Liver Flashcards

(204 cards)

1
Q

Liver functions?

A

Albumin production
Clotting factors
Storage (iron, vitamins, copper, glycogen)
Immunity
Metabolism of carbohydrates
Detoxification
Bilirubin metabolism
Oestrogen level regulation

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2
Q

LFTs specific to liver?

A
  • Bilirubin
  • Albumin
  • Clotting factora (PT/INR)
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3
Q

LFTs non-specific to liver function? Interpretation?

A
  • AST + ALT → Made in the liver and may be released into blood if hepatocytes are damaged
    • AST:ALT ratio normally 0.7-1.5
    • > 2 → Alcoholic liver disease (+ raised GGT)
    • <1 → NAFLD

GGT → Increased in ALD (differentiates increased ALP as a hepatic/bone cause)

ALP → Increased in biliary tree specific damage and bone pathology.

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4
Q

Bile components + physiology?

A

Contains bile acids, bile salts, water, cholesterol, phospholipid, bilirubin and electrolytes.

Stimulated by CCK which makes the gallbladder contract and relax the Sphincter of Oddi.

95% of bile salts reuptakes at the terminal ileum in portal vein for resuse.

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5
Q

Bilirubin cycle?

A

Spleen

  • Haemoglobin → Globin and Haem:
    • Haem → Iron and biliverdin:
      • Biliverdin → Unconjugated bilirubin (biliverdin reductase)

Unconjugated bilirubin is bound to albumin and travels to liver. UGT converts to conjugated bilirubin.

Liver - UGT converts to conjugated bilirubin.

Colon - Conjugated bilirubin is converted to urobilinogen.

  • Urobilinogen is converted to:
    • 90% stercobilin (poo - brown colour)
    • 5% urobilin (urine)
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6
Q

Jaundice?

A

The yellowing of skin and eyes due to accumulation of bilirubin which is a sign of liver dysfunction (unconjugated/conjugated).

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7
Q

Jaundice types? Presentation?

A

Pre-hepatic - Normal urine and stools, no itching and normal LFTs.

Hepatic/post-hepatic - Dark urine, pale stools, can itch, abnormal LFTs (more bilirubin is excreted in the urine and less is excreted in poo).

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8
Q

Pre-hepatic jaundice causes?

A

Haemolytic anaemias and Gilbert’s syndrome

Sickle cell, G6DPH def, autoimmune haemolytic, thalassaemia, malaria.

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9
Q

Intrahepatic jaundice causes?

A

Disease of the liver (HCC, ALD/NAFLD, hepatitis, hepatotoxic drugs).

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10
Q

Post-hepatic jaundice causes?

A

Conjugated hyperbilirubinaemia. Due to biliary obstruction.

Biliary tree pathology (pancreatic cancer, cholangiocarcinoma, choledocholiathis (gallstone in common bile duct), autoimmune (PBC, PSC)).

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11
Q

Acute liver failure?

A

Rapid decline in liver function (<weeks) in patients with previously healthy liver functions.

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12
Q

Acute liver failure timing?

A

Hyper-acute (<1w), acute (1-3w), subacute (4-26w).

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13
Q

Acute on chronic liver failure?

A

Abrupt decline in patients with chronic liver symptoms.

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14
Q

Fulminant liver failure?

A

Very severe acute liver failure with significant hepatic encephalopathy, mc due to paracetamol overdose, diagnose with biopsy and treat with urgent liver transplant.

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15
Q

Acute liver failure causes?

A

Paracetamol overdose
Viral (Hep A, E, B, CMV, EBV, HSV)
Metabolic
Autoimmune hepatitis
Acute fatty liver of pregnancy

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16
Q

Acute liver failure presentation?

A

Jaundice + coagulopathy + hepatic encephalopathy

Ascites, renal impairment

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17
Q

Acute liver failure investigations + findings?

A

Aim to identify underlying cause

LFTs, U+Es, clotting screen, albumin, serum paracetamol, hepatitis serology

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18
Q

Acute liver failure management?

A

Treat underlying cause and complications

Paracetamol: IV fluids and N-acetylcystine
Viral - supportive

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19
Q

Liver transplant requirements?

A

Paracetamol related → Arterial pH >7.3 or INR >6.5, creatinine >300 and H.E grade 3/4

  • Non-paracetamol related → INR >6.5 or 3/5 of:
    • Patient under 10/over 40, bilirubin over 300, INR >3.5, drug toxicity, comatose >7d after jaundice
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20
Q

Chronic liver disease?

A

Progressive liver disease over 6+ months due to repeated insults.

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21
Q

Chronic liver disease causes?

A

ALD (mc), NAFLD, viral (hep B/C/D).

Other - Metabolic, drugs, autoimmune, PBC +PSC, Budd Chiari.

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22
Q

Chronic liver disease presentation?

A

Jaundice
Spider naevi
Caput medusae
Telangiectasia
HE
Ascites
Portal hypertension and oesophageal varices
Gynecomastia
Palmar erythema
Clubbing

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23
Q

Alcoholic liver disease?

A

Affects 10-35% of heavy drinkers due to prolonged heavy alcoholism

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24
Q

Calculating alcohol units?

A

Strength (ABV) x volume (ml)/1000.

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25
Alcoholic liver disease progression?
Steatosis (fatty) → Hepatitis (mallory bodies) → Cirrhosis (micronodules)
26
Alcoholic liver disease presentation?
Initially asymptomatic. Later stages: Chronic liver symptoms and alcohol dependence
27
Screening questions for alcohol dependence?
CAGE (cut down? others annoyed? guilty? Early morning drinking?).
28
Alcoholic liver disease investigations?
LFTs (AST:ALT >2, raised GGT, bilirubin and ALP) FBC - Macrocytic non-megaloblastic anaemia. Decreased albumin USS → Fatty liver, hepatomegaly, portal hypertension Biopsy → Extent of cirrhosis or if just hepatitis.
29
Alcoholic liver disease management?
Alcohol abstinence, diet improvement, vitamin B1 supplements MDF score above 32 → Prednisolone 40mg/d Monitor and treat complications Severe → Referral and consider transplantation
30
MDF score?
Maddrey's Discriminant Function for Alcoholic Hepatitis Scores above 32 typically suggest poor prognosis and that these patients may be helped by steroid administration.
31
Alcoholic liver disease complications?
Acute liver failure, cirrhosis, pancreatitis, Wernicke-Korsakoff
32
Non-alcoholic fatty liver disease?
Chronic liver disease associated with metabolic syndromes (obesity, DM) not due to alcoholism.
33
Non-alcoholic fatty liver disease progression?
Hepatosteatosis (NAFLD) - Non-alcoholic steatohepatitis (NASH) - Fibrosis - Cirrhosis.
34
Non-alcoholic fatty liver disease presentation?
Typically asymptomatic; findings are incidental initially. Severe - may present with signs of liver failure.
35
NAFLD investigations?
Deranged LFTs (usually high ALT), macrocytic anaemia, coagulopathy 1st line - USS + FIB4 or NAFLD score to determine degree of fibrosis FIB4 >2.67 then refer to secondary care → fibroscan, biopsy
36
NAFLD management?
Lifestyle changes (lower BMI, eat healthier, vitamin E)
37
Liver cirrhosis? Types?
Micronodular liver affecting function and bloodflow through it (portal hypertension and oesophageal varcies) Compensated (liver function) or decompensated (very poor liver function - ESLF).
38
Liver cirrhosis investigations?
FBC, U+Es, LFTs, clotting, serology, albumin Fibroscan → NAFLD in secondary care, screening for ALD, heavy drinkers and hepatitis C USS + biopsy
39
Liver cirrhosis monitoring?
OGD in new patients (varices), USS liver 6m +AFP (HCC)
40
Liver cirrhosis prognostic scores?
Child Pugh A, B, C to assess severity MELD score → Assess mortality in transplant candidates
41
Liver cirrhosis complications?
Hepatocellular carcinoma Varices, HE, ascites, abscesses, SBP, hepatorenal syndrome
42
Biliary tract disease?
Spectrum of disease associated with gallstones - cholesterol (mc), pigment or mixed.
43
Biliary tract disease RFs?
Fat, fertile, female, fair, forty plus and family history
44
Biliary colic presentation?
Sudden RUQ pain worse after fatty meal (lasts a few hours)
45
Cholecystitis presentation?
RUQ pain + fever (positive Murphy sign - palpate gallbladder and inhale = pain + referred shoulder tip pain)
46
Murphy sign?
Palpate gallbladder and inhale = pain + referred shoulder tip pain. Inflammation
47
Ascending cholangitis presentation?
Charcot's triad: RUQ pain, fever + jaundice Reynold's pentad: Charcot’s + hypotension + confusion (critical condition)
48
Gallstones investigations + management?
- Dx - 1st line USS, normal bloods - Tx - NSAIDs, diet changes, weight loss - Laparoscopic cholecystectomy
49
Cholecystitis investigations + management?
- Dx - Raised WCC, normal LFT, USS shows >3mm thickened GB wall - Tx - Laparoscopic cholecystectomy <72h, NBM, IV fluids, antibiotics
50
Cholangitis investigation + management?
- Dx - Raised WCC, ALP, bilirubin, USS shows dilatation and stones - Tx - IV antibiotics and ERCP 24-48h
51
Biliary tract disease complications?
Gallstone ileus - Large gallstones obstructs GIT, mc at ileocaecal valve Gallbladder empyema - Cholecystitis related gallbladder pus accumulation
52
Viral hepatitis?
Viral induced intrinsic liver inflammation. Notify Public Health England for hepatitis A, B + C.
53
Types of viral hepatitis?
A, B, C, D, E
54
Hepatitis A?
RNA virus. Faeco-oral spread, pico-RNA virus. Acute only.
55
Hepatitis A immunity + cancer risk?
100% immunity after, no risk of HCC
56
Hepatitis A associations? How long does it take to resolve?
Associated with travel and shellfish with 2-4w incubation. Resolves <6w.
57
Most common hepatitis in the world?
Hepatitis A. Rare in the UK
58
Hepatitis A presentation?
Prodromal flu symptoms, then RUQ pain and cholestasis
59
Hepatitis B investigations?
HAV IgM
60
Hepatitis A management?
Supportive (travellers vaccine available for MSM, IVDU, liver disease)
61
Hepatitis A complication?
Fulminant liver failure
62
Hepatitis B?
Acute and chronic. Blood borne. DNA virus. Present worldwide.
63
Hepatitis B RFs?
Sex, IVDU, vertical
64
Hepatitis B presentation?
Incubation 1-6m then 1-2w prodrome of jaundice + hepatosplenomegaly
65
Hepatitis B investigations?
Hepatitis B serology: - HBsAg → Active infection. - Anti-HbsAg → Recovery and immunity (past infection or vaccination) - Anti-HbC: - IgM - Acute hepatitis - IgG - Chronic or resolved - HbeAg → Raised viral replication - Anti-HbeAg → Marker if they’ve been through active phase - HBV DNA → Direct count of viral load
66
Hepatitis B management?
Pegylated interferon-alpha, tenofovir
67
Hepatitis B complications?
If chronic; increased risk of cirrhosis and HCC.
68
Hepatitis C?
Acute and chronic. RNA flavivirus. Blood-borne. More common in UK.
69
Hepatitis C association?
Large association with IVDU and limited vertical/sexual transmission.
70
Hepatitis C presentation?
Acutely aSx, late symptoms of hepatosplenomegaly and chronic liver symptoms.
71
Hepatitis C investigations?
HCV serology.
72
Hepatitis C management?
Antiviral protease inhibitors (sofosbuvir +/- rivabarin)
73
Hepatitis C complications?
Increased risk of HCC - 25% recover, 75% develop chronic hepatitis C: - With 25% developing cirrhosis 20-30y later
74
Hepatitis D?
Acute and chronic. Incomplete RNA, depends on hepatitis B antigen for survival. Blood-borne. Rare in UK.
75
Hepatitis B + D superinfection?
If hepatitis B + D superinfection there is a risk of fulminant liver failure and increased chronic progression.
76
Hepatitis D management?
Hepatitis B treatment
77
Hepatitis E?
Acute only. RNA. Faeco-oral spread.
78
Hepatitis E associations?
Associated with undercooked pork, pigs, dogs and contaminated water.
79
Hepatitis E presentation?
Like HepA, self-limiting.
80
Hepatitis E investigations?
HEV IgM
81
Hepatitis E management?
Supportive, usually not required.
82
Hepatitis E complications?
Increased mortality in pregnancy ladies (fulminant liver failure).
83
Autoimmune hepatitis? Cause?
Very rare cause of chronic hepatitis. Unknown cause. Can cause cheek rash. MC is middle aged women.
84
Autoimmune hepatitis types + antibodies?
- Type 1 (mc) → Adults and children. Ani-SMA antibodies - Type 2 → Young people and children. Anti-LKM1 antibodies - Type 3 → Adult middle aged women. Anti-SLA
85
Autoimmune hepatitis RFs?
HLA-B8/DR3, autoimmune disease, hypergammaglobulinemia
86
Autoimmune hepatitis presentation?
Jaundice, RUQ pain, fatigue - May be acute or chronic - 25% asymptomatic
87
Autoimmune hepatitis investigations?
Deranged LFTs and serology
88
Autoimmune hepatitis management?
Immunosuppression: 1. Prednisolone 2. Azathioprine Last resort → Transplant
89
Primary biliary cholangitis?
Autoimmune interlobular bile duct damage and inflammation.
90
What is PBC associated with?
Associated with Sjogren’s syndrome
91
PBC rule of M's?
Rule of M’s → Middle aged F, raised IgM, anti-mitochondrial M2 antibodies
92
PBC presentation?
Pruritus and fatigue first then jaundice, hepatosplenomegaly and xanthelasma Or may be initially asymptomatic, routine test shows increase AMA.
93
PBC investigations + findings?
Deranged LFTs. 95% of patients show AMA M2 antibodies USS +/- MRCP
94
PBC management?
1st line - Ursodeoxycholic acid (reduces cholestasis). Symptom relief → Cholestyramine (binds to bile to prevent absorption in gut, reduces pruritus) End-stage - liver transplant
95
PBC complications?
Osteomalacia, raised HCC risk
96
Primary sclerosing cholangitis?
Atypical autoimmune intra and extra-hepatic duct damage.
97
Who does PSC affect? Association?
Affects middle aged men and associated with ulcerative colitis.
98
PSC presentation?
RUQ pain, obstructive jaundice + pruritus Initially asymptomatic then symptoms develop
99
PSC investigations + findings?
Deranged LFTs, raised pANCA (90%) GS → MRCP
100
PSC management?
Only symptomatic relief (cholestyramine) and vitamin supplements - Last resort if severe biliary damage: - ERCP dilation - Liver transplant
101
PSC complication?
Cholangiocarcinoma
102
Types of pancreatitis?
Acute and chronic
103
Acute pancreatitis?
Pancreatic autodigestion by enzymes (premature activation).
104
Acute pancreatitis causes?
IGETSMASHED: Idiopathic, gallstones, ethanol, trauma, steroids, mumps/malignancy, autoimmune, scorpion stings, hyperlipidaemia, ERCP (post), drugs (NSAIDs, corticosteroids, ACEi).
105
Most common causes of acute pancreatitis?
MC in order: gallstones, alcohol, idiopathic
106
Acute pancreatitis symptoms?
Sudden severe epigastric pain radiating to the back with N+V and fever
107
Acute pancreatitis signs?
- Grey turner sign (flank bleeding) - Cullen sign (periumbilical bleeding)
108
Acute pancreatitis investigations + findings?
Bloods (amylase, lipase → 3x upper limit of normal is diagnostic. FBC, CRP) USS, CT, ERCP
109
Acute pancreatitis severity scoring?
Modified Glasgow score for severity → PANCREAS: PaO2 <8, age >55, neutrophils >15, Ca <2, renal (urea >16), enzymes (AST >200, LDH >600), albumin <32, sugar >10.
110
Acute pancreatitis management?
A-E, analgesia, antibiotics, IV fluids NBM if vomiting
111
Acute pancreatitis local complications?
Pancreatic necrosis and pseudocysts
112
Acute pancreatitis systemic complications?
- SIRS → >2 of raised WCC, tachycardia, tachypnoea, pyrexia - ARDS due to acute CVR dysfunction
113
Chronic pancreatitis?
Chronic inflammation of pancreatic tissue leading to fibrosis and decreased function.
114
Chronic pancreatitis causes?
Most commonly due to alcoholism, also gallstones and CF.
115
Chronic pancreatitis presentation?
Chronic epigastric pain radiating to back and worse <30m after eating - Exocrine dysfunction → Steatorrhoea and failure to thrive - Endocrine dysfunction → DM
116
Chronic pancreatitis investigations?
GS is CT abdomen AXR may show pancreatic calcification
117
Chronic pancreatitis a management?
- Alcohol cessation - Analgesia - Pancreatic enzyme supplements
118
Are primary or secondary liver cancers more common?
Secondary liver cancer is more common than primary liver cancer
119
Hepatocellular carcinoma?
3rd most common worldwide cancer. MC cause in UK is hepatitis C and worldwide it’s hepatitis B
120
HCC RFs?
Liver cirrhosis due to HepB/C, alcohol, NAFLD, CLD, haemochromatosis.
121
HCC presentation?
- Cirrhosis, irregular hepatomegaly - Weight loss, fevers, night sweats
122
HCC investigations?
Alpha fetoprotein + USS liver GS - CT abdomen
123
HCC management?
Surgical resection or liver transplant If unresectable → sorafenib
124
Cholangiocarcinoma?
Adenocarcinoma of biliary tree associated with PSC. Presents like pancreatic cancer but rarer.
125
Cholangiocarcinoma presentation?
Pruritus, biliary colic + obstructive jaundice with palpable painless large gallbladder Lymphadenopathy - Virchow’s, sister Mary Joseph
126
Cholangiocarcinoma investigations?
Raised CA19-9 GS - ERCP
127
Cholangiocarcinoma management?
If resectable → Surgery
128
Pancreatic cancer?
Adenocarcinoma of exocrine pancreas (99%), of ductal origin typically affecting the head.
129
Pancreatic cancer RFs?
Higher age, DM, chronic pancreatitis, genetic (MEN, BRCA2 etc), alcohol
130
Pancreatic cancer presentation?
Painless jaundice Courvoisier sign - palpable painless large gallbladder Pale stools, dark urine Body + tail - Epigastric pain radiating to back and relieved when sitting forward.
131
Pancreatic cancer investigations?
Raised CA19-9 GS → CT pancreas
132
Pancreatic cancer management?
80% inoperable, very poor prognosis (5y survival = 3%). Surgery if possible; Whipple pancreaticoduodenectomy
133
Haemochromatosis?
Autosomal recessive mutation of HFE gene on chromosome 6. Results in iron overload.
134
Who does haemochromatosis affect?
More common in men (middle aged) and less likely in women due to iron loss from menstruation.
135
Haemochromatosis presentation?
40-50y with bronze/gray skin, fatigue, T2DM, liver cirrhosis - Joint pain, hypogonadism, dilated cardiomyopathy - Osteoporosis, hair loss, memory and mood disturbance
136
Haemochromatosis investigations?
1st → Transferrin sats >55% M/>50% F, raised ferritin and iron, low TIBC - LFTs, liver biopsy, MRI, genetic testing - XR - chondrocalcinosis
137
Haemochromatosis management?
1st line → Venesection (every 3-4 months, initially weekly until stable) 2nd: → Iron chelation
138
Haemochromatosis complications?
DM, liver cirrhosis, cardiomyopathy
139
Wilson’s disease?
Autosomal recessive mutation of ATP7B gene on chromosome 13 → excess body copper.
140
Wilson’s disease typical patient?
Typical patients are young at ~20y/o, FHx.
141
Wilson’s disease presentation?
Neurological → Parkinsonism, ataxia, tremor, dementia, dysarthria Liver cirrhosis symptoms (jaundice) Cornea → Kayser Fleischer rings (copper deposits in cornea).
142
Wilson’s disease investigations?
Low serum caeruloplasmin Raised 24h urinary copper GS → Liver biopsy
143
Wilson’s disease management?
D-penicillinamine (chelation)
144
Alpha 1 antitrypsin deficiency? Pathophysiology?
Deficiency of alpha 1 antitrypsin enzymes. Autosomal recessive mutation of SERPINA 1 mutation on chromosome 14 resulting in deficient A1AT (protects against neutrophil elastase.
145
A1AT presentation?
Young/middle aged male with little/no smoking Hx and with panacinar emphysematous COPD like symptoms (dyspnoea, chronic cough, sputum) - +/- liver dysfunction
146
A1AT investigations?
Serum A1AT decreased and deranged LFTs - CT - panacinar emphysema - PFT or spirometry shows obstruction
147
A1AT management?
Avoid/stop smoking, SABAs - Consider A1AT IV concentrate replacement - Last resort → Lung and/or liver transplant
148
Portal hypertension?
Pathophysiologically increased pressure in portal vein, complication of cirrhosis.
149
Portal hypertension causes?
- Pre-hepatic: Portal vein thrombosis - Hepatic: Cirrhosis (mc UK), schistomiasis (mc world) - Post-hepatic: Budd Chiari, RH failure
150
Portal hypertension presentation?
Mostly asymptomatic: Found when when oesophageal varices rupture (90% hypertension causes them, 1/3rd rupture).
151
Oesophageal varices?
Due to portal hypertension causing collateral vessel shunting, prone to rupture.
152
Oesophageal varices presentation?
Haematemesis with background of liver failure
153
Oesophageal varices investigations?
OGD is diagnostic
154
Oesophageal varices management?
Acutely → A-E, consider transfusion, stop bleeding: -Terlipressin, variceal banding, TIPS (SE = HE) -Prevent bleed → Propranolol, repeat binding, transplant
155
Ascites?
Accumulated free fluid in abdominal cavity, complication of cirrhosis.
156
How to classify ascites?
Serum-ascites albumin gradient (SAAG)
157
Ascites types + causes?
- High SAAG (>1.1g/dL) → Portal hypertension associated - Cirrhosis, thrombus, Budd-Chiari, RHF - Raised hydrostatic pressure - Low SAAG (<1.1g/dL) → Non-portal hypertension associated - Cancer, TB, nephrotic syndrome - Inflammation/decreased oncotic pressure
158
Ascites presentation?
Abdominal distension May have jaundice/other liver symptoms
159
Ascites investigations?
O/E → Shifting dullness, flank fullness, fluid thrill, distension Ascitic tap for SAAG + MC+S
160
Ascites management?
Treat underlying cause and decrease salt intake -Spironolactone (aldosterone antagonist) -Paracentesis
161
Ascites complications?
SBP (mc) due to E. coli most commonly Prophylactic ciprofloxacin to ascitic patients with a past history of SBP
162
Paracetamol overdose?
Excessive use of paracetamol (>75mg/kg). 50% self-poisoning cases in UK and mc cause of acute liver injury in the west.
163
Most common cause of acute liver injury in the Western world?
Paracetamol overdose
164
Paracetamol overdose pathophysiology?
- 90% phase II glucoronidation → excretion - 10% phase I CYP450 NAPQI → phase II with glutathione → excretion - In overdose → glucoronidation is saturated → shunting down CYP450 leading to an accumulation of NAPQI (toxic) → liver damage
165
Paracetamol overdose presentation?
May be asymptomatic N+V, loin/abdominal pain, jaundice, haematuria, proteinuria, coma
166
Paracetamol overdose investigations?
FBC, U+E, LFTs, clotting, albumin, VBG 4h later - check paracetamol levels
167
What is used to plot paracetamol levels over time?
Nomograms may be used to plot paracetamol concentration against time which helps guide treatment
168
Paracetamol overdose management?
<1h → Activated charcoal Staggered overdose (over 1h) → Start N-acetylcysteine STAT (infusion over 1h) Massive overdose (>150mg/kg) → NAC STAT
169
Liver transplant guidelines in paracetamol overdose?
Arterial pH >7.3 or INR >6.5 + creatinine >300 + H.E grade 3/4
170
Paracetamol overdose complications?
Fulminant liver failure
171
Gilbert’s/Criggler Najjar syndrome?
Autosomal recessive mutation in UDP1A1 gene - UGT enzyme deficiency. Causes unconjugated hyperbilirubinaemia.
172
Gilbert’s + Criggler Najjar syndrome frequency?
Gilbert’s is common whereas Criggler Najjar is very rare.
173
Most common cause of hereditary jaundice?
Gilbert's syndrome
174
Gilbert's vs Criggler Najjar?
Gilbert's - Mildly decreased UGT activity Criggler Najjar - Dramatically decreased/absent UGT activity
175
Gilbert’s syndrome presentation and management? Risks?
Mild bilirubin elevation with stress, illness, dehydration causing painless jaundice Supportive management NO risk of kernicterus
176
Criggler-Najjar presentation and management?
- Very raised bilirubin with risk of kernicterus in infancy - Presents with jaundice, lethargy and N+V Treat with phototherapy + liver transplant
177
Criggler-Najjar syndrome types?
- Type 1 - Don’t survive into adulthood - Type 2 - MC than type 1, phenobarbital may help
178
Hernia?
Protrusion of an organ through defect in its containing cavity. Typically the abdomen.
179
Reducible vs irreducible hernias?
Reducible → Pushed back into place. Irreducible → Obstructed (bowel), strangulated (ischaemic bowel), incarceration (no obstruction or ischaemia).
180
Inguinal hernia?
Spermatic cord herniates through inguinal canal (male). Or the bowel herniates.
181
Inguinal hernia types?
- Indirect (80%) → Not in Hesselbach triangle - Patent processus vaginalis, follows spermatic cord, younger patients - Commonly involves scrotum, higher strangulation risk - Direct (20%) → In Hesselbach triangle - Abdominal wall weakness and increased intra-abdominal pressure, older patients - Rarely involves scrotum, lower strangulation risk
182
Inguinal hernia presentation?
Groin bulge in M, inferolateral to pubic tubercle Positive cough impulse
183
Inguinal hernia management?
- Mesh surgery - In the meantime - hernia truss
184
Femoral hernia? Risks?
- Bowel herniates through femoral canal. - Very likely to strangulate due to rigid femoral canal borders.
185
Femoral hernia presentation?
Groin bulge in F, supero-lateral to pubic tubercle - Raised strangulation risk - Negative cough impulse
186
Femoral hernia management?
Surgery
187
Hiatal hernia? Cause?
- Stomach herniates through diaphragm aperture. - Mainly due to increased intra-abdominal pressure (pregnancy, raised BMI, COPD)
188
Hiatal hernia types?
- Sliding (80%) → LES slides into abdomen. - Rolling (20%) → LES stays in abdomen, part of fundus rolls into thorax.
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Hiatal hernia presentation, investigations + management?
- Sx - GORD, dysphagia. - Dx - Barium swallow (GS) - Tx - PPI, weight loss, surgery
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Wernicke’s encephalopathy?
Vitamin B1 (thiamine) deficiency commonly seen in alcoholics, poorly absorbed in alcoholics alongside poor diet.
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Wernicke’s encephalopathy vs Korsakoff syndrome?
Wernicke’s encephalopathy comes before Korsakoff syndrome.
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Wernicke’s encephalopathy pathophysiology?
Petechial haemorrhages occur in a variety of structures in the brain including the mamillary bodies and ventricle walls
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Wernicke’s encephalopathy presentation?
Nystagmus, ophthalmoplegia (lateral rectus palsy and conjugate gaze palsy), gait ataxia Encephalopathy: confusion, disorientation, indifference, inattentiveness
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Wernicke’s encephalopathy management?
Replace thiamine (vitamin B1)
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Wernicke’s encephalopathy complication?
Wernicke-Korsakoff syndrome
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Korsakoff syndrome?
A memory disorder that results from vitamin B1 deficiency and is associated with alcoholism - often irreversible.
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Korsakoff syndrome presentation?
Wernicke's encephalopathy AND: - Anterograde amnesia - Retrograde amnesia - Confabulation (false memory)
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Hepatic encephalopathy?
Brain changes in patients with advanced, acute or chronic liver disease due to the build up of toxins (ammonia).
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Hepatic encephalopathy presentation?
Personality changes, intellectual impairment, impaired memory, coma
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How to classify hepatic encephalopathy?
- West Haven 1-4: 1. Mood and sleep changes 2. Mild confusion and asterixis 3. Confused and decreased GCS 4. GCS3 - comatose
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Hepatic encephalopathy management?
Laxatives (help to clear the ammonia from the gut before being absorbed) Antibiotics (reduces the number of bacteria in the gut producing ammonia)
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Which electrolyte abnormality is caused by acute pancreatitis?
Hypocalcaemia
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