Physio Final

Front 1

Alveolar Ventilation Equation

Back 1

Alveolar Ventilation (VA) =

863(VCO2/PACO2)

Front 2

Alveolar Gas Equation

Back 2

PAO2 = PIO2 - (PACO2/R) + F

= 147 - (PACO2/0.8)

Front 3

respiratory quotient

Back 3

CO2 produded / O2 consumed
250 / 300
0.8

Front 4

PvCO2

Back 4

46

Front 5

PaCO2

Back 5

40

Front 6

PvO2

Back 6

40

Front 7

PaO2

Back 7

100

Front 8

CO probe to test for diffusion

Back 8

DL-CO = VCO/PACO

Front 9

LaPlace’s law

Back 9

P= 2(T/r)

Front 10

R =

Back 10

change in P / flow

Front 11

N2O

Back 11

- high permeability
- poor interaction with hemoglobin
- reaches equilibrium faster than O2

Front 12

CO

Back 12

- reacts well with hemoglobin
very well
- very slow to reach equilibration due to poor permeability

Front 13

HCO3—H2CO3 as buffers

Back 13

- pka = 6.1
- its abundant
- the effective pKa is >6.1 b/c of changes in ventilation
- lungs control PCO2
- kidneys control HCO3

Front 14

Na+/H+

Back 14

antiporter - extrudes H+ when pH is low

Front 15

Cl-/HCO3-

Back 15

antiporter - extrudes HCO3- when pH is high

Front 16

H+/K+ ATPase

Back 16

extrudes H+

Front 17

Na+/2HCO3-

Back 17

extrudes HCO3- by gradient

Front 18

respiratory acidosis

Back 18

- hypoexcretion of CO2 by the lung results in high PaCO2 and thus high [H+] → low pH
- compensate w/ renal excretion of fixed acids and generation of HCO3- to buffer blood - PCO2 stays high

Front 19

respiratory alkalosis

Back 19

- hyperexcretion of CO2 by lung through hyperventilation results in low PaCO2 and thus low [H+] and high pH
- compensate w/ renal excretion of HCO3- while PCO2 remains abnormally low

Front 20

metabolic acidosis

Back 20

- addition of fixed acids to blood or a loss of base
- compensate w/ pulmonary hyperventilation to increase excretion of CO2 (change in PCO2)

Front 21

metabolic alkalosis

Back 21

- loss of fixed acids from body or addition of base
- compensate w/ pulmonary hypoventilation to conserve CO2 (limited by O2 requirements)

Front 22

anatomical shunts

Back 22

bronchial veins which drain into the pulmonary veins and thebesian veins which drain into the left ventricle

Front 23

normal values of lung stuff

Back 23

- FEV1 = 4.0L
- FVC = 5.0L
- FEV1/FVC = 0.80
- FEF25-75% = 3.5L

Front 24

patients with obstructive disease

Back 24

- FEV1 = 1.3L
- FVC = 3.1L
- FEV1/FVC = 0.42
- FEF25-75% = 1.4L

Front 25

patients with restrictive disease

Back 25

- FEV1 = 2.8L
- FVC = 3.1L
- FEV1/FVC = 0.90
- FEF25-75% = 3.7L

Front 26

load with water

Back 26

- decrease in the osmolarity of ECF and ICF
- increase in the volume of ECF and ICF

Front 27

load w/ salt

Back 27

- increase in the osmolarity of ECF and ICF
- increase in the volume of ECF
- decrease in volume of ICF

Front 28

load w/ isomolar solution

Back 28

causes a rise in ECF volume only

Front 29

proximal convoluted tubule (PCT) basic info

Back 29

resorbs 2/3 of filtered salt and water, all filtered glucose, and secreted drug metabolites
- resorbs most water via A1

Front 30

descending loop of Henle basic info

Back 30

resorbs water and secretes NaCl

Front 31

ascending loop of Henle basic info

Back 31

impermeable to water, resorbs NaCl

Front 32

distal convoluted tubule and collecting ducts basic info

Back 32

- resorb water under the influence of ADH which controls aquaporin 2
- resorb Na+ and secrete K+ under the influence of aldosterone
- resorb or secrete H+ based on acid-base balance

Front 33

filtration fraction

Back 33

- equal to GFR/RPF
- normal value is 120/600 = 20%

Front 34

filtered load of y

Back 34

GFR X plasma [] of y

Front 35

excreted load of y

Back 35

V times urine [] of y

Front 36

reabsorption and secretion in terms of filtered load and excreted load

Back 36

- reabsorption is filtered load minus excreted load
- secretion is excreted load minus filtered load

Front 37

clearance equation

Back 37

- volume of plasma cleared of a solute per unit time
- Cy = (V x [y]urine)/[y]plasma
- = excreted load /[y]plasma

Front 38

normal GFR values

Back 38

- men: 95±20mL/min
- women: 120±mL/min

Front 39

RPF =

Back 39

- Clearance of PAH x (1/Effusion of PAH)
- (540) x (1/0.9) = 600mL/min

Front 40

glomerular filtration pressure (and normal values)

Back 40

- (PC - PBowman’s) – (COPC - COPBowman’s)

- (60 – 15) – (30 – 0) = 15mmHg

Front 41

MFP

Back 41

- (PC - PBowman’s) – mean COP

- mean COP = (COPafferent + COPefferent)/2

Front 42

GFR (mL/min) =

Back 42

Kf x MFP

Front 43

reabsorption of NaCl
transcellular movement

Back 43

- everywhere EXCEPT dLOH
- lumen to the cell (via apical surface) is passive
- can be coupled to 2o
- cell to interstitium (via basolateral surface) requires Na+/K+ ATPase (not in dLOH)

Front 44

reabsorption of NaCl
paracellular movement

Back 44

- via passive diffusion
- Na+ usually accompanied by HCO3- or Cl- to balance charge
- passive back-leak is para secretion of Na+ PCT, dLHO is leaky and allows water via aquaporin-1 - aLHO, DCT, CD are tight and use other aquaporins than A1

Front 45

aquaporin-3

Back 45

allows passage of water from the cell to the interstitium - it is unregulated

Front 46

K+/Na+ ATPase

Back 46

- moves Na to interstitium on PCT
- against electrochemical gradient
- sets up the gradient that allows passive movement of Na+ from the lumen into the cell

Front 47

transporters on apical PCT surface

Back 47

- Na+/Cl- co-transporter
- Na+/glucose co-transporter
- Na+/amino acid co-transporter
- aquaporin-1
- Na+/H+ antiporter

Front 48

transporters on basolateral PCT surface

Back 48

- Na+/K+ ATPase
- aquaporin-1
- glucose transporter

Front 49

bicarbonate reabsorption

Back 49

- H+ is secreted into lumen, combines /w HCO3 -> CO2, water
- CO2 rapidly enters, combines w/ water -> H+ and HCO3-
- HCO3 across basolater w/ passive exchange or by a HCO3-/Cl- transporter
- carbonic anhydrase on apical surface and in cell

Front 50

urea reabsorption

Back 50

- PCT resorbs around 50% - independent of ADH
- ADH stimulated resorption in CD

Front 51

LOH basic info

Back 51

- receives isosomolar from PCT
- reabsorbing more solute than water so that filtrate leaving it is hyposmolar and that interstitium is hyperosmolar
- helps water removal and urine concentration in DCT, CD
- ADH-independent

Front 52

dLOH trasport

Back 52

- no Na+/K+ ATPase
- aquaporin-1 - water reabsorb
- UT-2 (and passive diffusion) secrete urea
- passive diffusion of Na sec

Front 53

aLOH transport

Back 53

- no water transport!!
- NaCl actively reabsorbed to cell due to gradient via Na+/K+/2Cl (Lasix inhibits) co-trans - moves out K against gradient
- from cell to IS via Na+/K+ ATPase anti-transporter (against Na gradient)
- ROMK channels moves K out of apical membrane passivly

Front 54

UT-1

Back 54

transport urea on vasa recta

Front 55

descending vasa recta

Back 55

- blood entering is 300 mOsm/L
- solute is imported from the IS and water is exported
- at the bottom of the loop the osmolarity is 1200 mOsm/L

Front 56

ascending vasa recta

Back 56

- solute is exported to IS and water is imported
- water resorption is aided by high osmotic pressure and COP
- at end, osmolarity is 350

Front 57

DCT and CD transporters

Back 57

- Na goes from lumen to cell passivly then to IS via Na+/K+ ATPase (K+ moved INTO cell)
- a K+ channel lets K+ out of cell and into lumen
- ENA channel (amiloride blocks) is on apical surface and allows aldosterone mediated Na reabsorption

Front 58

α cells

Back 58

- secrete H+, line the tubule
- H combines with HCO3- -> water and CO2
- CO2 moves into cell and combines w/ water -> H+, HCO3-
- HCO3- into IS via a HCO3-/Cl- antiporter and H+ into lumen via H+/K+ ATPase and ATP primary transporter

Front 59

β cells

Back 59

- secrete HCO3-, line tubule
- active in alkalosis
- transport HCO3- from cell to lumen via a HCO3-/Cl- ATPase
- H+ moved into IS via ATP primary transporter

Front 60

medullary CD transporters

Back 60

- ADH-dependent water reabsorption via aquaporin-2
- ADH-dependent expression of UT-1 for urea reabsorption

Front 61

ADH

Back 61

- synthesized in hypo, secreted from pituitary IRT plasma osmolarity or drop in BV or BP
- vasoconstriction due to binding to V-1 receptor
- antidiuretic due to binding to V-2 receptor

Front 62

V-2 receptors

Back 62

- in DCT and CD
-> cAMP increase -> PKA increase which (P)s serine on aqua-2 -> moves them to apical membrane -> more water reabsorbed into cell
- activates UT-1 in MCD for urea resorption - moves into the interstitium via aqua-3

Front 63

aquaporin 4

Back 63

found on hypothalamic glial cells - possible role as osmosensors

Front 64

aquaporin-1 null

Back 64

- normal in basal state
- cant maximally concentrate urine in water restriction
- main effect in dLOH, little effect on the proximal tubule

Front 65

central vs. nephrogenic diabetes insipidus

Back 65

- mutation in the gene coding for ADH or damage or loss of ADH-producing neurons due to trauma or neoplasm
- cells dont respond to ADH (lithium overdose, excessive fluid intake, pregnancy)

Front 66

renal myogenic response

Back 66

increase in transmural P -> increase in Ca conductance and release of endothelial factors -> vasoconstriction

Front 67

tubuloglomerular feedback

Back 67

- increased MAP -> increased NaCl to macula densa
- causes granular cells to make renin and other vasoconstrictions like ATP and adenosine
- if MAP decreased, granular cells release NO and prostoglaind E (vasodilators)

Front 68

during increased Na+ intake ...

Back 68

- increased ECV (water retention) -> decreased COP
- also -> increased MAP -> increase hydrostatic P in PCs
- these favor decrease in fluid uptake and increase in sodium excretion

Front 69

renal sensors

Back 69

- cardiopulmonary sensors – sense circulating volume
- baroreceptors – sense MAP
- granular cells – sense renal perfusion pressure
- macula densa cells – sense delivery of NaCl in the distal tubule

Front 70

atrial natriuretic peptide (ANP)

Back 70

- synthesized in atria and released if increases in ECV
- inhibits Na+ reabsorption in the DCT and CD
- inhibits ENaC, indirectly inhibits Na+/K+ ATPase
- inhbits release of renin,
- dilates afferent arterioles to increase GFR

Front 71

renal sympathetic efferents

Back 71

- if ECV decreased, increased firing and activity
- constricts the afferent arteriole, decreasing GFR
- Na+/H+ antiporters on apical PCT stimulated, which increases Na+ uptake

Front 72

renin-angiotensin-aldosterone system

Back 72

- renin release if decreases in ECV and pressure - it catalyzes conversion of angiotensinogen to angiotensin I to angiotensin II by ACE
- angiotensin II is potent vasoconstrictor -> increase peripheral R and MAP and GFR, decreases hydrostatic P in PCs
- this favors Na+ reabsorption
- stimulates the Na+/H+ in PCT
- stimulates release of ADH and aldosterone and ADH
- stimulates thirst centers

Front 73

aldosterone

Back 73

- binds MR, also stimulated by cortisol but kidney enzymes make it inactive
- increases ENaC
- increases Na+ reabsorption
- increases K+ secretion
- makes colon epi increase Na absorption
- steroid hormone, ~90 minutes

Front 74

renal artery stenosis

Back 74

- input arteries narrow -> dec glom P, GFR, and RBF -> less NaCl to macula densa -> renin -> increase in AII -> inc MAP and peripheral R, efferent arterioles constrict
- maintains a minimal GFR in reduced RBF - ACE inhibitors dispose the effect -> renal failure from decreased GFR
- treat w/ surgery and diuretics

Front 75

glucocorticoid remediable aldosteronism

Back 75

- ald release stimulated by ACTH -> inc in ald -> inc Na+ reabsorption -> inc ECV
- treat w/ cortisol -> (-) feedback on ACTH release
- symptoms are increased BP, hypernaturemia, hypokalemia, and high aldosterone

Front 76

apparent mineralocorticoid excess

Back 76

- MC receptors stimulated by cortisol (renal enzyme messed up)
- treatment w/ spirolactone which blocks the MR
- present w/ hypokalemia and hypertension and decreased circulating aldosterone

Front 77

Liddle’s Syndrome

Back 77

- mutation in the gene for ENaC that increases its number and activity
- increased reabsorption of Na+ and secretion of K+
- treatment w/ amiloride, it blocks ENaC
- patients present with hypertension and hypokalemia

Front 78

acetazolamide

Back 78

- acts at the PCT
- inhibits carbonic anhydrase which decreases Na+/H+ activity

Front 79

furosemide (Lasix)

Back 79

- acts at the ascending loop of Henle
- inhibits activity of the Na+/K+/2Cl- transporter

Front 80

thiazide (HCTZ)

Back 80

- acts at the distal convoluted tubule
- inhibits the activity of the Na+/Cl- transporter

Front 81

amiloride

Back 81

- acts at the DCT and collecting ducts
- inhibits activity of ENaC channels

Front 82

spirolactone

Back 82

inhibits MR activity

Front 83

VIP

Back 83

- inhibits activation of the smooth muscle cells
- released by enteric neurons and hyperpolarizes the smooth muscle cells
- activates K+ channels to reduce the amplitude and duration of the slow waves

Front 84

chief cells

Back 84

- in bottom of gastric glands (pyloric and oxyntic)
- release pepsinogen and gastric lipase

Front 85

neck cells

Back 85

secrete mucus for lubrication and buffering functions

Front 86

parietal cells

Back 86

- found in oxyntic glands only
- secrete HCl
- secrete intrinsic factor
- stimulated by gastrin (weak), histamine (strong - induced by gastrin)
- inhibited by H+, somatostatin (induced by H+), and secretin (induced by H+)

Front 87

HCl

Back 87

- antibacterial
- denatures macromolecules
- catalyzes pepsinogen to pepsin

Front 88

intrinsic factor

Back 88

- helps absorption of B-12 in the large intestine - protects the vitamin from digestion
- deficiency results in pernicious anemia

Front 89

enteroendocrine cells

Back 89

- (<1%)secrete into interstitum
- gastrin (from pyloric glands only)
- somatostatin
- histamine
- ghrelin (only in oxyntic glands, does hunger)

Front 90

stomach interdigestive phase

Back 90

- stomach is empty, very acidic
- negative feedback - H+ stimulates somatostatin release -> inhibits release of gastrin and more H+
- H+ also directly inhibits gastrin and its own release

Front 91

stomach cephalic phase

Back 91

- sight thought of food
- vagas causes ACh release -> release pepsinogen from chief -> release of H+ and IF from parietal cells
- GRP (gastrin releasing peptide) release -> gastrin relese from enteroendocrines

Front 92

stomach gastric phase

Back 92

- food in stomach
- protein -> peptides (pepsin) and aa's buffers
- these activate chemo receptors and food bulk gets stretch receptors -> enteric nervous system to release more gastrin -> gets parietal cells, mast cells -> histamine which further gets parietal
- maximal release of H+ and intrinsic factor

Front 93

early intestinal phase

Back 93

- aa's enter SI first, fats last - carbs enter unchanged (no stomcah enzymes)
- duodenal gastrin cells -> gastrin -> more H+ in stomach
- CCK released -> pyloric contractionsphincter to slow stomach movement

Front 94

late intestinal phase

Back 94

- inhibitory gastric phase
- CCK release continues -> stimulates somatostatin in stomach
- enterogastromes (secretin and GIP) released -
- H+ in duodenum -> secretin -> inhibits H+ from parietals and releases HCO3- from pancrease (buffer)
- GIP -> inhibits H+ release

Front 95

HCl production by parietal cell

Back 95

- CA in cell catalyzes CO2 + water -> H+ and HCO3-
- H+ pumped into lumen by H+/K+ ATPase (both against gradient)
- HCO3- pumped across the base via HCO3-/Cl- antiporter -> alkaline tide in bloodstream (buffered by an acid tide from pancreas)
- Cl- driven across baso by a Na+/Cl- symporter and across apical by a K+/Cl- symporter
- large pool of K+ in lumen return via K+/H+ ATPase
- H+ and Cl- -> HCl

Front 96

histamine

Back 96

- binds receptor on parietal -> adenylate cyclase -> cAMP in cell -> fusion of vesicles w/ H+/K+ ATPase and IF onto apical membrane
- this creates canaliculi that empty into lumen
- inhibited by somatostatin, which lowers IC cAMP

Front 97

Zollinger-Ellison disease

Back 97

- gastrin-secreting tumor
- diagnosis by measuring plasma gastrin, then giving secretin and re-measuring
- the gastrin would normally decrease, but its increaseed
- acidity inhibits the activity of pancreatic enzymes which leads to diarhea

Front 98

ulcer medications

Back 98

- cant inhibit gastrin (too cose to CCK)
- H2 blockers – block histamine receptor
- antacids – buffer acids
- H+/K+ ATPase inhibitors (prevacid) block acid prod - will also reduce release of somatostatin -> increased gastrin -> risk of cancer (mitogen)

Front 99

Paneth cells

Back 99

- <1% - found at crypt base
- protect against bacteria by secreting lysozyme and alpha defensins

Front 100

M cells

Back 100

- <1%, line lumenal surface of Peyer’s patches
- antigen-presenting cells
- most common in the ileum

Front 101

columnar cells

Back 101

- (~90%)
- have absorptive and secretory function, depending on location

Front 102

goblet cells

Back 102

- (6-10%)
- secrete mucus

Front 103

acinar cells

Back 103

- ACh and CCK get basolateral receptors -> conversion of PIP2 to IP3 -> more IC [Ca++]
- Ca++ stimulates Cl- channels on apical -> fusion exocytosis
- movement of Cl- into lumen -> gradient to draw Na+ through paracellular channels into lumen -> osmotic gradient to draw in water

Front 104

pancreatic amylase

Back 104

- first enzyme in starch breakdown
- starch -> disaccharides and trisaccharides

Front 105

pancreatic lipases

Back 105

break up phospholipids, cholesterol esters and triglycerides

Front 106

pancreatic proteases

Back 106

- enterokinase (a brush border enzyme) catalyzes conversion of trypsinogen into trypsin
- trypsin catalyzes the conversion of chymotrypsinogen into chymotrypsin and procarboxypeptidase into carboxypeptidase

Front 107

central acinar cells

Back 107

- secrete water and NaHCO3
- cells use CA, then HCO3- is transported to lumen by a Cl-/HCO3- antiporter
- high Cl- in lumen via cAMP activated channel
- cAMP inc by secretin and dec by somatostatin
- H+/Na+ antiporter puts H across baso
- HCO3- and Cl- in lumen -> gradient to draws Na+ into lumen (paracellular) -> osmotic gradient to pull in water

Front 108

pancrease in interdigestive phase

Back 108

- there is little action
- the sphincter of Oddi is closed

Front 109

pancrease in cephalic phase

Back 109

- vagal stimulation increases
- ACh released -> weak stim of release of pancreatic enzymes
- some contraction of the gall bladder, Oddi relaxation

Front 110

pancrease in gastric phase

Back 110

- vagal stim continues
- gastrin released in the stomach -> weakly stimulates CCK receptors in pancreas -> inc secretion of pancreatic enzymes gall B contraction

Front 111

pancrease in early intestinal phase

Back 111

- movement of food into SI -> release of gastrin and CCK
- CCK gets CCK receptors -> strong contraction of gall B and relaxation of Oddi

Front 112

pancrease in late intestinal phase

Back 112

low pH in duodenum -> release of secretin -> release of electrolyte solution from pancrease and bile duct to buffer

Front 113

bile salt synthesis

Back 113

- form micelles around fats
- made from cholesterol thats esterified w/ gly or tau
- 7-hydroxylase, the first enzyme, is regulated by (-) feedback from cholic acid

Front 114

enterohepatic circulation

Back 114

- 99% bile salts recaptured
- in terminal ileum and returned to the liver
- aided by high affinity transporters in ileum & liver
- bile salts that remain in circulation are reabsorbed by the PCT
- hepatoctyes do de novo syn to keep bile salts constant

Front 115

phospholipids

Back 115

- amphipathic - form mixed micelles with bile salts
- these are also solubilizers

Front 116

cholestrerol

Back 116

- unclear if cholesterol in bile is just a means for the body to get rid of excess
- dissolves in the middle of micelles, thus insoluble

Front 117

bile pigments

Back 117

- in bile for excretion
- from the degradation of Hb -> bilirubin
- very insoluble, carried in blood bound to albumin ( so no renal clearance)
- conjugated with glucuronic acid in hepatocytes to increases solubility somewhat
- in interior of mixed micelle
- liver damage -> bilirubin in blood -> jaundice

Front 118

digestion of fats

Back 118

- fats -> smaller components from enzymes in mixed m's
- solubilized fats go to brush border and are released
- go across apical into columnar epi
- short chain FAs go across baso, other reassembled in SER -> lipoprotein particles in Golgi - exocytosed from baso and taken up by lacteals into lymphatic system -> thoracic duct -> stored in adipose and muscle tissue and the liver

Front 119

difestion of carbs

Back 119

- starch and complex sugars -> di and tri via amylase
- these -> monomers via brush border enzymes (close to apical transporters)
- ATs include SGLT-1 for gluclose and galactose, GLUT-5 for fructose (-> glucose)
- at the baso, glucose and galactose GLUT-2 (fac diff)
- in the systemic circulation, sugars travel to all tissues

Front 120

SGLT-1

Back 120

- sodium-dependent glucose transporter
- apical transporter that is able to transport glucose and galactose - high energy

Front 121

GLUT-5

Back 121

- transports fructose via energy-independent facilitated diffusion inside the cell
- fructose -> glucose immediatly the baso

Front 122

GLUT-2

Back 122

- on baso - transports glucose and galactose into systemic circulation
- huge gradiuent so via facilitated diffusion

Front 123

pancreatitis

Back 123

may result in a deficiency of amylase thus greatly interfering with the digestion of starches

Front 124

lactose malabsorption syndrome

Back 124

- there is a genetic defect in the lactase enzyme that does lactose -> galactose
- lactose accumulates in the lumen -> large gradient that draws water into the lumen
- diarrhea is primary symptom

Front 125

protein digestion

Back 125

- pancreatic proteases and pepsin -> peptides and aa's
- brush border enzymes do more breakdown
- aa's across apical via 1 of 7 transport molecules
- small peptides across apical via distinct transporter
- intact protein not taken up unless M cell as Ag
- at baso, 3 transporters for facilitated diffusion for aa's
- in blood, aa's enter the circulatory pool and various tissues

Front 126

Hartnup’s disease

Back 126

- defect in transporter that moves neutral aa's
- seldom nutritional def since neutral aa's can be transported by small peptide transporters

Front 127

aquaporin 8

Back 127

- found on both the basolateral and apical membranes of SI

Front 128

crypt cell secretion
basolateral membrane

Back 128

- Na+/K+ extrudes Na+ into the interstitium and K+ into cell
- Na+/K+/2Cl- symporter (like LOH) pumps ions into the cell, increasing IC [Cl-]
- there are leak channels to let K+ move down gradient -? (-) RMP thats close to EK+
- this electrical and chemical gradient drive Cl- out of cell

Front 129

crypt cell secretion
apical membrane

Back 129

- lots of CFTR channels activated by (P) of PKA (via cAMP)
- cAMP stimulated by VIP binding baso, inhibited by somatostatin
- open CFTR allows Cl- to move out into lumen

Front 130

movement of water into lumen

Back 130

- as [Cl-] in lumen increases -> electrical gradient that draws in Na+ from interstitium through ion-specific paracellular channels
- Na+ in lumen restores driving force on Cl-
- NaCl creates an osmotic gradient draws in water via AQP-8 channels into the lumen

Front 131

movement of water out of lumen

Back 131

- due largely to the osmotic gradient set up by the absorption of nutrients
- SGLT-1 moves glucose into the cells, and specific transporters move amino acids

Front 132

colon

Back 132

- in distal colon, ENaC on apical (aldosterone makes them take up Na+)
- typically absorbs NaCl and secretes KHCO3 (regulated by the body’s K+ status K+ through varied expression of leak channels and H+/K+ ATPase designed to recapture the ion)

Front 133

cholera

Back 133

- high levels of cAMP activate CFTR channels, and there is a flood of Cl- into the lumen
- so Na+ then water are drawn into the lumen a lot more

Front 134

pancreatic cholera

Back 134

- when a non β-islet cell tumor secretes too much VIP
- that activates the CFTR pathway too much
- can be treated w/ an analog of somatostatin (inhibits CFTR pathway and VIP tumor release

Front 135

cGMP pathway

Back 135

- receptor is on apical and is guanylate cyclase (GCC) - similar to GCA, a ANP receptor
- natural ligand is guanylin (found in intestinal extracts)
- guanylin similar to that of the HS toxin of E. coli - expressed in goblet cells of the colon
- coexpression of guanylin and mucin by goblet cells ensures mucin is properly hydrated

Front 136

ventromedial hypothalmus

Back 136

– satiety center
- electrode stimulation suppresses food intake
- lesions lead to uncontrolled food intake

Front 137

lateral hypothalmus

Back 137

- lateral – hunger center
- electrode stimulation triggers food intake
- lesions cause anorexia

Front 138

CCK and hunger

Back 138

- gives inhibitory signals
- injection -> reduced intake but only short term – it signals the end of a meal, no long term control over the set point of body weight
- injection alos decreases meal size, but not meal number

Front 139

ghrelin and hunger

Back 139

- stimulatory signals
- injection -> increased appetite and food intake
- natural peaks just before a meal
- short term, no long term control over the set point
- obese people have low ghrelin
- gastric bypass removes many ghrelin-producing cells

Front 140

adipose tissue and hunger

Back 140

- adipose tissue provides a signal that lowers the set point - so increase gives (-) feedback where metabolic rate is increased
- sympathetic-mediated response, so mice w/out β adrenergic receptors lose this loop and gain weight uncontrolably on high fat diet

Front 141

leptin

Back 141

- product of obese gene - controls the set point
- secreted by white adipose tissue
- ob-/ob- mice are obese - if given leptin, they will be thin from loss of adipose
- decrease in intake and increase in metabolic rate
- most obese have a LOT of leptin due to resistance

Front 142

estrogen and obesity

Back 142

- female athletes have little adipose tissue so less leptin
- leptin has a stimulatory effect estrogen release, so thats decreased too
- amenorrhea in female athletes