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Block 0ne sem one > Liver disorders > Flashcards

Liver disorders Flashcards

1
Q

where is the liver located

A

under the diaphragm in the upper right quadrant

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2
Q

how many lobes does the liver have and what are they made up of

A

4 lobe made up of thousands of lobules which are the functional units of the liver

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3
Q

what are the two sources of blood supply to the liver

A
  • oxygenated blood flows in via the hepatic artery

- venous blood flows in via the hepatic portal vein carrying nutrients and toxic materials

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4
Q

what are sinusoids

A

vascular channels allowing exchange between blood and hepatocytes

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5
Q

outline the flow of bile out of the liver

A
  • bile is produced in the hepatocytes and drains into the canaliculi
  • exits into the lobules via the bile ducts
  • exists the liver via the hepatic duct
  • enters the duodenum via the common bile duct
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6
Q

what are 9 functions of the liver

A
  • carbohydrate metabolism
  • protein metabolism
  • synthesis of bile
  • fat metabolism
  • breaking down toxic substances
  • conjugation of bilirubin
  • converting ammonia into urea (urea cycle)
  • steroid metabolism
  • storage of some vitamins and minerals
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7
Q

how is liver disease diagnosed

A
  • patient history
  • patient signs and symptoms
  • physical examination
  • lab tests (blood, urine)
  • other diagnostics eg liver biopsy, abdominal ultrasound, ct scan
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8
Q

What is hepatocellular injury? What happens? what is the major symptom?

A
  • injury to the hepatocytes leading to cell necrosis (death)
  • causes a decrease in synthetic/metabolic activity of the liver and the release of intracellular contents
  • major symptom high levels of bilirubin in the blood (hyperbilirubinemia) causing jaundice
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9
Q

jaundice is usually the first and sometimes the only sign of liver disease, what is it

A

it is a yellow discolouration of the skin and sclera due to abnormally high levels of serum bilirubin accumulating in the blood.

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10
Q

why is bilirubin bad and how do we normally control it

A

bilirubin is toxic to cells

- it is usually excreted in the urine when kidneys are functioning normally

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11
Q

What is Kernicterus, why is it bad and how does it happen?

A
  • high bilirubin which has crossed the blood brain barrier in neonates
  • may lead to permanent and fatal brain damage
  • happens cos in premature babies, immature liver function unable to form conjugated bilirubin leading to an accumalation
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12
Q

there are 3 types of jaundice which are based on location and which part of the bilirubin conjugation process they impact what are these 3 types called

A

prehepatic (hemolytic) jaundice
intrahepatic jaundice
posthepatic (obstructive) jaundice

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13
Q

explain what happens during prehepatic (hemolytic) jaundice

A
  • increased rate of RBC breakdown = excess uncojugated bilirubin is produced fatser than liver is able to conjugate it.
  • unconjugated bilirubin is insoluble and is not able to be excreted from body in urine
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14
Q

explain what happens during intrahepatic jaundice

A
  • hepatic injury impeded conjugation of bilirubin and/or its secretion = accumalation of unconjugated bilirubin in blood stream
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15
Q

posthepatic (obstructive) jaundice

A
  • bile flow is obstructed between the liver and intestine impairing bile formation and/or bile flow by blockage of bile ducts = build up of bilirubin and bile salts in the blood
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16
Q

what is hepatitis

A
  • inflammation of the liver
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17
Q

what are two common causes of hepatitis and what can happen if inflammation persists?

A
  • causes : viral infection (hepatitis virus) and alcoholism

- if inflammation perisists = fibrosis = cirrhosis

18
Q

explain what is happening with fatty liver disease (steatosis)

A
  • fat content of liver is greater than 10%

- liver is enlarged due to macrovesicular changes leading to inflammation may progress to fibrosis/cirrhosis

19
Q

explain what is happening with non alcoholic fatty liver disease

A
  • absence of alcohol use and hepatitis viral infection
  • instead associated with insulin reisistance/metabolic syndrome/obesity
  • ranges from steatosis, inflammation with steatosis, hepatocyte necrosis, cirrhosis
20
Q

explain what cirrhosis is

A
  • chronic end stage liver disease
  • marked by degeneration of cells, inflammation, and fibrous thickening of tissue.
  • characterised by portal hypertension often leading to ascities ( build up of fluid in peritoneal cavity)
  • It is typically a result of alcoholism or hepatitis.
21
Q

what are the clinical manifestations of cirrhosis (5)

A
  • diffuse fibrosis with nodules of hepatocytes
  • fibrosis disrupts vascular flow and bilary ducts in liver
  • leads to portal hypertension and associated complications such as ascities and varicxes, bilary channel obstruction and bile stasis
  • results in hepatomegaly, weight loss, cachexia, weakness, anorexia and RUQ pain
  • later stages = portal hypertension and liver failure
22
Q

what is portal hypertension

A

increased pressure in hepatic portal system due to cirrhosis

23
Q

what is ascities and what may cause it

A
  • increased fluid in the peritoneal cavity

- may be caused by , obstruction of lymphatic flow, portal hypertension or elevated adh and aldosterone

24
Q

why would elevated ADH (antidurietic hormone) and aldosterone lead to ascities

A
  • adh and aldosterone are normally inactivated and removed by the liver
  • impaired liver function = increase in adh and aldosterone = fluid retention
25
Q

what are oesophageal varices

A
  • enlarged veins in the esophagus. They’re often due to obstructed blood flow through the portal vein, which carries blood from the intestine, pancreas and spleen to the liver.
  • submucosa is thin walled so may hemorrhage into stomach = bleeding varices
26
Q

when does liver failure occur

A

when 80-90% of liver function is lost

27
Q

the liver is reponsible for production of bile salts and acids which are secreted in bile and are important for normal fat digestion. In regrds to this what would happen if your liver failed

A
  • person would have difficulty digesting fat, indigestion = fat exercreted in faeces
  • leads to fat intolerance and steatorroea (pale greasy stools)
28
Q

the liver is responsible for detoxification reactions of drugs and alcohol what would happen in regards to this if the liver failed

A
  • impaired liver function = deficient detoxification reactions = toxic degardation of cells in the body
29
Q

the liver is responsible for formation of lipo proteins, sysnthesis and metabolism of steroid hormones, in regards to this how might we detect abnormal liver function

A
  • lowered serum cholesterol levels
  • gynecomastia, testicular atrophy in males
  • amenorrhea in females
30
Q

the liver is responsible for glycogenensis during the absorptive state and maintaining blood glucose during the post absorptive state through glycogenolysis and gluconeogensis, in regards to carbohydrate metabolism what might happen with impaired liver function

A
  • impaired liver function = impaired carbohydrate metabolism = risk of hypoglycemia
31
Q

the liver store vitamins A,B12,D,E&K what may happen in regards to this if liver disease is present

A
  • in liver disease there is impaired fat absorption and reduced storage of fat-soluble vitamins thus it may lead to some deficiences in these particular vitamins
32
Q

in regards to protein metabolism the liver is responsible for synthesis of plasma proteins (e.g albumin) and some clotting factors (e.g prothrombin) aswell as the deamination of of proteins and formation of urea from ammonia, what would happen in regards to these identified factors if the liver was to fail

A
  • decreased albumin contributes to ascities (albumin important for maintaining normal fluid distribution)
  • bleeding tendancy if inadequate sysnthesis of clotting factors
  • without formation of urea from ammonia= increased levels of ammonia in blood which is highly toxic to cells and may cause hepatic encephalopathy
33
Q

what does hepatic encephalopathy result from and what are the stages of it

A
  • results from complete liver failure

- stages; changes in personality, memory, confusion, stupor, convulsions and then coma

34
Q

what are two factors that lead to a coma with hepatic encephalopathy

A
  • hypoglycemia due to failure of normal blood glucoes homeostasis by liver
  • bilud up of ammonia; severe liver impairment = ammonia not converted to urea = build up of blood ammonia which is toxic to tissues especially brain = coma (encephalopathy)
35
Q

how do liver function tests work ?

A

they combine markers of function (albumin and bilirubin) with markers of liver damage (alanine transaminase (ALT), asparate aminotransferase (AST), alkaline phosphate (alk phos) and y-glutamyl transferase (GGT))

36
Q

ALT and AST are used to assess hepatocyte function as being markers of liver damage. what would suggest hepatocyte process?

A

ALT and AST are also found in other organs so raised levels would suggest functioning hepatocytes

37
Q

explain cholestasis and what can happen

A
  • impaired bile formation by hepatocytes or implaired bile flow by blockage of bile ducts
  • causes build up in the blood of substances that are normally excreted - bile can accumalate and form plugs in the ducts which lead them to rupture an damage liver cells also increased bile acids in the blood and skin cause pruitis (itiching)
38
Q

what is intrahepatic cholestasis

A
  • wide spread blockage of small ducts/canaliculi
39
Q

what is extrahepatic (posthepatic) cholestasis

A

blockage of bile from gallbladder to duodenuem.

40
Q

what are gallstones (cholelithiasis), what are common sysmptoms and how are they diagnosed

A
  • gallstones are made up of 80% cholesterol
  • cholesterol is hydrophobic and precipitates in crystals unless it is held in solution by bile salts
  • presents with localised pain, nausea and vomiting after eating a fatty meal
  • diagnosed by an ultrasound
41
Q

what is cholecytisis

A

and inflammed gallbladder

Block 0ne sem one (5 decks)

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