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Phase 3 > Liver Disease > Flashcards

Liver Disease Flashcards

1
Q

What is meant by Acute on chronic inflammation?

A

Where chronic liver disease often presents with acute exacerbation plus evidence of underlying chronicity - i.e fibrosis

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2
Q

What the most common “target” of inflammation in the liver, and how does this impact other structures?

A

Liver Parenchyma (hepatocytes, bile apparatus and blood vessels) - specifically the hepatocytes are usually the key target

the problems is - when one part of the parenchyma is targeted - usually the rest will also become damaged

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3
Q

Define end stage liver cirrhosis:

A

Diffuse
Nodular
Fibrotic

*to avoid this is the aim of treatment

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4
Q

Outline the very basic clinical approaches to liver damage:

A

LFTs

  • AST
  • ALT
  • ALK Phos
  • GGT

Haematology

  • haemolysis
  • Iron levels

Viral serology

Autoimmune serology
- Anti - mitochondrial (PBC)

  • Anti ANA (auto Hep)

Radiology
- ultrasound

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5
Q

Histologically: what does acute hepatitis look like?

A

Diffuse cellular swelling
with areas of necrosis
- spotty necrosis

with inflammatory infiltrate in all places

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6
Q

If there is paracetamol overdose, what is the AST/ALT levels going to be?

A

> 1000s

- very high

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7
Q

What colour does bile turn in histology staining?

A

Brown

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8
Q

Histologically, what does the hep B virus in the liver look like?

A

Ground glass cytoplasm

- due to accumulation of surface antigen

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9
Q

What may co-amoxiclav cause?

A

Acute Cholestatic hepatitis

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10
Q

Name a biliary Hamartoma:

A

Von Meyenberg complex

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11
Q

If there is haemochromatosis and you take a biopsy - how do you differentiate between Lipofucin (a normal wear and tear deposit within the liver) and Iron?

A

Prussian Blue stain

- stains Iron blue

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12
Q

What are the most common causes of Abnormal Liver blood tests?

A

Fatty Liver

  • alcohol
  • non alcohol

Chronic viral Hepatitis

Autoimmune

  • primary Biliary Cholangitis
  • Autoimmune Hepatitis

Haemochromatosis

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13
Q

What is non- alcoholic fatty liver disease often associated with, and what may it become?

A

Metabolic syndrome:

  • obesity
  • insulin resistance
  • Hyperlipidaemia

there severity of the steatohepatitis increases the metabolic risk factors

NASH
- non alcoholic Steatohepatitis

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14
Q

Outline the pathological changes that occur in alcoholic and nonalcoholic liver fatty liver disease

A

Alcohol:
Alcoholic Steatosis > Alcoholic Hepatitis > Alcoholic Cirrhosis

Non - Alcoholic:
Steatosis > NASH ?
NAFLD Cirrhosis

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15
Q

Name some key lab findings that differentiate between Fatty liver disease and non fatty liver disease:

A

AST:
Higher in Alcoholic

AST:ALT ratio:
much higher in alcoholics

GGT:
Much higher in alcoholics

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16
Q

Outline some classical clinical features of newly jaundiced ALD patient:

A

Hepatomegaly

Fever

Leukocytosis

Hepatic Bruit

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17
Q

In liver fibrosis - where does the fibrosis start?

A

Portal tract then moves into the septa and spreads diffusely

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18
Q

What non-invassive scan can be done for Liver fibrosis?

A

Fibroscan
- measures the firmness of the liver.

Blood based Assessment:
- ELF test

  • Fib-4 score
  • NAFLD Fibrosis Score
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19
Q

What assessment is used to asses the degree of liver damage?

A

Child’s Turcotte- Pugh Score

Grade A: 5-6
- mild

Grade B: 7-9
- moderat e

Grade C: 10-15
- Severe

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20
Q

What is the model for End staged liver failure, and what is it also used for?

A

Model for End stage Liver Disease

Used to allocate donor organs

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21
Q

What are the two main alcohol metabolic pathways within the liver?

A

Alcohol Dehydrogenase
- cytosol

Microsomal Ethanol Oxidase System
- Smooth endoplasmic

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22
Q

Where does fibrosis first start in alcohol disease?

A

Perivenular area

- zone 3

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23
Q

When assessing Ascites what things must you assess?

A

Cell count
- high white blood cell count (>250) suggests: Spontaneous Bacterial Peritonitis

Albumin:
- Serum ascites albumin Gradient

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24
Q

What is the Serum Ascites Albumin gradient?

A

Is it important to understand where the fluid within the peritoneum has come from:
- portal hypertension (transudate)

  • Infection within the peritoneum (exudate) (Spontaneous bacterial peritonitis)

This is worked out by assessing the amount of albumin in the ascites.
[Serum Ascites Albumin Gradient]
it involves:
- Serum Albumin MINUS Ascites Albumin

> 11g/l = Portal hypertension

Since portal hypertension produced transudate - you would expect a greater difference between the plasma and peritoneal fluid.
- thus an increase of over >11g/L is suggestive of transudate

25
Q

If there is a high Lymphocytes within the ascites - what does this suggest?

A

TB

or

Peritoneal Carcinomatosis

26
Q

What is the management of Ascites?

A

Low salt diet

Spironolactone

Furosemide

paracentesis

Transjugular intrahepatic portosystemic shunt (TIPSS)

27
Q

List some precipitating factors to hepatic encephalopathy and name some key things not to make it worse:

A

Encephalopathy comes about due to the build up of waste products in the blood namely - ammonia NH3.
anything that will increase the level of this will make it worse.

Gastrointestinal bleeding
- direct spillage of NH3

Infections
- production of NH3

Constipation
- increased break down of Urea to NH3 by bacteria

electrolyte imbalance
- hyponatremia makes it worse

Excess protein
- more substance for bacteria

Alkalosis
- holds the NH3 - as there is a reduction in H+ ions to bind with it

Things to avoid:

Avoid sedation
- opiates

Avoid Hyponatremia

28
Q

What score is used to assess Mental state in Hepatic Encephalopathy?

A

Conn Score

score 0 = no changes

Score I = lack of awareness

Score II = Lethargy or apathy

Score III = Somnolence

Score IV = coma

29
Q

List the common things Cirrhosis is associated with:

A

Ascites

Encephalopathy

Variceal bleeding

Hepatocellular carcinoma

30
Q

List some investigation you would carry out in suspected Liver disease:

A

LFTs

FBC

  • clotting factors
  • Vitamin K

Bilirubin

autoimmune antibodies

  • ANA
  • Anti - mitochondrial

Conn Score

Liver ultrasound

31
Q

Name an important benign tumour of the liver that shouldn’t be biopsied due to the risk of bleeding.

A

Haemangioma

32
Q

What serum marker can be seen in Hepatocellular carcinoma?

A

Alpha fetal Protein

33
Q

What is a high Alpha Fetal protein indicative off?

A

Hepatocellular carcinoma

34
Q

If IgG levels are elevated in liver disease, what is this suggestive off?

A

Autoimmune hepatitis

35
Q

If the IgM levels are elevated in liver disease, what is this suggestive off?

A

Primary biliary cholangitis

36
Q

In someone with chronic liver disease, what viruses would you check for?

A

Hep B

Hep C *this is the most common

these are the only ones that lead to chronic states.

37
Q

In chronic liver disease - what investigations would you do?

A

Ultrasound

Autoimmune test

Viral tests

  • HCV
  • HBV

Metabolic functions

  • ferritin levels
  • Ceruloplasmin - Wilson’s
  • Alpha -1 - antitrypsin
38
Q

List some Stigmata (obviously) chronic liver failure signs:

A

Encephalopathy

Foetor on the breath - smells like rich tea biscuits

Prolonged prothrombin

Hypoalbuminemia

Portal hypertension

39
Q

What are the combined pathologies that lead to increased Encephalopathy?

A

Inflammation induced by liver failure

Increased levels of ammonia - which is leaking out from the shunting portal veins.

**important not to give benzodiazepines and opioids

40
Q

What is the classical diagnostic sign seen in hepatic encephalopathy?

A

1Hz flapping tremor

41
Q

Treatment of Hepatic encephalopathy?

A

increase bowel Movements
- lactulose

Antibiotics

42
Q

In the context of liver disease, itchy skin can be indicative of what?

A

Primary Biliary cholangitis

43
Q

What blood test can help diagnose Wilson’s disease?

A

Ceruloplasmin

Copper and protein bind to make ceruloplasmin. In the presence of kidney disease or wilson’s disease the protein won’t be made, lead to free copper. as such if there is LOW ceruloplasmin then it is suggestive of wilson’s

44
Q

What is the screening marker for Hepatocellular carcinoma?

A

Alpha Fetal protein

45
Q

What tests would you do to assess the functioning of the liver?

A

Prothrombin time

Albumin levels

Bilirubin levels

*these demonstrate the functioning of the liver much more over the LFTs

46
Q

Name come clinical signs that may be seen in chronic hepatic failure:

A

Spider navei
- above the SVC

Palmer erythema

Axthanomas

Gynecomastia in males

47
Q

What are some key lab findings for auto immune hepatitis, and what is the treatment?

A

Anti smooth muscle antibodies
Anti nuclear antibodies

Treatment:
- steroids
+/- Azathioprine

48
Q

In suspicion of colorectal cancer, what blood tests would you carry out?

A

FBC

U&Es

LFTs
- often metastasis from the liver can arrive there.

49
Q

What is used to stage colorectal cancers:

A

CT

MRI - very useful for pelvis

50
Q

What is the treatment of colorectal cancer:

A

Neo Adjunctive therapy (for some patients)

Surgical resection

  • this is primary choice.
  • abdominal peri- anal resection may need to be done and results in need for colostomy bag
51
Q

What stage is used for Colorectal cancer?

A

Dukes

A - tumour confined to mucosa

B1 - Growth into muscular propia
B2 - Full thickness - through mucosa
**Through the muscular propia

C1 - Tumour spread to 1-4 lymph nodes
C2 - > 4 lymph nodes
**local lymph nodes

D - Distant metastasis - liver, bone

52
Q

Where would you expect to see obstruction from a colon cancer and why?

A

Left sided colon involvement

- this is because the bowel is narrower here resulting in decreased space.

53
Q

What polyps are usually stalked, and why is this, and name one that isn’t:

A

Adenomatous Polyps

Tubulovillous Polyps

these are stalked due to the waves of peristalsis which drag the polyp along into the shape of it.
there is also extreme pressures within the colon which may lead to bleeding

Villous adenoma

54
Q

What kind of epithelial, lines the serosa?

A

Non keratinised squamous epithelium

55
Q

What is the stages that cause the Adenomatous polyps to become malignant:

A

APC mutation development (either sporadic or Familial poly polyposis adenoma)

this leads to KRAS mutations - which causes the mutation

this then leads to p53 mutation = cancer

56
Q

What medication protects against polyps forming cancer?

A

Aspirin

57
Q

What is the management of Ascites?

A

*Spironolactone +/- Furosemide

58
Q

What is refractory ascites? and what is the management?

A

Sodium restriction
Spironlactone
furosemide

Paracentesis
- drainage of the fluid

for every 3L drained albumin needs to be given. this is because there can be massive fluid shifts that occur as fluid from the extravascular space come into the space that was the ascites.

59
Q

What is the destruction that occurs in primary biliary cholangitis?

A

Granulomatous destruction of the intrahepatic bile ducts

Phase 3 (50 decks)

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