Pathophysiology

End stage of cronic liver disease where functional tissue is replaced by fibrous tissue. Diffuse fibrosis and formation of nodules (3mm up to several cm large), that consticts the vascular channels and bilary duct system.
Balance between regeneration and construction activity lead to scarring

Asymptomatic to liver failure. Symptoms show when advanced.

Weight loss, anorexia and weakness, diarrhea, enlarged liver and jaundice is common (bilirubin buildup). Abdominal pain due to liver stretching and enlargement. hypertension and liver cell failure lead to enlarged spleen, abdominal swelling due to fluid accumulation. Bleeding due to dicreased clothing factors. Enlargement of brests (men and women) and feminising pubic hair (testicular atrophy)

Most common primary liver tumor (HCC). Large problem in less developed regions due to hepatitis B,C,D, cirrhosis, long-term exposure to environmental agents or drinking conatminated water (arsenik)

Unclear how agents contribute to cancer. With viruses it could be that the DNA integrates ino the reproduction of cells causing cancer mutations

Similar/same to cirrhosis or chronic hepatitis.

Weakness, anorexia, weight loss, fatigue, abdominal swelling and pain, jaundice, increased liver size,.... Can be more rapid progressive if cirrhosis already present (restoration of tissue impaired).

Hypoglycemia due to hormones produced by tumor, or hypocalcemia

Bile duct cancer. Quite rare.
Increased age or inflammatory bowel disease are risk factors
Presents with pain, weightloss, abdominal swelling, Jaundice if bile duct is obstructed

metastatic tumors!
Spred from brest, colon, lung or urogenital cancers. 

Diffuse inflammation of the gallbladder. Mostly associated with gallstones

Gallstones, sepsis, severe traume or infections can cause it. Either acute or chronic (repetitive episodes of inflammation)

Obstuction of cystic duct by gallstones leads to release of phospholipase from epithelium in gallbladder. This enzyme hydrolizes lecithin and releases a membrane-active toxin. Additionally disruption of protective mucous lining increases cell vulnerability (also due to concentrated bile salts)

Mild Fever, nausea, anorexia, vomitting (GI-trac is connected to vomitting center). Emotional factor can lead to loss of apetite. 

Elevated WBC count, and slightly elevated bylirubin

Cholangitis is an inflammation of the common duct which can form spontaneously. Symptoms are similar to those of gallstones

Choledocolithiasis=stones in common duct

Acute: Reversible inflammatory process by premature activation of pancreatic enzymes. Due to Gallstones of alcohol abuse. Associated by hypercalcemia, hyperlipidemia, infections and trauma or drugs

Chronic: Progressive destruction by fibrosis (first exocrine then endocrine pancreas). irreversible. Long term alcohol abuse, long standing, chronic pancreatitis, inflammatory bowel disease or hereditary pancreatitis can be factors

Inflammation of pancreas, or serum amylase/lypase much higher than normal.

Autodigestion of pancreatic tissue begins with activation of trypsin which activates digestive enzymes. Bilary tract obstruction (gallstones) or bilary reflux can activate enzymes in pancreatic duct system

(Chronic: progressive fibrotic destruction)

Mild to severe organ dysfunction. Abdominal pain.

Fever, tachycardia, hypotension, respiratory distrress, thirst, poor urine output,

Tachycardia can lead to hypoxemia, confusion, rising hematocrit levels

Can lead to necrosis and organ failure

Alpha cells in the pancreas. Secrete into the liver.

Increases the blood sugar levels

Start using the (glucose?) reserves by activating liver processes (ketones,...)

Autoimmune disease, destruction of beta-cells, genetic or virus-caused. Shows up in children.

If untreated it results in dehydration and acidosis (death)

Either genetic or caused by a virus

???

Thirst, hunger and dehydration

obesity, not enough exercise, old age

beta-cells malfunction and hyperglycemia, increased glucose output in the liver

Insulin resistance

lower blood glucose levels, because increased insulin sensitivity due to exercise

At old age due to high glucose levels, usually because blood test for other disease/by chance

1: no insulin production because beta-cells are degraded

2: beta-cells are "exhausted" because of reduced insulin sensitivity

Usually in type 1 diabetes, Hyperglycemia -> lypolysis (increased free fatty acids and uses ketoacids to generate energy, despite of abundance of glucose)

Acidosis forms and dehydration cintiniues to get rid of acids -> osmolarity increases --> (and all over again...)

rapid destruction of pancreatic beta-cells that produce insulin. Mots of the time immune mediated (detection of antibodies possible).
Genetic causes or viral (much less common)

Elevation in blood glucose (hyperglycemia)
Breakdown of body fats and proteins (lipolysis) -> Ketoacidosis develops  (liver converts fatty acids into ketones)