30/04 Flashcards
causes post-hepatic jaundice
due to biliary obstruction by a stone in the common bile duct or by carcinoma of the pancreas. Pancreatic pseudocyst, chronic pancreatitis, sclerosing cholangitis, a bile duct stricture, or parasites in the bile duct are less common causes.
Pre-hepatic jaundice
caused by conditions that heighten your blood’s rate of hemolysis. This is the process through which red blood cells are broken down, releasing hemoglobin and converting into bilirubin. Because the liver can only process so much bilirubin at once, bilirubin overflows into bodily tissues
Hepatocellular jaundice
bilirubin is unable to leave the liver cells and cannot be removed from the body by the kidneys. Hepatocellular jaundice is usually caused by liver failure, liver disease (cirrhosis), hepatitis (inflammation of the liver), or by taking certain types of medication.
sickle cell disease and jaundice causes
Patients with sickle cell disease are prone to haemolytic crises, in which sickled red blood cells pool in the spleen and are haemolysed. This is particularly common when patients are exposed to hypoxia or infection. Bilirubin is a breakdown product of haem, and therefore levels will increase if there is increased haem present in the blood following haemolysis.
transporting peptides into enterocytes from the intestinal lumen?
Peptide transporter-1 (PepT1)
alcohol cirrhosis / hepatitis
Consistent damage to the liver can impair bilirubin uptake by hepatocytes, leading to accumulation in the blood and resultant jaundice.
what absorb iron
only mechanism by which the body can regulate iron absorption is by altering the extent of iron absorption. Hepcidin is a peptide that is secreted by hepatocytes, and it acts to decrease the number of iron transporters in the basolateral membrane of enterocytes. Therefore, reducing hepcidin secretion allows the body to increase iron absorption and restore iron levels in the blood.
excessive bruising and recurrent nosebleeds due to
Following digestion, monoglycerides and fatty acids associate with bile salts (not bilirubin) and phospholipids, forming micelles. They also contain fat-soluble vitamins and cholesterol.
Vitamin K is a fat-soluble vitamin and due to its role in clotting factor synthesis, a deficiency leads to excessive bleeding (presenting with symptoms such as excessive bruising and recurrent nosebleeds). Malabsorption of micelle components including vitamin K would explain this patient’s symptoms.
intermittent right upper quadrant pain, pain may be a result of biliary colic secondary to gallstones.
Cholecystokinin (CCK) increases the flow of bile by stimulating gallbladder emptying. This patient has obstruction of the bile duct by gallstones, and pain will result when there is contraction of the gallbladder if the bile duct is obstructed.
what does omeprazole block
Omeprazole is a proton pump inhibitor (PPI) which blocks the action of the H+/K+ ATPase pump in gastric parietal cells. H+/K+ ATPase typically exchanges potassium from the intestinal lumen with cytoplasmic hydronium. It is responsible for the acidification of the stomach contents. By blocking these enzymes, PPIs reduce the amount of stomach acid produced, alleviating symptoms of acid reflux.
cells is unaffected by atropine administration?
Enterochromaffin-like cells release histamine when stimulated by gastrin. Gastrin is released from G-cells that are stimulated via vagal stimulation through the neurotransmitter gastrin releasing peptide (GRP) not by acetylcholine (the primary neurotransmitter of the parasympathetic nervous system). Atropine is an antagonist of muscarinic receptors, and blocks the action of acetylcholine typically released by post-ganglionic neurones in the parasympathetic branch of the autonomic nervous system. As acetylcholine is not involved in the stimulation of enterochromaffin-like cells, they will be unaffected by atropine poisoning.
What is the mechanism of action of oral rehydration therapy in the treatment of cholera
Oral rehydration therapy consists of fluid administration, in combination with sodium and glucose. Action of the sodium-glucose transporter increases in order to increase sodium and glucose absorption. The presence of increased sodium and glucose in the epithelial cells lining the GI tract increases their osmolality, and creates an osmotic gradient acting into the cells, along which water passively diffuses. Water absorption is increased, which reduces water loss in the stool and therefore dehydration risk.
stimulates the gastric phase of secretion
Gastric secretion is stimulated by the presence of ingested food (mainly peptides and amino acids). Ingested food stimulates gastric secretion in 2 ways:
Stretching the stomach - This activates a short reflex, mediated through the myenteric nerve plexus, and a long reflex mediated via the vagus nerve.
Raising pH of its contents
What is the mechanism of dehydration in cholera
Cholera toxins bind to chloride channels on the apical membrane of enterocytes lining the small intestine, resulting in chloride (and subsequently sodium) efflux into the lumen. This increase in ion concentration in the lumen increases osmolality of the lumen, and creates an osmotic gradient by which water passively diffuses into the lumen. Not all this fluid can be reabsorbed in the large intestine, resulting excessive fluid loss and dehydration.
What effect does a higher salivary flow rate have on the ionic composition of saliva
higher salivary flow rates there is less time for duct cells to reabsorb bicarbonate ions, the main determinant of salivary pH. Therefore, the saliva will be more alkaline (less acidic
