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169 Cards in this Set
- Front
- Back
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What are the main symptoms of liver failure?
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Jaundice, ascites and encephalopathy
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What are the two types of liver failure?
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Acute and chronic
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How can you distinguish acute from chronic liver failure?
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Acute usually presents with encephalopathy, confusion etc, jaundice and ascites do not have time to develop. Chronic is the opposite.
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What are some typical causes of acute liver failure?
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Paracetamol, ecstacy, Isoniazid (TB), hepatisis, epstein barr
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What are some typical causes of chronic liver failure?
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Cirrhosis, alcohol, viruses (HBV, HCV), some autoimmune conditions
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In cirrhosis, what is the 50% rule?
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50% of the liver can be fibrous tissue, which means the functioning mass of the liver is reduce by over 50%, whihc means remaining liver cells function at less than 50% efficiency
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What is bilirubin?
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The tetrapyrrole ring of haem is linearised to yield bilirubin, part of the breakdown of red blood cells
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Why is bilirubin transported to the liver and how is it excreted?
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Bilirubin is insoluble, so must be transported to the liver, here it is made soluble and then it can be excreted as bile.
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Which cells break down red blood cells and where are they found?
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Kupffer cells in the liver (specialised macrophages) and other macrophages in the spleen and bone marrow break down old red blood cells
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How is unconjugated (insoluble) bilirubin transferred to the hepatocytes?
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Boiund to plasma albumin
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What are the classic signs of jaundice?
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Yellow skin and sclera, dark urine
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Is the bilirubin secretory pathway rate limited by liver damage?
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No, the liver's ability to excrete bilirubin is not reduced even in extensive liver damage, this means that patients will always present with jaundice in liver failure.
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Classify glands according to whether they have ducts or not.
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Ducted glands are exocrine. Endocrine glands have no ducts.
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What is merocrine secretion, and give an example in the body?
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Also known as eccrine, this is secretion by exocytosis - the contents of the vesicle leave the cell without a membrane. Example, sweat glands.
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What is apocrine secretion, and give an example in the body?
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This secretion occurs via a membrane bound vesicle. Example, mammary glands.
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What is holocrine secretion, and give an example in the body?
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In this secretion, the whole cell ruptures, releasing it's contents into the lumen. Examples are sebaceous glands in the skin.
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Classify salivary glands.
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Exocrine (ducted), and merocrine (modified sweat glands), branched acinar structure
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Why do some acinar cells stain dark or light?
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Light staining cells secrete mucus, dark staining cells secrete serous/watery
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What are serous demilunes?
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Dark staining serous cells, squidged to the outside of the light staining mucus cells. Probably an artifact, in life they are arranged equally.
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What are the various secretions of the salivary glands?
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Parotid - serous. Sublingual - mucus. Submandibular - mixed.
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What are myoepithelial cells and what do they do?
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Myoepithelial cells surround acinar glandular cells, and aid secretion by contraction.
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What is the order of the ducts in an acinus gland?
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Acinar cells secrete 1) into an intercalated duct 2) then a striated duct and 3) and excretory duct
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What are striated ducts and how do they gain their appearance?
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Infoldings of basal membrane and vertically aligned mitochondria form the striations, they are the site of Na+ pumps for reabsorption of Na+ and Cl-. Also secretion of K+ and HCO3- to make a hypotonic secretion.
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Which antibodies are secreted by plasma cells?
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IgA class anitbodies.
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How does the pancreatic acinar duct differ from that found in the parotid gland?
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Have centroacinar cells, and no striated ducts.
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What are centroacinar cells?
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Sit inside the acinar cells in the pancreas, secreting mucus and bicarbonate. Not found in the parotid gland.
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Which cells secrete what in the pancreatic Islets of Langerhan?
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Alpha cells - Glucagon
Beta cells - Insulin Delta cells - Somatostatin |
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What structures make up the portal triads?
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Hepatic portal vein, hepatic artery, and bile duct (plus lymphatics)
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Which direction does fluid flow in the liver?
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Oxygenated blood (hepatic artery) and venous blood (hepatic vein) flow towards the central vein. Lymph and bile flow out to the portal triad.
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Where are the sinusoids?
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Form channels between hepatocytes.
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Where do the Kupffer cells lie?
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In sinusoids with endothelial cells
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What is secreted by hepatocytes?
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Albumin, fibrinogen and clotting factors (2, 7, 9 and 10)
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What is typically absorbed in hepatocytes?
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Nutrients and drugs.
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Which channels aid in the secretion of bile from hepatocytes?
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Bile canneliculi.
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What is bile?
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Thick alkaline fluid containing salts such as sodium glycocholate, deoxycholate and taurocholate, plus bile pigments such as bilirubin and biliverdin.
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What is a lobule?
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The hexagonal structure demarcated by portal triads arranged around a central vein.
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What shape is a liver acinus?
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Diamond shape, links 2 central veins via the two intermediate portal triads.
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Describe the zones of a typical liver acinus
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Zone 1 lies between 2 triads, half way between central veins. This is where most oxygenated blood is, and is the site for toxicity.
Zone 2 lies more lateral to this. Zone 3 is near the central veins. Blood here is least oxygenated, this is the last site for toxicity, but the first for ischaemia. |
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What is the epithelium of the gall bladder?
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Tall, simple columnar with a brush border. Also heavily folded to allow for expansion.
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Which neural and hormonal stimuli promote the production and release of bile?
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PNS (Vagus) is the main nerve
Acidic chyme in the duodenum stimulates release of secretin and CCK Secretin enhances the flow of bile from the liver hepatocytes CCK causes contraction of the gallbladder |
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Does blood pressure affect biliary secretion?
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Not in the first instance. Bile production can increase to maximum without any rise in blood flow in the liver.
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Is secretion of a bile a consequence of raised hydrostatic pressure in the blood over the bile ducts?
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No, in fact it can be the other way round, and bile will still pass out of the blood.
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Describe the path of bile from the hepatocytes to the gall bladder.
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Collects in bile canaliculi and then into perilobular ducts, then terminal ducts and finally interlobular ducts,. Next it passes into the right and left hepatic ducts, then the common hepatic duct (pre-gall bladder), then the common bile duct (post gall bladder)
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When does hepatic bile collect in the gall bladder?
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Interdigestive state (between meals)
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What is the rough composition of liver bile?
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Cholic, chenodeoxycholic and deoxycholic salts, isotonic to plasma although Na+ is higher due to osmotically active micelles sequestering cations.
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Why does liver bile contain a higher Na+ concentration than plasma?
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Bile forms osmotically active micelles which sequester cations such as Na+
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How does the gall bladder concentrate bile?
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Between meals the bile duct opening to the duodenum is closed. Bile backs up into the gall bladder. Here it is concentrated 20x by removal of Na+, Cl- and H2O.
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What happens to secreted bile salts?
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Reabsorbed, mostly in the lower ileum and is transported back to the liver.
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Does bile secretion have a temperature coefficient and what doe this say about the process?
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It has a high temperature coefficient and this indicates it is a metabolically active process requiring energy.
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Is bile just salts?
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No, contains acids, fatty acids, bilirubin and cholesterol in high concentrations
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Where does the bilirubin in bile come from?
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85% from breakdown of RBC, 15% recycled from ileum
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Why is toxic bilirubin not damaging in the blood?
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Tightly bound to plasma albumin until it is conjugated in the liver.
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How is bilirubin conjugated in the liver?
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UTP and glucose form UDP-glucaronic acid, this is conjugated with bilirubin by enzyme Glucuronyl transferase, to form bilirubin (conjugated) and UDP
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How is cholesterol, normally insoluble, incorporated into bile?
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Forms vesicles with phospholipids.
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What might cause a painless jaundice?
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Obstruction of bile duct (e.g. by cancer), anorexia, or increased bilirubin production (haemolysis, transfusions), or decreased clearance (hereditary defects)
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Where is Lipoprotein Lipase found, how is it activated, and what is it's role in the storage of fatty acids?
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Lipoprotein Lipase is present in capillaries. It is activated by insulin and it is responsible for the hydrolysis of triacylglycerol (TAG) present in chylomicrons prior to its storage in adipose tissue.
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What happens to remnant chylomicrons in the liver?
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Cholesterol is used in VLDLs and in bile, new TAGs synthesised.
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Which enzymes break down lipids in the stomach?
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Lingual and gastric lipase
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What happens to medium and short chain fatty acids in the stomach?
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Diffuse freely into the blood, hence 15% of fat absorption happens in the stomach.
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How do short and medium chain fatty acids diffuse into enterocytes?
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Soluble in water.
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What continues the breakdown of fats in the proximal small intestine?
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Pancreatic juices (secretio stimulated by secretin, gastrin and CCK)
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What stimulates the release of CCK by duodenal mucosal cells?
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Arrival of acidic chyme from the stomach into the duodenum.
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Where is pancreatic lipase active and why?
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At the interface of the triglyceride droplet. Both bile salt and phopholipid micelles inhibit it's action elsewhere.
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What happens to emulsion droplet as fat is broken down?
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They get smaller and smaller, eventually forming unilamellar vesicles composed of bile salts and mixed lipids.
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How are fatty acids absorbed from bile salt and mixed lipid micelles?
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Bile salt/mixed lipid micelles reach the enterocyte brush border they encounter a low pH, the FFA are protonated and pass into the enterocyte either by diffusion or collision
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What happens to bile salts once fatty acids are absorbed?
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Pass along and are absorbed into the small intestine passively and via active transport in the distal ileum.
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What happens to absorbed fats in the SER of enterocytes?
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Long chain fatty acids, monoglycerides, lysophospholipids and cholesterol are re-esterified in the SER.
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Where are apoproteins formed in enterocytes?
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RER.
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Where are apoproteins glycolysated in enterocytes?
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Golgi.
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What happens to nascent chylomicrons and VLDLs in enterocytes?
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Gain apoproteins in their membranes.
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How are VLDLs and chylomicrons absorbed and why?
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Lacteals, so pass into the lymph. They are too big to pass through fenestrations in the capillaries.
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How does absorbed fat enter the blood stream?
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Lacteals, thoracic duct, subclavian vein.
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What are the 5 lipoprotein particles found in blood, in order of size?
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Chylomicrons, VLDL, IDL, LDL, HDL.
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What is pharmacokinetics concerned with?
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ADME - Absorption, Distribution, Metabolism and Excretion of drugs.
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What are enteral and parenteral routes of drug administration?
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Enteral - mouth and bum, parenteral, anywhere else.
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Why would you go via a parenteral route?
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Speed/high concentration required quickly - nerve block for surgery, oral route not possible
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Why would you go oral?
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Sterility not required, non-invasive, no skill/training to administer, cheap, gradual absorption.
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What is bioavailability of an orally administered drug and how is it calculated?
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AUC - Area Under Curve for drug plasma concentration. Bioavailability is the ratio of availability of a drug orally/IV x 100%
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What processed are involved in the subsequent decline in plasma concentration following IV administration?
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Distribution. Drug is distributed to fluid compartments (vasculature, tissues)
Kidney clearance - GFR, secretion Liver clearance - metabolism, biliary excretion |
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Give reasons why an orally administered drug might fail to achieve a satisfactory plasma concentration?
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Too insoluble to dissolve in GIT
Not stable in acid pH in stomach Broken down by stomach enzymes Drug not lipophilic so cannot be absorbed in GIT Pumped back into lumen by enterocyte transporters Metabolised too quickly in first pass (first pass effect) |
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Where are basic drugs best absorbed?
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Alkaline conditions of the intestine (cannot be absorbed in ionised form)
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Where are acidic drugs best absorbed?
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Acidic conditions in the stomach (cannot be absorbed in ionised form)
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Which forms of drugs are not absorbed in the GIT?
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Ionised forms - so basic drugs are not absorbed in the stomach, and acidic drugs are not absorbed in the small intestine.
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How do chemicals enter hepatocytes?
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If lipophilic they can diffuse from sinusoids into hepatocytes. Otherwise they need transporter proteins.
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What are the two phases of drug metabolism?
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Phase 1 - Oxidation e.g. N- and O- reactions,
Phase 1 - Reduction e.g. ketone conversion Phase 1 - Hydrolytic reactions e.g. de-esterification Phase 2 - enzyme mediated conjugation e.g. glucuronide, glutathione, sulphate |
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What is the reaction most typical of phase one drug metabolism?
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Oxidation.
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What are some non-Cytochrome P450 enzymes?
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Alcohol dehydrogenase, MAO, esterases
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Where are cytochrome P450 enzymes found?
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Lipid membrane of ER.
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What is first pass effect?
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Term used to describe a drug which after oral administration is absorbed but fails to appear in the blood, or appears in a much lower concentration - due to excretion directly into bile by hepatocytes, or is metabolised by phase 1/2 enzymes.
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Give examples of drugs which have a near complete first pass effect and state whether this is desirable.
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GTN - under tongue vasodilator, used in angina so good effect
Inhaled corticosteroids for asthma, again, good Testosterone - bad so administer in lipid soluble form |
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How do hepatocyte transporters deal with high molecular weight conjugates?
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Transport into bile canaliculi, too hydrophilic to diffuse back so excreted into small intestine
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How do hepatocyte transporters deal with low molecular weight conjugates?
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Actively transported into sinusoidal blood, pass to kidney and are excreted.
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Why might some enteral and parenteral administration routes be preferable to standard oral therapy?
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Faster enter to blood stream, e.g. GTN under the tongue
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Give two examples of pharmacological inactivation.
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Corticosteroid inhaled for asthma is inactivated in the liver. If swallowed it is used for Crohns, it is an antiinflammatory in the gut, but is then metabolised in the liver 'first pass' so doesn't enter systemic circulation.
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Give an example of phamacological activation.
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Enalapril is de-esterified to form the active ACE inhibitor, Enalaprilat.
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Give an example of activation to a toxic metabolite.
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Paracetamol if taken in overdose quantities saturates the usual defensive pathways leading to the formation of a toxic metabolite.
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Give three types of hepatoctoxicity due to drugs.
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Paracetamol, which in overdose saturates usual defensive pathways to become a toxic metabolite
Some drugs can form metabolites which in some patients can stimulate an immune response on second exposure The third type binds to bile transporters, preventing secretion of bile |
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What is cholestasis?
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Any condition which causes blockage of bile from the liver.
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Which of the two processes are saturable in paracetamol overdose?
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Glucuronyl conjugate, and sulphate conjugate.
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What happens to any toxic metabolites formed after normal doses of paracetamol?
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Conjugated by glutathione
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What happens to normal routes of conjugation in paracetamol overdose?
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Normal routes of conjugation are saturated, toxic P450 metabolite is formed, glutathione runs out and the toxic metabolite binds to liver proteins inactivating them, leading to cell damage and vulnerability to ROS.
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What can be given to patients after a paracetamol overdose?
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Within 12 hours treatment with a glutathione precursor can raise levels and protect liver cells
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How much is a unit of alcohol (g and ml)?
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10ml, 8g
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How many units in a pint of lager (normal strength), a pint of premium strength, a 175ml glass of wine @ 14% and a pub measure (25ml) of 40% vodka?
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Normal strength lager - 2 units
Premuim strength - 3 units 175ml glass of wine - 2.5 units 40% Spirit, 25ml - 1 unit |
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What is the DoH guidelines for alcohol for men and women?
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Men, 3-4 units per day, women 2-3 units per day
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What are the three routes of (phase 1) ethanol metabolism to acetaldehyde by liver cells?
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Main route - Alcohol Dehydrogenase in cytosol
Second route - Cytochrome P450 type 2E1 (CYP2E1) - in Endoplasmic Reticulum Third route, not at all really - Catalase |
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What is the toute of metabolism of acetaldehyde in liver cells, and to what?
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Acetaldehyde is metabolised to acetate by aldehyde dehydrogenase (ALDH)
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What is the energy source for the metabolism of ethanol by liver cells?
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NAD+ - NADH
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What is NAD?
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Nicotinamide Adeninde Dinucleotide - a proton carrier for redox reactions.
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What are the two key differences in the way alcohol is metabolised by men and women?
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Women have a slower metabolism, so they achieve higher BAC and it takes longer to diffuse out of their system.
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How does disulfiram (Antebuse) work and why is it crap?
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Stops the second stage metabolism of acetaldehyde to acetate by inhibiting aldehyde dehydrogenase. Causes 'flushing'/hangover symptoms immediately after drinking; high BP, dizzyness, headache, feinting etc. Crap because it makes you feel so shit no alcoholic would ever take it voluntarily.
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How is methanol toxic, and what 2 options are available for treatment?
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Methanol in metabolised to formaldehyde, then formic acid - which disturbs neuronal mitochondrial function. Ethanol prolongs the half life of methanol, so if you get drunk, you can stave off the toxic effect long enough to have dialysis to remove the toxin. Now treatment is with fomepizol (a long acting ADH antagonist)
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How does alcohol alter energy metabolism in liver cells?
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NAD is needed for Acetyl CoA to enter the citric acid cycle, and for fatty acid oxidation. When alcohol is consumed, NAD is used to metabolise the alcohol. Acteyl CoA cannot enter citric acid cycle, so is used for fatty acid synthesis, and because these are not oxidised they form triglycerides.
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Acetaldehyde is chemically active and toxic in what ways?
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Formation of neoantigens (modified proteins) can lead to an immune response and alteration of protein secretion and endocytosis mechanisms.
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What is blood alcohol content?
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Grams of ethanol/100ml of blood.
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What is the drink drive limit?
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80mg/100ml = 0.08BAC
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At what level BAC would you expect to find gross motor impairment, blurred vision and major loss of balance, dysphoria and impaired judgement and perceptions
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0.13-0.15BAC (130-150mg/100ml)
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On average, how quickly is ethanol metabolised so it is removed from the blood?
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7-10g per hour
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What symptoms would you expect at 0.2BAC?
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Dazed/confused, disorientated, desensitised to pain, nausea and vomiting, gag reflex impairment, blackouts
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At what BAC level would you expect coma and possible death due to respiratory arrest?
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0.4BAC (although coma can result at 0.35BAC)
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What is the drink drive limit in mM?
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17.4mM
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What are the likeliest sites of intoxicating action in the CNS for low/medium dose ethanol?
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GABA channels (neuronal inhibition)
Glutamate NMDA receptor channels (inhibits neuronal excitation) slo-1 potassium channels - (inhibits neuronal excitation) Thalamic T-type calcium channels - concentration |
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Why is the effect of alcohol on concentration said to be biphasic?
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Low doses enhance concentration, high doses inhibit
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Explain how alcohol is thought to affect GABA receptors.
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GABA channels are principally inhibitory in the CNS - they make up ion channels for chloride, which keeps neurones in their -ive or off state when allowed into the cell. Alcohol is thought to enhance GABA effects at low doses
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Explain how alcohol is thought to affect thalamic T-type calcium channels at low and high doses.
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Alcohol enhances activity of Thalamic T-type calcium channels at low doses, and inhibits their activity at high doses
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Explain how alcohol is thought to affect NMDA receptors.
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NMDA receptors mediate neuronal excitability, alcohol is thought to suppress these receptors
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What does alcohol do to slo-1 potassium channels?
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Stimulates them, inhibiting neuronal excitability.
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Which area of the brain is thought to be involved in the mechanism for alcohol dependence?
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Nucleus accumbens (ventral striatum)
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What are some of the features of foetal alcohol syndrome?
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Thin upper lip, indistinct philtrum, short palpebral fissures (slitty eyes), railroad ears
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What teratogenic effects (disturbing foetal development) are seen with alcohol abuse by pregnant mothers?
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Reduction in size of the corpus callosum, pre-frontal cortex (cognitive) and parietal cortex (including language interpretation)
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What level BAC is shown to affect neurones in the foetus?
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200mg/dl (more than double the drink drive limit) for a few hours can cause significant cell loss
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What effects are caused by first trimester and third trimester drinking?
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First trimester - craniofacial, third trimester, neuronal
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What are spider naevi and what do they symbolise?
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Spider naevi are caused by failures of cutaneous arteriole sphincters caused by the failure of the liver to metabolise oestrogen - only found in SVC areas (so face, neck, arms and hands)
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Alcohol affects liver cell synthesis of proteins, what symptom would this cause?
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Low albumin causes a loss of oncotic pressure, leading to peripheral oedema.
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Which proteins are notably produced by the liver?
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Albumin and prothrombin.
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Why does liver damage cause ascites?
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Damage to liver cells and resulting fibrosis causes portal hypertension, this combined with low plasma albumin causes build up of fluid in the peritoneal space (due to Starlings hypothesis relating to hydrostatic v oncotic pressure)
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How does the failure of the liver to synthesise prothrombin (clotting factor 2) affect patients?
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Bleeding and bruising. Also INR (International Normalised Ratio) is raised - as half life of prothrombin is 6hours this
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Liver failure causes the failure of metabolism of certain key hormones, which ones?
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Aldosterone - leads to salt and water retention
Ascites and oedema are exacerbated Oestrogen - gynaecomastia, impotence and spider naevi |
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What causes hepatic encephalopathy?
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Failure of the liver to synthesise urea leads to a build up of ammonia and aromatic amino acids, these lead to cerebral dysfunction, disordered mood, violent and aggressive behaviour, confusion.
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What causes the aromatic smell to some patients?
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Build up of aromatic amino acids due to failure of liver to synthesise urea.
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Failure of liver metabolism leads to hyper- or hypoglycaemia, and why?
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Reduced insulin clearance by liver (as with oestrogen), also decreased breakdown of glycogen, and inability to synthesise glucose (gluconeogenesis) - all lead to hypoglycaemia.
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Why might autocannibalism occur in chronic liver disease?
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Lack of glucose leads to fat and muscle breakdown, this autocannibalism causes a negative nitrogen balance.
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What are some of the side effects of autocannibalism?
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Increased resting energy expenditure, which causes inflammation and increase in levels of inflammatory mediators.
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What hormones are raised in hypermetabolism due to liver failure?
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Adrenalin and NA raised as they are not metabolised, causing increase CO
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Why are liver disease patients more at risk of infections?
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Loss of Kupffer cells - specialised liver macrophages, result is frequent bacterial infections from the GIT.
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What do alanine and aspartate play a major role in?
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Nitrogen metabolism:
Alanine - Nitrogen transport Aspartate - Urea synthesis |
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What might raised levels of alanine amino transferase (ALT) and asparate amino transferase (AST) indicate and why?
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Present in liver cell cytosol and mitochondria, if found in blood there is evidence for liver cell damage
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List some tests for liver function.
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Bilirubin, ALT and AST, alkaline phosphatase, albumin levels, INR
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What is Child-Pugh grading?
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A measure of severity in chronic liver disease.
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What factors are accounted for in Child-Pugh grading?
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Encephalopathy, ascites, bilirubin levels, albumin levels and INR.
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Which types of hepatitis virus cause chronic infection?
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B, C and D. A and E do not.
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What percentage of 5 years olds have hepatitis A in resource poor countries?
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80-90%
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What is the route of transmission for hepatitis A?
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Faeco-oral
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If a patient with Hepatitis A has jaundice are they still infectious?
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No
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How is Hep E transmitted and what is the incubation period?
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Enterically. 6 weeks.
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How is Hep B transmitted and what is the incubation period?
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Sexual intercourse, blood born. 6 weeks to 6 months incubation, mean period is 2.5 months
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What are the clinical features of an acute Hep B infection?
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Jaundice, usual acute symptoms, but these resolve, and then the chronic infection persists causing cirrhosis.
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What factors put you at increased risk of developing chronic complications from a Hep B infection?
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Age of infection, worse if young
Immune compromised If acute infection was asymptomatic |
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What is the best way to stage a Hep B infection, assess infectivity or the effectiveness of anti-virals?
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Hep B DNA test
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List four measures to prevent, control or treat Hepatitis B.
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Passive immunisation with Hep B Ig, active immunisation with a recombitant vaccine, antiviral therapy and immunomodulators.
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What is delta hepatitis?
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A 'super infection' - a defective virus which can only survive if also infected with Hep B, so Hep B immunisation is effective.
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How is Hep C transmitted and what is the incubation period?
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Blood products, transfusions. 6 - 12 week incubation period.
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What are some of the risks of a Hep C infection?
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Anicteric. 50% of patients may develop liver damage and 20% can develop cirrhosis.
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What is the duodenal cap and why is it relevant?
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The smooth walled initial part of the duodenum. This is readily identifyable on x-ray.
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What is a feature of gall stones on an ultrasound?
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Echo streaks
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What are the 4 main ways to visualise the duct system of the biliary tract?
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Drugs, vascular injection, liver injection and retrograde investigation via the duodenum.
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What is the difference between a cholecystogram and a choleangiogram?
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Cholecystogram = tablets. Choleangiogram = IV dye.
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Which part of the small intestine appears more flocular on x-ray, and why?
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Upper 2/5ths = jejunum, appears this way due to plica circulares.
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How can you take a double contrast view of the colon?
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Inflate with air.
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