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145 Cards in this Set
- Front
- Back
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By convention, what part of the patient is on the left side of the screen/image for transverse views?
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the patient’s right will be on the right side of the ultrasound image and the patient’s left on the left side of the image
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By convention, what part of the patient is on the left side of the screen/image for longitudinal (sagittal) views?
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then the ultrasound image should have the patient’s head to the right side of the image and patient’s feet to the left side of the image.
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What does gain adjust in reference to ultrasound mean?
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Gain is adjusted to provide enough sound to create an image without over filling it with noise
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Describe the Aorta as seen on ultrasound?
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Bright walled structure, seen as a black tube running slightly left of midline, from deep at the level of the diaphragm to superficial at the level umbilicus where it usually bifurcates
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What is meant by the following Ultrasound terms …
interface acoustic enhancement Attenuation |
interface - Strong echoes that delineate the boundary of organs, caused by the difference between the acoustic impedance of the two adjacent structures
acoustic enhancement - Sound is not weakened (attenuated) as it passes through a fluid-filled structure and therefore the structure behind appears to have more echoes than the same tissue beside it Attenuation - A decrease in amplitude and intensity, as sound travels through a medium |
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What causes Shadowing?
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strong reflectors, or attenuating structures, i.e. bone, gas, calcifications and air
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What is meant by the following Ultrasound terms ….
anechoic isoechoic hypoechoic hyperechoic |
anechoic – A structure that does not produce any internal echoes
isoechoic - echo similarity of 2 or more tissues as measured by ultrasonography hypoechoic - tissues or structures that reflect relatively few of the ultrasound waves directed at them. hyperechoic producing an increased amplitude of waves returned in ultrasonography which is characteristic of bone and dense tumor tissue. |
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What are the landmarks for identifying the pancreas on ultrasound?
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It is a comma like structure with relationships to the SMA, Splenic Vein, Portal / Splenic Confluence, inferior border of the left lobe of liver.
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On ultrasound how do you tell the difference between the aorta and inferior vena cava?
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IVC unlike the aorta can change in diameter depending on respiration and compression.
You also cant see branches entering the IVC like you can see with the aorta |
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What does a pancreas look like on ultrasound when pancreatitis is present, and when else does it look like this?
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Increases in echogenicity (brightness) with age and with pathologic process such as pancreatitis.
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How do you tell the difference between hepatic veins and portal veins on ultrasound?
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The hepatic veins a thin walled and there are 3 main branches – right middle and left
Whereas the Bright walled vessels that cross the liver in a more transverse direction ALSO - Portal vein has a flat forward flow, demonstrating some respiration influence Whereas Hepatic veins have forward and reverse flow with respiration, mostly in the reverse direction |
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Describe a hepatic artery on ultrasound?
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A Hepatic artery is small, has a forward systolic and diastolic wave form
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what is meant by A diffusely echogenic liver?
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When the liver has homogenous increase in brightness (echogenicity) and it is detected by comparing it to the right kidney (usually the same echogenicity/brightness)
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what are the common causes of a diffusely echogenic liver?
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Fatty liver disease
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Describe what gall bladder stones look like on Ultrasound vs polyps?
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Gall stones appear as bright echogenic structures that produce a shadow and where as polyps do not as they are attached to the gall bladder wall, Polyps do not shadow
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What is gall bladder sludge and when is it seen?
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A mixture of microscopic particulate matter in bile that occurs when particles of material precipitate from bile. It is often seen in patients who have been fasted for a long time, such as patients in intensive care
Usually moves when patient is rolled |
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What causes pre-hepatic causes of jaundice and what sort is it?
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Pre-hepatic jaundice is caused by anything which causes an increased rate of hemolysis (breakdown of red blood cells). i.e. malaria, sickle cell anaemia, spherocytosis, thalassemia and glucose 6-phosphate dehydrogenase deficiency, Haemalytic uraemic syndrome, Gilbert's syndrome (a genetic disorder of bilirubin metabolism) and Crigler-Najjar syndrome.
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Describe the blood and urine findings in pre-hepatic uncongugated jaundice?
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Urine: no bilirubin present (because uncongugated is not water soluble) and urobilinogen > 2 units
Blood - increased unconjugated bilirubin |
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What are the causes of hepatic jaundice?
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Hepatocellular (hepatic) jaundice can be caused by acute or chronic hepatitis, hepatotoxicity, cirrhosis, drug induced hepatitis and alcoholic liver disease.
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What sort of hyperbilirubinaemia is seen in hepatic jaundice and why?
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Mixed type and the ratio of conjugated to uncongugated hyperbilirubinaemia depends what is the cause of hepatic jaundice – If there is Cell necrosis this reduces the liver's ability to metabolize and excrete bilirubin leading to a buildup of unconjugated bilirubin in the blood.
If there is primary biliary cirrhosis there is an increase in plasma conjugated bilirubin because there is impairment of excretion of conjugated bilirubin into the bile. |
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What is the cause of newborn jaundice and what sort of hyperbilirubinaemia is it?
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In a new born hepatic machinery for the conjugation and excretion of bilirubin does not fully mature until approximately two weeks of age so it is an unconguagated hyperbilirubinaemia.
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What is post-hepatic jaundice also known as?
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also called obstructive jaundice
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What are the 2 most common causes of obstructive jaundice?
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gallstones in the common bile duct, and pancreatic cancer in the head of the pancreas
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In kidney ultrasound what is normal?
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Hypoechoic medulla compared to the echogenic cortex
Generally the same echogenicity as the liver |
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True or False? The ureter does not display a Doppler shift
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TRUE
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What are the features of a simple kidney cyst on ultrasound?
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Walled, anechoic, posterior enhancement not always seen in the surrounding tissue
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Describe liver cirrhosis?
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Diffuse process characterised by fibrosis and the conversion of the entire liver
architecture into structurally abnormal nodules
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Describe the 3 elements of liver cirrhosis?
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Death of hepatocytes
Extra-cellular matrix deposition Vascular re-organisation |
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Decribe the process by which there is extracellular matrix deposition in cirrhosis?
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Damaged hepatocytes and Kupffer cells (plus endothelial cells) stimulate stellate cells (in space of Disse)
Stellate cells then deposit collagens in space of Disse |
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Name the 5 porAtal-systemic anastomoses?
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Describe the liver architecture in cirrhosis?
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Normal liver cells are replaced by spherical parenchymal nodules consisting of regenerating liver cells confined by fibrous septa
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What are the 8 clinical signs of portal hypertension?
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How does ascities develop?
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Sinusoidal hypertension and hypoalbuminaemia cause leakage of intra- vascular fluid into space of Disse
Which then leads to fluid leakage from hepatic interstitium into peritoneal cavity Also there is Renal retention of sodium and water due to 2o hyperaldosteronism |
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Why is there 2o hyperaldosteronism in liver cirrhosis?
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2o hyperaldosteronism in oedematous states (eg hepatic cirrhosis) is adaptive response to perceived hypovolaemia &/or low intra-renal perfusion
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Describe alcoholic cirrhosis?
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It is a fine micronodular cirrhosis
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Describe the cirrhosis due to chronic hepatitis B?
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Extensive fibrous bands of scar tissue bridging between Portal tracts and separating disorderly nodules of regenerating hepatocytes
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Where and why do you see Ground-glass hepatocytes?
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In chronic hepatits B due to accumulation of HBsAg in endoplasmic reticulum
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What is this?
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Macronodular cirrhosis and malignant hepatocarcinoma
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What is this?
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LIVER - METASTASES FROM BRONCHIAL CARCINOMA
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What can you see in this slide of liver?
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Fatty change
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What colour is fluid on ultrasound?
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Black
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What proteins are made by the liver?
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plasma proteins – namely albumin
Coagulation factors – fibrinogen and all factors except factor VIII (comes from epithelial cells instead) Transport protiens – i.e. thyroid binding globulin, steroid binding globulin, retinyl binding protiens, transferrin and vit D binding protein. |
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Why is there a deficiency in fat soluble hormones in liver failure?
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the liver synthesizes transport protiens important for binding and transporting fat soluble horomones i.e. ADE and K
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As well as synthesizing hormone transport protiens, the liver is important for activation/inactivation of particular hormones, name and wether they are activated or inactivated by the liver?
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Thyroxine– activated in the epithelial cells of the liver
Vitamin D – activated via conversion to 25 Vit D Ecosionoid – activated Insulin- Inactivated Glucagon – inactivated Growth Hormone – inactivated Steroid hormones – inactivated Catecholamines - inactivated |
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What dietary factors are metabolised in the liver?
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Carbohydrates – all dietary CHOs are converted to glucose in the liver
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What are the minimum dimension of the pelvic inlet for a natural birth?
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5” wide X 4” deep (12.5 X 10cm)
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Describe the general blood supply to the pelvis?
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There is an anterior division of the internal iliac which has 9 branches and there is a posterior division with 3 branches
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Which GLUT transporter is used to take up glucose into the hepatocyte?
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GLUT 2
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What drives the glucose uptake through GLUT2 in the hepatocyte?
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passive transport driven by the concentration of glucose inside the hepatocyte (chemical gradient)
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What are the ‘fates” of G-6-P (trapped flucose) in the hepatocyte?
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Conversion to glycogen
Broken down to pyruvate To then go into the citric acid cycle to be converted to ATP To be converted to amino acids for protein Or converted to Acetly CoA which can then be converted to Fas or Ketone bodies |
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What are the actions of glucagon in the hepatocyte and what two other factors have this same effect?
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Breakdown Glycogen to Glucose and Pyruvate to Glucose
Catecholamines and Steroids have this same effect |
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What is the shared actions of glucagon, catecholamines and steroids?
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Breakdown Glycogen to Glucose and Pyruvate to Glucose in the hepatocytes
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What action does insulin have on hepatocytes?
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Cause the conversion of glucose to glycogen and pyruvate
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What physiological change has the same action as insulin on glucose in the hepatocyte?
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Hepatocyte swelling – causes glucose to be converted to glycogen and pyruvate
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What physiological change has the same action as glucagon on glucose in the hepatocyte?
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Hepatocyte shrinkage– causes glycogen and pyruvate to be converted to glucose
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What are ketogenic amino acids vs glycogenic amino acids?
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Glycogenic amino acids are the amino acids that can be converted to pyruvate and then back to glucose
Where as the ketogenic amino acids are those that are too far metabolized to be converted to pyruvate and hence are converted to Acetyl CoA which can only be converted to FAs or Ketone bodies (note – not glucose) |
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Describe the why there needs to be a way to remove NH4+ (ammonia) and how the body does?
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The liver has NH4+ as a by product of all the metabolism that occurs.
This can be toxic and hence is either converted to urea by addition to HCO3 (but this requires a lot of energy) by the liver, or excreted by the kidney which relies on a pH gradient and glutamine conversion to glutamate |
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During alkalosis which is the most important way to remove ammonia?
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the Urea cycle as it uses HCO3- and NH4+ to convert to urea
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During Acidosis what mechanism is important for removing ammonia?
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Renal excretion
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The visceral surface is characterised by an H-shaped arrangement. Describe what makes up the H?
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The upright parts of the H are formed by the fissures for ligamentum venosum and teres on the left, and the fossae for the inferior vena cava and gall bladder on the right. The porta hepatis, forms the cross-bar of the H, and separates the caudate lobe above from the quadrate lobe below.
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Which Structures enter and leave the liver at the porta hepatis?
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Enter: L & R branches of portal vein and proper hepatic artery, autonomic nerves (efferent)
Leave: L & R hepatic ducts, lymphatic vessels, visceral afferent fibres |
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The caudate and quadrate lobes are part of which anatomical lobe?
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right
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The liver receives a dual blood supply. What are the two supplies and what % of total do they provide?
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The proper hepatic artery (30% of supply) carries oxygenated blood from the aorta.
The portal vein (70% of supply) brings deoxygenated blood containing products of digestion from the alimentary tract, and waste products of red cell destruction from the spleen which contribute to bile pigments. |
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What is the function of the ductus venosus?
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It carries shunted blood from the left umbilical vein to the inferior vena cava in the fetus, short-circuiting the liver.
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When hepatic circulation is slowed what cells are effected and why?
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Oxygen tension is greatest close to the portal triads and lowest near the central vein. Therefore anything that slows the hepatic circulation will affect cells close to the central vein.
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What can cause damage to the cells closest to the portal triad as supposed to those near the central vein?
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poisons entering the liver (by portal vein or hepatic artery) will tend to damage cells close to the portal triad.
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describe what happens after a carbohydrate-rich meal if blood glucose concentrations begin to rise above 5mM and why?
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Above a blood glucose concentration of 5mM the capacity of hexokinase (low Vmax) is exceeded in many tissues so liver glucokinase (high Vmax) phosphorylates excess glucose to produce glucose 6-phosphate for conversion to glycogen and storage.
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Under normal metabolic conditions, and when carbohydrate intake results in the synthesis of sufficient glycogen, what happens to the excess carbohydrate?
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It is channelled through glycolysis and the pyruvate which is ultimately produced, is converted to acetyl CoA and in turn, is converted into long-chain fatty acids (LCFAs).
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What happens to Ingested long chain fatty acids?
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Ingested LCFAs are converted into triglycerides, which are transported to adipose tissue as Very Low Density Lipoproteins (VLDLs) for storage.
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When energy demand by tissues increases, LCFAs are released from adipocytes and are degraded within the liver to give acetyl CoA. What are the 2 fates of Acetyl CoA?
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Acetyl CoA may be completely oxidised by the citric acid cycle to produce ATP or it may be converted into HMGCoA which is the building block for two key groups of compounds, cholesterol (in the cytoplasm) and ketone bodies in mitochondria
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What happens to Nitrogen-containing compounds that are ingested in excess of normal requirements?
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they are processed by the liver.
The Amino acids are de-aminated and their carbon skeletons made into either glucose (gluconeogenic amino acids) or acetyl CoA (ketogenic amino acids including leucine and lysine). |
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Describe the metabolism of purine and pyrimidine bases?
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Purine bases are either oxidised to uric acid or re-cycled to generate purine nucleotides by salvage pathway enzymes including adenine and guanine/hypoxanthine ribosyltransferases.
Pyrimidine bases are degraded to ammonium. This ammonium, and that derived from the transamination of amino acids coupled to the deamination of glutamate, is processed by the urea cycle and the urea excreted via the kidney. |
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_________ is the end-product of glucose metabolism by erythrocytes and actively metabolising white muscle?
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Lactate
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How is lactate processed?
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it is taken up by the liver and, on average, ~30% is processed by oxidation (lactate-->pyruvate-->acetyl CoA-->CO2 ) and ~70% is converted to glucose.
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Acute liver failure usually results from what pathological event?
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massive necrosis of hepatocytes- but note the aetiology of the massive necrosis is usually not able to be detected from routine pathology.
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Describe Cirrhosis?
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Cirrhosis is characterised by bands of fibrous tissue surrounding nodules of hepatocytes. The cause of cirrhosis can often be implied from the pathology. Describe the pathology associated with hepatitis B?
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The cause of cirrhosis can often be implied from the pathology. Describe the pathology associated with hepatitis C ?
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Cirrhosis due to hepatitis C is characterised by fat deposits in hepatocytes - lobular steatosis and varying degrees of liver fibrosis associated with nodular portal tract infiltrates
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The cause of cirrhosis can often be implied from the pathology. Describe the pathology associated with Alcoholic liver disease?
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Cirrhosis due to Alcoholic Liver Disease is associated a neutrophilic inflammatory infiltrate, pericellular fibrosis and Mallory's hyaline in hepatocytes.
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Why are Liver biopsies in chronic HCV infection (and HBV) performed?
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in order to establish the degree of liver injury (inflammation and fibrosis). Such information often influences treatment decisions.
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An important disease to recognize on liver biopsy is autoimmune hepatitis. Describe the identifying pathology?
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Autoimmune hepatitis is characterized by an inflammatory portal tract infiltrate that is enriched with plasma cells. There is also an interface hepatitis where the border between the portal tract and the liver lobule is obscured
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In Australia, what % of adults have chronic hepatitis B?
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1-2%
Note - Rates in indigenous Australians and in migrants (from Asia, Africa, and Pacific Islands in particular) are much higher – up to 10-15%. |
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Replication of the hepatitis B virus is mainly in the hepatocyte but also occurs where?
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in salivary glands, pancreas and testis.
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Both the acute and chronic liver disease associated with HBV infection are mainly caused by what?
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the host response
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What causes the Fibrosis (cirrhosis) associated with HBV?
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It is caused by a local HBc antigen-specific cytotoxic T cell response. This process is greatly accelerated by concomitant liver injury by other agents - including alcohol or other viral infections such as HCV.
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Which virus is more infective HBV or HIV?
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The hepatitis B virus is 50 to 100 times more infectious than HIV and can survive outside the body for 7 days or more.
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Describe the presentation of acute hepatitis due to HBV?
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most patients are jaundiced and have high level HBsAg, and HBV DNA in the blood.
Anti-HBc is present and specific IgM Anti-HBc is detectable usually at high titre and HBeAg is usually present. |
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Describe the “liver” in someone with acute hepatitis due to HBV?
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In the liver HBV DNA is high and apoptotic liver cells as well as 'ground glass hepatocytes' containing very high levels of HBs are seen. There is also lymphocytic infiltration mainly in the portal tracts
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Describe the 4 phases of HBV infection?
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The immune tolerance phase occurs during the initial 15 to 30 years of life and is marked by HBeAg positivity, high-level hepatitis B viraemia but no active hepatitis (ie normal alanine aminotransferase level).
The immune clearance phase follows, with fluctuating HBV DNA and elevated ALT levels. During this phase, patients may spontaneously seroconvert from HBeAg positive to HBeAg negative with development of antibodies to HBeAg (anti-HBe). (Note - Spontaneous seroconversion before the age of 30 years confers a favourable long-term prognosis.) However, if this immune clearance phase is prolonged, fibrosis and cirrhosis may develop. Then the immune control phase when patients are HBeAg negative, anti-HBe positive and have low or undetectable HBV DNA (usually less than 2000 IU/mL) and normal liver enzymes. Some patients then progress to an immune escape phase with HBeAg negative chronic hepatitis and increased HBV DNA (more than 2000 IU/mL) and therefore have increased infectivity and inflammation. Such patients are at high risk of progression to cirrhosis, hepatic decompensation and hepatocellular carcinoma. |
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Describe the HBV vaccine and the protocols associated with it?
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The Hepatitis B vaccine consists of recombinant HBs antigen expressed in yeast. It assembles into virus like particles analogous to the defective HBs in serum. The vaccine is very effective and relatively affordable so that it is now WHO policy to offer vaccination to all neonates globally.
To prevent HBV transmission from infected mothers to their babies, hepatitis B vaccine plus specific hepatitis B immune globulin is given to the neonate within 12 hours of birth. |
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Liver transplantation is now rarely performed for patients with liver failure due to hepatitis B. why?
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Because of the effectiveness of antiviral treatment
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When are Serum ALT levels raised?
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ALT is raised due to release of this enzyme from the liver when hepatocytes are damaged. ie. hepatocellular necrosis, as in hepatitis.
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In most liver diseases, ALT values exceed AST, but what is one important exception and a few others?
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alcoholic hepatitis in which AST is >ALT.
Note - AST is also higher than ALT in diseases like chronic hepatitis at the stage of cirrhosis. |
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Alkaline phosphatase (SAP) and gamma-glutamyl transpeptidase (GGT) are present on the where in the hepatocyte?
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In the plasma membrane.
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When do you see commonly see raised plasma levels of SAP and GGT?
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in cholestasis - Note SAP and GGT are often referred to as 'biliary enzymes' because cholestasis is a common cause.
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Alcohol or drug ingestion (eg anticonvulsants) What can stimulate synthesis and release of GGT in the absence of liver injury?
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Alcohol or drug ingestion (eg anticonvulsants)
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why do you look at ALT more commonly than AST if your testing liver function?
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While AST is raised in acute liver damage, it is also present in red blood cells, and cardiac and skeletal muscle and is therefore not specific to the liver
Although note that AST is raised (above ALT) in alchsolic hepatitis |
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Describe what raised ALP in liver function tests suggests?
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Alkaline phosphatase (ALP) is an enzyme in the cells lining the biliary ducts of the liver. – so will rise with large bile duct obstruction, intrahepatic cholestasis or infiltrative diseases of the liver.
Note - ALP is also present in bone and placental tissue, so it is higher in growing children (as their bones are being remodelled) and elderly patients with Paget's disease. |
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Describe the use of GGT as a liver function test and its limitations?
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It is a plasma membrane enzyme which is reasonably specific to the liver and a more sensitive marker for cholestatic damage than ALP, but GGT may be elevated with even minor, sub-clinical levels of liver dysfunction.
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Describe the bilirubinaemia in general liver disease?
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Liver disease impairs both conjugation and secretion of bilirubin and is therefore associated with mixed conjugated and unconjugated hyperbilirubinemia.
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What sort of bilirubinaemia do you see in Cholestasis?
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Cholestasis produces conjugated hyperbilirubinemia.
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What is the commonest cause of mild unconjugated hyperbilirubinemia?
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Gilbert's syndrome- a genetic disorder of bilirubin metabolism that can result in mild jaundice, found in about 5% of the population
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What is Gilberts Syndrome?
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a genetic disorder of bilirubin metabolism that can result in mild jaundice, found in about 5% of the population which is the most common cause of unconjugated hyperbilirubinemia
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How can Vitamin K deficiency be caused by cholestasis?
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because of the resultant malabsorption of long chain fatty acids
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In acute liver failure what is the most useful test to show impaired liver function and why?
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a prolonged PT is the most useful test of impaired liver function (as opposed to the other tests for liver disease ) because of the rapid turnover of clotting factors
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In chronic liver disease, the serum albumin concentration may be low reflecting impaired hepatic synthesis. Is the same true in regards to total serum globulins?
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No – in chronic liver disease total serum globulins are often increased due to dysregulation of their synthesis.
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In Chronic liver disease, while there is low serum albumin, there is often raised total serum globulins (due to dysregulation). The types of globulins that are increased can be a clue to diagnosis, What do raised IgM, IgG and IgA each suggest?
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IgG will be raised with autoimmune hepatitis
IgM with primary biliary cirrhosis IgA with alcoholic liver disease. |
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In which liver disease do you see raised serum ferritin?
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haemochromatosis
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In which liver disease do you see low caeruloplasmin?
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Wilson's disease
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What is wilsons disease?
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Wilson's disease or hepatolenticular degeneration is an autosomal recessive genetic disorder in which copper accumulates in tissues
It manifests as neurological or psychiatric symptoms and liver disease |
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Chronic liver injury is usually defined as liver injury lasting for longer than six months. The terms, ' acute ' and ' subacute ' define liver injury lasting…..?
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less than six weeks and for six weeks to six months respectively.
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What are the 2 Autoimmune chronic cholestatic diseases?
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primary biliary cirrhosis (PBC) and primary sclerosing cholangitis (PSC).
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Which 3 Drugs may damage the biliary system?
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anti-psychotic drugs (chlorpromazine) and antibiotics (flucloxacillin, augmentin).
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True or False? Autoimmune hepatitis is the only primary immunologic disorder of the liver amenable to immunosuppressive therapy
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TRUE. - Corticosteroids (usually prednisone), usually given with azathioprine (imuran) improves the 5-year mortality from 40% without treatment to below 10%.
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How do you treat metal storage disorders?
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“bleeding” (venesection) to deplete body iron stores in haemochromatosis, and use of copper chelating agents like d-penicillamine for Wilson's disease.
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While endstage chronic liver disease was once uniformly fatal, liver transplantation is now a treatment that is highly effective in appropriately selected individuals. What are the Survival rates following liver transplant?
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~ 80% in adults and 90% in children.
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Describe the type of virus, the spread, the incubation period, the type of disease, if there is a risk of HCC and if there is a vaccine for HAV – Hepatitis A?
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Describe the type of virus, the spread, the incubation period, the type of disease, if there is a risk of HCC and if there is a vaccine for HBV – Hepatitis B?
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Describe the type of virus, the spread, the incubation period, the type of disease, if there is a risk of HCC and if there is a vaccine for HCV – Hepatitis C?
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Describe the type of virus, the spread, the incubation period, the type of disease, if there is a risk of HCC and if there is a vaccine for HDV – Hepatitis D?
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Describe the type of virus, the spread, the incubation period, the type of disease, if there is a risk of HCC and if there is a vaccine for HEV – Hepatitis E?
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What mode of transmission is responsible for the global prevalence of HBV?
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Maternal transmission
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Why is the HAV vaccination effective worldwide?
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Because there is a single serotype worldwide
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How do you test for recently acquired Hep A?
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IgM antibody against HAV – i.e. anti-HAV IgM
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What is the most common cause of acute hepatitis globally?
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HEV
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True or False? The main mode of tramission for HEV is person to person?
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FALSE – there is no person to person spread – it is a fecal transmission
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What is the fatality rate for those with HEV?
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1-3% in the general pop but 15-25% in pregnant women
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What are the 2 most common genotypes that predominate in Australia?
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1b and 3a
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Why is there a huge prevalence of viral hepatitis in Egypt and which type?
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HCV 3a – which is due to the shistosomaisis vaccination along the nile using the same needle
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What is the case fatality rate, and the mortality rate from chronic liver disease associated with HCV?
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low case fatality rate, and 3% mortality rate from chronic liver disease
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What % of HCV infections develop into chronic infection, and chronic hepatitis?
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60-80% leads to chronic infection and then 70% leads to chronic hepatitis
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How do you test for acute HCV infection and why?
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HCV serum RNA – which is evident within 1-3 weeks
Note – antibodies to HCV are unreliable as they take a while to develop |
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Name 11 fats the predict poor response to anti-viral therapy for HCV?
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Describe the serology for someone with resolved HBV infection?
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Describe the serology for someone vaccinated against HBV?
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Describe the serology for someone susceptible to HBV?
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Describe the serology for someone with acute HBV infection?
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Describe the serology for someone susceptible to HBV?
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Describe the serology for someone with chronic HBV infection?
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describe what you need for hep d infection and what results?
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HDV is considered to be a subviral satellite because it can propagate only in the presence of the hepatitis B virus (HBV).[1] Transmission of HDV can occur either via simultaneous infection with HBV (coinfection) or superimposed on chronic hepatitis B or hepatitis B carrier state (superinfection).
Both superinfection and coinfection with HDV results in more severe complications compared to infection with HBV alone. These complications include a greater likelihood of experiencing liver failure in acute infections and a rapid progression to liver cirrhosis, with an increased chance of developing liver cancer in chronic infections |
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Describe the 4 aspects of severe drug induced liver injury?
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Jaundice
bleeding (prothrombin >50%) Hepatic encephalopathy progresses fulminantly and rapidly |
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Describe hepatic encephalopathy?
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Hepatic encephalopathy is a worsening of brain function that occurs when the liver is no longer able to remove toxic substances in the blood.
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Identify the 9 drugs that can frequently causes drug induce liver injury?
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In order from most frequent to least….
Isoniazid, Chlorphromazine, Flucloxacillin (for staph), Dantrolene, Valproic acid, Halothane, Ketoconazole, Phenytoin, dicoflenac (NSAID) and Amoxycilin/Clavulanic acid (Augmentin) |
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What dose of paracetamole is associated with hepatotoxicity?
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12g – 24 tablets
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Why does fasting make paracetemol toxicity worse?
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Because fasting decreases your glutathione which is needed for detoxification of NAPQI
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What 3 drugs can cause hepatic fibrosis?
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Methotrexate
Arsenic Hypervitaminosis A |
