23/05 Flashcards
what does omeprazole act on
Parietal cells are located in the epithelium lining the fundus and body of the stomach, and secrete HCl into the stomach using the H+/K+-ATPase pump. Omeprazole is a proton pump inhibitor (PPI) and therefore inhibits the H+/K+-ATPase pump.
2 primary bile acids
Cholic acid
Chenodeoxycholic acid
bile salts
cholic acid
Chenodeoxycholic acid
When these bile acids are conjugated with amino acids they form bile salts.
Bile salts are amphipathic which means they have a hydrophobic end (which is lipid soluble) and a hydrophilic end (which is water soluble).
This structure allows bile salts to emulsify fats which allows pancreatic lipase digest fats.
hepatotoxic drug eg
Amiodarone is a hepatotoxic drug. This means it is likely to cause damage to the hepatocytes and impair its ability to conjugate bilirubin, leading to hepatic jaundice.
used for bad ventricular tachy
Metoclopramide
Metoclopramide is a dopamine-receptor antagonist which causes relaxation of the lower oesophageal sphincter and increases gastric motility, leading to increased gastric emptying. Patients on these drugs may experience an increased appetite
Enterogastric reflex
The enterogastric reflex is stimulated by distension of the small intestine by the presence of chyme. Inhibitory signals are sent to the stomach via the enteric nervous system as well as signals to the medulla. Vagal stimulation of the stomach is reduced and gastric acid secretion is reduced.
feedback mechanism to regulate the rate at which partially digested food (chyme) leaves the stomach and enters the small intestine.
Brunner’s gland
Submucosa of the duodenum only
Brunner’s gland provide abundant alkaline mucous to neutralise the chyme entering from the stomach.
Gastric Inhibitory Peptide
Gastric Inhibitory Peptide (GIP) mediates the ileal brake reflex. This delays gastric emptying to prevent unabsorbed nutrients entering the lower ileum, and is mainly triggered by high levels of fat. The aim of the ileal brake reflex is to slow small intestine bolus transit, to increase absorption in the small intestine. If GIP is disrupted, this will therefore exacerbate malabsorption by interrupting this reflex.
What is mainly responsible for gastric-inhibitory peptide (GIP) secretion?
GIP belongs to a family of metabolic hormones called incretins. Incretins are released after eating a meal containing glucose. They cause beta cells of the pancreatic islets to release insulin and lower blood glucose levels.
excess insulin production and secretion continues after the glucose derived from the meal has been digested, causing the amount of glucose in the bloodstream to fall to a lower-than-normal level.
what does CCK do
Chole = “bile”, cysto = “sac”, kinin = “move” –> move the bile-sac (gallbladder).
The presence of fatty acids in chyme that passes through the duodenum stimulates gallbladder contraction and release of stored bile into the duodenum via CCK. Bile plays a key role in digestion of fat in the duodenum.
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Frank-Starling curve of the heart shows
Stroke Volume and Preload
reason for oedema in heart failure?
Aldosterone promotes sodium and anion reabsorption, which increases the osmolality of the extracellular fluid. Thus, osmoreceptors in the hypothalamus detect this increase and stimulate ADH secretion, which acts to increase fluid retention and oedema.
Venous return =
(Mean systemic filling pressure - Right atrial pressure) / Resistance to venous return.
Muscarinic receptors
G-protein coupled receptors. (M1-M5)
M1 is excitatory and found in neural tissue, gastric parietal cells and salivary glands.
M2 is inhibitory and found in cardiac tissue.
M3 is excitatory and is principally found in exocrine and smooth muscle tissue.
Muscarinic receptors are involved in parasympathetic neural pathways, as well as sympathetic stimulation of the sweat glands. They are usually stimulated by acetylcholine (although they can be stimulated by muscarine) and they are inhibited by atropine.
Adrenoceptors
G-protein coupled receptors. sympathetic nervous system
Alpha1, Alpha2, Beta1 and Beta2.
Alpha1 (located in blood vessels and when stimulated cause vasoconstriction),
Beta1 (located in the heart and when stimulated cause increased heart rate and contractility)
Beta2 (located in the lungs and when stimulated cause bronchodilatation).
They are stimulated by adrenaline (typically acts on Beta adrenoceptors) and noradrenaline (typically acts on Alpha adrenoceptors).