Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Phase 2a Sheffield Medicine > Liver > Flashcards

Liver Flashcards

1
Q

What are the 4 functions of the Liver?

A
  1. Glucose and fat metabolism
  2. Detoxification and excretion
  3. Protein synthesis e.g. albumin and clotting factors
  4. Defence against infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Where is most of the blood supplied to from the liver?

A

The portal vein.

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

What are the 3 Liver function tests?

A
  1. Serum bilirubin
  2. Serum albumin
  3. Pro-thrombin time
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the 4 fat soluble vitamins?

A

ADEK

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

Give an example of a transamine?

A

AST and ALT

They increase in hepatocellular disease

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

When does Alkaline phosphatase increase in the serum?

A

In cholestatic (duct and obstructive) disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is budd chiari syndrome?

A

Vascular disease associated with occlusion of hepatic veins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are some pathological changes in the liver associated with excessive alcohol consumption?

A
  1. Fatty liver
  2. Alcoholic hepatitis
  3. Cirrhosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What condition is associated with the liver and oedema?

A

Hypoalbuminaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the causes of haemolytic anaemia?

A
  1. Sickle cell disease
  2. Hereditary spherocytosis
  3. GP6D Deficiency
  4. Hypersplenism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is ascites?

A

An accumulation of fluid in the peritoneal cavity that leads to abdominal extension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the signs of ascites?

A
  • Flank swelling

- Dull to percuss and shifting dullness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the pathological causes of Ascites?

A
  1. Local inflammation e.g. peritonitis
  2. Leaky vessels e.g. imbalance between hydrostatic and oncotic pressures
  3. Low flow e.g. cirrhosis, thrombosis and heart failure
  4. Low protein e.g. hypalbuminaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the physiological factors that contribute to ascites?

A
  • High portal venous pressure

- Low serum albumin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe the pathogenesis of ascites

A
  1. Increased intrahepatic resistance causes portal hypertension –> Ascites
  2. Systemic vasodilation leads to RAAS, NAd and ADH secretion –> Fluid retention
  3. Low serum albumin also causes ascites
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What investigation would you use in ascites?

A
  • Ultrasound

- Ascitic tap – important to rule out bacterial peritonitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What would be the management of ascites?

A
  • Fluid and salt restriction
  • Diuretics – spironolactone
  • Large volume paracentesis and albumin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the two different types of ascites?

A

Exudative ascites

Transudative ascites

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

What are Exudative ascites?

A

Increased vasc permeability to infection; inflammation or malignancy

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

What are transudative ascites?

A

Increased venous pressure due to cirrhosis, cardiac failure or hypoalbuminaemia

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

If neutrophils are present in ascites, what is this indicative of?

A

Spontaneous bacterial peritonitis

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

What is chronic liver disease?

A

A wide range of conditions affecting the liver characterised by disease of over 6 months and progressive destruction of the liver.

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

What are the causes of Chronic liver disease?

A
  1. Alcohol
  2. Non-Alcoholic fatty liver disease (NAFLD)
  3. Viral Hep (B,C,E)
  4. AI diseases
  5. Metabolic e.g. haemochromatosis
  6. Vascular e.g. budd-chiari
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the signs of chronic liver disease?

A
  1. Ascites
  2. Oedema
  3. Malaise
  4. Anorexia
  5. Bruising
  6. Itching
  7. Clubbing
  8. Palmar erythema
  9. Spider naevi
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the outcomes of chronic liver disease?

A
  1. Cirrhosis

2. Liver failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the management of chronic liver disease?

A

Dependent on the cause

  • Steroids, interferon, antivirals
  • Supportive therapy for complications – Albumin, vit K, diuretics
  • Possible transplant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What should you ask a patient with expected drug induced liver injury?

A

If they are on any medications or have began taking any new medications recently.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are drugs that can cause induced liver injury?

A
  • Co-amoxiclav
  • Flucloxacillin
  • Erythromycin
  • TB drugs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are drugs that do not cause induced liver injury?

A
  1. Low dose aspirin
  2. NSAIDs
  3. Beta blockers
  4. HRT
  5. CCB
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is Glutathione Transferase?

A

Mops up reactive intermediate of paracetamol and thus prevents toxicity and liver failure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What 4 features would you see in a paracetamol overdose?

A
  1. Metabolic acidosis
  2. Prolonged thrombin time
  3. Raised creatine (renal failure)
  4. Raised ALT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is the treatment for paracetamol overdose?

A

IV N-Acetyl-cysteine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are the symptoms of acute liver disease?

A
  • Malaise
  • Lethargy
  • Anorexia
  • Jaundice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are the causes of acute liver disease?

A
  1. Viral hepatitis
  2. Drug induced hepatitis
  3. Alcohol induced hepatitis
  4. Vascular
  5. Obstruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are the outcomes of acute liver disease?

A
  1. Recovery

2. Liver failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are the investigations in acute liver disease?

A

Blood test - prothrombin response time.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are the treatments in acute liver disease?

A

Dependent on the cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is hepatitis?

A

Inflammatory condition of the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

How long must hepatitis be present for it to become chronic?

A

6 months or more.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are the symptoms of acute hepatitis?

A
  1. General malaise
  2. Myalgia – pain
  3. GI upset
  4. Abdo pain
  5. Raised AST,ALT
  6. Possible jaundice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are the causes of acute hepatitis?

A
  1. Viral e.g. A,B,C,D,E
  2. Drug induced
  3. Alcohol Induced
  4. Autoimmune
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

How long does HBsAg be present in the serum post infection?

A

6-18 weeks.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

When could you detect Anti-HBV core (IgM)

A

Rises from 6 weeks and peaks at 18.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

How can you tell if a patient has been vaccinated or previously been accepted?

A

If they have anti-HBV’s IgC in their serum.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What are the infective causes of acute hepatitis?

A
  1. Hepatitis A to E infection
  2. EBV
  3. CMV
  4. Toxoplasmosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What are the non infective causes of acute and chronic hepatitis?

A
  1. Alcohol
  2. Drugs
  3. Toxins
  4. Autoimmune
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are the infective causes of chronic hepatitis?

A
  • Hep B +-D
  • Hep C
  • Hep E
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What are the complications of chronic hepatitis?

A

Uncontrolled inflammation –> Fibrosis –> Cirrhosis –> HCC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Is Hep A a DNA virus or RNA virus?

A

RNA virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

How can Hep A virus be prevented?

A

Vaccination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

How is Hep A transmitted?

A

Faeco-orally e.g. contaminated food and water

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

How can you diagnose Hep A?

A

Viral serology initally –> anti-HAV IgM then Anti-HAV IgG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is the management of Hep A?

A
  • Supportive
  • Monitor liver function to ensure no fulmiant hepatic failure
  • Manage close contacts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Is Hepatitis B an RNA or DNA virus?

A

DNA virus which replicates in hepatocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

How is Hep B transmitted?

A

Blood borne –> needle stick injury.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

How many cases of Hep B go onto chronic infection?

A

5%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What is the natural history of Hepatitis B?

A
  1. Immune tolerance phase –> unimpeded viral replication –> High HBV DNA levels
  2. Immune clearance phase –> IS wakes up, liver inflammation and high ALT
  3. Inactive HBV Carrier phase –> HBV DNA low, No inflammation and normal ALT
  4. Reactivation Phase –> ALT and HBV, DNA levels are intermittent and inflame is seen on liver due to fibrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What does HBV Trigger in the immune system?

A

Core proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

How would you diagnose HBV?

A

Viral serology –> HBV surface antigen from 6th week to 18th week or anti-HBV core IgM after 3 months.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

How would you manage Hepatitis B?

A
  1. Supportive
  2. Liver function monitoring
  3. Manage contacts
  4. Follow up at 6 months to see if HBV surface Ag has cleared –> if present chronic hepatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

How could you tell if someone has a chronic HBV?

A

A follow up appointment in 6 months to see if HBV surface antigen had cleared.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What are the consequences of chronic HBV infection?

A
  1. Cirrhosis
  2. HCC
  3. Decompensated cirrhosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

How can HBV infection be prevented?

A

Vaccination - inactivated HbsAg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What is the treatment for HBV?

A
  • Alpha interferon- boosts immune system

- Antivirals e.g. tenofovir –> inhibit viral replications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What are the side effects of alpha interferon?

A

Myalgia, malaise, lethargy, thyroiditis, mental health issues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Is Hepatitis C a RNA or DNA virus?

A

Blood borne RNA Virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

How much of Hep C passes on to be a chronic infection?

A

70%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What are the risk factors for HBV/HCV

A
  1. IVDU
  2. People who have required blood results
  3. Needles stick injuries
  4. Unprotected sex
  5. Materno-foetal transmission
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

How would you diagnose HCV?

A

Viral serology - presence of Anti-HCV and IgM/IgC RNA.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

How can you prevent HCV?

A
  1. Screen blood products
  2. Lifestyle modification
  3. Needle exchange
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Does HCV infection confer immunity?

A

No. There is no vaccine either.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What is the current treatment for HCV?

A

Direct acting antivirals e.g. NS5A and NS5B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Is Hep D an RNA virus or DNA virus?

A

RNA virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What does Hep D require to survive?

A

Hep B infection as it is protected by HbsAg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

How is Hep D caused?

A

Blood borne transmission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

How do you treat Hep D?

A

Get rid of Hep B.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

How is Hep E caused?

A

Faeco-oral RNA virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

When can Hep E be chronic?

A

In patients with compromised immune systems.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

How would you diagnose Hepatitis E?

A

Viral serology for initially anti-HEV IgM then Anti-HEV IgG.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What is the primary prevention for Hep E?

A

Good food hygiene and a vaccine is in development

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What are the symptoms of spontaneous bacterial peritonitis?

A
  • Dull to percussion
  • Temp
  • Abdo pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What are the causes of peritonitis?

A
  • Stomach ulcer
  • Infection
  • Abdo wound/injury
  • Cirrhosis of liver
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What investigations are necessary in peritonitis?

A
  • Blood tests – raised WCC, platelets, CRP, Amylase, reduced blood count
  • CXR – Look for air under the diaphragm
  • Abdo x-ray –> bowel obstruction
  • CT scan – inflammation, ischaemia, cancer
  • ECG - Epigastric pain could be related to heart
  • B-HCG –> Hormone secreted by pregnant women
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What are the complications for peritonitis?

A
  1. Hypovolaemia
  2. Kidney failure
  3. Systemic sepsis
  4. Paralytic ileus
  5. Pulmonary atelectasis (lung collapse)
  6. Portal pyaemia (pus in portal vein)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

How can the paralytic ileus cause resp problems?

A
  • Peristaltic Waves stop –> dilation of bowel –> distended abdo therefore increased pressure
  • Pushes on diaphragm –> respiration affected
86
Q

What is the management of peritonitis?

A
  1. ABC
  2. Treat underlying cause
  3. Call a surgeon
  4. Set up post-management
87
Q

What are the causes of liver failure?

A
  1. Infection e.g. viral hep b,c
  2. Induced e.g. alcohol, drug toxicity
  3. Inherited e.g. autoimmune
88
Q

What are the symptoms of liver failure?

A
  • Jaundice
  • Pain in URQ
  • Nausea/swelling
89
Q

What are the appropriate investigations in Liver failure?

A
  • FCB, WCC, CRP/ESR + Prothrombin time.
  • CT/MRI abdo
  • Liver biopsy
90
Q

What are the complications of Liver failure?

A
  1. Hepatic encephalopathy
  2. Abnormal bleeding
  3. Jaundice
  4. Ascites
91
Q

What is the management of liver failure?

A
  1. Nutrition
  2. Supplements
  3. Treat complications
  4. Liver transplant
92
Q

How is hepatic encephalopathy a complication of liver failure?

A
  • Liver can’t get rid of ammonia so ammonia crosses the BBB

- Cerebral Oedema

93
Q

Why are liver failure patients vulnerable to infection?

A
  1. Impaired reticulo-endothelial function
  2. Reduced opsonic activity
  3. Leukocyte function is reduced
  4. Permeable gut wall
94
Q

What are the prehepatic causes of jaundice?

A

unconjugated –> haemolysis, gilberts

95
Q

What are the hepatic causes of jaundice?

A

Conjugated –> Hepatitis, ischaemia, neoplasm, Drugs, cirrhosis

96
Q

What are the post hepatic causes of jaundice?

A

Conjugated –> Gallstones, bile duct, malignant, ischaemic, inflame, mirizzi stricture.

97
Q

What would the stools and urine look like in a pt with prehepatic jaundice?

A

Urine and stools are normal, no itching and LFT’s are normal

98
Q

What would the stools and urine look like in a pt with cholestatic jaundice?

A

Dark urine and pale stools, itching and LFT’s are abnormal

99
Q

What is raised conjugated bilirubin an indicator of?

A

cholestatic problem e.g. hepatic liver disease or bile duct obstruction.

100
Q

What investigations would be neccesary in Jaundice?

A
  • History
  • Urinalysis for bilirubin
  • LFTs
101
Q

What is the management of Jaundice?

A

Manage the underlying cause.

102
Q

What is cirrhosis of the liver?

A

A chronic disease of the liver resulting from necrosis of liver cells leading to fibrosis

Characterised by nodular regeneration

End result is impairment of hepatocyte function and distortion of liver architecture

103
Q

How is cirrhosis of the liver caused?

A
  1. Alcoholic
  2. Hep B and C
  3. Any chronic liver disease e.g. autoimmune, metabolic or vascular
104
Q

What are the symptoms of liver cirrhosis?

A
  • Fatigue
  • Easy bleeding/bruising
  • Jaundice and oedema
  • Loss of periods/sex drive
  • Confusion and slurred speech –> hepatic encephalopathy!
105
Q

What investigations should you order in liver cirrhosis?

A

LFT
INR –> blood ability to clot
Biopsy
Creatinine

106
Q

What are the risk factors of liver cirrhosis?

A

Obesity
viral hep
alcohol abuse

107
Q

What is the treatment of Liver cirrhosis?

A
  1. Deal with underlying cause
  2. Screening for HCC
  3. Consider transplant
108
Q

What is a consequence of hepatocyte regeneration in cirrhosis?

A

Neoplasia and thus HCC

109
Q

What are some common serious infections in those with liver cirrhosis?

A

Spontaneous bacterial peritonitis

Can also be caused by E.coli and S. pneumoniae

Can be diagnosed through looking for the presence of neutrophils in ascitic fluid

110
Q

What are gallstones made out of?

A

Cholesterol, phospholipid and bile pigment.

111
Q

What are the risk factors of gallstones?

A
  1. Female
  2. Obese
  3. Fertile
112
Q

What are the symptoms of gallstones?

A
  1. Pain in RUQ of abdo and centre
  2. Pain in right shoulder and between shoulder blades
  3. Nausea or vomiting
  4. Asymptomatic
113
Q

What are the complications of gallstones?

A
  1. Biliary pain
  2. Obstructive jaundice
  3. Cholangitis (infection of biliary tract)
  4. Pancreatitis
114
Q

What investigations should be ordered in gallstones?

A
  • Ultrasound

- ERCP

115
Q

What is the treatment for gallstones?

A
  • Laparoscopic cholecystectomy
116
Q

What is cholecystitis?

A

Inflammation of the gallbladder caused by blockage of the bile duct –> obstruction to bile emptying

117
Q

What are the symptoms of cholecystitis?

A
  1. RUQ pain
  2. Fever
  3. Raised inflammatory markers
  4. NO JAUNDICE
118
Q

What is the cause of cholecystitis?

A

blockage of the bile duct causing obstruction to bile emptying.

119
Q

What are the risk factors of cholecystitis?

A

Obesity and diabetes

120
Q

What are the investigations used in diagnosing cholecystitis?

A
  • FBC –> WCC look for infection
  • CRP/ESR –> inflammatory
  • HIDA scan
  • Abdo/endoscopic US
121
Q

What is the appropriate management for cholecystitis?

A
  • Fluids
  • Analgesia
  • ERCP procedure to remove stones.
  • Cholecystectomy = gallbladder removal.
122
Q

What is ascending cholangitis?

A

Obstruction of biliary tract causing bacterial infection  EMERGENCY!

123
Q

How is ascending cholangitis different from the presentation of cholecystitis?

A

It presents with jaundice!

124
Q

What are the symptoms of ascending cholangitis?

A

Charcot’s triad

  1. Fever
  2. RUQ
  3. Jaundice
125
Q

What investigations would you order in suspected ascending cholangitis?

A
  1. Ultrasound
  2. Blood tests -LFT
  3. ERCP – definitive investigation
126
Q

What is the appropriate treatment of ascending cholangitis?

A
  • IV Fluid
  • IV antibiotics e.g. Cefotaxime and metronidazole
  • ERCP to remove stone
  • Stenting
127
Q

What is the pathology of sclerosing cholangitis?

A
  • Inflammation of the bile duct  structures harden
  • Progressive obliterating fibrosis of bile duct branches
  • Leading to cirrhosis and liver failure.
128
Q

What are the symptoms of primary sclerosing cholangitis?

A
  1. Itching
  2. Rigor
  3. Pain
  4. Jaundice
  5. 75% have IBD
129
Q

What condition is associated with sclerosing cholangitis?

A

Reynolds pentad

130
Q

What is reynold’s pentad characterised by?

A
  • Charcot’s pentad
  • Hypotension
  • Altered mental state
131
Q

Are most liver cancers primary or secondary?

A

Secondary - from the GI tract, breast and bronchus

132
Q

What is Wernicke’s encephalopathy?

A

An acute neurological syndrome which is caused by a lack of thiamine presenting with a triad of symptoms.

133
Q

What is the cause of WE?

A

Lack of B1 seen in alcohol usage

134
Q

What are the symptoms of WE?

A
  1. Ataxia
  2. Ophthalmoplegia
  3. Confusion
135
Q

What are the investigations of WE?

A
  • Clinical history
  • MRI scan
  • LFTs
136
Q

What is the treatment of WE?

A

IV thiamine.

137
Q

What is alcohol liver disease associated with?

A

Macrocytic anaemia.

138
Q

What would be seen on a biopsy in alcohol liver disease?

A

Lots of mallory bodies.

139
Q

What are the symptoms of ARLD?

A
  1. Abdo pain
  2. Loss of appetite
  3. Fatigue
  4. Feeling sick/diarrhoea
140
Q

What are the phases of ARLD?

A
  1. Fatty change – hepatocytes contain triglycerides
  2. Alcoholic hepatitis
  3. Alcoholic Cirrhosis – destruction of liver architecture and fibrosis
141
Q

What investigations could you order in ARLD?

A
  • LFT
  • Blood test for serum albumin
  • Prothrombin time –> clotting factors indicates liver damage
  • A Good history.
  • Liver biopsy
142
Q

What is the treatment for ARLD?

A
  • STOP DRINKING
  • Psychological therapy to encourage stopping.
  • Symptom management –> corticosteroids
  • Liver transplant
143
Q

What is Non-alcoholic steato-hepatitis?

A

An advanced form of non-alcoholic fatty liver disease

144
Q

What are the causes of non-alcoholic steato-hepatitis?

A
  1. T2DM
  2. Hypertension
  3. Obesity
  4. Hyperlipidaemia
145
Q

A 4-year-old girl presents with diarrhoea and is hypotensive. What is the physiological reason that fluid moves from the interstitium to the vascular compartment in this case?

A

Reduced hydrostatic pressure. Fluid will move from the interstitium into the plasma if there is an increase in osmotic pressure or a decrease in hydrostatic pressure. As this patient is hypotensive it is more likely to be the latter.

146
Q

How is haemoglobin broken down?

A
  1. Haem is broken down into Fe2+ and Biliverdin
  2. Biliverdin reductase converts biliverdin to unconjugated bilirubin
  3. Glucuronosyltransferase converts unconjugated bilirubin to conjugated in the liver.
  4. Conjugated bilirubin forms urobilinogen via intestinal bacteria.
147
Q

What is the function of glucuronosyltransferase?

A

Transfers glucuronic acid to unconjugated bilirubin to form conjugated bilirubin

148
Q

Why can’t unconjugated bilirubin travel in the blood without albumin?

A

Unconjugated bilirubin binds to albumin as it isn’t H2O soluble so needs to bind to albumin so it can travel to the blood in the liver.

149
Q

What is the 3 things that urobilinogen can do?

A
  1. Go back to the liver via enterohepatic system
  2. Can go to the kidneys forming urinary urobilin
  3. Can form stercobilin which is excreted in the faeces
150
Q

What is diverticulitis?

A

Infection and inflammation of diverticula (pouches) along the digestive tract.

151
Q

What is the epidemiology of diverticulitis?

A

Diverticular disease most commonly affects older patients with low fibre diets

152
Q

What is most commonly affected in diverticulitis?

A

descending colon.

153
Q

What is the pathophysiology of diverticulitis?

A

Outpouching of bowel mucosa –> faeces get trapped and obstruct the diverticula

This causes abscess and inflammation leading to diverticulitis

154
Q

What are the signs of diverticulitis?

A
  • Similar to appendicitis but on the left side
  • Pain in left iliac fossa region, fever and tachycarida.
  • Diarrhoea/constipation –> rectal bleeding with blood and mucus
155
Q

What is acute diverticulitis?

A

a sudden attack and swelling in the diverticula, can be due to surgery.

156
Q

What are the causes of diverticulitis?

A
  • Surgery (acute)

- Infection

157
Q

What are the investigations for diverticulitis?

A
  • Colonoscopy
  • CT
  • Bloods –> CRP for inflammation and possible WBC for infection.
158
Q

What is the treatment for diverticulitis?

A
  • High fibre diet
  • Paracetamol –> not aspirin and ibuprofen as can cause stomach upsets.
  • Surgery –> severe cases.
159
Q

What are oesophageal varices?

A

Abnormal, enlarged veins in the oesophagus prone to bleeding.

160
Q

What are the symptoms of varices?

A
  1. Haematemesis
  2. Melaena
  3. Abdo pain
  4. Dysphagia
  5. Anaemia
161
Q

What investigations would you order in varices?

A
  • Abdo CT/Doppler US of splenic/portal veins
  • Capsule endoscopy
  • Endoscopic exam
162
Q

What is the treatment for varices?

A
  • Endoscopic therapy –> Banding

- Beta blockers e.g. propranolol to reduce portal hypertension.

163
Q

What is the pathophysiology of oesophageal varices?

A

Obstruction to portal blood flow leads to portal hypertension

Blood is diverted into collaterals e.g. gastro-oesophageal junction so causes varices

164
Q

What is a major risk associated with oesophageal varices?

A

Haemorrhages if they rupture

165
Q

What is primary biliary cirrhosis?

A

autoimmune disease where there is progressive lymphocyte mediated destruction of intrahepatic bile ducts –> cholestasis –> cirrhosis

166
Q

What is the epidemiology of primary biliary cirrhosis?

A
  • Females affected more then men

- Familial trend

167
Q

What is the pathophysiology of primary biliary cirrhosis?

A
  • Lymphocyte mediated attack on bile duct epithelial

- Destruction of bile ducts –> cholestasis and then cirrhosis

168
Q

What diseases are associated with primary biliary cirrhosis?

A

Thyroiditis, RA, Coeliac disease, Lung disease

169
Q

What are the symptoms of primary biliary cirrhosis?

A
  1. Itching and dry eyes
  2. Fatigue
  3. Joint pains
  4. Variceal bleeding
170
Q

What would be the blood results in primary biliary cirrhosis?

A
  • Raised IgM
  • Raised ALP
  • Positive AMA
171
Q

What is the treatment for primary biliary cirrhosis?

A

Ursodeoxycholic acid –> improves liver enzymes, reduces inflame and portal pressure so reduces the rate of variceal development

172
Q

What is biliary colic?

A

A gallbladder attack –> RUQ pain due to gallstone blocking the bile duct.

173
Q

What are the symptoms of biliary colic?

A
  • RUQ pain

- Itching – due to build-up of bilirubin

174
Q

What are the risk factors?

A

Female, obese, over 40, have a condition that affects bile flow, IBD/IBS, taking ceftriaxone.

175
Q

What is the main difference between biliary colic and acute cholecystitis

A

Acute cholecystitis has an inflammatory component

176
Q

What are 3 metabolic disorders of the liver?

A
  • Haemochromatosis – iron overload
  • Alpha 1 anti-trypsin deficiency
  • Wilsons disease – Disorder of copper metabolism
177
Q

What is the mechanism of Alpha 1 anti-trypsin deficiency leading to chronic liver disease?

A

results in protein retention –> causing cirrhosis.

178
Q

What are the general symptoms of alpha 1 anti-trypsin deficiency?

A

Frequent chest infection, wheezing, chronic cough, breathlessness during exercise, associated with jaundice and cirrhosis.

179
Q

What is the treatment for Alpha 1 anti-tryspin deficiency?

A

Treat the conditions it causes e.g. COPD or liver cirrhosis.

180
Q

What is wilson’s disease?

A
  • Autosomal recessive disorder of copper metabolism
181
Q

How does wilsons disease cause hepatic failure and cirrhosis?

A

Excessive deposition of copper in the liver, causing hepatic failure and cirrhosis

182
Q

What is the treatment of Wilsons disease?

A
  • Life treatment with pencillamine
183
Q

What are the causes of portal hypertension?

A
  1. Cirrhosis and fibrosis (Intra-hepatic causes)
  2. Portal vein thrombosis (Pre-hepatic causes)
  3. Budd-chiari (post-hepatic cause)
184
Q

What are the symptoms of portal hypertension?

A
  1. Ascites
  2. GI Bleeding –> black tarry stool
  3. Reduced level of platelets
  4. Hepatic encephalopathy
185
Q

What investigations would you order in portal hypertension?

A
  • Endoscopic
  • Splenomegaly
  • Ultrasound
  • Patient history
  • Bloods –> clotting factors (prothrombin)
186
Q

What are the complications of portal hypertension?

A
  • Splenomegaly

- Varices

187
Q

What is the treatment for portal hypertension?

A
  • Propanolol –> prevention of bleeding and varicies –> reduces portal pressure.
188
Q

What are the causes of duct obstruction?

A
  1. Gallstones
  2. Stricture (narrowing) e.g. malignant, inflammatory
  3. Carcinoma
  4. Blocked stent
189
Q

What are the symptoms of duct obstruction?

A
  • Abdo pain in RUQ
  • Dark urine
  • Fever
  • Jaundice
190
Q

What investigations are neccesary in duct obstruction?

A
  • Abdo CT and US
  • ERCP
  • Blood tests –> alkaline phosphatase, liver enzymes and bilirubin level.
191
Q

What is the treatment of duct obstruction?

A
  • Dependent on the cause –> stop the blockage
192
Q

What are the complications of duct obstruction?

A

sepsis, liver disease, biliary cirrhosis.

193
Q

What is haemochromatosis?

A

Inherited condition –> iron overload.

194
Q

What histological stain would you use to test for haemochromatosis?

A

Perl’s stain

195
Q

What is the cause of haemochromatosis?

A

90% of people have a mutation in the HFE gene –> Autosomal recessive inheritance

196
Q

What is the protein, controlling iron absorption, which is lacking in Haemochromatosis called?

A

Hepcidin

197
Q

What are the symptoms of haemochromatosis?

A
  1. Hepatomegaly
  2. Cardiomegaly
  3. Diabetes mellitus
  4. Hyperpigmentation of skin
  5. Lethargy
198
Q

What is the pathophysiology of haemochromatosis?

A

Uncontrolled intestinal iron absorption leads to deposition in heart, liver and pancreas –> fibrosis –> organ failure

199
Q

What is an indicator for the diagnosis of haemochromatosis?

A
  • Raised ferritin
  • HFE Genotyping
  • Liver biopsy
200
Q

What are the causes of iron overload?

A
  1. Genetic disorders e.g. haemochromatosis
  2. Multiple blood transfusions
  3. Haemolysis
  4. Alcoholic liver disease
201
Q

What is druggability?

A

the ability of a protein target to bind with molecules with high affinity.

202
Q

What are 4 drug targets?

A
  • Receptors
  • Enzymes
  • Transporters
  • Ion channels
203
Q

What is a receptor?

A

a component of a cell that interacts with a specific ligand –> can be exogenous (drug) or endogenous (hormones)

204
Q

How can cells communicate?

A
  • Neurotransmitters –> Acetylcholine
  • Autacoids – cytokines
  • Hormones – testosterone
205
Q

Give 4 types of receptors.

A
  • Ligand gated ion channels (nicotinic ACh receptor)
  • G protein coupled receptors (Beta adrenoceptors)
  • Kinase-linked receptors (Growth factors)
  • Nuclear receptors (steroid receptors)
206
Q

Describe ligand gated ion channels

A
  • Binding causes transformational protein change to allow ion through.
207
Q

Describe G protein coupled receptors

A
  • GPCR are a group (7) of receptors in the eukaryotic membrane.
  • G proteins (GTPases) act as molecular switches
  • When activated it transduces a signal.
208
Q

Describe kinase-linked receptors

A
  • Transmembrane receptors are activated when binding of EC ligand
  • This causes enzymatic activity on IC side.
209
Q

Describe nuclear receptors

A
  • IC receptors, modify gene transcription, causing a conformational change
  • This causes Zinc fingers in which can bind to the genome –> switching on transcription.
210
Q

Define affinity

A

how well a drug binds to a receptor

Agonists –> high affinity and efficacy

211
Q

Define efficacy

A

how well a ligand activates to a receptor and induces a conformational change.

Antagonists –> high affinity but no efficacy

Phase 2a Sheffield Medicine (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions