U10C3 Domestic Violence And Liver Cirrhosis

Question 1

What is domestic violence and how may it look?

Answer 1

Any incident or pattern of incidents of controlling, coercive, threatening behaviour, violence or abuse between those aged 16 or over who are, or have been, intimate partners or family members regardless of gender or sexuality

o Coercive control (a pattern of intimidation, degradation, isolation)
o Psychological and/or emotional abuse
o Physical abuse
o Sexual abuse
o Financial abuse
o Harassment and stalking, online or digital abuse

Question 2

What are the risk factors for victims and perpetrators of domestic violence ?

Question 3

What is the I3 theory of aggression?

Answer 3

Question 4

How does intimate partner violence IPV impact health?

Answer 4

o Experienced IPV ↑ health care episodically and ↓ preventive health care.
o IPV is a significant cause of morbidity and mortality across all socioeconomic groups but risk of IPV ↑ when poor, young, socially isolated, learning difficulties, or experiencing chronic mental illness.
o Both direct and second-hand exposure to IPV are associated with an increased risk of illness during and after the period of violence.
o Women reporting domestic abuse in pregnancy have been found to be at a higher risk for high blood pressure or oedema, vaginal bleeding, severe nausea, vomiting or dehydration, kidney infection or urinary tract infection.

Question 5

What support is available?

Answer 5

Domestic Abuse Charities:

• Refuge: Provides support and safe houses for domestic abuse victims.
• Women’s Aid: Works to end domestic abuse against women and children.

Campaigns:

• 16 Days of Activism: An international campaign against gender-based violence.
• White Ribbon Campaign: Engages men in the prevention of violence against women.

Question 6

How is bilirubin metabolised?

Answer 6

Question 7

How is alcohol metabolised?

Answer 7

Question 8

What is the effect of alcohol on the body?

Answer 8

Question 9

What is the mechanism of alcohol withdrawal symptoms?

Answer 9

Question 10

What are the symptoms of liver failure?

Answer 10

Question 11

What is the Pathophysiology of the symptoms?

Answer 11

Question 12

What is the Pathophysiology of pitting oedema?

Answer 12

Question 13

What are oesophageal varices and how are they graded?

Answer 13

Question 14

What is the Pathophysiology of liver cirrhosis?

Answer 14

• Liver cirrhosis involves progressive scarring of the liver tissue, disrupting its normal structure and function. Chronic liver injury, often caused by conditions like chronic hepatitis, alcohol abuse, or fatty liver disease, triggers inflammation and fibrosis. As liver cells are damaged, the body attempts to repair the tissue, leading to the formation of fibrous scar tissue.
• The pathophysiology includes activation of hepatic stellate cells, which play a key role in collagen deposition, leading to fibrosis. As cirrhosis advances, nodules of regenerating hepatocytes surrounded by fibrous bands replace normal liver tissue. This disrupts blood flow through the liver, impairing its functions like detoxification, synthesis of proteins, and regulation of metabolism.
• Complications may arise, such as portal hypertension due to increased resistance to blood flow, leading to esophageal varices and ascites. The impaired liver function also results in decreased synthesis of clotting factors, potentially causing coagulopathy. Additionally, cirrhosis increases the risk of hepatocellular carcinoma. Overall, the pathophysiology of liver cirrhosis involves a complex interplay of inflammation, fibrosis, and structural changes in the liver tissue.

Question 15

What is the Pathophysiology of ascites?

Answer 15

Question 16

What is the reversibility of alcoholic liver disease?

Answer 16

Is alcoholic liver disease reversible?

• Early stages - steatosis and hepatitis - can be reversed by stopping alcohol consumption.
• Cirrhosis is irreversible because of the loss of functional hepatocytes and build up of fibrotic tissue.

Liver Stages of regeneration:

1. Initiation - damage
2. Priming - activation of genes in preparation for growth factors
3. Proliferation - growth factors bind to complementary receptors i.e. EGFR and c-MET, activating them
4. Termination - TGF-beta

Question 17

How is liver cirrhosis diagnosed?

Answer 17

• Raised bilirubin - clinical jaundice - excretory function of the liver has been damaged so not getting released in bile
• Raised alanine aminotransferase (ALT) - hepatocellular damage
• Reduced serum albumin - impaired synthetic of the liver function
• Elevation of the INR (international normalised ratio- ratio of patient to normal, above 1.1 is abnormal) - damage to synthetic function of the liver
• Raised gamma glutamyltransferase (GGT) - biliary damage
• Low level of platelets - spleen enlarges and causes platelet
  consumption

Question 18

What are the anatomical and histological changes in the progression of liver disease?

Answer 18

Question 19

What is the progression from normal to liver cancer?

Answer 19

Question 20

How is liver cirrhosis treated?

Answer 20

IV vitamins
Diuretics
B-blockers
Lactulose

Question 21

What is the eligibility criteria for a liver transplant?

Answer 21

• MDT meeting
• 2 main conditions: Without transplant likely lifespan would be shorter than normal or with a poor quality of life. Expected to have at least a 50% survival rate for 5 years after transplant
• UKLED score- From blood tests, needs to be at least 49
• Assessing Qol- Subjective. Main areas: persistent tiredness, ascites, debilitating shortness of breath, persistent itchiness
• Not eligible if: Severe malnutrition, infection, AIDS, heart failure, COPD, serious mental health condition, advance liver cancer, continuing use of alcohol and drugs

Question 22

How does jaundice develop?

Answer 22

• If liver cells are damaged/dead and can no longer conjugate bilirubin/release their bilirubin, conjugated or unconjugated bilirubin starts to leak back into the plasma where it accumulates to high concentrations than usual.
• This high plasma bilirubin concentration allows this yellow pigment to accumulate in the collagen rich skin and sclera, giving a yellow complexion in patients with jaundice.
• In addition, the higher conjugated bilirubin concentration leads to excess bilirubin being excreted in the urine, turning it a darker colour than normal.