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Belle Phase 2a > Liver And Friends > Flashcards

Liver And Friends Flashcards

1
Q

Definitive treatment if symptomatic gallstones

A

Cholecystectomy

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2
Q

ERCP

A

Endoscopic retrograde cholangiopancreatography

Endoscope and X-Ray to look T the bile duct and pancreatic duct to search for and remove present gallstones

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3
Q

Presentation of pancreatitis

A

Epigastric pain radiating to the back
Vomiting
Pain may be relieved by leaning forward

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4
Q

Bile acid sequestrants

A

Bind to bile acids in the small intestine
Prevent their reabsorption into enterohepatic circulation
Reduction in bile acid levels causes hepatic conversion of LDL cholesterol to bile acids

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5
Q

Three biliary tract diseases

A

Gallstones (biliary colic)
Cholecystitis
Cholangitis

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6
Q

Distinguish between biliary colic, acute cholecystitis and ascending cholangitis using Charcot’s triad

A

Charcot’s triad: RUQ pain, fever, jaundice

Biliary colic: RUQ pain

Acute cholecystitis: RUQ pain, fever & increased WCC

Ascending cholangitis: RUQ pain, fever & increased WCC, Jaundice

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7
Q

Biliary colic pathophysiology

A

Gallstone blocks the cystic or common bile duct

Without signs of cystic inflammation

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8
Q

Components of bile

A

cholesterol, pigments and phospholipids

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9
Q

Types of gall stone

A

Cholesterol: excess production (obesity and fatty diets)

Pigment: (haemolytic anaemia)

Mixed: made of both of the above

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10
Q

Presentation of biliary colic

A

COLICKY RUQ PAIN

worse after eating large or FATTY meals (triggers gallbladder to contract AGAINST the blockage)

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11
Q

Five risk factors of gallstones

A 
5 F's:
Fat
Fertile
Forty
Female
FHx
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12
Q

Investigations for gallstones

A

Rule out:

  • FBC & CRP: inflammatory response (cholecystitis)
  • Amylase: pancreatitis can also give RUQ pain
  • LFTs: raised ALP (bilirubin and ALT normal)

Diagnostic: ULTRASOUND

1) Stones
2) Gallbladder wall thickness (due to inflammation)
3) Duct dilation (distal blockage)

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13
Q

Gallstone differential diagnoses

A 
RUQ pain:
cholecystitis 
cholangitis 
IBD
pancreatitis 
GORD 
peptic ulcers
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14
Q

Gallstone treatment

A

NSAIDs/analgesia

Cholecystectomy (optional to prevent recurrence)

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15
Q

Cholecystitis pathophysiology

A

Inflammation of the gallbladder wall (cholecyst-itis) usually caused by a stone blocking the duct causing bile to build up and distend the gallbladder

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16
Q

Presentation of cholecystitis

A

Generalised epigastric pain migrating to severe RUQ pain, fever
Pain associated with tenderness and guarding (inflamed gallbladder, local peritonitis)

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17
Q

Murphys sign

A

elicited in acute cholecystitis: ask patient to take in and hold a deep breath whilst palpating RUQ

positive = pain on inspiration when the gallbladder comes into contact with examiners hand

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18
Q

Ix cholecystitis

A

Positive Murphy’s sign
Inflammatory markers
Ultrasound (thick gallstone walls from inflammation)

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19
Q

Cholecystitis treatment

A

IV Abx
Heavy analgesia
IV fluids
Cholecystectomy (if needed)

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20
Q

Cholangitis

A

Bile DUCT inflammation caused by prolonged bile duct blockage

Bacteria can travel from the GI tract and not be flushed out with the bile, causing biliary tree infection

Jaundice: bile cannot enter the GI tract

Infection can travel to the pancreas as it shares the gallbladder ducts

Mortality: 5-10%

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21
Q

Cholangitis presentation

A

severe RUQ pain with fever and jaundice

may also present with:
sepsis
pancreatitis

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22
Q

Cholangitis investigations

A

FBC, LFTs, CRP: leukocytosis, raised ALP and bilirubin, raised CRP

Blood cultures/MC&S: for pathogen detection to use correct Ab

Ultrasound +/- ERCP (endoscopic retrograde cholangiopancreatography) = biliary tree contrast X-Ray

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23
Q

Cholangitis treatment

A

Treat SEPSIS
ERCP + stenting to mechanically clear the blockage
Surgery/cholecystectomy (if possible)

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24
Q

SEPSIS 6

A
  1. GIVE oxygen
  2. TAKE blood cultures
  3. GIVE IV Abx
  4. GIVE fluids
  5. TAKE lactate measurement
  6. TAKE urine output measurement
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25
Q

Causes of acute pancreatitis

A 
I GET SMASHED
Idiopathic
Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune (prevalent in Japan)
Scorpion venom
Hyperlipidaemia
ERCP
Drugs - NSAIDs, corticosteroids, ACEis
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26
Q

Two main causes of acute pancreatitis and the pathophysiology

A

GALLSTONES: BLOCKAGE of bile duct = back up of pancreatic juices
- change in luminal concentration causes calcium release inside pancreatic cells = activated trypsinogen early = AUTODIGESTION OF PANCREAS

ALCOHOL: CONTRACTS THE AMPULLA OF VATER obstructing bile clearance = calcium homeostasis disrupted = trypsinogen = AUTODIGESTION OF PANCREAS

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27
Q

Why does Grey Turner’s sign occur in acute pancreatitis

A

leaky and damaged pancreas = AUTODIGESTION to nearby structures = haemorrhage and Grey Turner’s sign (abdominal skin discolouration from retroperitoneal bleeding)

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28
Q

Why does hyperglycaemia occur in pancreatitis

A

disrupted insulin production

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29
Q

Acute pancreatitis presentation

A

SEVERE EPIGASTRIC PAIN RADIATING TO THE BACK

Anorexia, fever, jaundice, Grey Turner’s sign (flank bruising), N&V, tachycardia

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30
Q

Acute pancreatitis investigations

A

Serum amylase: raised
Urinalysis: raised urinary amylase
Serum lipase: raised (more specific than amylase)
CRP and FBC: raised CRP
Erect CXR: exclude gastroduodenal rupture
Abdo ultrasound, CT, MRI

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31
Q

Two scores used in acute pancreatitis

A

APACHE 2

Glasgow & Ranson

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32
Q

Acute pancreatitis treatment

A

Nil by Mouth (decrease pancreatic stimulation)
Analgesics
Prophylactic Abx
Treat gallstones if underlying cause

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33
Q

causes of chronic pancreatitis

A

CHRONIC ALCOHOL USE
Hereditary
Autoimmune
CKD

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34
Q

Presentation of chronic pancreatitis

A

EPIGASTRIC PAIN ‘BORING’ THROUGH THE BACK: worse after alcohol, better on leaning forward

Typical patient: 50 odd year old MALE with an appropriate SHx (drinking)

N&V, decreased appetite, malabsorption (painless weight loss)

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35
Q

Chronic pancreatitis investigations

A

Serum amylase and lipase: may be raised if enough cells remain to make them
Ultrasound abdo, CT, MRI

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36
Q

Treatment of chronic pancreatitis

A 
Stop drinking
Pancreatic enzyme supplements
PPI to help digestion
Insulin for DM
Duct drainage
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37
Q

Haemochromatosis

A

inherited condition where IRON LEVELS build up in the body

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38
Q

Pathophysiology of haemochromatosis

A

mutation in autosomal recessive HFE gene (c6)

causes increased intestinal iron absorption

iron accumulates in liver, joints, pancreas, heart, skin, gonads

ORGAN DAMAGE: liver fibrosis, cirrhosis, HCC (hepatocellular carcinoma)

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39
Q

Presentation of haemochromatosis

A

Fatigue, arthralgia (joint stiffness), weakness
Hypogonadism e.g erectile dysfunction
Slate-grey skin (brownish/bronze)
Chronic liver disease, heart failure, arrythmias

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40
Q

haemochromatosis investigations

A

Bloods: iron study, LFTs
Genetic testing
GOLD STANDARD: liver biopsy
MRI: detects iron overload

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41
Q

Wilson’s disease

A

error of COPPER metabolism = copper deposition in organs, including liver, basal ganglia, cornea

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42
Q

Presentation of Wilson’s disease

A

KAYSER-FLEISCHER RING: copper in cornea (green/brown pigment at outer edge)
Psychiatric: depression, neurotic behavioural patterns
CNS: tremor, dysarthria, involuntary movements, dysphagia
Liver: hepatitis, cirrhosis

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43
Q

Wilson’s disease investigations

A

serum copper and ceruloplasmin reduced (but can be normal)
24 hour URINARY copper excretion HIGH
DIAGNOSTIC: LIVER BIOPSY

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44
Q

Wilson’s disease management

A

Avoid high copper foods (liver, chocolate, nuts, mushrooms, shellfish)
Chelating agent: PENICILLAMINE
Liver transplant

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45
Q

Ascites

A

Excessive buildup of fluid in the peritoneal cavity

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46
Q

Ascites pathophysiology

A

Poor liver function = low albumin = low blood oncotic pressure = fluid leaks out into peritoneal cavity

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47
Q

Main cause of ascites

A

Liver failure/cirrhosis

48
Q

Presentation of ascites

A

LARGE DISTENDED ABDOMEN

Shifting dullness

  • DULLNESS OVER FLUID
  • RESONANCE OVER AIR
49
Q

Ascites treatment

A

Low sodium diet
Diuretics: Spironolactone + Furosemide
Identify cause + treat accordingly

50
Q

Peritonitis aetiology

  • Primary
  • Secondary
  • Causative organisms
A

Primary: spontaneous bacterial infection, ascites

Secondary: perforation (bowel, appendix, peptic ulcer), gastritis, ectopic pregnancy

Most common causative organisms: S. Aureus, Klebsiella, E.coli

51
Q

Presentation of peritonitis

A

Perforations: SUDDEN ONSET SEVERE ABDO PAIN with generalised shock/collapse

Secondary: gradual onset: generalised abdo pain&raquo_space; localised severe pain (visceral&raquo_space; parietal)

Rigid abdomen
Pyrexia, tachycardia, potential confusion, N&V
Guarding, rebound tenderness, rigidity, SILENT ABDO

52
Q

Peritonitis investigations

A

Bloods: FBC & CRP, Amylase (pancreatitis), hCG (ruptured ectopic pregnancy)

Erect CXR for air below the diaphragm, AXR to exclude bowel obstruction, CT for abdo ischaemia

Ascitic tap and blood cultures: pathogen

53
Q

Treatment of peritonitis

A

ABCDE
Find and treat underlying cause (e.g. may be surgery for perforated bowels)
IV fluids
IV Abx (broad spec&raquo_space; specific)
Peritoneal lavage (clean the cavity surgically)

54
Q

Hernias

A

protrusion of organ through defect in wall of its containing cavity

55
Q

Hernia classifications

A
  • Reducible (flattens when you lie down or push against it)
  • Irreducible (loop of intestine becomes trapped and the bulge cannot flatten out) - requires immediate medical attention&raquo_space; Obstructed (intestinal flow stopped)

-Strangulated (tightly trapped intestine causing blood supply to be cut off) > ischaemia > gangrene

56
Q

Inguinal hernia

A

protrusion of abdominal contents through inguinal canal

presents superior and medial to pubic tubercle

  • swelling in groin
  • impulse

20% are direct (medial to inferior epigastric artery through a weakened area)
80% are indirect (lateral to inferior epigastric artery through deep inguinal ring)

57
Q

Femoral hernia

A

bowel comes through femoral canal

58
Q

Hiatus hernia

A

herniation of stomach through oesophageal aperture of diaphragm

59
Q

Incisional hernia

A

hernia through surgical scar

60
Q

Epigastric hernia

A

hernia through linea alba above umbilicus

61
Q

Management of hernias

A

SURGERY

62
Q

Risk factors for inguinal hernia

A

Male
Chronic cough
Heavy lifting
Past abdo surgery

63
Q

Investigations for an inguinal or femoral hernia

A

Clinical diagnosis

USS/CT/MRI

64
Q

Most likely classification in femoral hernia

A

Irreducible and strangulation (due to rigidity of canals borders)

65
Q

Presentation of a femoral hernia

A

Mass in upper medial thigh
Neck of hernia is inferior and lateral to pubic tubercle
May be cough impulse

66
Q

Types of hiatus hernia

A

Rolling: 20% - GOJ remains in abdo, part of fundus rolls up through hiatus, LOS

Sliding: 80% - GOJ and part of stomach slides up into chest, LOS less

67
Q

Risk factors for hiatus hernia

A 
Obesity
Female
Pregnancy
Ascites
Age
68
Q

Hiatus hernia presentation

A

Heartburn/GORD

Dysphagia

69
Q

Hiatus hernia investigation

A 
CXR
Barium swallow (oesophagogram) 
Endoscopy
Oesophageal manometry
70
Q

Functions of the liver

A 
Oestrogen regulation
Detoxification
Carbohydrate metabolism
Albumin production
Clotting factor production
Bilirubin regulation
Immunity (Kupffer cells in reticuloendothelial system)
71
Q

Pathophysiology of spider naevi and palmar erythema

A

Oestrogen dysregulation

72
Q

Acute presentation of liver disease

A

Malaise
Nausea
Anorexia
Jaundice

73
Q

Chronic presentation of liver disease

A 
Ascites
Oedema
Pruritus
Clubbing
Palmar erythema
Xanthelasma
Spider naeivi
Hepatomegaly
Bleeding (haematemesis, bruising)
74
Q

Causes of acute liver disease

A 
Viral (Hep A, Hep B, EBV)
Drugs
Alcohol
Vascular
Obstruction
Congestion
75
Q

Causes of chronic liver disease

A

Alcohol
Viral (Hep B, Hep C)
Autoimmune
Metabolic (Iron, Copper)

76
Q

Causes of liver failure

A 
Toxins (Paracetamol, ALCOHOL - most common cause)
Infection (viral HEPATITIS)
Metabolic (Wilson's/A1AT)
Autoimmune (PBC, PSC)
Neoplastic (HCC)
Vascular (Budd Chiari, ischaemia)
77
Q

Signs of liver failure

A

Jaundice
Coagulopathy
Hepatic encephalopathy (altered mood, dyspraxia, asterixis)
Fetor hepaticus (sweet and musty breath/urine)

78
Q

Characteristics of liver failure decompensation

A

Abnormal bleeding
Ascites
Hepatic encephalopathy
Jaundice

79
Q

Investigations of liver failure

A

Clinical examination
Bloods (increased PT, increased AST/ALT, toxicology, FBC, U&E)
If ascites: peritoneal tap with MS&C

80
Q

Management of liver failure

A

Conservative (fluids, analgesia)

Medical: treat complications

  • Ascites: diuretics
  • Bleeding: vitamin K
  • Cerebral oedema: mannitol
  • Encephalopathy: lactulose
  • Sepsis: SEPSIS 6 (Abx)
  • Hypoglycaemia: dextrose

Surgical: transplant

81
Q

Hep A

A 
Spread: faecal-oral (vowels = bowels)
Virus: RNA
Infection: acute + mild
Test: Bloods show raised AST/ALT, raised IgG and IgM
Management: supportive
Vaccine available
82
Q

Hep B

A

Spread: blood products + bodily fluids (unprotected sex)
Virus: DNA (the only DNA one)
Infection: can be severe
Test: Hep B serology
Management: pegylated interferon alpha 2a, tenofovir (inhibits viral replication)
Vaccine available

83
Q

Hep C

A

Spread: blood products + bodily fluids (IVDU)
Virus: RNA
Infection: very slow progressing
Test: HCV RNA, Anti-HCV serology
Management: direct acting anti-virals, ribavirin, sufosbuvir

84
Q

Hep D

A 
Spread: blood products + bodily fluids
Virus: RNA (requires Hep B)
Infection: makes HBV worse, likely to progress to cirrhosis or HCC
Test: HDV RNA, Anti-HDV
Management: treat HBV
85
Q

Hep E

A 
Spread: faecal-oral (vowels = bowels)
Virus: RNA
Infection: normally mild
Test: HVE RNA, Anti-HVE
Management: supportive
  • only really get symptoms if PREGNANT
86
Q

Complications of hepatitis (B, C, D, E)

A

Cirrhosis

HCC

87
Q

Hep B serology:

Vaccinated

A

HB core Ab: -ve
HB surface Ab: +ve
HB surface Ag: -ve

88
Q

Hep B serology:

Previous HBV

A

HB core Ab: +ve
HB surface Ab: +ve
HB surface Ag: -ve

89
Q

Hep B serology:

Chronic HBV

A

HB core Ab: +ve
HB surface Ab: -ve
HB surface Ag: +ve
IgM negative, IgG positive = chronic

90
Q

Paracetamol metabolism and toxicity

A
  1. Glucuronidation = excretion
  2. Sulfation = excretion
  3. p450 > NAPQI [toxic] > NAPQI + glutathione = excretion

Overdose: too much toxic NAPQI without enough glutathione = liver damage
- nausea, vomiting, anorexia, RUQ pain

Treatment: activated charcoal, N-acetylcysteine

91
Q

Non-alcoholic fatty liver disease (summary)

A

Healthy > Steatosis > Steatohepatitis > Fibrosis > Cirrhosis

Px: asymptomatic, nausea, vomiting, diarrhoea, hepatomegaly

Dx: biopsy (diagnostic), imaging

Tx: weight loss (reduce fat)

92
Q

Alcoholic liver disease

A

Fatty liver > alcoholic hepatitis > cirrhosis

Ix:

  • GGT high, AST and ALT mildly raised
  • FBC: macrocytic anaemia
93
Q

Calculation for units of alcohol

A

Strength (ABV) x volume (ml) / 1000 = units

94
Q

Complications of alcoholic liver disease

A

Wernicke-Korsakoff encephalopathy (ataxia, confusion, nystagmus, memory; Tx: IV thiamine)

Acute/chronic pancreatitis

Mallory-Weiss tear

95
Q

GGT (LFT)

A

Gamma-glutamyl transferase

96
Q

Common causes of cirrhosis

A

Chronic alcohol abuse
NAFLD
Hepatitis (B & C)

97
Q

Clinical Px of cirrhosis

A 
Ascites
Clubbing
Palmar erythema
Xanthelasma
Spider naevi
Hepatomegaly
Peripheral oedema
98
Q

Ix cirrhosis

A

Low platelets, high INR, low albumin
US + CT: hepatomegaly
Liver biopsy

99
Q

Tx cirrhosis

A 
Alcohol abstinence 
Good nutrition
Liver transplantation
Screen for HCC every 6 months (increased AFP)
Symptoms e.g. spironolactone for ascites
100
Q

Causes of portal hypertension

A

Prehepatic (portal vein thrombosis)
Intrahepatic (schistosomiasis, cirrhosis, Budd Chiari)
Post-hepatic (RH failure, IVC obstruction)

101
Q

Pathophysiology of oesophageal varices

A

Portal hypertension pushes blood into surrounding vessels i.e. oesophageal varices

These are thin vessels and not meant to transport high pressure blood = easily ruptured

Rupture > haematemesis > digested blood > melaena

102
Q

Tx oesophageal varices

A

Beta blocker (reduce CO > reduce portal HT)
Nitrate (reduce portal HT)
Terlipressin

Surgical: band ligation, TIPS shunt

103
Q

Causes of prehepatic jaundice

A

Haemolytic anaemia = excessive red cell breakdown which overwhelms the liver’s ability to conjugate bilirubin = unconjugated hyperbilirubinaemia (jaundice)

104
Q

Causes of hepatocellular jaundice

A 
Liver failure
Liver disease
Hepatitis 
Iatrogenic (toxicity) 
Gilbert’s syndrome
105
Q

Causes of post hepatic jaundice

A

Gallstones

106
Q

Acute HBV infection serology

A

HB core Ab: +ve
HB surface Ab: -ve
HB surface Ag: +ve
IgM positive = acute

107
Q

Blood results associated with alcoholic liver damage

A

Raised GGT
High AST:ALT ratio
Mallory bodies

108
Q

Cholestatic picture

A

Dark urine

Pale stools

109
Q

Complications of acute pancreatitis

A

ACUTE RENAL FAILURE (due to dehydration)
Sepsis
Acute respiratory syndrome
Chronic pancreatitis

110
Q

Pancreatic cancer Px

tumour at head of pancreas

A

Painless obstructive jaundice

Steatthorea

111
Q

RBC breakdown

A

Heme
Biliverdin
Bilirubin

Large intestine: Urobilinogen > Urobilin (urine) / Stercobilin (faeces)

112
Q

What is ERCP?

A

Endoscopic retrograde cholangio-pancreatography

113
Q

Primary biliary cholangitis

A

Intrahepatic ducts

114
Q

Primary sclerosing cholangitis

A

Intra and extra hepatic ducts

Strong link with UC

115
Q

Acute liver failure definition

A

Onset of less than 26 weeks duration and no previous liver disease

116
Q

Medication used for delirium tremens/alcohol withdrawal

A

Chlordiazpoxide

IV B-vitamins

117
Q

How does cirrhosis cause

1) Splenomegaly
2) Upper GI bleed

A

1) Portal hypertension

2) Oesophageal varices

Belle Phase 2a (14 decks)

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