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137 Cards in this Set
- Front
- Back
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what demarcates a "lobule" in the kidney?
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interlobular arteries (running vertically)
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what are the 2 layers mediating filtration at the glomerulus?
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fenestrated endothelium
podocytes w/ filtration slits |
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where/how are proteins in the filtrate reabsorbed?
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in the proximal convoluted tubule
via endocytosis |
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urine leaves the medulla and enters the minor calices at...
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medullary papilla via area cribrosa
medullary papilla has a transitional epithelium |
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all circulating blood passes through the two kidneys every...
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5 minutes!
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where is filtered glucose reabsorbed?
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in hte proxial convoluted tubule
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what is the function of mesangial cells?
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they are in the glomerular endothelium, they phagocytose particles in the basal lamina of the glomerulus
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what are the size limits for filtration at the glomerulus?
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<7,000 daltons: freely filtered
700-7,000 daltons: variable dependent on charge >70,000: excluded |
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what is the charge of the glomerular basement membrane, and what is the consequence for plasma proteins?
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negatively charged
negatively charged proteins are excluded |
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what is the clearance equation?
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clearance (a %) = urine concentration x urine flow rate / plasma concentration
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what is an artificial and natural way to calculate GFR?
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artificial: inulin (only filtered)
natural: creatinine (mostly filtered) |
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what is hte problem with using creatinine to measure GFR?
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between 100-50% kidney function there is very little change in creatinine levels
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what is a normal GFR?
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180 L/day
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what are the main functions of tubular secretion?
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removal of drugs
removal of excess K from blood urea excess H+ |
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does filtrate osmolality change in the proximal convoluted tubule?
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no, it is free isoosmotic diffusion with solutes and H20 proportionately
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what is the key transporter for Na to go from intracellular to interstitium on the basolateral tubular cells?
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Na-K ATPase
located at most (all?) tubule cells basolateral side |
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how does the TAL create dilute filtrate?
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reabsorption of solutes but impermeable to water
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what 2 transporters are responsible for Na reabsorption in the thick ascending limb
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Na-K-2Cl on the apical/lumenal (all going in)
Na-K ATPase on the basolateral side |
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where do furosemide's act?
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on the Na-K-2Cl transporters in the Thick Ascending limb
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where do thiazide's act?
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on the Na-Cl symporter in the intial part of the distal tubule
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what transporter is responsible for solute reabsorption at the initial part of the distal tubule?
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Na-Cl symporter
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what are the two types of cells in the distal tubule and collecting duct and what are their functions
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principal cells:
1. reabsorb Na 2. Secrete K 3. reabsorb water in presence of ADH intercalated cells 1. secrete H 2. generating new HCO3 3. reabsorb K |
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what effect does dopamine have at the kidney?
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increased Na excretion
a natriuretic |
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what effect does increased SNA have on the kidney?
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increased renin secretion
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what is the cellular effect of Atrial Natriuretic Peptide at the kidney?
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decreased reabsorption of Na by principal cells of the collecting ducts
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plasma osmolality is closely defended at what value?
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290 mosm/kg
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what is the difference between an effective osmole and an ineffective osmole?
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an effective osmole is impermeable at the membrane, so it creates osmotic pressure
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what are the most contributors to plasma osmolality?
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Na, BUN, and glucose
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what is "insensible water loss"
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water lost to evaporation at respiratory tract and skin
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what hypothalamic nuclei secrete ADH?
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paraventricular and supraoptic nuclei release it at the posterior pituitary
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the body is more sensitive to changes in (volume/osmolality)
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volume (so baroreceptor stimulated release of ADH supercedes osmoreceptor stimulated release of ADH)
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ADH stimulates...
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aquaporin insertion into the apical membrane
water reabsorption in the DCT and collecting duct urea reabsorption in the medullary collecting duct |
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what is the half life of aquaporins?
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15 minutes
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what is the cause of diabetes insipidus?
what are the signs? |
failure to produce ADH or failure to respond to ADH (dilute polyuria, polydipsia)
hypernatremia/hyperosmolarity |
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what is the consequence of inappropriate ADH secretion
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volume expansion
hypoosmolality/hyponatremia |
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what solutes contribute to osmolarity in the kidney medulla?
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Na
Cl Urea (urea contributes more and more the deeper you go) |
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how does ADH change urea flow?
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it increases permeability, and urea moves OUT into the interstitium (further contributing to water reabsorption)
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what is Urea recycling?
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Urea is reabsorbed to interstitium by collecting duct
urea RE-ENTERs ascending loop of henle (100% remains after 50% of filtered load had been reabsorbed) |
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how do you exam a patient for water vs. Na homeostasis?
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water: blood test
Na: physical exam (BP) |
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Na determines what physiologic parameters?
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blood volume
ECF vs. ICF water flow |
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what is the effective circulating volume?
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the amount of blood in the arteries
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the kidneys alter Na and Cl excretion in response to...
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changes in effective circulating volume (volume of arterial blood)
at peripheral baroreceptors and at juxtaglomerular apparatus |
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what 3 things stimulate release of renin?
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decreased perfusion pressure
increased SNA decreased NaCl delivery to macula densa (a signal of decreased filtration) |
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what are the 3 main effects of Angiotensin II?
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increased Na reabsorption
vasoconstriction thirst/ADH release |
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what is the effect of SNA on the kidney?
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increased water and Na reabsorption
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thiazides block Na reabsorption at the....
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distal convoluted tubule
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what is the response of the Juxtaglomerular apparatus to decreased lumen NaCl
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causes afferent arteriolar resistance, turning GFR down
release of renin |
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what do you give to a hypovolemic, hyponatremc patient?
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normal saline (a volume expander)
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what do you give to a hypernatremic patient?
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D5W
it has a sugar in it, but is metabolized to H20 so it is dilute while still expanding volume |
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what are the levels for hyperkalemia and hypokalemia in serum?
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hyper >5.0 meq/l
hypo <3.5 meq/l |
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what is the distribution of intakes/outputs of K daily?
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dietary intake: 100 mmole
feces output: 10 mmole urinary output: 90 mmole 50 mmole secreted 40 mmole of filtered load not reabsorbed |
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what is the most inportant factor regulating K distribution and how does it work?
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insulin activates Na-K ATPase
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what are the two ways (receptors) that epinephrine can affect K balance?
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alpha receptors: binding causes release of K from ICF to ECF
Beta receptors: activates Na-K ATPase pump, causes cells to uptake K |
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how does acidosis (organic vs. inorganic) change K balance?
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inorganic causes K to egress out of cells into ECF
organic has no effect |
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beta-agonists can cause (hypo/hyper)kalemia.
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hypokalemia (stim beta receptors stimulates Na-K ATPase)
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how can diabetes cause hyperkalemia?
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high glucose draws water out
solvent drag => K goes with |
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what is the region of the nephron responsible for the excreted K?
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distal tubule secretion
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what is unique about K excretion
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you can't make K free urine
you can excrete 150% of the filtered load! |
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what cell is responsible for K reabsorption? what channels allow for K reabsorption?
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intercalated cell
K-H ATpase on apical side K channel on basolateral side |
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what cells are responsible for K secretion? what channels allow for K secretion?
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principal cells
Na-K ATPase on the BL membrane K channel on the lumenal side |
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how does Aldosterone change K balance in the nephron?
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Aldosterone increases the number of Na-K ATPase in the Bl membrane
increased Na reabsorption leads to increased K secretion |
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the pH of ECF is tightly controlled at...
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7.38-7.42
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what happens with bicarbonate formation in the kidney?
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the H formed goes into the lumen, the HCO3 enters the circulation
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what is the equation for net acid secretion
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excreted titratable acid
+ excreted ammonium - excreted HCO3 |
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how is filtered HCO3 reabsorbed at the proximal tubule?
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converted to CO2 and OH by CA-IV (on apical border)
OH + H CO2 and H2O reabsorbed CAII in cytosol HCO3 reabsorbed into interstitium |
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how is new HCO3 formed in the kidney?
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H20 => H and OH
H added to titratable acid in the lumen OH adds to CO2 by CAII in cytosol to make HCO3 |
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what is the source of ammonium in the urine?
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2 ammonium made from 1 glutamine
2 HCO3 also made in the process |
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what are the three causes of renal tubular acidoses?
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defect in proximal tubule H secretion
defect in distal tubule H secretion defect in NH4 production |
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what is the main renal defense against acidosis?
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increased NH4 secretion
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what are the levels of HCO3, pCO2, and pH in metabolic acidosis?
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HCO3 low
pCO2 low pH low |
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what are the levels of HCO3, pCO2, and pH in respiratory acidosis?
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HCO3 high
pCO2 high pH low |
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how does aldosterone alter H and HCO3 balance in nephron?
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increases H secretion into urine
increases reabsorption of new HCO3 |
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parietal cells secrete...
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intrinsic factor and acid
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chief cells secrete
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pepsinogen
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What are enteroendocrine cells...what do they secrete?
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G cells: gastrin
D cells: somatostatin Ghrelin cells: ghrelin |
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what is barret's esophagus?
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when you have lots of GERD, you can get esophageal metaplasia turning the esophagus into gastric pits/glands
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what do paneth cells secrete?
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lysozome and alpha defensin
antimicrobial |
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of the anal sphincters, which is SMC and which is skeletal?
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inner is smooth muscle
outer skeletal |
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what is the function of myoepithelial cells?
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they are a thin (simple squamous like) layer surrounding acini which squeeze out secretions
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what is the difference in location and function of striated ducts and intercalated ducts?
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intercalated ducts: right next to acini
secrete lysozome and lactoferrin striated ducts: reabsorb Na and secrete K (make hypotonic sol'n) |
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what is the space of disse?
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the space between hepatocytes and sinusoids
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how is the hepatic acinus oriented?
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the bile ducts are central. bile flows periphery to central, blood flows centrally to periphery
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in the hepatic acinus organization, which hepatocytes are highest in oxygen/nutrients?
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zone 1 (closest to hepatic arteries)
zone 3 is near the central vein and are susceptible to ischemia |
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what is the function of the sphincter of oddi
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it controls bile release from the gall bladder
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how are the ducts of the sublingual gland different than the parotid and submandibular?
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they have no striated or intercalated ducts, only intralobular
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what is the principal NT of the PS to the GI tract?
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ACh
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how does stretch of GI tract wall induce peristalsis?
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leads to contraction of circular layer upstream and contraction of longitudinal downstream
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what are the 3 stages of the migrating motor complex?
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phase 1: no contractions
phase 2: contractions, some propogate downstream phase 3: high amplitude contractions which propagate downstream |
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what is absorbed in the colon?
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fluid and electrolytes
short chain FAs |
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what is hirschprung's disease?
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no meissner's or auerbach's plexuses in distal colon...no relaxation for peristalsis
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what is the difference between primary and secondary peristalsis?
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primary is from swallowing
secondary is from leftover bolus causing stretching |
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what is the channel responsible for acid secretion by Parietal cells?
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H-K ATPase
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what is the target of PPIs?
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H-K ATPase in parietal cells
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what are the different subunits of H-K ATPase and what are their functions?
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alpha-pump function
beta - targets to apical membrane (not basolateral so you only pump acid into lumen |
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what is the source of protons for acid secretion by parietal cells and what is the consequence?
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CA makes bicarb and H
so, when you eat a big meal and secrete a lot of acid, there is an alkaline tide in your venous blood from a lot of bicarb |
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what are the 3 stimulants of stomach acid secretion and which is the strongest?
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HISTAMINE
gastrin ACh |
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how does gastrin increase acid production by parietal cells
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it acts directly on parietal cells
more importantly... it acts on enterhchromaffin cells (ECLs) to secrete histamine |
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what inhibits gastric acid secretion?
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acid in stomach\
SECRETIN it inhibits gastrin release, increases somatostatin from D cells, and inhibits parietal cell H secretion |
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what is the pH of the stomach in a state of acid secretion?
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<1
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what ligands can bind the CCKb receptor?
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gastrin and CCK
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what are the intracellular signals activated by CCKb activation?
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Ca and Protein Kinase C (PKC)
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what drives solute secretion by pancreatic acinar cells?
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Na-K ATPase
Na-K-2Cl symporter both on the BL membrane sodium goes paracellularly intracellular Cl goes out apical channels |
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what is the function of pancreatic duct cells?
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they release Cl (CFTR)
they make HCO3 (H pumped out BL membrane via ATP H pump) they exchange HCO3 out for Cl in |
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what stimulates pancreatic duct secretion of HCO3
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ACh, secretin
they stimulate PKA which stimulates double phosphorylation of CFTR |
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how does the pancreas prevent autodigestion?
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trypsinogen (master on switch) is secreted as a zymogen
enterokinase activates trypsinogen to trypsin (located in SI mucosa) co-secrets "Pancreatic trypsin inhibitor" |
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what is the "master on switch" of pancreatic enzymes and what turns the on switch ON
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trypsinogen is cleaved to trypsin by enterokinase
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how is parotid gland duct secretion different than pancreatic duct secretion?
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pancreatic: Na-bicarb
parotid: K-bicarb |
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what happens with the R122H mutation of trypsinogen?
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trypsin can no longer inactivate other trypsin molecules
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what types of pancreatic enzymes are secreted as zymogens?
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peptidases
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what are the 4 mechanisms of sodium reabsorption in the GI tract?
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1. cotransport with glucose or AAs
2. parallel Na-H exchange and Cl-HCO3 exchange 3. Na-H exchange 4. Na channel ALL rely on Na-K ATPase in the BL membrane!! |
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what is the major Na reabsorption mechanisms in the GI tract during fasting?
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Na-H exchange parallel with
Cl-HCO3 exchange |
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what are the 3 mechanisms of Cl reabsorption in the GI tract?
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1. Cl channel / paracellular
2. Cl-HCO3 exchange 3. Na-H exchange parallel with Cl-HCO3 exchange |
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where in the GI tract is K absorbed and secreted?
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absorbed in the SI only
secreted in the colon only |
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how is K absorbed in the SI?
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solvent drag
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what are the two ways that K is secreted in the colon?
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passive paracellular
active Na-K ATPase |
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what is an exotoxin?
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a bacterial product that produces symptoms (even if the bac isn't present)
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what is an enterotoxin?
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an exotoxin that stimulates intestinal secretion
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what is the effect of all secretagogues?
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increased Cl secretion
inhibition of electroneutral NaCl absorption (parallel pathway) |
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what are the 3 mechanisms of secretagogues?
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increased cAMP
increased Ca increased cGMP |
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what is the effect of mineralcorticoids (i.e.aldosterone) on GI solute balance?
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increases Na absorption, increases K secretion in colon
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what is the effect of glucocorticoids (i.e. cortisol) on GI solute balance?
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increased electroneutral (parallel NaCl) sodium uptake in SI and colon
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what is the effect of somatostatin on GI solute balance?
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increased electroneutral NaCl absorption
inhibits electrogenic HCO3 secretion |
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what is the difference between amylose, amylopectin, and glycogne?
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amylose (alpha 1-4 only)
amylopectin (some alpha 1-6) glycogen (many alpha 1-6) |
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what is the catalytic activity of alpha amylase (pancreatic and salivary)?
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it cleaves alpha 1-4 linkages flanked by OTHER alpha 1-4 linkages (therefore it makes maltose and limit dextrins)
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what can cleave terminal alpha1-4 linkages?
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maltase
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what can cleave alpha 1-6 linkages?
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sucrase-isomaltase
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what is the transporter responsible for Na-Glucose cotransporter?
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SGLT1
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how does insulin affect glucose transport in the GI tract?
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it decreases Glut2 in the apical membrane (Glut2 is ALWAYS present in the basolateral membrane)
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what transporter is responsible for fructose absorption and hwere is this transporter?
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Glut5
jejunum |
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what is the difference between an endopeptidase and an exopeptidase?
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an endopeptidase goes from the middle between specific AAs
an exopeptidase goes from the C-terminus carboxypeptidases A and B |
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how are luminal, secreted exopeptidases different than brush border exopeptidases?
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luminal secreted can only go from carboxy term
brush border exopeptidases can go from N or C-term |
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what transporter is responsible for short peptide absorption and what other transporters does it rely on?
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PepT1
cotransports with H Na-H exchange on apical membrane provides H N-K ATPase on BL membrane allows for Na gradient |
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why are short and medium chain FAs easier to absorb?
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they do not need to be packaged into chylomicrons by enterocytes
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what is the form of dietary folate?
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folate conjugated to a string of glutamate residues
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where is B12-IF absorbed?
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terminal ileum ONLY
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what is the cause of pernicious anemia?
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autoimmune loss of parietal cells...so no IF production, B12 deficiency that is refractory to B12 administraiton
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where/how is calcium actively transported?
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in the duodenum, it enters enterocytes passively, binds calbindin in the cytosol (to keep gradient) and is pumped out BL membrane by a pump and a Ca-Na exchanger
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