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Medicine Phase 2A (OWN) > Liver and Friends > Flashcards

Liver and Friends Flashcards

1
Q

How does the presence of fatty acids lead to the release of bile into the duodenum?

A

Enteroendocrine cells release cholecystokinin (CCK) which relaxes the sphincter of oddi and stimulates the gallbladder to contract

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2
Q

How is fat broken down in the duodenum?

A

Bile is a fat emulsifier

Pancreatic lipase further breaks down micelles so they can be absorbed by the villi

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3
Q

Give 4 risk factors for developing gallstones

A 
Female
Obesity
Pregnancy
Age
Rapid weight loss
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4
Q

Where does pain occur in a gallbladder attack?

A

Sudden sharp pain in R upper quadrant or epigastrum which radiates to the right shoulder

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5
Q

Describe the pattern of pain with a gallbladder attack

A

Pain starts several hours after a meal and increases in severity for 15 minutes then plateaus for around 6 hours
After this it improves as the gallstone dislodges

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6
Q

How would you diagnose gallstones?

A

Recurrent symptoms

US

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7
Q

How would you treat biliary colic?

A

Manage pain and other symptoms

Cholecystectomy

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8
Q

Give the components of bile

A 
70% bile salts and acids (amphiphilic components of cholesterol metabolism)
10% cholesterol
5% phospholipids
5% proteins
1% bilirubin
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9
Q

Give the percentage of conjugated and unconjugated bilirubin in the bile

A

98-99% conjugated

1-2% unconjugated

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10
Q

Why might cholesterol stones form?

A

Precipitated cholesterol due to:
Supersaturation
Not enough salts/ acids or phospholipids
Gallbladder stasis

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11
Q

How might bilirubin stones form?

A

Increased unconjugated bilirubin in bile is in anionic form due to low pH, binds to calcium ions to form calcium bilirubinate

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12
Q

How might brown stones form?

A

Bacteria such as E.coli bring in hydrolytic enzymes which hydrolyse conjugated bilirubin to unconjugated bilirubin and phospholipids to hydrolysed phospholipids which precipitate out

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13
Q

How can gallstones lead to acute cholecystitis?

A

Bile is not moving due to stone blocking the cystic duct and so acts as a chemical irritant
Mucosa in the walls starts secreting mucus and enzymes causing:
Inflammation
Distention
Pressure build-up

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14
Q

Give 3 types of bacteria that can cause acute cholecystitis

A

E.coli
Enterococci
Bacteroides fragilis
Clostridium

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15
Q

Describe the pattern of pain with acute cholecystitis

A

Pain may shift from midepigastric to R upper quadrant (dull achey pain) which may radiate to the shoulders
Positive Murphy’s sign

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16
Q

Describe what is meant by a positive Murphy’s sign

A

Pressure on the abdomen preventing abdo contents moving, patient takes a deep breath so the diaphragm pushes down on the gallbladder, if there is pain then this is a positive Murphy’s sign

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17
Q

How might acute cholecystitis secondary to gallstones lead to sepsis?

A

Increased pressure compressed the blood vessels
Gallbladder ischaemia leads to gangrenous cell death, weakening the walls which may perforate, allowing bacteria into the blood

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18
Q

How can gallstones in the common bile duct cause jaundice?

A

Bile backs up into the liver and increases pressure in the bile duct
This forces bile into the blood through narrow cell junctions and therefore increases serum conjugated bilirubin

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19
Q

Why would you see an increase in alkaline phosphatase in acute cholecystitis?

A

ALP is an enzyme found in high amounts in the liver and bile ducts
It is released by dead cells due to damage

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20
Q

How would you diagnose acute cholecystitis?

A

US:
Gallbladder wall thickening
Sludge
Distention of the gallbladder/ bile duct

Endoscopic Retrograde Cholangiopancreatography (ERCP)

Cholescintigraphy: radiolabeled marker

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21
Q

How would you treat acute cholecystitis?

A

IV fluids
pain management
Abx
Cholecystectomy

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22
Q

Describe chronic cholecystitis

A

Repeated/ constant inflammation due to gall stones repeatedly lodging/ dislodging in the cystic duct, inflammation damages the gallbladder walls

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23
Q

Describe the damage to the mucosa as a result of chronic cholecystitis

A

Pockets of mucosa rather than smooth and flat

Rokitansky-Aschoff sinus

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24
Q

What changes occur to the gallbladder in chronic cholecystitis?

A

Gallbladder becomes more sensitive
Epithelial tissue of the gallbladder can undergo fibrosis and calcification leading to a “porcelain gallbladder” usually treated with a cholecystectomy

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25
Q

Describe ascending cholangitis

A

Inflammation of the bile ducts from bacteria that travel up the duct from the duodenum

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26
Q

Give the medical term for gall stones in the common bile duct

A

Choledocholithiasis

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27
Q

How might the flow of bile become blocked causing ascnding cholangitis?

A

Choledocholithiasis

Stricture due to cancerous growth or laparoscopic injury

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28
Q

Give the 3 bacterial causes of ascending cholangitis

A

E.coli
Klebsiella
Enterococcus

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29
Q

How might bacteria and bile in the bile ducts, from ascending cholangitis, enter the blood stream?

A

Spaces between cells due to high pressure from bile build-up allows bile and bacteria into the blood

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30
Q

Give the 3 symptoms in Charcot’s triad for ascending cholangitis

A

Fever
R upper quadrant pain
Jaundice

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31
Q

How would you diagnose ascending cholangitis?

A

Blood tests: evidence of infection, jaundice and shock
Imaging:
US
ERCP

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32
Q

How would you treat ascending cholangitis?

A

Manage symptoms: Abx and rehydration
Remove the obstruction: ERCP/ shockwave lithotripsy
Widen ducts: stent
Cholecystectomy

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33
Q

What is the exocrine function of the pancreas?

A

Secrete enzymes to break down proteins, lips, carbs

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34
Q

What is the endocrine function of the pancreas?

A

Alpha and beta cells secrete hormones into the bloodstream: insulin and glucagon

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35
Q

How does the pancreas protect itself from self-digestion?

A

Enzymes are produced as zymogens stored in vesicles with protease inhibitors

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36
Q

How can pancreatitis occur?

A

Zymogens become active in the small intestine by trips
If trypsinogen is activated early it can cause acute pancreatitis as a result of acinar cell injury and impaired secretion of proenzymes

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37
Q

What are the two leading causes of pancreatitis?

A

Alcohol: thickens pancreatic juices which form plugs that block ducts, juices back up
Gallstones: blocks release of pancreatic juices

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38
Q

Give 5 complications of pancreatitis

A 
Pancreatic pseudocyst
Pancreatic abscess
Haemorrhage from damaged blood vessels
Hypovolemic shock
DIC 
Acute respiratory distress syndrome
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39
Q

Give 5 signs and symptoms for the diagnosis of pancreatitis

A 
Hypocalcaemia: used up by fat necrosis
Bruising around umbilicus: Cullen's sign
Bruising along the flank: Grey Turner's sign
Epigastric pain radiates to back
Labs: Increased serum amylase and lipase
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40
Q

How would you treat acute pancreatitis?

A

Pain management
Hydration
Electrolytes
Rest of bowels

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41
Q

Give 2 key causes of chronic pancreatitis

A

Cystic fibrosis

Repeated bouts of acute pancreatitis

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42
Q

Describe chronic pancreatitis

A

Persistent inflammation leading to fibrosis, atrophy and calcification

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43
Q

How would you diagnose chronic pancreatitis?

A

XR/ CT: calcifications

ERCP of ducts

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44
Q

Describe the consequences of chronic pancreatitis including symptoms

A

Acinar cells are impaired: loss of digestive enzymes means trouble absorbing food/ fat
This causes weight loss
Fat soluble vitamin deficiencies
Steatorrhoea

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45
Q

Give the 3 enzymes involved in the metabolisation of alcohol in the hepatocytes and what is the product?

A

CP450
Alcohol dehydrogenase
Catalase
Product: Acetaldehyde

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46
Q

How do levels of NAD+ and NADH vary with alcohol metabolism and how does this affect fat production in the liver?

A

NAD+ –> NADH when alcohol is metabolised
An increase in NADH stimulates cells to make more fatty acids
A decrease in NAD+ levels leads to less fatty acid oxidation

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47
Q

How can high levels of acetaldehyde lead to alcoholic hepatitis?

A

It can bind to macromolecules, enzymes etc. and inhibit these molecules, forming acetaldehyde adducts
This leads to the destruction of hepatocytes by neutrophilic infiltration

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48
Q

Give 3 signs and symptoms of alcoholic liver disease

A 
Hepatomegaly 
Neutrophilic leukocytosis
Perivenular fibrosis
Enzymes leak out: high ALT and AST
Thrombocytopenia
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49
Q

How would you treat alcoholic liver disease?

A

Stop alcohol consumption

Corticosteroids- suppress the immune system

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50
Q

What is the normal function of stellate cells?

A

Store vitamin A in the liver

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51
Q

What happens when stellate cells are activated by paracrine factors secreted by injured hepatocytes in cirrhosis?

A

They lose vitamin A, proliferate and secrete TNF-beta

and produce collagen

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52
Q

Describe the problems that can be caused by compression of the central veins and sinusoids due to fibrotic tissue buildup in liver cirrhosis

A

Portal HTN meaning fluid in the vessels is more likely to be pushed into and across tissues into space leading to:

Portosystemic shunt, renal vasoconstriction and hepatorenal failure
Ascites
Congestive splenomegaly

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53
Q

Explain the consequences of decreased liver detoxification in cirrhosis

A

Toxins can enter the brain causing hepatic encephalopathy

In particular ammonia which is usually metabolised by the liver, can cause asterixis and coma

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54
Q

Explain the consequences of decreased oestrogen metabolism in liver cirrhosis

A

Increased oestrogen in the blood can cause:
Gynecomastia
Spider angiomata
Palmar erythema

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55
Q

Give 3 consequences of decreased liver function other than liver detoxification and oestrogen metabolism

A

Decreased bilirubin conjugation
Decreased albumin production
Decreased clotting factor production

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56
Q

Give 4 symptoms of extensive liver fibrosis

A

Jaundice and pruritus
Ascites
Hepatic encephalopathy- confusion
Easy bruising

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57
Q

How would you diagnose liver cirrhosis?

A 
Liver biopsy
Lab test:
Increased bilirubin
Increased enzymes
Thrombocytopenia
58
Q

How would you treat liver cirrhosis?

A

Treat the underlying cause

Transplant

59
Q

What are varices and what are they most commonly associated with?

A

Abnormally dilated vessels, most commonly associated with portal HTN

60
Q

What symptoms may present with varices?

A

Vomiting
Melena
Shock

61
Q

How would you diagnose varices?

A

Upper endoscopy

Labs: Decreased RBC count and platelets

62
Q

How would you treat oesophageal varices?

A

Therapeutic endoscopy

Vatical ligation or banding

63
Q

How does viral hepatic infection lead to liver damage?

A

MHC I presents the abnormal protein which attracts cytotoxic CD8+ T-cells causing cytotoxic killing and apoptosis

64
Q

Give 6 symptoms of viral hepatitis

A 
Fever
Malaise
Nausea
Hepatomegaly
Inflamed liver
Pain
65
Q

Which blood transaminases increase with viral hepatitis?

A 
Alanine aminotransferase (ALT)
Aspartate aminotransferase (AST)
66
Q

Why is jaundice a symptom of viral hepatitis?

A

Conjugated bilirubin leakage from ductules into the blood

Unconjugated bilirubin cannot be conjugated by dead hepatocytes so levels in the blood increase

67
Q

Why would you have dark urine with viral hepatitis?

A

High levels of soluble conjugated bilirubin in the urine

68
Q

Why are there high levels of urobilinogen in the urine with viral hepatitis?

A

Bilirubin is converted to urobilinogen in the gut which cannot be converted back to bilirubin/ bile by the liver and is therefore redirected to the kidneys and excreted

69
Q

What is the criteria for chronic hepatitis?

A

Greater than 6 months
Inflammation of the portal tract
Post necrotic cirrhosis

70
Q

What is the common group at risk of acquiring HepA?

A

Travelers

71
Q

Which antibody would be used in a HepA vaccination?

A

IgG antibody

72
Q

How is HepC transmitted?

A

Childbirth, IVDU, unprotected sex

73
Q

How might you test for HepC?

A

Enzyme immunoassay: HCV IgG
HCV RNA test (with PCR):
Early detection
Viral DNA in blood

74
Q

How is HepE transmitted?

A

Focal-oral: undercooked seafood/ infected water

75
Q

What is the risk with HepE during pregnancy?

A

Acute liver failure/ fulminant hepatitis

76
Q

How is HepB transmitted?

A

Childbirth, IVDU, sex

77
Q

Which types of antigens are targeted by IgG and IgM antibodies in HepB?

A

Surface antigen targeted by IgG

Core antigen targeted by IgM

78
Q

What is the difference between chronic “healthy” and chronic infective?

A

Chronic “healthy” is non-replicating and less contagious

Chronic Infective: Increase in post necrotic cirrhosis and increase risk of hepatocellular carcinoma

79
Q

Which strand of hepatitis must occur as a co-infection?

A

HepD with HepB

80
Q

How does cholera cause diarrhoea?

A

Gram neg. bacteria produces a toxin allowing Cl- into the lumen of the intestine and water follows by osmosis

81
Q

How does E.Coli 0157 bacteria cause damage?

A

Toxin attacks the lining of the colon causing liver and kidney damage

82
Q

Where is cryptosporidium commonly found and what is it resistant to?

A

Protozoa commonly found in calf/ lamb faeces

83
Q

Which antibiotics is C.diff associated with?

A

‘C abx’ e.g Clindamycin

84
Q

What is C.diff resistant to and how does it cause damage?

A

Resistant to chlorination and alcohol

Kills top layer of the gut lining which starts to slough off

85
Q

Where are the common places to acquire norovirus and at which time of year?

A

Hospitals, schools, cruise ships

Mainly during winter

86
Q

Give 6 symptoms of norovirus

A

Vomiting, diarrhoea, nausea, cramps, headaches, fever

87
Q

Describe the Bristol stool scale

A

1-7, 1: separate hard lumps, 3-4 is normal, 7:liquid

88
Q

Roughly how much copper do we consume in the diet each day and how much of this is needed?

A

Consume 1-2mg/day

Need about 0.75mg/day

89
Q

What happens to excess copper in the body?

A

90% bile (faecal copper)

10% urine

90
Q

In Wilson’s disease, what happens to excess copper in the body?

A

It is converted to Cu2+ + OH- + hydroxide free radical

91
Q

How is copper usually absorbed and exocytosed to bile?

A

Absorbed by enterocytes and carried to the liver where, though ATP7B, it either binds to ceruloplastimin or is packaged into vesicles for exocytosis to bile

92
Q

How does copper buildup inside the hepatocytes in Wilson’s disease?

A

There is an autosomal defect in the ATP7B gene meaning copper cannot bind to ceruloplastin or be packaged into vesicles, so it builds up and produces free radicals

93
Q

In Wilson’s disease, what can occur if copper deposits in the following locations:
Basal ganglia
Cerebral cortex
Descemet’s membrane

A

Movement disorder
Dementia
Kayser-fleishcher rings

94
Q

What would the blood test results be for Wilson’s disease?

A

Low ceruloplasmin

High free Cu in the blood and urine

95
Q

How would you treat Wilson’s disease?

A

Penicillamine (copper-chelating agent)
Meds to decrease Cu reabsorption
Liver transplant

96
Q

What is the key role of alpha-1 antitrypsin?

A

Inhibiting the action of elastase on elastin

97
Q

Give 4 symptoms of alpha-1 antitrypsin deficiency in the lungs

A

SOB, wheezing, mucous production, cough

98
Q

Give 5 signs and symptoms of alpha-1 antitrypsin deficiency in the liver

A

Inability to make coagulant factors, buildup of toxins, oesophageal variecs (portal HTN), hepatocellular carcinoma, jaundice

99
Q

How would you diagnose alpha-1 antitrypsin deficiency?

A

CXR/ CT: hyperinflation/ damaged tissue
Pulmonary function
Blood test
If suspected cirrhosis: liver US/ biopsy

100
Q

How would you treat alpha-1 antitrypsin deficiency?

A 
Augmentation therapy 
IV infusion of normal A1AT protein: slows/ halts progression
Supplemental O2
Inhalers
Standard treatment for cirrhosis
101
Q

Where is the most common place for a liver malignancy to metastasise to?

A

Lungs

102
Q

Where do secondary hepatic tumours often originate from?

A

Colon
Pancreas
Lungs
Breast

103
Q

Give 5 causes of liver cirrhosis which can lead to malignancy

A 
Alpha-1 antitrypsin deficiency
Alcoholic hepatitis
Primary biliary cirrhosis
Haemachromatosis
HBV and HCV
104
Q

How can aspergillus moulds cause liver malignancy?

A

Toxins produced are metabolised in the liver and form a DNA adduct, causing a mutation in the P53 tumour suppressor gene

105
Q

What is Budd-Chiari syndrome?

A

Liver tumour has spread to portal and hepatic veins

The veins are blocked, increasing pressure in the portal system causing ascites and hepatomegaly

106
Q

What proportion of liver cancer is asymptomatic? Give 2 potential symptoms

A

1/3 asymptomatic
Fever
Abdominal pain

107
Q

What blood test results might you see with liver cancer?

A

High AFP (produced by tumour cells)
High ALP and GGT (liver enzymes released with damage)
High erythropoietin
High insulin-like GF

108
Q

How would you diagnose liver cancer?

A

CT/ US

Angiography to see tumour vascularity

109
Q

How would you treat liver carcinoma?

A

20% are surgically removable

Transplant

110
Q

Where are 95% of pancreatic tumours found?

A

Exocrine glands, mainly the epithelial cells lining the ducts

111
Q

Where are 5% of pancreatic tumours found?

A

Acinar cells

112
Q

Give 3 modifiable and 3 non-modifiable risk factors for pancreatic cancer

A

Smoking
Obesity
Diet high in red meat

Male
Afro-caribbean
>65y/o

113
Q

Give 3 diseases associated with pancreatic cancer

A

Diabetes
Chronic pancreatitis
Liver cirrhosis

114
Q

Give 2 genes which may predispose someone to pancreatic cancer

A

BRCA2

PALB2

115
Q

Give 5 symptoms of pancreatic cancer

A 
Nausea
Vomiting
Fatigue
Weight loss
Midepigastric pain: radiates to mid/ lower back, worse when lying flat
116
Q

What is Trousseau’s sign of malignancy?

A

Blood clots felt as small lumps under the skin

117
Q

What is Courvoisier sign in pancreatic cancer?

A

Gallbladder enlarged and palpable but not tender

118
Q

What problems may arise if there is a tumour in the head of the pancreas?

A

It may obstruct the common bile duct and cause obstructive jaundice

119
Q

Give 4 symptoms of obstructive jaundice

A

Loss of appetite
Darker urine
Lighter stools
Pruritis

120
Q

How would you stage pancreatic cancer?

A

1: <2cm
2: >2cm
3: grown into neighbouring tissue
4: metastases

121
Q

How would you treat pancreatic cancer?

A

Surgery and adjuvant chemotherapy

122
Q

Give 3 causes of ascites

A 
Low protein (can't pull fluid into vessels)
Local inflammation (= more fluid)
Low flow (fluid can't move through system therefore causing an increase in pressure)
123
Q

Give 2 causes of low protein which then causes ascites

A

Malnutrition

Hypoalbuminaemia

124
Q

Give 2 causes of local inflammation which then causes ascites

A

Peritonitis

Abdominal cancers

125
Q

Give 3 causes of low flow which then causes ascites

A

Cardiac failure
Cirrhosis
Constrictive pericarditis

126
Q

Give 3 features of ascites you may find on examination

A

Distended abdomen
Dull percussion
Scratching= jaundice

127
Q

How would you diagnose ascites?

A

Ascitic tap

USS

128
Q

What is the difference between transudate and exudate ascitic fluid and when would you find either one?

A 
Transudate (<30g/l)
Cirrhosis
Constrictive pericarditis
Cardiac failure
Hypoalbuminaemia

Exudate (>30g/l)
Malignancy
Peritonitis
Pancreatitis

129
Q

Give 2 causes of peritonitis

A

Bacteria: Gram +ve (Staph)

Gram -ve (Coliforms)

130
Q

How would you differentiate between parietal and visceral peritonitis?

A

Parietal (abdo wall)- well localised pain

Visceral (organs)- poorly localised

131
Q

Where would you get pain with peritonitis of the:
Foregut
Midgut
Hindgut

A

Epigastric
Periumbilical
Suprapubic

132
Q

Give 3 typical findings in a history of a patient with peritonitis

A

Sudden onset
Pain lying stil
Improve when apply pressure
Speedbumps hurt

133
Q

How would you diagnose peritonitis?

A

Bloods: signs of infection/ inflammation/ amylase/ low Hb
CXR: air under diaphragm = perforation
Abdo XR: foreign body/ intestinal block
CT: Ischaemia/ cancer

134
Q

How would you treat peritonitis?

A

ABC

Treat underlying cause

135
Q

What is an inguinal hernia and what is it associated with?

A

Fatty tissue/ bowel pokes through into your groin at the top of the inner thigh
Associated with ageing and repeated abode strain

136
Q

Which type of hernia is more common in men and which in women?

A

Inguinal: men
Femoral: women

137
Q

What is an umbilical hernia and how can it occur in neonates?

A

Fatty tissue/ part of bowel pokes through near naval

In neonates, the opening through which the cord passes may not seal properly after birth

138
Q

What is a hiatus hernia and what symptom may it cause?

A

Part of the stomach pushes up through an opening in the diaphragm
Can cause heartburn

139
Q

If strangulation/ obstruction occurs due to a hernia which symptoms can it cause?

A

Sudden/ severe pain
Vomiting
Constipation

140
Q

How would you treat a hernia?

A

Surgery

Medicine Phase 2A (OWN) (10 decks)

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