Physiology Test 3

Front 1

what class of hormones enhance the effect of glucose on insulin secreion? give some examples

Back 1

incretins, such as Gluco-insulinotropic peptide (GIP) and proglucagon-derived peptides 1/2 (GLP 1/2)

Front 2

Where is secretin secreted? what is its function?

Back 2

from S cells in the duodenum, increases pancreatic HCO3- and H20 secretion, decreases gastric acid secretion

Front 3

Where is gastrin secreted? what is its function?

Back 3

G cells of the gastric antrum. stimulates gastric acid and histamine secretion (which also increases gastric acid)

Front 4

where is CCK secreted? what is its function?

Back 4

from I cells of the duodenum. inhibits gastric emptying and acid secretion, stimulates pancreatic ENZYME secretion, induces gallbladder contraction, inhibits food intake

Front 5

Where is GIP secreted, what is its function?

Back 5

from K cells of the intestine, stimulates insulin secretion (an incretin)

Front 6

where is peptide YY secreted, what is its function

Back 6

L cells of the intestine, all effects are inhibitory: gastric emptying and acid secretion, pancreatic secretion, intestinal motility (the ileal brake), food intake

Front 7

where is motilin secreted, what is its function?

Back 7

M cells in the proximal intestine, increases contraction of the LES, increases gastric emptying, increases intestinal motility

Front 8

where is ghrelin secreted, what is its function?

Back 8

X/A cells in the stomach and intestine - stimulates gastric emptying, increaes appetite, decreases energy expenditure

Front 9

where is somatostatin secreted? what is its function?

Back 9

D cells in stomach and duodenum, inhibits gastrin release, favors net absorption, increases smooth muscle tone and decreases pancreatic secretion

Front 10

where is serotonin secreted? what is its function?

Back 10

from enterochromaffin cells. opposes somatostatin (inhibits electrolyte and fluid absorption, favors secretion)

Front 11

describe acinar (initial) salivary fluid

Back 11

similar to plasma - isotonic

Front 12

how is saliva modified by ductal cells?

Back 12

NaCl is absorbed and KHCO3 is secreted, with more NaCl absorbed -> results in hypotonic solution

Front 13

how does salivary composition change with flow rate?

Back 13

all transfer except for HCO3- is diminished at high flow rates - high flow rate will have more NaCl and HCO3-, less K+

Front 14

what is sjorgen syndrome?

Back 14

autoimmune disease that attacks Cl/HCO3- exchanger in ductal cells in salivary glands - dry mouth, poor dentition

Front 15

how does pancreatic secretion vary with flow rate

Back 15

remember that HCO3- is exchanged for Cl- -> at high flow rates HCO3- is higher and Cl- lower

Front 16

describe acinar (initial) pancreatic secretion content

Back 16

High in NaCl, low in KHCO3. acinar cells secrete H20, Cl-, and Na+. Remember Na+ is paraccellular while Cl- in transcellular

Front 17

what is the strongest hormonal control of pancreated HCO3- secretion?

Back 17

secretin - activates CA -> increases cAMP -> PKA -> phosphorylates CFTR -> more Cl- secretion and exchange for HCO3-

Front 18

what is the main hormone responsible for pancreatic enzyme secretion? What hormone has an additive effect with it?

Back 18

CCK - VIP increases its effect

Front 19

which surface of hepatocytes faces the sinusoidal space?

Back 19

basolateral

Front 20

which 2 compounds were given as examples of secondary bile acids?

Back 20

lithocholic acid and deoxycholic acid

Front 21

what signals increased canalicular choleresis? ductular secretion

Back 21

bile acids increase canalicular secretions while secretin increasing ductular secretions

Front 22

describe neural stimulation of stomach secretions

Back 22

parasympathetic neurons release ACh which acts on ECL cells to release histamine -> parietal cells -> release HCL. They also directly synapse on parietal cells. GRP releasing neurons synapse on G cells -> release gastrin -> upregulates ECL and parietal cells

Front 23

describe the process of acid secretion inhibition in the stomach

Back 23

acid in the duodenum prompts D cells to release somatostatin which both inhibits gastrin and blocks G cells from releasing gastrin

Front 24

name three stimulatory signals for gastric acid secretion, 2 inhibitory signals

Back 24

stimulatory - gastrin and ACh (Through Gq), histamine (Gs). Inhibitory - somatostatin and prostaglandins (Gi)

Front 25

describe the role of GRP

Back 25

a neurotransmitter released from vagal nerves which causes gastrin release and SM relaxation in the stomach as part of the vasavagal reflex

Front 26

what is zollinger-ellison syndrome?

Back 26

overproduction of gastrin, often due to hormonally active tumors causes ulceration of the duodenum

Front 27

describe the absorption of monosaccharides

Back 27

glucose and glactose are absorbed by apical SGLT channels, fructose enters through GLUT5. Both diffuse passively through basal GLUT2

Front 28

what is enterokinase?

Back 28

membrane bound protease in intestine that activates pancreatic propeptidases

Front 29

why can people with specific AA transporter defects still absorb some of the deficient amino acid?

Back 29

short peptides (2 or 3 residues) can be absorbed via HP (proton/peptide) transporters and these can include the lacking AA

Front 30

describe the absorption of folate

Back 30

absorbed by specialized folate transporter, then converted intracellularly to TH4 before secretion into interstitium

Front 31

what is calbindins role in calcium absorption?

Back 31

buffers intracellular calcium to favor absorption. vitamin D stimulates expression of calbindin

Front 32

describe iron absorption

Back 32

Fe2+ binds to transferrin, which then complexes with transferrin receptor, both are endocytosed. Fe2+ can also enter as a heme or through H+/Fe2+ symporter

Front 33

which nephrons are primarily responsible for dilution and concentration of urine? describe them

Back 33

juxtamedullary nephrons

long loops of henle which descend to deep medulla and are supplied by vasa recta

Front 34

where are juxtaglomerular cells located?

Back 34

on the afferent (incoming) arteriole

Front 35

what is the equation for renal clearance? what must be true of substances that follow these dynamics

Back 35

clearance = (urine flow x urine concentration) / plasma concentration

substance must not be synthesized or metabolized in kidneys

Front 36

which substances are used to measure glomerular filtration rate? what qualities do these meet?

Back 36

inulin or creatinine

-not synthesized or metabolized
-freely filtered
-not secreted or absorbed

Front 37

which substance(s) are used to measure renal plasma flow? what qualities do these meet?

Back 37

para-aminohippuric acid (PAH)

-not synthesized or metabolized
-freely filtered
-doesnt alter RPF
-100% filtered or secreted

Front 38

what equation calculates GFR?

Back 38

remember amount filtered = amount excreted

GFR = ([inulin]u x urine flow)/ [inulin]p

Front 39

what equation calculates RPF? RBF?

Back 39

RPF:
RPF = ([PAH]u x urine flow)/ [PAH]p

RBF = RPF / (1-hematocrit)
remember RBCs are the main unfilterable constituent in blood

Front 40

what is the filtration fraction? give examples that will increase or decrease it

Back 40

GFR/RPF

will increase with renal artery stenosis
will decrease with filtration dysfunction - systemic lupus erythematosus, rhabdomyolysis

Front 41

what is clearance ratio? give examples for high and low value

Back 41

ratio to clearance of inulin (fully and only filtered)

high value (great than 1) indicates secretion, ie PAH
low value (less than 1) indicates reabsorption, ie Na+

Front 42

how large of particles can be filtered in the glomerulus?

Back 42

anionic proteins up to 20 angstroms and cationic proteins up to 42 angstroms

Front 43

describe the mechanism of tubuloglomerular feedback during high flow in the distal tubule

Back 43

increased calcium in MD cells -> adenosine and ATP to JGA cells -> calcium in smooth muscle cells of afferent arteriole -> vasoconstriction

also decreases renin release (this causes vasodilation, but is mostly active in efferent arteriole -> decreases GFR)

Front 44

what is a typical GRF? Filtration fraction?

Back 44

180 L/day, 16%

Front 45

describe changes in transepithelial voltage gradient in the nephron

Back 45

very early PT lumen is negative, becomes postive due to paracellular absorption of Cl-, favors absorption of Na+

In the distal nephron (DT and collecting duct), the lumen is negative from high amounts of remaining Cl- following lots of cation reabsorption -> favors K+ and H+ secretion

Front 46

describe the function and location of aquaporins

Back 46

AQP1 - apical in PT
AQP2 - regulated by ADH in collecting tubule
AQP3/4 - basal in PT

Front 47

describe how absorptive gradient acts a feedback to counter changes in GFR

Back 47

increased GFR -> increased filtered load -> capillary blood has lower volume and higher osmolarity -> favors absorption of Na+ and H20 (~constant ratio)

Front 48

how does the thick ascending limb of the LOH dilute urine?

Back 48

absorbs electrolytes, mainly NaCl without H20

Front 49

what is bartter's syndrome?

Back 49

variety of mutations (can be NKCC2, ClC-Kb or ROMK) in thick ascending limb

malabsorption of sodium in TAL -> polyuria and salt depletion -> hyperaldosteronism and hyopkalemic metabolic acidosis

Front 50

where in the nephron do thiazide diuretics act?

Back 50

on NaCl symporter in distal tubule

Front 51

where are principal cells found? what is their function?

Back 51

found in late distal tubule / collecting ducts

Absorb Na+, secrete K+
regulate H20 absorption (ADH responsive)

Front 52

where are intercalated cells found? what is their function?

Back 52

found in late distal tubule and collecting duct

regulate acid base balance
reabsorb K+ (exhanged with H+)

Front 53

what is insulins role in K+ regulation?

Back 53

causes intracellular uptake of K+ (remember most K+ is stored intracellularly)

in diabetes mellitus -> hyperkalemia with low intracellular concentration

Front 54

how are H+ and K+ regulation related?

Back 54

H+/K+ exchanger on intercalated cells (and other cells not in kidney)

during acidosis, plasma will hyperkalemia to buffer acidity

Front 55

where are the main sites of K+ absorption and regulation

Back 55

mostly absorbed in PT

regulated by SECRETION when elevated in the DT and CD (principal cells)

Front 56

where in the nephron is Ca2+ excretion regulated?

Back 56

in the distal tubule - sensitive to PTH

also, local regulation in the TAL via CaSR/NKCC2 regulation

Front 57

which calcium regulating hormone affects GI absorption of calcium?

Back 57

calcitriol (vitamin D)

Front 58

how is the filtered load of calcium measured?

Back 58

.6 x [plasma Ca2+] x GFR

remember that ~40 percent of plasma calcium is protein bound

Front 59

name 4 cells types which express CaSR

Back 59

Distal tubule and TAL cells -> CaSR upregulates NKCC2 channel, increases Ca absorption

Chief cells in parathyroid -> secrete PTH

Proximal tubule cells -> convert vit D -> calcitriol -> increase GI calcium absorption

Parafollicular cells in thyroid -> regulate calcitonin secretion

Front 60

which hormone inhibits excretion of both calcium and phosphate?

Back 60

calcitriol

Front 61

where in the nephron is phosphate transport regulated?

Back 61

in the proximal tubule, where its absorption is inhibited by PTH

remember that PTH is primarily trying to raise Ca2+, inhibiting Na/Pi symporter increases positive transepithelial electrical gradient for Ca absorption

Front 62

what factors affect effective circulating blood volume?

Back 62

blood volume, cardiac output, total peripheral resistance

Front 63

what hormone opposes the RAA system

Back 63

ANP

Front 64

give an example of a loop diuretic. describe their action

Back 64

furosemide

inhibits the NKCC2 pump, reduces Na+ absorption and lessens the positive epithelial voltage -> mg2+ and ca2+ excretion due to decreased paracellular absorption

Front 65

give an example of distal tubule duretics. describe their action

Back 65

thazides

block NaCl symport in the early distal tubule. increases K+ excretion, but decreases Ca2+ excretion

Front 66

give an example of K+ sparing diuretics

Back 66

Amelioride

Act in the late distal tubule, block the ENaC channels - increased Na+ excretion. K+ is retained as Na intracellular is reduced, lowing the Na/K pump which drives secretion

Front 67

what is the normal range for pH? what are the normal values for HCO3- and pCO2

Back 67

7.38-7.42

HCO3- = 24
pCO2 = 40

Front 68

what channels are involed in HCO3- absorption?

Back 68

NHE-3 = apical Na/H exchanger

NBC-1 = basal Na+/HCO3- symporter

Front 69

how does effective circulating volume affect HCO3- absorption

Back 69

it will be absorbed more during volume contraction because H+ secretion is tied to Na+ absorption

Front 70

why does aldosterones action of principal cells cause K+ excretion?

Back 70

-upregulates basal Na/K pump
-Increased Na absorption makes distal nephron lumen more negative, favors secretion of K+ (and H+ from intercalated cells)