrates 
Glomuleronephritis
129
Q

What diseases are associated with autoimmune hepatitis?

A

Autoimmune thyroiditis
DM
Pernicious anaemia
PSCUC

130
Q

What results would you see from the investigations of someone who you suspect has autoimmune hepatitis?

A

Raised LFTs - increased bilirubin, AST, ALT, ALP
Hypersplenism = low WCC and platelets
Autoantibodies = +ve anti-nuclear antibody
Liver biopsy = mononuclear infiltrate

131
Q

How is autoimmune hepatitis treated?

A

Prednisolone - immunosuppression

Liver transplant

132
Q

What is primary biliary cirrhosis?

A

An autoimmune disease where intra-hepatic bile ducts are destructed by chronic granulomatous inflammation –> cholestatis (bile in liver) –> cirrhosis, fibrosis, portal hypertension

133
Q

Describe 2 features of the epidemiology of primary biliary cirrhosis

A
  1. Females > males

2. Familial - 10 fold risk increase

134
Q

Give 3 disease associated with primary biliary cirrhosis

A
  1. Thyroiditis
  2. RA
  3. Coeliac disease
  4. Lung disease
    Other autoimmune diseases
135
Q

Give 3 symptoms of primary biliary cirrhosis

A
  1. Pruritis
  2. Fatigue
  3. Hepatosplenomegaly
  4. Obstructive jaundice
  5. Cirrhosis and coagulopathy
136
Q

What would investigations show in someone with biliary cirrhosis?

A

Bloods = AMA antibody, LFT - GGT and ALP raised
Positive anti-mitochondrial antibody = diagnostic
low albumin
Liver biopsy = epithelial disruption and lymphocyte infiltration

137
Q

What is the treatment for primary biliary cirrhosis?

A

early stage = Ursodeoxycholic acid + steroids + Cholestyramine
ADEK vitamins

severe = Liver transplant

138
Q

What is Primary sclerosing cholangitis?

A

Autoimmune inflammation and narrowing of intra and extra hepatic bile ducts

139
Q

Describe the pathophysiology of primary sclerosing cholangitis

A

Inflammation of the bile duct –> stricture and hardening –> progressive obliterating fibrosis of bile duct branches –> cirrhosis –> liver failure

140
Q

Give 3 causes of primary sclerosing cholangitis

A
  1. Primary = unknown causes
  2. Infection
  3. Thrombosis
  4. Iatrogenic trauma
141
Q

Give 3 symptoms of primary sclerosing cholangitis

A
  1. Pruritus
  2. Charcot’s triad = fever with chills, RUQ pain, obstructive jaundice
  3. Cirrhosis
  4. Liver failure
  5. Fatigue
142
Q

What would the investigations show in someone with primary sclerosing cholangitis?

A

Bloods = increased Alk phos, elevated ALP, bilirubin and Ig, AMA negative
Imaging = ERCP and MRCP
Liver biopsy = fibrous and obliterative cholangitis

143
Q

What is the treatment for primary sclerosing cholangitis?

A
  • Cholestyramine for pruritus
  • Ursodeoxycholic acid - may protect against colon cancer and improve LFT
  • ADEK vitamins
  • Liver transplant
144
Q

What complications might occur due to primary sclerosing cholangitis?

A

Increased risk of bile duct, gallbladder, liver and colon cancer

145
Q

What is ascending cholangitis?

A
  • Obstruction of biliary tract causing bacterial infection
  • usually caused by bacteria ascending from its junction with the duodenum
  • Regarded as a medical emergency
146
Q

Give 3 causes of ascending cholangitis?

A

Gallstone
Primary infection (Klebsiella, E. coli)
Strictures following surgery
Pancreases head malignancy

147
Q

Name the triad that describes the 3 common symptoms of ascending cholangitis

A

Charcot’s triad

  1. Fever
  2. RUQ pain
  3. Jaundice
148
Q

What other symptoms can present with Charcot’s triad with ascending cholangitis?

A

Reynolds pentad

  • Charcot’s triad (fever, RUQ pain, jaundice)
  • Hypotension
  • Confusion/altered mental state
149
Q

What investigations might you do in someone who you suspect might have ascending cholangitis?

A
  1. USS
  2. Blood tests - LFTS
  3. CT - excludes carcinoma
  4. ERCP - definitive investigation
150
Q

Describe the management of ascending cholangitis

A 
Fluid resuscitation 
Treat infection with broad spectrum antibiotics (cefotaxime, metronidazole)
ERCP to clear obstruction
Stenting 
Laparoscopic cholecystectomy
151
Q

What is the difference between the clinical presentation of ascending cholangitis and acute cholecystitis?

A

A patient with acute cholecystitis would not have signs of jaundice

152
Q

What is the main difference between biliary colic and acute cholecystitis?

A

Acute cholecystitis has an inflammatory component

153
Q

What complications can occur due to acute ascending cholangitis?

A 
Sepsis
Biliary colic
Acute cholecystitis
Empyema
Carcinoma 
Pancreatitis
154
Q

What is peritonitis?

A

Inflammation of the peritoneal lining

155
Q

what are the different types of peritonitis?

A
  1. Primary = spontaneous bacterial peritonitis, ascites, immunocompromised
  2. Secondary = Bowel perforation, abdomen organ inflammation, TB, bowel ischaemia
156
Q

Give 3 symptoms of peritonitis

A
  1. Abdominal pain and tenderness
  2. Nausea and vomiting
  3. Chills
  4. Rigors
  5. Fever
157
Q

Give 3 signs of peritonitis on an abdomen examination

A
  1. Guarding
  2. Rebound tenderness
  3. Rigidity
  4. Silent abdomen
  5. lying still
158
Q

What investigations might you do in someone who you suspect could have peritonitis?

A
  1. Blood tests: raised WCC, platelets, CRP, amylase, reduced blood count
  2. CXR: look for air under the diaphragm
  3. Abdominal x-ray: look for bowel obstruction
  4. CT: can show inflammation, ischaemia or cancer
  5. ECG: epigastric pain could be related to the heart
  6. B-HCG: a hormone secreted by pregnant ladies
159
Q

What is the management for peritonitis?

A
  1. ABCDE
  2. Treat the underlying cause - might be surgery if perforated bowel
  3. IV fluids
  4. IV antibiotics - first broad spectrum then specific
  5. peritoneal lavage (clean the cavity surgically)
160
Q

Give 5 potential complications of peritonitis

A
  1. Hypovolaemia
  2. Kidney failure
  3. Systemic sepsis
  4. Paralytic ileus
  5. Pulmonary atelectasis (lung collapse)
  6. Portal pyaemia (pus in portal vein)
161
Q

What is the commonest serious infection in those with cirrhosis?

A

Spontaneous bacterial peritonitis

162
Q

Name a bacteria that can cause spontaneous bacterial peritonitis

A
  1. E. coli

2. S. pneumoniae

163
Q

How can spontaneous bacterial peritonitis be diagnosed

A

By looking for the presence of neutrophils in ascitic fluid

164
Q

Describe the treatment for spontaneous bacterial peritonitis

A

Cefotaxime and metronidazole

165
Q

What investigation is it important to do in someone with chronic liver disease and ascites? Explain why it is important

A

Ascitic tap to rule out spontaneous bacterial peritonitis

166
Q

You do an ascitic in someone with ascites. The neutrophil count comes back as - Neutrophils > 250/mm3. What is the likely cause of the raised neutrophils?

A

Spontaneous bacterial peritonitis

167
Q

What is acute pancreatitis?

A

An inflammatory process with release of inflammatory cytokines (TNF alpha, IL-6) and pancreatic enzymes (trypsin, lipase)
the pancreas returns to functionally and structurallynormal after the episode
Occurs as isolated or recurrent attacks

168
Q

Describe the pathophysiology of acute pancreatitis

A

Main two causes are alcohol and gallstones:–

Gallstones:
Blockage of bile duct = backup of pancreatic juices. This change in luminal concentration causes Ca2+ release inside pancreatic cells and cause them to activate trypsinogen early which digests the pancreas.

Alcohol:
Contracts the Ampulla of Vater obstructing the bile clearance and also messes with Ca2+homeostasis causing the same as above.
• Leaky and damaged pancreas an auto digest nearby structures causing haemorrhage and Grey
Turner’s sign abdominal skin discolouration from retroperitoneal bleeding.
• Deranges pancreatic function so can cause hyperglycemia from reduction of insulin production

169
Q

What are the causes of acute pancreatitis?

A 
I GET SMASHED – remember 
I = Idiopathic
G = Gallstones (60%)
E = Ethanol = alcohol (30%)
T = Trauma
S = Steroids
M = Mumps
A = Autoimmune
S = Scorpion venom
H = Hyperlipidaemia/ hypothermia/ high Ca
E = ERCP (endoscopic retrograde cholangiopancreatography) 
D = Drugs (furosemide, corticosteroid, NSAIDs, ACEi)
170
Q

Give 4 symptoms of acute pancreatitis

A
  1. Severe epigastric pain that radiates to the back
  2. Anorexia
  3. Nausea, vomiting
  4. Signs of septic shock - fever, dehydration, hypotension, tachycardia
  5. Necrotising - umbilical (Cullens sign) vs flank (Grey Turners sign)
171
Q

What investigations are done on someone you think has acute pancreatitis?

A

Raised serum amylase and lipase urinalysis - raised urinary amylase
Erect CXR
Contrast CT
MRI

172
Q

Describe the treatment for acute pancreatitis

A
  • analgesia
  • nil by mouth
  • IV fluids
  • prophylactic antibiotics
173
Q

Give 2 potential complications of acute pancreatitis

A
  1. Systemic inflammatory response syndrome
  2. Multiple organ dysfunction
  3. Pancreatic necrosis- hyperglycaemia- hypocalcaemia- renal failure- shock
174
Q

Why is morphine contraindicated in acute pancreatitis?

A

Morphine increases sphincter of Oddi pressure and so aggravates pancreatitis

175
Q

What is chronic pancreatitis?

A

Chronic inflammation of the pancreas leads to irreversible damage
- Progressive loss of exocrine pancreatic tissue which is replaced by fibrosis

176
Q

Describe the pathogenesis of chronic pancreatitis

A

Pancreatic duct obstruction leads to activation of pancreatic enzymes –> necrosis –> fibrosis

177
Q

Name 3 causes of chronic pancreatitis

A
  1. Excess alcohol - most common
  2. CKD
  3. Idiopathic
  4. Recurrent acute pancreatitis
  5. hereditary
  6. CF - all have it from birth
  7. autoimmune
  8. tropical
178
Q

Describe how alcohol can cause chronic pancreatitis

A

Alcohol –> proteins precipitate in the ductal structure of the pancreas (obstruction) –> pancreatic fibrosis

179
Q

what is the clinical presentation of chronic pancreatitis?

A
  1. Severe epigastric pain that radiate through to the back - worse after alcohol/meal and better on leaning forward
  2. Weight loss, malabsorption
  3. Nausea, vomiting
  4. Steatorrhea (lack of lipase)
  5. Exocrine/endocrine dysfunction (DM)
  6. jaundice
180
Q

A sign of chronic pancreatitis is exocrine dysfunction, what can be consequence of this?

A
  1. Malabsorption
  2. Weight loss
  3. Diarrhoea
  4. Steatorrhoea
181
Q

A sign of chronic pancreatitis is endocrine dysfunction, what can be consequence of this?

A

DM

182
Q

What immunoglobulin might be elevated in someone with autoimmune chronic pancreatitis?

A

IgG4

183
Q

How is autoimmune chronic pancreatitis treated?

A

Steroids

184
Q

What is the treatment for chronic pancreatitis?

A

Alcohol cessation
Analgesia (NSAIDs, tramadol)
Pancreatic enzyme (creon) and vitamin replacement
pancreatin + omeprazole
If DM = insulin
Surgery - local resection, for unremitting pain and duct draining

185
Q

Why can pancreatitis cause malabsorption?

A

Pancreatitis result in pancreatic insufficiency and so lack of pancreatic digestive enzymes
Defective intra-luminal digestion leads to malabsorption

186
Q

What 2 enzymes, if raised, suggest pancreatitis?

A

LDH (lactate dehydrogenase) and AST

187
Q

Give 3 complications of chronic pancreatitis

A
  1. Diabetes
  2. Pseudocyst
  3. Biliary obstruction –> obstructive jaundice, cancer
188
Q

Name a drug that can cause drug induced liver injury

A
  1. Co-amoxiclav
  2. Flucloxacillin
  3. Erythromycin
  4. TB drugs
189
Q

Give 5 causes of diarrhoea infection

A
  1. Traveller’s diarrhoea
  2. Viral - (rotavirus/norovirus)
  3. Bacterial (E. coli)
  4. parasites (helminths, protozoa)
  5. Nosocomial (C. diff)
190
Q

Give 5 causes of non-diarrhoeal infection

A
  1. Gastritis/peptic ulcer disease (H. pylori)
  2. Acute cholecystitis
  3. Peritonitis
  4. Thyphois/paratyphoid
  5. Amoebic liver abscess
191
Q

Give 3 ways in which diarrhoea can be prevented

A
  1. Access to clean water
  2. Good sanitation
  3. Hand hygiene
192
Q

What is the diagnostic criteria for travellers diarrhoea?

A

> 3 unformed stools per day and a least one of:
- abdominal pain
- cramps
- nausea
- vomiting
Occurs within 2 weeks (usually 3 days) of arrival in a new country

193
Q

give 3 causes of travellers diarrhoea

A
  1. Enterotoxigenic E. coli
  2. Norovirus
  3. Giardia
194
Q

Describe the pathophysiology of traveller’s diarrhoea

A

Heat labile ETEC modifies Gs and it is in a permanent ‘locked on’ state
Adenylate cyclase is activated and there is increased production of cAMP
Leads to increased secretion of Cl- into the intestinal lumen, H2O follows down as osmotic gradient –> diarrhoea

195
Q

Which type of E. coli can cause bloody diarrhoea and has a shiga like toxin?

A

Enterohaemorrhagic E.coli (EHEC)

196
Q

What does EIEC stand for?

A

Enteroinvasive E. coli

197
Q

What type of E. coli is responsible for causing large volumes of watery diarrhoea?

A

Enteropathogenic E.coli (EPEC)

198
Q

What does EAEC stand for?

A

Enteroaggregative E. coli –> infantile diarrhoea

199
Q

What does DAEC stand for?

A

Diffusely adherent E. coli

200
Q

What is the leading cause of diarrhoea illness in young children?

A

Rotavirus

There is a vaccine = rotary

201
Q

Name a helminth responsible for diarrhoea infection?

A

Schistosomiasis

Strongyloides

202
Q

Give 5 symptoms of helminth infection

A
  1. Fever
  2. Eosinophilia
  3. Diarrhoea
  4. Cough
  5. Wheeze
203
Q

Why is c. diff infectious?

A

Spore forming bacteria (gram positive)

204
Q

Give 5 risk factors for c.diff infection

A
  1. Increasing age
  2. Comordities
  3. Antibiotic use
  4. PPI
  5. Long hospital admission
  6. NG tube feeding and GI surgery
  7. Immunocompromised - HIV, anti-caner drugs
205
Q

Name 5 antibiotics that can cause c. diff infection

A
  1. Ciprofloxacin (quinolones)
  2. Co-amoxiclav (penicillins)
  3. Clindamycin
  4. Cephlosporins
  5. Carbapenems

RULE OF C’s

206
Q

Describe the treatment for c. diff infection

A

Metronidazole and vancomycin (PO)
Rifampicin/rifaximin
Stool transplant

207
Q

What can helicobacter pylori infections cause?

A

H. pylori produces urease –> ammonia –> damage to gastric mucosa –> neutrophil recruitment and inflammation

Causing gastritis, peptic ulcer disease, gastric cancer

208
Q

Describe H. pylori

A

A gram negative bacilli with a flagellum

209
Q

Describe the treatment for H. pylori infection

A

Triple therapy = 2 antibiotics and 1 PPI

Omeprazole, clarithomyocin and amoxicillin

210
Q

Define biliary colic

A

Pain associated with the temporary obstruction of the cystic or common bile duct by a stone

211
Q

what investigations should be undertaken for jaundice?

A
  • liver enzymes - very high ALT/AST- MRCP or ERCP
  • urine - bilirubin absent in pre-hepatic, in obstructive urobilinogen absent
  • FBC
  • ultrasound
212
Q

what is the treatment for jaundice?

A

treat the underlying cause

213
Q

what is the clinical presentation of biliary colic?

A

● Recurrent episodes of severe and persistent pain in the upper abdomen which subsides after several hours
● Pain may radiate to right shoulder and suprascapular region
● Vomiting
● Normal examination

214
Q

what investigations should be undertaken for biliary colic?

A

● History and US showing gallstones
● Increases of serum alkaline phosphatase and bilirubin during an attack support the diagnosis of biliary pain
● Absence of inflammatory features differentiates this from acute cholecystitis

215
Q

what is the management of biliary colic?

A

● Analgesics and elective cholecystectomy
● Abnormal liver biochemistry or a dilated CBD on US is an indication for preoperative MRCP
● CBD stone removed at ERCP

216
Q

what is cholecystitis?

A

inflammation of the gallbladder
● Follows the impaction of a stone in the cystic duct or neck of the gallbladder
● Can occasionally occur without stones

217
Q

what is the clinical presentation of cholecystitis?

A
  • Generalised epigastric pain migrating to severe RUQ pain.
  • Signs of inflammation like a fever or fatigue.
  • Pain associated with tenderness and guarding from inflamed gallbladder and local peritonitis.

Tenderness worse on inspiration (Murphy’s sign)

218
Q

what are the investigations for cholecystitis?

A
  • Positive Murphy’s Sign = Severe pain on deep inhalation with examiners hand pressed into the RUQ.
  • Inflammatory markers - FBCs, CRP
  • Ultrasound: Thick gallstone walls from inflammation
219
Q

what is the management of cholecystitis?

A

• Antibiotics IV,
heavy analgesia,
IV fluids
an eventual Cholecystectomy if needed.

220
Q

what is the pathophysiology of cholecystitis?

A

• Stone is blocking the ducts. Bile builds up, distending the gallbladder. Vascular supply may be reduced from this distension.
Inflammation follows these events secondary to the retained bile, inflaming the gall bladder.

221
Q

what are the complications of cholecystitis?

A

● Empyema (pus)

● Perforation with peritonitis

222
Q

what is the pathophysiology of primary biliary cholangitis?

A
  • Due to prolonged bile duct blockage, bile isn’t ‘flushing’ out the tubes so bacteria can climb up from the GI tract and cause biliary tree infection and consolidation.
  • This prevents bile entering the GI tract and causes jaundice.
  • 5-10% mortality and infection can affect the pancreas too since it shares ducts with the gallbladder.
223
Q

what is the clinical presentation of primary biliary cholangitis?

A
  • Severe RUQ pain, with fever (rigors) AND jaundice.

* Patient may present as septic and/or have developed some level of pancreatitis.

224
Q

what are the investigations for primary biliary cholangitis?

A
  • FBCs, LFTs, CRP - Leukocytosis, Raised ALP and Bilirubin, raised CRP
  • Blood cultures/MC&S: work out what the pathogen is so you can use the trust’s advised ABs
  • Ultrasound +/- ERCP (Endoscopic Retrograde Cholangiopancreatography) (basically a biliary treecontrast x-ray)
225
Q

what is the treatment for primary biliary cholangitis?

A

• Treat sepsis, ERCP and stenting to mechanically clear the blockage, surgery/cholecystectomy possible

226
Q

what is primary biliary cholangitis?

A

● Infection of the biliary tree

● Most often occurs secondary to CBD obstruction

227
Q

what are the causes of primary biliary cholangitis?

A

● CBD obstruction
● Benign biliary strictures
● Pancreatic or bile duct carcinoma

228
Q

what is ascending cholangitis?

A

bile duct infection, usually caused by bacteria ascending from its junction with the duodenum

229
Q

what is the clinical presentation of ascending cholangitis?

A

RUQ pain, jaundice, & rigors (Charcot’s triad’)

230
Q

what is the treatment for ascending cholangitis?

A

Cefuroxime IV & Metronidazole IV/PR.

231
Q

what is primary sclerosing cholangitis?

A

a disease of the bile ducts that causes inflammation and obliterative fibrosis of bile ducts inside and/or outside of the liver.
- This pathological process impedes the flow of bile to the intestines and can ultimately lead to cirrhosis of the liver, liver failure, and bile duct and liver cancer

232
Q

what is the epidemiology of alcoholic liver disease?

A

● Most common cause of liver disease in the Western World
● Men > women
● Usually presents in 4th and 5th decades

233
Q

what are the causes of alcoholic liver disease?

A

Alcohol abuse, genetic predisposition, immunological mechanisms

234
Q

what happens to fatty liver on cessation of alcohol intake?

A

the fat disappears

235
Q

what are the pre-hepatic causes of portal hypertension?

A

portal vein thrombosis

236
Q

what are the intrahepatic causes of portal hypertension?

A
  • schistosomiasis
  • cirrhosis
  • budd-chiari syndrome
237
Q

what are the post-hepatic causes of portal hypertension?

A
  • RH failure

- IVC obstruction

238
Q

what is the pathophysiology of portal hypertension?

A
  • Increased resistance to blood flow leads to portal hypertension causes splanchnic vasodilation
  • This results in a drop in BP
  • CO increases to compensate for BP resulting in salt and water retention
  • Hyperdynamic circulation/increased portal flow leads to the formation of collaterals between portal and systemic systems
239
Q

what is the treatment of GI varices?

A

● fluid resuscitation until haemodynamically stable
● If anaemic – blood transfusion
● Correct clotting abnormalities – vitamin K and platelet transfusion
● Vasopressin – IV terlipressin or octreotide
● Prophylactic antibiotics
● Variceal banding
● Balloon tamponade
● TIPS

240
Q

what is the clinical presentation of varices?

A 
o Haematemesis
o Abdominal pain
o Shock
o Fresh rectal bleeding
o Hypotension and tachycardia
o Pallor
o Suspect varices as cause of GI bleeding if alcohol abuse or cirrhosis
Splenomegaly and hyponatraemia
241
Q

what investigations should be done for varices?

A

endoscopy - find source

242
Q

what is the prevention of varices?

A

o Nonselective B blockade – propranolol – reduced resting pulse and decrease portal pressure
o Variceal banding repeated to obliterate varices
o TIPSS
o Liver transplant

243
Q

what is ascites?

A

accumulation of fluid in peritoneal cavity

common complication of cirrhosis and common post op

244
Q

what are the risk factors for developing ascites?

A
  • high sodium diet
  • HCC
  • splanchnic vein thrombosis causing portal hypertension
245
Q

what are the causes of ascites?

A 
● liver failure - cirrhosis
● Portal hypertension e.g. cirrhosis
● Hepatic outflow obstruction
● Budd-Chiari syndrome
● Peritonitis
● Pancreatitis
● Cardiac failure
● Constrictive pericarditis
246
Q

what are the clinical features of ascites?

A
  • large distended abdomen
  • mild pain and discomfort
  • shifting dullness - classic sign, percuss abdomen and observe dullness over fluid versus resonance over air. Ask the patient to roll on to one side, wait a good few seconds for fluid to settle at a new level then percuss on the side and observe the dullness has shifted.
247
Q

what investigations should be done for ascites?

A

● Diagnostic aspiration of 10-20ml of ascitic fluid
o Raised white cell count indicates bacterial peritonitis
o Gram stain and culture
o Cytology for malignant cells
o Amylase to exclude pancreatic ascites
● Protein measurement of ascitic fluid
o Transudate (low protein) - Portal hypertension, constrictive pericarditis, cardiac failure, Budd-Chiari syndrome
o Exudate (high protein) BAD!! - Malignancy, peritonitis, pancreatitis, peritoneal tuberculosis, nephrotic syndrome

248
Q

what is the management of ascites?

A
  • treat underlying cause
  • low sodium diet
  • spironolactone and furosemide
  • drain fluid - paracentesis
249
Q

what can be a complication of ascites?

A

spontaneous bacterial peritonitis

250
Q

what investigations are undertaken for chronic pancreatitis?

A
  • serum amylase and lipase - may be raised

- abdominal US, CT and MRI

251
Q

what is alpha 1 antitrypsin deficiency?

A
  • rare cause of cirrhosis
  • autosomal recessive condition
  • mutation of alpha-1-antitrypsin gene on chromosome 14
252
Q

what is the pathophysiology of alpha-1-antitrypsin deficiency?

A

● A mutation in the alpha-1-antitrypsin gene on chromosome 14 leads to reduced hepatic production of alpha-1-antitrypsin which normally inhibits the proteolytic enzyme, neutrophil elastase
● Deficiency results in emphysema, liver cirrhosis and hepatocellular carcinoma

253
Q

what are the investigations for alpha-1-antitrypsin deficiency?

A

Serum alpha-1-antitrypsin levels are low

254
Q

what is the treatment for alpha-1-antitrypsin deficiency?

A

● No treatment
● Treat complications such as liver disease
● Stop smoking
● Those with hepatic decompensation should be assessed for liver transplant
● Manage emphysema

255
Q

what is the treatment for gallstones?

A

● Analgesics and elective cholecystectomy

● CBD stone removed at ERCP

256
Q

what investigations are undertaken for gallstones?

A

FBC and CRP: Looking for signs of an inflammatory response - suggestive of cholecystitis
• LFTs: Raised ALP - Bilirubin and ALT usually normal.
• Amylase: Check for pancreatitis
• Ultrasound = diagnostic:
1.Stones
2.Gallbladder wall thickness (inflammation)
3.Duct dilation (suggests distal blockage)

257
Q

what are the side-effects of chelating agents?

A

skin rash,
fall in WCC, HB and platelets,
haematuria,
renal damage

258
Q

what are the investigations for wilsons disease?

A
  • Serum copper and ceruloplasmin reduced (but can be normal)
  • 24hr urinary copper excretion high
  • Liver biopsy – diagnostic
259
Q

what are the causes of peritonitis?

A

bacterial = most common

  • gram -ve coliforms - e.coli
  • gram +ve staphylococcus

chemical - bile, old clotted blood

260
Q

what is the clinical presentation of HAV?

A

nausea,
anorexia,
distaste for cigarettes
some become jaundiced - dark urine and pale stool

261
Q

what is the epidemiology of HEV?

A

● Common in Indochina
● More common in older men
● Commoner than Hep A in UK
● High mortality rate in pregnancy

262
Q

what is the management of HEV?

A

● Prevention via good sanitation and hygiene, vaccine also available
● Once you’ve had it once you cannot become infected again

263
Q

what are the test results for HBV?

A

● HBsAg is present 1-6 months after exposure
● HBsAg presence for more than 6 months implies carrier status
● Anti-HBs – antibodies

264
Q

what are the clinical features of HDV?

A

similar to HBV

265
Q

what are the investigations for HDV?

A

similar to HBV
HDV-RNA
anti-HDV

266
Q

what is the treatment for HDV?

A

treat HBV

SC pegylated interferon-alpha-2a

267
Q

what is the epidemiology of HCV?

A

● High incidence in Egypt due to failed public health initiative
● Transmitted by blood and blood products
● Very high incidence in IV drug users
● Limited sexual transmission
● Vertical transmission is rare

268
Q

how do you remember the viral hepatitis information?

A

● A is Acquired by mouth from Anus, is Always cleared Acutely and only ever Appears once
● E is Even in England and can be Eaten (found in pigs), if not always beaten
● B is Blood-Borne and if not Beaten can be Bad
● B and D is DastarDly
● C is usually Chronic but Can be Cured at Cost

269
Q

what are the risk factors for non-alcoholic fatty liver disease?

A 
Obesity, 
diabetes, 
hyperlipidaemia, 
parental feeding, 
jejuno-ileal bypass, 
wilsons disease, 
drugs - Amiodarone, Tetracycline ,Methotrexate, Tetracycline
270
Q

which drugs increase the risk of developing non-alcoholic fatty liver disease?

A

Amiodarone, Tetracycline ,Methotrexate

271
Q

what are the clinical features of non-alcoholic fatty liver disease?

A

Usually no symptoms; liver ache in 10%

Fat, sometimes with inflammation & fibrosis

272
Q

what are the investigations for non-alcoholic fatty liver disease?

A

Fat, sometimes with inflammation & fibrosis

Need biopsy to distinguish NAFL from NASH

273
Q

what is the treatment for non-alcoholic fatty liver disease?

A

control risk factors, bariatric surgery - to treat obesity

274
Q

what is the pathophysiology of fatty changes of the liver?

A

o Most common biopsy finding in alcoholic individuals
o Symptoms usually absent and on examination there may be hepatomegaly
o Lab tests often normal although elevated MCV indicates heavy drinking
o GGT level usually elevated
o Fat disappears on cessation of alcohol

275
Q

what is the pathophysiology of alcoholic hepatitis?

A

o Generally, occurs years after heavy drinking
o Ballooned hepatocytes often contain amorphous eosinophilic material
o Rapid onset of jaundice

276
Q

what is the pathophysiology of alcoholic cirrhosis?

A

o Classically of the micronodular type but mixed pattern is also seen accompanying fatty change, and evidence of pre existing alcoholic hepatitis may be present

277
Q

what are the clinical features of fatty liver?

A

o No symptoms or signs

o Vague abdominal symptoms are due to general effects of alcohol on the GI tract

278
Q

what are the clinical features of alcoholic hepatitis?

A

o May only be apparent on liver biopsy
o Occasionally mild jaundice and signs of chronic liver disease (ascites, bruising, clubbing)
o If severe the patient will have jaundice and ascites, abdominal pain, high fever

279
Q

what are the clinical features of alcoholic cirrhosis?

A

o Final stage of liver disease from alcohol
o Patients can be well with very few symptoms
o Usually signs of chronic liver disease
o Diagnosis confirmed by liver biopsy
o Features of alcohol dependency

280
Q

what are the investigations for fatty liver?

A

o Elevated MCV indicates heavy drinking
o Raised ALT and AST
o Ultrasound or CT/liver histology will demonstrate fatty infiltration

281
Q

what are the investigations for alcoholic hepatitis?

A

o FBC – leucocytosis, elevated MCV, thrombocytopenia
o Serum electrolytes abnormal – elevated serum creatinine
o Elevated AST, ALT, bilirubin, prothrombin time
o Microscopy and culture of blood, urine and ascites to search for infection
o Liver and biliary US used to identify obstruction

282
Q

what is the management for fatty liver?

A

if alcohol is stopped fat disappears

283
Q

what is the management for alcoholic hepatitis?

A

o Nutrition maintained with enteral feeding and vitamin supplements
o Steroids show short term benefit – reduce inflammation
o Infections treated and prevented

284
Q

what is the management for alcoholic cirrhosis?

A

o Reduce salt intake, stop drinking for life
o Avoid aspirin and NSAIDS
o Liver transplant

285
Q

what is the epidemiology of alcoholic liver disease?

A

● Most common cause of liver disease in the Western World
● Men > women
● Usually presents in 4th and 5th decades
● Only 10-20% of people who drink alcohol develop cirrhosis

286
Q

what are the causes of alcoholic liver disease?

A

Alcohol abuse, genetic predisposition, immunological mechanisms

287
Q

which condition is associated with primary sclerosing cholangitis?

A

IBD - especially ulcerative colitis

288
Q

what do the following serological markers indicate in HBV infection?

  • HBsAg
  • HBeAg
  • HBV-DNA
  • anti-HBs
  • anti-HBc IgM
  • anti HBc IgG
  • anti HBe
A
  • HBsAg = acute infection (persistence after >6months implies chronic infection)
  • HBeAg = acute infection (persistence implies active viral replication) - can distinguish between active and inactive chronic infection
  • HBV-DNA = implies viral replication (present in acute and chronic)
  • anti-HBs = immunity to HBV from immunisation or previous cleared infection
  • anti-HBc = implies previous or current infection
  • anti-HBc IgM = recent infection within last 6 months
  • anti-HBc IgG = persists long term
  • anti-HBe = seroconversion and is present for life
289
Q

what do the following liver function tests indicate?

ALT, ALP, AST, GGT

A 
ALT = liver specific
ALP = bile duct specific
AST = alcohol specific
GGT = differentiate between bone and liver
290
Q

what are the primary bile salts?

A

colic acid and chenodeoxycholic acid`

291
Q

what are the secondary bile salts?

A

deoxycholic acid and lithocholic acid

292
Q

how are primary bile salts turned into secondary bile salts?

A

Primary bile salts turn into secondary bile salts by dehydroxylation by bacteria in the gut

293
Q

where is bile synthesised?

A

in the liver and stored in the gallbladder

294
Q

what is the role of bile?

A

emulsification of lipids to aid absorption

295
Q

where is the primary site of lipid digestion and absorption?

A

small intestine

296
Q

what is the process of lipid absorption?

A

Bile salts emulsify fats and pancreatic lipase hydrolyses fats into monoglycerides and fatty acids
Pancreatic lipase makes fatty acids form micelles which diffuse through epithelial cells
This forms chylomicrons which are absorbed into lymphatic system

297
Q

what structures make up the portal triad?

A

portal vein
hepatic artery
hepatic bile duct

298
Q

what are the investigations for NAFLD?

A

1st line

  • enhanced liver fibrosis test (<7.7 = non-mild, >7.7-9.8 = moderate, >9.8 = severe)
  • LFTs - increased AST and ALT (AST:ALT ratio close to 1)
  • FBC - anaemia or thrombocytopenia

gold standard

  • liver US (diffuse fatty infiltration and abnormal echotexture)
  • liver biopsy (required for diagnosis)
299
Q

how can you tell the difference between NAFLD and alcoholic liver disease?

A

AST:ALT ratio

ratio close to 1 = NAFLD
2:1 ratio = alcoholic liver disease

300
Q

what are the symptoms of pre-hepatic jaundice?

A

pallor
fatigue
exertional dyspnoea

301
Q

what are the symptoms of intra-hepatic jaundice?

A

anorexia
fatigue
nausea
abdominal pain

302
Q

what are the symptoms of post-hepatic jaundice?

A 
pale stools
dark urine
pruritus
steatorrhea
RUQ pain
hepatomegaly
303
Q

what conditions are associated with primary biliary cholangitis?

A

IBD

304
Q

which vitamins are people with chronic pancreatitis at risk of becoming deficient in?

A

fat soluble vitamins

ADEK

305
Q

what are the investigations for chronic pancreatitis?

A

CT or MRI - pancreatic duct dilation, calcification, atrophy or pseudocysts
endoscopic ultrasound
fecal elastase test - decreased elastase

306
Q

what cancer marker is present in hepatocellular carcinoma?

A

alpha-fetoprotein

Phase 2A revision (38 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions