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38 Cards in this Set
- Front
- Back
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Membrane transporters of the GI tract
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- Na + - K + ATPase
- NKCC symporter - Cl - - HCO 3 - antiporter - Na + - K + antiporter - H + - K + ATPase - NA + , K + , Cl - channels Apical |
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ions in CFTR (cystic fibrosis channel
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CL- out. drives Cl in / HCO3 out antiporter
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what does CCK do
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constriction of gall ladder and bile secrtetion
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describe pepsin
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- Secreted as pepsinogen
- Conversion occurs at pH<5 - Optimal activity pH<3 - Gastrin, Ach, CCK, secretin increase secretion - Can digest up to 20% of protein in meal |
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what activates trisinogen (into what)
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Enteropeptidate activates tripsinogen into trypsin aka enterokinase
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what happens at brush border
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• Brush Border
– Enzymes on enterocytes ’ luminal surface • Disaccharides etc - sucrose, maltase, lactase • Small peptides - peptidases • |
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what happens in Intracellular digestoin
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Intracellular
– Enzymes inside enterocytes • Peptidases - di - or tri - peptides - > amino acids |
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glucose carrier is dependent on gradient of what ion
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Na
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fructose carrier is powered how?
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facilitated diffusion glut 5
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sugar transporter on basolateral pole of the cell? powered by what?
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GLUT 2 facilitated diffusion
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difference between endo and exo peptidase
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exopeptidases break down the end AA bonds
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di and tri peptides are cotransported (and antiported) with what ion? single AAs?
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H+
AA's with Na+ |
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lipase breaks triglycerides to
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2 fatty acids and a monoglyceride
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describe enterohepatic circulation
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about 90% of bile acids are reabsorbed by active transport by the ileum
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whats i a chylomicron what does it do
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fats, cholesterol and protein, gets packaged into vesicles at the Golgi and exit to the lymphatic system via lacteals
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important fat soluble vitamins
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ADEK
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how is B12 absorbed
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in the ileum, only in complex with "intrinsic factor" secreted in stomach
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hepcidin acts how
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master regulating hormone of iron absorption which acts by inhibiting ferroportin
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what senses hi or low blodd pressure
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volume receptors and endocrine cells in the atria; baroreceptors in the carotid and aorta
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what channels are added or modified i nresponse to aldosterone?
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ROMK (K secretion); ENaC; Na/K ATPase (Na reabsorption)
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what causes increased bicarb and result?
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hyperventilation; increased pH (alkalosis)
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what causes increased carbonic acid; result?
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hypoventilation; decreased pH (acidosis)
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hallmark of metabolic acidosis?
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decrease in HCO3- (bicarbonate) (it gets used up in buffering the acid)
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most likely mechanism for ventilatory compensation
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progressive increase in the sensitivity of carotid body chemoreceptors
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explain: Ventilatory Adaptation
Carbonic Anhydrase Inhibition Promotes Acclimatization |
Carbonic anhydrase inhibition with acetazolamide
(Diamox) inhibits secretion of [H + ] into the renal tubular fluid which causes LESS reabsorption of [HCO 3 - ] – net effect is an acidosis that facilitates natural acclimatization – stimulating ventilation. |
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describe the shift of oxygen hemoglobin dissociation curve at elevations above 1500 ft
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left shift, O2 loading in the lungs is enhanced and blood carries more oxygen (in response to low PCO2 due to hyperventilation)
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"hypoxic pulmonary vasoconstriction"
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This promotes redistribution of blood in the lungs. There
is a greater perfusion of the lung apices and thereby causes a more uniform overall perfusion of the lungs. |
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Na linked secondary active transport is used for:
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glucose, amino acids, ions, various organic metabolites
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where t=does paracellular reabsorption happen most
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proximal tubule where tight junctions between cells are more leaky
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give an example of primary and secondary active transport in reabsorption
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Na/K ATPase in basolateral prox tubule; Na/glucose symporter as luminal side
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major sites of Mg / Ca regulation
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loop of henle / distal tubule
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where is 60 to 65% NaCl and H20 and 90% of filtered HCO3 reabsorbed
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the proximal tubule
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in metabolic alkalosis how/where is HCO3 secreted
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Intercalated cells in the collecting duct secrete H+, reabsorb K+ and secrete HCO3 in metabolic alkalosis
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trace the path of vasopressin
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low bp or hi blood osm. produces ADH in hypothalmus, release by pituitary, G-protein membrane receptor on CD cell, cAMP 2nd messnger, aquaporin vesicles attach to luminal wall of cell.
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link between Na and hi BP
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eat salt. release ADH. conserve H20 and drink H20; increase ECF volume causes hi BP. (slow response of kidney is to excrete H20 with the salt)
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trace the path of aldosterone
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released by adrenal cortex. hits hormone receptor in P cell in cortical 1/3 of distal tubule. increases transcription of K secretion and Na reabsorption pumps and modifies existing pumps and channels.
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what stimulates aldosterone release?
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drop in BP; increased K+; secondarily: decreased sodium
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natruretic peptides do what? how?
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cause NaCl and H20 excretion they are relased by atrial myocardial cells in response to increased stretch (hi BV/BP) decreasing vasopressing and aldosterone
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