LIVER & FRIENDS Flashcards

1
Q

JAUNDICE
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
2
Q

GALLSTONES
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
3
Q

PORTAL HYPERTENSION
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
4
Q

PORTAL HYPERTENSION
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
5
Q

ASCITES
what are the causes of ascites with serum ascites albumin gradient (SAAG) >11g/L?

A

Indicates portal hypertension
LIVER (most common cause)
- cirrhosis/alcoholic liver disease
- acute liver failure
- liver mets

CARDIAC
- right HF
- constrictive pericarditis

OTHER
- budd-chiari syndrome
- portal vein thrombosis
- veno-occlusive disease
- myxoedema

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

ASCITES
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
7
Q

ASCITES
Describe the treatment for ascites

A
  1. Restrict sodium and fluids
  2. Aldosterone antagonist (SPIRONOLACTONE) +/- loop diuretic (FUROSEMIDE)
  3. Paracentesis
  4. prophylactic antibiotics (CIPROFLOXACIN or NORFLOXACIN) to prevent spontaneous bacterial peritonitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

HEPATITIS
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
9
Q

HEPATITIS
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
10
Q

HEPATITIS
Describe the treatment for HCV

A

Direct acting antivirals (sofosbuvir or daclatasvir)
contact tracing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

BUDD-CHIARI SYNDROME
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
12
Q

HAEMOCHROMATOSIS
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
13
Q

HAEMOCHROMATOSIS
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
14
Q

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

A
Tremor
Dysarthria 
Dyskinesia 
Ataxia
Parkinsonism 
Dementia 
Depression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

WILSONS DISEASE
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

AUTOIMMUNE HEPATITIS
How does autoimmune hepatitis present?

A
Fatigue, fever, malaise 
Hepatitis 
Hepatosplenomegaly
Amenorrhoea 
Polyarthritis 
Pleurisy 
Lung infiltrates 
Glomuleronephritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

AUTOIMMUNE HEPATITIS
What diseases are associated with autoimmune hepatitis?

A

Autoimmune thyroiditis
DM
Pernicious anaemia
PSCUC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

PRIMARY BILIARY CHOLANGITIS
what other conditions are associated with primary biliary cholangitis?

A

sjogrens syndrome
raynauds disease
autoimmune thyroid disease
rheumatoid arthritis
systemic sclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

PRIMARY BILIARY CHOLANGITIS
what are the clinical features of primary biliary cholangitis?

A

classic presentation = significant itching in middle-aged female

SYMPTOMS
- pruritus
- fatigue + weight loss
- dry mouth + eyes (sjogrens)
- obstructive jaundice (icteric, pale stool + dark urine)

SIGNS
- skin hyperpigmentation (increased melanin)
- clubbing
- mild hepatosplenomegaly
- xanthelsma + xanthomata
- scleral icterus

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

PRIMARY BILIARY CHOLANGITIS
What are the investigations?

A
  • antimitochondrial antibodies (AMA)
  • antinuclear antibodies (ANA)
  • smooth muscle antibodies
  • LFTs = obstructive jaundice (raised ALP, GGT + bilirubin, AST + ALT mildy deranged)
  • coagulation profile = deranged in advanced disease
  • serum immunoglobulin = raised IgM
  • transabsominal USS (exclude other causes)

to consider:
- MRCP
- liver biopsy

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

PRIMARY BILIARY CHOLANGITIS
What is the treatment for primary biliary cholangitis?

A

1st line:
- ursodeoxycholic acid
- fat-soluble vitamin supplement (ADEK)
- cholestyramine (for symptomatic relief of pruritus)

2nd line
- liver transplantation (indicated in severe disease)

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

PRIMARY SCLEROSING CHOLANGITIS
what are the investigations?

A

-LFTs = raised ALP + GGT, raised conjugated bilirubin, ALT/AST may or may not be elevated
- albumin = decreased in later disease
- viral hepatitis screen
- pANCA
- anti-mitochcondrial antibodies (AMA) (to rule out PBC)
- abdominal USS (to exclude other causes)
- MRCP = beaded appearance (due to multiple biliary strictures)

to consider
- ERCP (gold standard)
- liver biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

PRIMARY SCLEROSING CHOLANGITIS
What is the treatment for primary sclerosing cholangitis?

A

1st line
- observation + lifestyle optimisation (alcohol cessation, exercise)
- cholestyramine for pruritus (rifampicin = 2nd line)
- ADEK vitamin supplement

END STAGE LIVER DISEASE
- liver transplant

24
Q

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

A
  • trans-abdominal USS
  • Blood tests - LFTS (ALP>ALT + raised bilirubin), CRP, FBC,
  • MRCP = gold standard
25
Q

ASCENDING CHOLANGITIS
Describe the management of ascending cholangitis

A

INITIAL
- IV broad spectrum antibiotics (cefotaxime + metronidazole)
- IV fluids

BILIARY DECOMPRESSION
- ERCP (first line)
- surgical drainage

ELECTIVE CHOLECYSTECTOMY

26
Q

PERITONITIS
What is the management for peritonitis?

A

1st line:
- broad spectrum antibiotics (piperacillin-tazobactam or metronidazole with cetriaxone)
- fluid resuscitation via IV fluids
- analgesia (paracetamol + opioids)
- NG tube for feeding

2nd line
- surgery +/- peritoneal lavage

27
Q

SPONTANEOUS BACTERIAL PERITONITIS
Name a bacteria that can cause spontaneous bacterial peritonitis

A
  1. E. coli
  2. S. pneumoniae
28
Q

SPONTANEOUS BACTERIAL PERITONITIS
Describe the treatment for spontaneous bacterial peritonitis

A

Cefotaxime and metronidazole

29
Q

ACUTE PANCREATITIS
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

30
Q

ACUTE PANCREATITIS
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)
~~~

31
Q

CHRONIC PANCREATITIS
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
32
Q

CHRONIC PANCREATITIS
what is the clinical presentation of chronic pancreatitis?

A

SYMPTOMS
- epigastric pain (dull, radiating to back, improved by leaning forwards, occurs 15-30 mins after eating)
- steatorrhoea + diarrhoea (foul smelling + difficult to flush)
- N+V
- weight loss + fatigue
- features of diabetes (polydipsia + polyuria)

SIGNS
- epigastric tenderness
- signs of liver disease (jaundice + ascites)
- skin nodules

33
Q

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

34
Q

CHRONIC PANCREATITIS
What 2 enzymes, if raised, suggest pancreatitis?

A

LDH (lactate dehydrogenase) and AST>ALT

35
Q

CHOLECYSTITIS
what is the management of cholecystitis?

A

1st line
- IV fluids + analgesia
- IV antibiotics (CERFUOXIME or METRONIDAZOLE)
- early laparoscopic cholecystectomy (within 1 week of diagnosis, often within 72hrs)

2nd line
- urgent cholecystectomy (if sepsis/gangrene/perforation suspected)

36
Q

PORTAL HYPERTENSION
what are the pre-hepatic causes of portal hypertension?

A

portal vein thrombosis

37
Q

PORTAL HYPERTENSION
what are the intrahepatic causes of portal hypertension?

A
  • schistosomiasis
  • cirrhosis
  • budd-chiari syndrome
38
Q

PORTAL HYPERTENSION
what are the post-hepatic causes of portal hypertension?

A
  • RH failure

- IVC obstruction

39
Q

PORTAL HYPERTENSION
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
40
Q

WILSONS DISEASE
what are the side-effects of chelating agents?

A

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

41
Q

NON-ALCOHOLIC FATTY LIVER
which drugs increase the risk of developing non-alcoholic fatty liver disease?

A

Amiodarone, Tetracycline ,Methotrexate

42
Q

NON-ALCOHOLIC FATTY LIVER
what are the investigations for non-alcoholic fatty liver disease?

A
  • LFTs = raised ALT
  • liver USS = confirm hepatic steatosis (seen as increased echogenicity)
  • enhanced liver fibrosis (ELF) blood test = 1st line (>10.51= advanced fibrosis)
  • NAFLD fibrosis score
  • fibrosis-4 score
  • fibroscan
  • liver biopsy = gold standard
43
Q

ALCOHOLIC LIVER DISEASE
what is the pathophysiology of alcoholic liver disease?

A

chronic excessive alcohol consumption leads to liver impairment
- alcohol is metabolised into acetaldehyde and then to acetate
- excessive NADH leads to greater fatty acid oxidation and subsequently fatty infiltration of the liver
- the production of free radicals results in increase in TNF-alpha causing hepatic inflammation
- chronic inflammation leads to liver fibrosis and eventually cirrhosis

44
Q

HEPATITIS
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
45
Q

CHRONIC PANCREATITIS
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

46
Q

ACUTE PANCREATITIS
what are the risk factors?

A
  • advancing age
  • afro-caribbean ethnicity
  • sex (female = gallstone related, male = alcohol related)
  • high glycaemic diet
  • obesity
  • T2DM
  • family history
47
Q

ACUTE PANCREATITIS
how is the severity calculated?

A
  • modified Glasgow score
  • PANCREAS
  • P02 <8kpa
  • Age >55
  • Neutrophils >15x109/L
  • Calcium <2mmol/L
  • Renal function (urea >16mmol/L)
  • Enzymes (AST>200U/L or LDH>600U/L)
  • Albumin <32g/L
  • Sugar (blood glucose>10mmol/L)
48
Q

CHRONIC PANCREATITIS
what are the investigations?

A
  • LFTs
  • HbA1c
  • transabdominal USS = first line imaging
  • CT abdomen

to consider
- faecal elastase
- IgG4
- MRCP
- ERCP

49
Q

PBC VS PSC
what are the differences between primary biliary cholangitis + primary sclerosing cholangitis

A

PRIMARY BILIARY CHOLANGITIS
- more common in middle aged women
- destruction of intrahepatic ducts only
- associated with autoimmune conditions
- often asymptomatic or fatigue, pruritus, jaundice + hepatomegaly
- raised ALP + GGT +/- conjugated bilirubin, anti mitochondrial antibodies (AMA)
- diagnosed via cholestatic LFTs, abdominal USS, history + exam
- treat with ursodeoxycholic acid, colestyramine + ADEK vita

PRIMARY SCLEROSING CHOLANGITIS
- more common in middle aged men
- inflammation of intrahepatic + extrahepatic ducts
- associated with ulcerative cholitis (UC)
- has symptoms of IBD + ascending cholangitis
- raised ALP + GGT +/- conjugated bilirubin, pANCA
- diagnosed via cholestatic LFTs, MRCP, history + exam
- treat with observation, colestyramine + ADEK vits

50
Q

PANCREATIC CANCER
what are the risk factors?

A
  • increasing age (65-75yrs)
  • male
  • smoking
  • diabetes
  • chronic pancreatitis
  • genetic (hereditary non-polyposis colorectal cancer, BRCA1 + 2
  • multiple endocrine neoplasia
51
Q

PANCREATIC CANCER
what are the clinical features?

A

SYMPTOMS
- painless jaundice
- epigastric or atypical back pain
- anorexia
- weight loss
- new onset diabetes (thirst, polyuria, nocturia)
- nausea + vomiting
- steatorrhoea
- pale stool + dark urine

SIGNS
- positive Courvoisier’s sign (palpable gallbladder in the presence of painless jaundice)
- Trousseau sign of malignancy (migratory thrombophlebitis, blood vessels get inflamed with associated clot)

52
Q

PANCREATIC CANCER
what are the investigations?

A
  • LFTs = obstructive (raised ALP + GGT + bilirubin)
  • coagulation profile (assess for liver mets)
  • abdominal USS
  • CT (or MRI) pancreas = double duct sign (simultaneous dilation of pancreatic + common bile ducts)
  • CA 19-9

to consider:
- PET scan (for staging)
- endoscopic USS
- ERCP

53
Q

PANCREATIC CANCER
when would you refer someone for 2ww?

A
  • over 40 with jaundice = 2ww
  • over 60 plus one of following (diarrhoea, back pain, abdo pain, N+V, constipation or new diabetes) = direct access CT abdomen

NOTE - pancreatic cancer is the only situation where a GP can do a direct access CT abdomen referral

54
Q

PANCREATIC CANCER
where does it tend to spread to?

A

liver
peritoneum
lungs
bones

55
Q

HEPATITIS
what is the management of HDV?

A

pegylated interferon alpha

56
Q

NON-ALCOHOLIC FATTY LIVER
what are the different stages?

A
  1. non-alcoholic fatty liver disease
  2. non-alcoholic steatohepatitis (NASH)
  3. fibrosis
  4. cirrhosis
57
Q

ASCITES
what are the causes of ascites that cause serum ascites albumin gradient (SAAG) <11g/L?

A

HYPOALBUMINAEMIA
- nephrotic syndrome
- severe malnutrition (e.g. kwashiorkor)

MALIGNANCY
- peritoneal carcinomatosis

INFECTION
- Tuberculous peritonitis

OTHER CAUSES
- pancreatitis
- bowel obstruction
- biliary ascites
- postoperative lymphatic leak
- serositis in connective tissue diseases