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Sandra Phase 2a > Liver & Friends > Flashcards

Liver & Friends Flashcards

1
Q

What pathways can alcohol take once in the hepatocytes?

A

1.Involves enzyme alcohol dehydrogenase (ADH). Happens in the cytosol

2.Involves catalase in peroxisomes

3.Alcohol is converted by enzyme Cytochrome P450 2E1

=all pathways lead to the conversion of alcohol to acetaldehyde

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2
Q

Why is there an increase of NADH in the hepatocytes if someone drinks excessive amount of alcohol and what is the consequence of this

A

Once ADH enzyme is used to convert alcohol, it needs NAD+. This is then converted to NADH

As NADH levels increase, NAD+ levels decrease.

Effects:
1.Higher NADH levels tell cell to start producing more fatty acids
2.Lower NAD+ levels result in less fatty acid oxidation
=More fat production in the liver

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3
Q

What is excessive fat in the liver also known as

A

Fatty change/fatty liver

The liver becomes large, heavy, greasy, tender. Also yellowish in appearence due to fat deposits (Steatosis)

Other symptoms are not present

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4
Q

When alcohol dehydrogenase is converted to acetaldehyde what does it produce.

A

Reactive oxygen species e.g:
Hydrogen peroxide
Hydroxyl radical
Superoxide anion

Can react with DNA + proteins damaging cells

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5
Q

How are acetaldehyde adducts created?

A

Acetaldehyde binds to macromolecules, enzymes, cell membrane forming acetaldehyde adducts, inhibitng the cell.

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6
Q

What happens when acetaldehyde adducts are formed

A

Immune system recognises acetaldehyde adducts as foreign.

This means that hepatocytes get destroyed via neutrophil infiltration

Cells become inflamed and damged, patients have developed alcoholic hepatits

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7
Q

Histological appearence in a patient developing alcoholic hepatitis

A

Formation of mallory bodies: damaged intermediate filaments located in the cytoplasm

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8
Q

What can you find in someone with alcoholic liver disease

A

Perivenular fibrosis: Scar tissue around central veins

Hepatomegaly: Causing pain and enzymes to leak out (ALT,AST). More AST in hepatatis. Elevated ALP + GGT.

Neutrophilic leukocytosis

Thrombocyopenia

Hypoglycaemia

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9
Q

Treatment for alcoholic liver disease

A

Stop alcohol consumption

Corticosteroids: suppress immune system

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10
Q

Complications of alcohol-induced liver disease

A

Cirrhosis
Liver Failure

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11
Q

Diagnosis for alcohol-induced liver disease

A

Ultrasound
CT scan
MRI
Liver Function test

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12
Q

What is non-alcoholic fatty liver disease

A

Spectrum of diseases

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13
Q

What causes non-alcoholic fatty liver disease

A

Results from fat deposition in the

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14
Q

Who is affected by non-alcoholic fatty liver disease

A

Affects individuals with metabolic syndrome with 3 of 5 folowing diagnoses:

Obesity
Hypertension
Diabetes
Hypertriglyceridemia
Hyperlipidemia

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15
Q

What plays an important role in the development of non-alcoholic fatty liver disease

A

Insulin Resistance

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16
Q

Appearence of a fatty liver

A

Widespread steatosis
-Liver appears large
-Soft
-Yellow
-Greasy

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17
Q

Pathology of non-alcoholic fatty liver disease

A
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18
Q

Histological appearence of pateint with non-alcoholic fatty liver disease

A

Bloating/Dying hepatocytes

Mallory-Denk Bodies: tangles of intermediate filaments

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19
Q

How does fibrosis in the liver occur

A

Chronic steatohepatitis can cause stellate cells to lay down fibrotic tissue

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20
Q

What does fibrosis lead to?

A

Cirrhosis

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21
Q

Symptoms of non-alcoholic liver disease

A

+Because hepatocytes are being destroyed there can be an increase in liver enzymes:
Aspartate transaminase (AST)
Alanine transaminase (ALT)

Can also get increased ALT & sometimes AST

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22
Q

Diff of liver enzyme levels in non-alcoholic fatty liver disease vs. alcoholic fatty liver disease

A
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23
Q

Diagnosis of non-alcoholic fatty liver disease

A
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24
Q

Treatment for non-alcoholic fatty liver disease

A
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25
Q

Progression of non-alcoholic fatty liver disease

A
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26
Q

What is hepatitis

A

Inflammation of the liver

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27
Q

Lifecycle of Hepatitis A virus

A

Hepatitis A virus binds to receptors on hepatocytes and Kupffer cells entering via endocytosis.

The virus reproduces and exits via exocytosis

After exiting the cell the viral particles are secreted into bile and excreted via GI tract

Cells are recruited to liver. (See pic)

Immune cells are secreted against virus. B cells create IgM & IgG antibodies

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28
Q

What is the result of Hepatits A viral infection?

A

Liver Damage

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29
Q

On a biopsy what would liver damage look like

A

Ballooning hepatocytes
Councilman Bodies
Monocyte infiltration

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30
Q

Life cycle of hepatitis E

A

Life cycle unknown
Thought to be similar to Hepatitis A

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31
Q

What patients with Hepatitis E develop chronic disease

A

Immunocomprimised patients esp.Organ Transplant

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32
Q

Complications of hepatitis E

A
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33
Q

How long does infection of hepatitis A & E last

A

Last 2-4 weeks
Most infected individual recover

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34
Q

Diagnosis of Hepatitis A & E infection

A
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35
Q

Treatment for Hepatitis A & E

A
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36
Q

Prevention of Hepatitis A & E infection

A
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37
Q

What virus is Hep B virus

A

Hepadnavirus (DNA virus)

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38
Q

What virus is Hep D virus

A

Deltavirus (RNA virus)

Needs Hep B to replicate

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39
Q

What are sources of Hep B virus

A

Blood
Milk
Amniotic fluid
Vaginal secretions
Semen

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40
Q

Routes of transmission for the Hep B virus

A

Birth, placenta barrier

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41
Q

How is a Hep D virus disease only caused?

A

Active Hep B infection

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42
Q

Hep B virus summary

A
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43
Q

Hep D virus summary

A
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44
Q

Hep C virus summary

A
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45
Q

Hep A & E virus summary

A
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46
Q

What is autoimmune hepatitis

A

Resulting inflammation of liver tissue, because they’re being attacked by your own immune cells

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47
Q

Causes of autoimmune hepatitis

A

Unknown
Environmental triggers
Genetic predisposition: young women. F:M = 4:1

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48
Q

Other associations of Autoimmune hepatitis

A

Hashimoto’s thyroiditis
Graves’ Disease

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49
Q

Symptoms of Autoimmune hepatitis

A
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50
Q

Types of autoimmune hepatitis and diagnosis for them

A
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51
Q

Treatment for autoimmune hepatitis

A
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52
Q

What is liver cirrhosis

A

When the liver becomes seriously scarred + damaged to the point where it’s no longer reversible, at which point it becomes fibrotic. This is known as cirrhoisis

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53
Q

What is liver cirrhosis referred to as

A

“End-stage” liver damage

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54
Q

What are classic signs of cirrhosis

A

regenerative nodules
fibrosis

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55
Q

What cells mediate fibrosis

A

stellate cells

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56
Q

Complications of liver cirrhosis 1

A

Portal hypertension
Ascites
Congestive Splenomegaly
Hepatorenal failure
Coma
Asterixis

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57
Q

Complications of liver cirrhosis (2)

A
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58
Q

Symptoms of liver cirrhosis

A

Jaundice

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59
Q

Diagnosis of liver cirrhosis

A
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60
Q

Treatment of liver cirrhosis

A

Liver transplant
Treat underlying cause

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61
Q

What is acute liver failure/fulminant hepatic failure

A

When the liver loses function rapidly in some days/weeks

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62
Q

Complications of liver failure

A

Oedema
Jaundice
Coagulopathy
Encephalopathy

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63
Q

What causes acute liver failure

A

Due to extensive damge to liver cells

Can include:
1.Taking too much paracetemol
2.Usage of prescription medication: antibiotics, NSAIDs
3.Infected by hepatitis A,B,E
4.Epstein-Barr, Herpes simplex viruses, cytomegalovirus
5.Autoimmune disease
6.Fatty liver
7.Wlson’s disease
8.Budd Chiari-syndrome

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64
Q

Symptoms of acute liver failure

A

1.Nausea & vomiting
2.Jaundice
3.Sleepiness
4.Pain in upper right abdomen
5.Tremors
6.Confusion
7.Abdominal swelling
8.Yellowing of the eyes
9.Skin become tender

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65
Q

Diagnosis of liver failure

A

CT scan
Ultrasound
MRI

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66
Q

Treatment for acute liver failure

A

Liver transplant
Medications to reverse poisoning

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67
Q

Causes of chronic liver failure

A

Alcoholic liver Disease
Viral Hepatitis
NASH

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68
Q

What is jaundice?

A

Yellowing of the skin and conjuctiva. Jaundice is caused by elevated serum bilirubin levels.

Jaundice is only detected when serum bilirubin levels are greater than 2mg/dL

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69
Q

What is the earliest sign of jaundice and increased bilirubin in blood

A

1.Looking at sclera of eyes

2.Looking at skin

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70
Q

What are two types of disorders that have increased unconjugated bilirubin and similar presentation of jaundice

A

Extravascular haemolytic anaemia

Ineffective haematopoesis

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71
Q

Breakdown of Hb

A

1.Blood cells near end of lifespan (120 days) are phagocytosed by macrophages in the reticuloendothelial system

  1. Haemglobin if broken down into heme and globin. Globin is further broken down into amino acids. Heme is broken down into iron and protoporphyrin.
  2. Protoporphyrin is converted into UCB

4.Albumin binds to UCB (lipid soluble) and taken up by hepatocytes

5.UCB is conjugated by enzyme uridine glucuronyl transferase (UGT) into conjugated bilirubin.

6.Conjugated bilirubin is secreted out the bile canaliculi where it drains into the bile ducts and sent to gallbladder for storage as bile

7.When food is ingested, the gallbladder secretes bile and CB, it moves through the common bile duct to the duodenum of the small intestine and is converted to urobiliongen (UBG) by intestinal microbes in the gut. Urobilinogen is reduced to stercobilin which is excreted. Urobilinogen is recycled into blood and spontaneously oxidise into urobilin and excreted or goes back to liver

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72
Q

Disorders with increased UCB

A

1.Physiologic jaundice of the newborn. Treatment: phototherapy
2.Dyserythropoesis
3.Extravascular haemolysis
4.intravascular haemolysis
5.Extravasation
6.Medications

Genetic defects:
2.Gilbert’s syndrome
3.Crigler Najjar syndrome

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73
Q

Disorders associated with increased CB

A

Intrahapatic causes:
Viral hepatitis
Alcoholic hepatitis
Non-alcoholic sigatohepatitis
drugs & toxins
sepsis
TPN
Post operative patients

Post hepatic causes:
Gall bladder carcinoma
Cholelithcasis
Parasites
Lymphoma
Pancreatic tumour
ERCP

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74
Q

Jaundice with increased CB & UCB

A

Viral hepatitis

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75
Q

Investigations for jaundice

A

Initial Investigations:
Liver Function Test: Bilirubin, Albumin
INR

Jaundice with UCB:
LFT is not deranged. Consider haemolytic screen:
FBC
Blood Film
Reticulocytes
Haptoglobin
LDH
Coombs test

Jaundice with CB intrahepatic:
AST & ALT elevated
If liver injury hepatitis screen

Jaundice with CB obstructive:
ALP is elevated
Need imaging

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76
Q

In obstructive jaundice where would gallstones be located?

A

In the common bile duct.

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77
Q

What is pre-hepatic jaundice?

A

When a condition or infection speeds up the breakdown of red blood cells. This causes bilirubin levels in the blood to increase, triggering jaundice.

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78
Q

What conditions can cause pre-hepatic jaundice?

A

Malaria, sickle-cell anaemia, thalassaemia.

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79
Q

What is intra-hepatic jaundice?

A

When there is a problem in the liver – for example, damage due to infection or alcohol, this disrupts the liver’s ability to process bilirubin.

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80
Q

What can cause intra-hepatic jaundice?

A

HepatitisA/B/C, alcoholic liver disease, Gilbert’s syndrome, drug misuse.

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81
Q

What is Gilbert’s syndrome?

A

A genetic syndrome where the liver has problems breaking down bilirubin at a normal rate. The conjugated bilirubin is normal but the unconjugated bilirubin levels will be elevated.

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82
Q

What is post-hepatic jaundice?

A

When the bile duct system is damaged, inflamed or obstructed, which results in the gallbladder being unable to move bile into the digestive system.

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83
Q

What can cause post-hepatic jaundice?

A

Gall stones, pancreatic cancer, gallbladder cancer, pancreatitis

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84
Q

What is Wernicke’s encephalopathy

A

Acute and reversible encephalopathy due to deficiency of thiamine (Vitamin B1)

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85
Q

Risk Factors of Wernicke’s encephalopathy

A

Patients with poor nutritional absorption, intake or loss
1. Chronic alcoholism
2. Anorexia nervosa
3. Hyperemesis
4. Prolonged fasting/starvation
5. GI surgery
6. Systemic malignancy
7. Transplantation
8. AIDS

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86
Q

Symptoms of Wernicke’s Encephalopathy (WE)

A

Triad of Symtpoms (CAN)
Confusion (Encephalopathy): Profound disorientation, indifference, inattentiveness

Ataxia: Stance and gait, polyneuropathy, cerebellar involvement

Oculomotor dysfunction Nystagmus:

Other:
Coma
Hypotension
Hypothermia

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87
Q

Treatment for Wernicke’s Encephalopathy

A

IV thiamine
DO NOT administer glucose BEFORE thiamine can worsen WE

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88
Q

Complication of Wernicke’s encephalopathy

A

Korsakoff’s syndrome: chronic condition that is a consequence of Wernicke’s encephalopathy

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89
Q

What is Korsakoff’s syndrome

A

chronic condition that is a consequence of Wernicke’s encephalopathy.

Neurological Disorder with a thiamine deficiency

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90
Q

Symptoms of Korsakoff syndrome

A

Amnesia
Confabulation

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91
Q

What are examples of bilary tract diseases

A

Biliary colic
Cholecystitis
Ascending cholangitis

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92
Q

When does bilary colic (“gallbladder attack”) happen

A

When gallstones get lodged in the bile ducts causing temporary severe abdominal pain

Usually after a fatty meal

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93
Q

Risk Factors for developing gallstone

A

4 F’s
Female sex
Age- Forty
Obesity- Fat
Pregnancy - Fertile

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94
Q

Clinical Presentation of biliary colic

A
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95
Q

Complication of biliary colic

A

If gallstone stays in the cystic duct for longer stretches, can lead to acute cholecystitis or inflammation

Can also lead to fever

96
Q

Diagnosis of biliary colic

A

Based on recurrent symptoms
Confirmed by ultrasound

97
Q

Treatment for biliary colic

A

Manage pain & other symptoms
Cholecystectomy

98
Q

What is cholecystitis

A

Inflammation of the gallbladder because of an obstruction of the cystic duct by a gallstone

Most common complication of cholelithiasis (formation of stones in the gallbladder)

99
Q

Define the following terms:
1.Cholelithiasis
2.Choleoocholithiasis

A

1.Cholelithiasis: Formation of stone in the gallbladder
2.Choleoocholithiasis: Formation of stone in common bile duct

100
Q

What is the difference between the bilary tract diseases:
1.Biliary Colic
2.Acute cholecystitis
3.Cholangitis

A

1.Biliary Colic: temporary obstruction of the gallstone at the neck of the gallbladder

2.Acute cholecystitis: Gallstone stuck at the cystic duct causing inflammation of the gallbladder

3.Cholangitis: Complication of gallstones where infection develops in the common bile duct. This is life threatening

101
Q

Signs and synptoms of acute cholecystitis

A

Fever
Nausea
Vomiting
RUQ pain
Pain which may radiate to right side

102
Q

Examination of acute cholecystitis

A

Postive Murphy’s sign

103
Q

What is Murphy’s sign

A

Where a hand is placed at the mid-inferior border of the liver.
The patient is then asked to take a deep breath in. The diahragm lowers during inspiration and with the hand being placed where it is this will irritate the gallbladder as the diaphtagm pushes the gallbladder down.

104
Q

Diff between bilary tract diseases regarding: Pain, Fever, Jaundice

A
105
Q

Complications of acute cholecystitis

A

Gallbladder Carcinoid
Chronic cholecystitis
Mucocele
Empyema
Mirizzi’s syndrome
Perforation
Gallstone ileus at the terminal ileum
Pancreatitis
Bile backflow -> Obstructive Jaundice

106
Q

What is Courvoisier’s Law

A

Presence of enlarged gallbladder and painless jaundice is u likely due to gallstones rather carcinoma of the head of the pancreas

107
Q

Investigations for acute cholecystitis

A

Ultrasound is diagnostic

108
Q

Management for acute cholecystitis

A

Surgery is only done for symptomatic patients

Nill by mouth, IV antibiotic and pain relief is given before surgery

Surgery: Laprocopic cholecystectomy -> Open cholecystectomy

109
Q

Chronic cholecystitis vs Acute Cholecystitis

A

Acute: Stone lodged in cystic duct/common bile duct -> acute inflammation. 90% is resolved within 1 month

Chronic: Obstruction of cystic duct -> inflammation of gallbladder wall. Constant state of inflammation

110
Q

What is the result of chronic inflammation in chronic cholecystits

A

Changes gallbladder wall
gallbladder is sensitive -> Pain after meals

Pain is felt in RUQ and right scapula and shoulder

111
Q

Complication of chronic cholecystitis

A

Porcelain gallbladder
Increase risk of gallbladder cancer

112
Q

Treatment for chronic cholecystitis

A

Cholecystectomy

113
Q

What is ascending cholangitis?

A

Acute infection of the bile duct caused by intestinal bacteria ascending from the duodenum

114
Q

Why does flow of bile become blocked in ascending cholangitis

A

Choledocholithiasis
Stricture

115
Q

Complications of ascending cholangitis

A

Septic shock

116
Q

Signs and symptoms of Ascending cholangitis

A

Charcot’s triad: RUQ pain, jaundice, fever/chills

Reynold’s pentad: Charcot’s triad + hypotension/shock, altered consciousness

117
Q

Diagnosis for ascending cholangitis

A

Blood tests: evidence of infection, jaundice or shock

Medical Imaging: ultrasound, endoscopic retrograde cholangiopancreatography (ERCP)

118
Q

Treatment for ascending cholangitis

A
119
Q

What are cholestatic liver diseases

A

Primary sclerosing cholangitis
Primary biliary cholangitis

=both lead to cirrhosis and liver failure

120
Q

What is primary sclerosing cholangitis

A

Chronic, progressive condition characterised by inflammation and scarring of intrahepatic + extrahepatic bile ducts

121
Q

What is a charactersitc feature in the appearence of bile ducts in primary sclerosing cholangitis

A

Beads on a string appearance.

This is due to some parts of being unaffected

122
Q

Significance of primary sclerosing cholangitis

A

Prevalence 6/100,000
2:1 Male to Female
30-40 age peak
80% also affected by IBD (UC)

123
Q

Pathophisiology of primary sclerosing cholangitis

A
124
Q

Prognosis of primary sclerosing cholangitis

A

15 years from diagnosis

125
Q

Complications of primary sclerosing cholangitis

A
  1. Cholangiocarcinoma (1/5)
  2. Hepatocellular carcinoma
  3. Gallbladder malignancy
  4. Colorectal cancer
  5. Pancreatic cancer
126
Q

Signs and symptoms of primary sclerosing cholangitis

A
127
Q

Diagnosis of primary sclerosing cholangitis

A
128
Q

Treatment of primary sclerosing cholangitis

A
129
Q

What is primary biliary cholangitis

A

Chronic, progressive autoimmune condition leading to destruction of small intrahepatic bile ducts

130
Q

Significance of primary biliary cholangitis

A

Prevalence 35/100,000
9:1 Female to male

131
Q

Pathogenesis of primary biliary cholangitis

A

True autoimmune condition
-F>M
-Association with coeliac’s, Sjogren syndrome, thyroiditis

132
Q

Prognosis of primary biliary cholangitis

A

Slow progression/remission in some cases
Average survival 15-20y from diagnosis

133
Q

What are the complications of primary biliary cholangitis

A

1.Hepatocellular carcinoma
2.Osteoporosis

134
Q

Signs and symptoms primary biliary cholangitis

A
135
Q

Diagnosis of primary biliary cholangtitis

A
136
Q

Treatment of primary biliary cholangitis

A
137
Q

What is acute pancreatitis

A

Acute inflammation of the pancreas

10-25% mortality

138
Q

Functions of the pancreas

A

Endocrine (release into blood)
-Insulin
-Glucagon
-Somatostatin

Exocrine (Secretion via duct)
-Pancreatic Juice: Bicarbonate - neutralises acid. Digestive enzymes - trypsinogen , elastase, lipase, amylase

139
Q

Pathophisiology of acute pancreatitis

A

Early Activation -> Inflammation -> Oedema -> Vascular Compromise -> Ischaemia -> Necrosis

1) Mild/Interstitial pancreatitis: Inflammation due to cell injury
2) Severe/necrotising pancreatitis: Predominantly necrosis

140
Q

Acute pancreatitis causes

A

I - idipoathic
G - gallstones (Most common)
E - ethanol (alcohol)
T - trauma
S - steroids
M - microbiological (Mumps, hepatitis, TB)
A - Autoimmune
S - scorpion stings
H - Hypercalcemia, hypertrigylceridemia
E - ERCP, emboli
D- Drugs: Diuretics, gliptins, opiates, VPA, oestrogen

141
Q

Signs and symptoms of acute pancreatitis

A
  1. Abdominal Pain: Epigastric with back radiation. “Band Like”
  2. Nausea + Vomiting
  3. Fever
  4. Loss of appetite
  5. Features of Gallstone disease
142
Q

Physical examination in acute pancreatitis

A
  1. Epigastric tenderness
    -Rebound tenderness
    -Guarding
  2. Distension
  3. Cullens/Gray Turner signs
    -retroperitoneal haemorrhage

Secondary manifestations
Hypovolemia/shock
ARDS
DIC
Multiorgan failure

143
Q

Diagnosis of acute pancreatitis

A

2/3 of:
1.Abdominal pain
2.Elevated lipase/amylase
3. Indicative imaging findings:
-US/CT
-Imaging more reliable after 48 hours

Other investigations:
Deranged liver function tests
Hypocalcemia - Fat necrosis -> Free fatty acid release -> Bind calcium
Hyperglycemia

144
Q

What is used to predict the severity of pancreatitis

A

Glasgow Imrie Score: (PANCREAS)

145
Q

What is used to predict the severity of pancreatitis

A

Glasgow Imrie Score: (PANCREAS)

146
Q

Treatment of acute pancreatitis

A

Surgery is indicated in some cases:
1. Infected Pancreatic necrosis
2. Non resolving pancreatic pseudocyst
3. Abscess
4. Obstruction
5. Vascular complications
6. Diagnostic uncertainty

147
Q

What is chronic pancreatitis

A

Persistent, chronic inflammation of pancreas due to autodigestion -> irreversible injury of exocrine, endocrine pancreas

This leads to pancreatic insufficiency & difficulty producing hormones like insulin

148
Q

Causes of chronic pancreatitis

A
149
Q

Complications of chronic pancreatits

A

Pancreatic pseudocyst
Ascites
Pancreatic insufficiency
Diabetes Mellitus
Vitamins (ADEK) deficiency
Pancreatic cancer

150
Q

Signs and symptoms of chronic pancreatitis

A

Severe abdominal pain radiating to back
Nausea
Vomiting
Weight loss
Steatorrhoea
Oedema due to malabsorption

151
Q

Diagnosis of chronic pancreatitis

A

CT scan
Ultrasound
ERCP/MRCP
Mildly elevated serum amylase,alkaline, phosphatase, bilirubin

152
Q

Treatment for chronic pancreatitis

A
153
Q

What is ascites?

A

Abnormal build up of fluid in the peritoneal cavity. Specific 25ml <=

154
Q

What is ascitic fluid made up of

A

Proteins (Albumin)
Lipids
Bile Acids
WBCs

155
Q

What is SAAG

A

Serum Ascites Albumin Gradient (SAAG)

Test where we compare the albumin conc in the ascitic fluid with the albumin conc in the serum of the patient

SAAG = Serum Albumin conc - Ascites Albumin conc

High SAAG: >=1.1mg/dL
Low SAAG: <=1.1mg/dL

Useful as it shows whats occuring with the Starling forces bewtween the ascitic fluid and the serum. It shows us whether the imbalance is due to hydrostatic pressure imbalance or oncotic pressure imbalance which are caused by different pathophisiology.

156
Q

Ascites pathophisiology

A

Ascites with a high serum ascites albumin gradient tells us that fluid is being pushed out of circulation causing an increase in the conc of albumin in the serum because albumin is normally too large to pass through the peritoneum. While the conc in the ascitic fluid is low. Therefore this is a hydrostatic pressure imbalance

Ascites with low serum ascites gradient. Conc of albumin in the ascitic fluid and in serum are similar meaning that the peritoeum is more permeable than usual allowing albumin to pass through. This is an oncotic pressure imbalance

157
Q

Signs and symptoms of ascites

A
158
Q

Diagnosis of ascites

A
159
Q

Treatment for ascites

A
160
Q

What is hepatic encephalopathy

A

Decline in brain function that occurs as a result of liver failure

161
Q

Pathophisiology of hepatic encephalopathy?

A
162
Q

What are the causes of hepatic encephalopathy

A
163
Q

What are the stages of hepatic encephalopathy

A

West Haven criteria

164
Q

What are the signs and symptoms of hepatic encephalopathy

A
165
Q

Diagnosis of hepatic encephalopathy

A
166
Q

Treatment of hepatic encephalopathy

A

Depends on type of hepatic encephalopathy

Grade 3/4 -> Airway protection due to loss of gag reflex
Type A (Acute) : Even Grades 1/2 may require a liver transplant
Type B (Shuntig) : Often resolves spontaneously. Lactulose, rifaximin, vancomycin
Type C (chronic) : Find underlying cause. Often infection

167
Q

What is portal hypertension

A

Elevated bp in the portal system
Portal hypertension = 5mmHg MORE than inferior vena cava

Normal Range: 5-10 mmHg

168
Q

Causes of portal hypertension

A

Portal hypertension happens when blood flow from the portal system to inferior vena cava meets resistance

Can be broken down into:
1.Prehepatic
2.Intrahepatic
3.Posthepatic

169
Q

Prehepatic portal hypertension causes

A

Portal vein thrombosis
Splenic vein thrombosis
AV malformation
Splenomegaly

170
Q

Intrahepatic causes of portal hypertension

A

Cirrhosis: Alcohol, viral hepatitis, metabolic (Haemachromatosis, Wilson’s NAFLD/NASH)

Primary sclerosing cholangitis

Schistosomiasis

Nodular regenerative hyperplasia

171
Q

Posthepatic causes of portal hypertension

A

IVC obstruction
Right sided heart failure
Budd Chiari syndrome

172
Q

Signs and symptoms of portal hypertension

A
173
Q

Complications of portal hypertension

A

1.Variceal Rupture - bleeding
2.Hepatic encephalopathy
3.Ascites
- Spontaneous bacterial peritonitis
- Hepatorenal syndrome

174
Q

Diagnosis of portal hypertension

A
175
Q

Treatment for portal hypertension

A
  1. Treat underlying cause

2.Reduce portal pressure
-Transjugular intrahepatic portosystemic shunt (TIPS)

  1. Prevent complications
    -Bleeding: beta blockers, nitrates, terlipressin. Variceal ligation
    -Hepatic encephalopathy
    -Ascites: Symptatic relief, salt reduction, diuretics, paracentesis
176
Q

What is spontaneous bacterial peritonitis

A

Ascitic fluid infection

Most common bacterial infection in patients with cirrhosis
Has poor prognosis if missed

177
Q

Clinical presentation of spontaneous bacterial peritonitis (FBI)

A

Fever
Belly Pain
Increasing Ascites

178
Q

Pathogenesis of spontaneous bacterial peritonitis

A

Spread of intestinal bacteria into the portal circulation and then ascitic fluid

Most common pathogen is E.Coli

Liver cirrhosis predisposes people to bacterial translocation due to:
1. Bacterial overgrowth
2. Intestinal permeability
3. Acquired Immune deficiency

179
Q

Risk Factors for Spontaneous Bacterial Peritonitis

A

Varices
Advanced cirrhosis
Prior SBP
Malnutrition
Usage of proton pump inhibitor

180
Q

Investigations for spontaneous bacterial peritonitis

A
181
Q

Diagnosis of spontaneous bacterial peritonitis

A

+ SAAG score

182
Q

Management of spontaneous bacterial peritonitis

A

Ceftriaxone
Albumin
Trimethoprim

183
Q

Metabolic liver disease examples

A
  • Haemochromatosis
  • Wilson’s disease
  • Alpha 1 antitrypsin deficiency
184
Q

What is haemochromatosis

A

metabolic disorder where the body absorbs too much iron in the body - iron overload

185
Q

Pathology & Cause of haemochromatosis

A
186
Q

Types of haemochromatosis

A

1.Primary (hereditary: autosomal recessive)

2.Secondary (not genetic):
Multiple blood transfusions
Chronic haemolytic anaemias
Excessive iron intake

187
Q

Complications of haemochromatosis

A
188
Q

Signs and symtpoms of haemochromatosis

A
189
Q

Diagnosis of haemochromatosis

A

Lab Results:
High levels of serum iron
Elevated ferritin
High transferrin saturation
Decreased total iron binding capacity

Liver Biopsy

190
Q

Treatment of haemochromatosis

A

Deferoxamine
Surgery: Advanced liver damage -> transplantation
Phlebotomy

191
Q

What is Wilson’s disease

A

Wilson’s disease or hepatolenticular degeneration is a rare autosomal recessive inherited disorder of copper metabolism characterised by excessive deposition of copper in the liver, brain and other tissues

192
Q

Pathogenesis of Wilson’s disease

A

The transport of copper by the P-type ATPase is defective due to one of several mutations (>300 identified) occurring within the ATP7B gene

This gene has been mapped to chromosome 13q14.3

Intestinal copper absorption and transport into the liver are intact, whilst incorporation into caeruloplasmin and excretion into bile are impaired

193
Q

Diagnostic tests of Wilson’s disease

A
194
Q

Management of Wilson’s disease

A
195
Q

Clinical Features of Wilsons disease

A
196
Q

What is alpha-1 antitrypsin deficiency (liver)

A

Genetic condition where the alpha-1 antitrypsin gene is defective

197
Q

Clinical presentation of alpha-1 antitrypsin deficiency

A
198
Q

Dignosis of alpha-a antitrypsin deficiency

A

Cirrhosis
-Liver Ultrasound
-Liver biopsy: Period Acid Schiif (PAS+). Diastase Resistant

199
Q

Treatment for alpha-1 antitrypsin deficiency

A

Augmentation therapy
-IV infusion of normal A1AT protein
Slows or halts progression of disease

Standard treatments for cirrhosis

200
Q

Pathology of alpha 1 antitrypsin deficiency

A

Misfolded alpha 1 antitrypsin builds up, killing hepatocytes and leading to cirrhosis

201
Q

Hepatobiliary cancers examples

A

Pancreatic cancer (including Courvoisier’s sign)

Hepatocellular carcinoma

Cholangiocarcinoma

202
Q

Pathology and causes of pancreatic cancer

A

Highly lethal malignancy of exocrine pancreas

Usually unresectable at presentation

203
Q

Risk Factors for pancreatic cancer

A
204
Q

Symptoms of pancreatic cancer

A
205
Q

Diagnosis of pancreatic cancer

A

Medical imaging + biopsy confrim diagnosis

Staging depends on: Size & location
1. less than 2cm
2. greater than 2cm
3. grown into neighbouring tissue
4. metastatic ~ spreads through blood & lymph

206
Q

Treatment for pancreatic cancer

A
207
Q

Pathology and causes of hepatocellular carcinoma

A

Hepatic malignancy commonly disagnosed in presence of chronic liver disease

208
Q

Signs and symptoms of hepatocellular carcinoma

A
209
Q

Risk Factors for developing hepatocellular carcinomas

A
210
Q

Complications of hepatocellular carcinoma

A

Paraneoplastic syndrome
Extrahepatic metastasis

211
Q

Hepatocellular carcinoma aetiology

A
212
Q

Diagnosis for hepatocellular carcinoma

A

Ultrasound with biopsy, CT scan, MDCT, arteriography, portography, MRI:
Tumour visulaisation, histopathological analysis, grading, TNM staging, potential for resection

MRI angiography

Elevated alpha-fetoprotein (most common serum marker)

213
Q

Treatment for hepatocellular carcinoma

A
214
Q

Pathology and causes of cholangiocarcinoma

A
215
Q

Types of cholangiocarcinoma

A
216
Q

Risk Factors for cholangiocarcinoma

A

Primary:
Existing liver/gallstone disease, PSC, chronic liver disease

Congenital abnormalities of biliary tree
Genetic disorders
Obesity
Liver Fluke infection
Increasing age

217
Q

Signs and symptoms of cholangiocarcinoma

A

Abdominal pain
Fatigue
Unintended weight loss
Intensely itchy skin
Jaundice
Changes in colour of stool/urine

218
Q

Diagnosis of cholangiocarcinoma

A
219
Q

Treatment for cholangiocarcinoma

A
220
Q

Paracetemol toxicity pharmacology

A
221
Q

Clinical Presentation of paracetemol toxicity

A
222
Q

Treatment for paracetemol overdose

A
223
Q

Diagnosis of paracetemol overdose

A

+ bilirubin, lipase
- PTT, INR
+BUN, creatinine, ammonia
-Glucose

224
Q

What is Gilbert’s syndrome

A

Benign, genetic condition involving recurrent episodes of jaundice.

It is an unconjugated hyperbilirubinemia

225
Q

Causes of Gilbert syndrome

A

Autosomal dominant/recessive condition
-70% of cases caused by mutation in UGT gene

Caused by a mild decrease in activity of UDP

226
Q

Clinical Presentation of Gilbert syndrome

A
227
Q

Treatment and Diagnosis for Gilbert syndrome

A
228
Q

Diif types of hernias

A
  • Inguinal
  • Femoral
  • Umbilical
  • Incisional
  • Epigastric
  • Hiatal
229
Q

Inguinal hernias

A

INGUINAL HERNIA
Protrusion of abdo contents through inguinal canal

Patho
Both direct/indirect present above + medial to pubic tubercle (mostly)
- Direct – 20%, medial to inferior epigastric artery, enters inguinal canal through weakness in posterior wall, rarely strangulates
- Indirect – 80%, lateral to inferior epigastric artery, enters inguinal canal through deep inguinal ring, can strangulate

RFs (risk factors)
Male, chronic cough, heavy lifting, past abdo surgery

Px
Swelling in groin/scrotum
Maybe painful – ‘dragging’ sensation (pain tends to indicate strangulation)
Impulse – swelling increase on coughing
May be reducible

Ix
Clinical dx
Imaging if in doubt (USS/CT/MRI)

Mx
If small, reassure
Surgery (if strangulated, urgent referral)
Truss

230
Q

Femoral hernia

A

FEMORAL HERNIA
Bowel comes through femoral canal

Patho
Likely to be irreducible and strangulate – due to rigidity of canal’s borders

Px
Mass in upper medial thigh
Neck of hernia inferior and lateral to pubic tubercle (inguinal hernias are superior and medial to this point)
May be cough impulse

Ix
Clinical dx
Imaging if in doubt (USS/CT/MRI)

Mx
Surgical repair

231
Q

Umbilical hernia

A

At umbilicus

232
Q

Hiatal hernia

A

HIATUS HERNIA
Herniation of stomach through oesophageal aperture of diaphragm

Patho
- Sliding – (80%), GOJ (gastroesophageal junction) and part of stomach slides up into chest, acid reflux often, LOS (lower oesophageal sphincter) less competent
- Rolling – (20%), GOJ remains in abdo, part of fundus rolls up through hiatus, LOS intact, reflux uncommon

RFs
Obesity, female, pregnancy, ascites, advanced age, skeletal deformities (scoliosis, kyphosis)

Px
Heartburn, especially on lying/bending
GORD
Dysphagia

Ix
CXR
Barium swallow – dx
Upper GI endoscopy if indicated
Oesophageal manometry (mostly used when surgery is being considered)

Mx
Lose weight
PPI
Surgery to prevent strangulation – indications: therapeutic regimes not working, resp complications of reflux, eg asthma

233
Q

Incisional hernias

A

Tissues or organs protrude through the site of an incision or a scar, which has caused a weakness in the underlying muscle.

234
Q

Epigastric hernias

A

through linea alba above umbilicus

235
Q

What is the treatment for hernias

A

Surgery

Sandra Phase 2a (17 decks)

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