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142 Cards in this Set

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Alveolar Ventilation Equation
Alveolar Ventilation (VA) =

863(VCO2/PACO2)
Alveolar Gas Equation
PAO2 = PIO2 - (PACO2/R) + F

= 147 - (PACO2/0.8)
respiratory quotient
CO2 produded / O2 consumed
250 / 300
0.8
PvCO2
46
PaCO2
40
PvO2
40
PaO2
100
CO probe to test for diffusion
DL-CO = VCO/PACO
LaPlace’s law
P= 2(T/r)
R =
change in P / flow
N2O
- high permeability
- poor interaction with hemoglobin
- reaches equilibrium faster than O2
CO
- reacts well with hemoglobin
very well
- very slow to reach equilibration due to poor permeability
HCO3—H2CO3 as buffers
- pka = 6.1
- its abundant
- the effective pKa is >6.1 b/c of changes in ventilation
- lungs control PCO2
- kidneys control HCO3
Na+/H+
antiporter - extrudes H+ when pH is low
Cl-/HCO3-
antiporter - extrudes HCO3- when pH is high
H+/K+ ATPase
extrudes H+
Na+/2HCO3-
extrudes HCO3- by gradient
respiratory acidosis
- 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
respiratory alkalosis
- 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
metabolic acidosis
- addition of fixed acids to blood or a loss of base
- compensate w/ pulmonary hyperventilation to increase excretion of CO2 (change in PCO2)
metabolic alkalosis
- loss of fixed acids from body or addition of base
- compensate w/ pulmonary hypoventilation to conserve CO2 (limited by O2 requirements)
anatomical shunts
bronchial veins which drain into the pulmonary veins and thebesian veins which drain into the left ventricle
normal values of lung stuff
- FEV1 = 4.0L
- FVC = 5.0L
- FEV1/FVC = 0.80
- FEF25-75% = 3.5L
patients with obstructive disease
- FEV1 = 1.3L
- FVC = 3.1L
- FEV1/FVC = 0.42
- FEF25-75% = 1.4L
patients with restrictive disease
- FEV1 = 2.8L
- FVC = 3.1L
- FEV1/FVC = 0.90
- FEF25-75% = 3.7L
load with water
- decrease in the osmolarity of ECF and ICF
- increase in the volume of ECF and ICF
load w/ salt
- increase in the osmolarity of ECF and ICF
- increase in the volume of ECF
- decrease in volume of ICF
load w/ isomolar solution
causes a rise in ECF volume only
proximal convoluted tubule (PCT) basic info
resorbs 2/3 of filtered salt and water, all filtered glucose, and secreted drug metabolites
- resorbs most water via A1
descending loop of Henle basic info
resorbs water and secretes NaCl
ascending loop of Henle basic info
impermeable to water, resorbs NaCl
distal convoluted tubule and collecting ducts basic info
- 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
filtration fraction
- equal to GFR/RPF
- normal value is 120/600 = 20%
filtered load of y
GFR X plasma [] of y
excreted load of y
V times urine [] of y
reabsorption and secretion in terms of filtered load and excreted load
- reabsorption is filtered load minus excreted load
- secretion is excreted load minus filtered load
clearance equation
- volume of plasma cleared of a solute per unit time
- Cy = (V x [y]urine)/[y]plasma
- = excreted load /[y]plasma
normal GFR values
- men: 95±20mL/min
- women: 120±mL/min
RPF =
- Clearance of PAH x (1/Effusion of PAH)
- (540) x (1/0.9) = 600mL/min
glomerular filtration pressure (and normal values)
- (PC - PBowman’s) – (COPC - COPBowman’s)

- (60 – 15) – (30 – 0) = 15mmHg
MFP
- (PC - PBowman’s) – mean COP

- mean COP = (COPafferent + COPefferent)/2
GFR (mL/min) =
Kf x MFP
reabsorption of NaCl
transcellular movement
- 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)
reabsorption of NaCl
paracellular movement
- 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
aquaporin-3
allows passage of water from the cell to the interstitium - it is unregulated
K+/Na+ ATPase
- 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
transporters on apical PCT surface
- Na+/Cl- co-transporter
- Na+/glucose co-transporter
- Na+/amino acid co-transporter
- aquaporin-1
- Na+/H+ antiporter
transporters on basolateral PCT surface
- Na+/K+ ATPase
- aquaporin-1
- glucose transporter
bicarbonate reabsorption
- 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
urea reabsorption
- PCT resorbs around 50% - independent of ADH
- ADH stimulated resorption in CD
LOH basic info
- 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
dLOH trasport
- no Na+/K+ ATPase
- aquaporin-1 - water reabsorb
- UT-2 (and passive diffusion) secrete urea
- passive diffusion of Na sec
aLOH transport
- 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
UT-1
transport urea on vasa recta
descending vasa recta
- 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
ascending vasa recta
- solute is exported to IS and water is imported
- water resorption is aided by high osmotic pressure and COP
- at end, osmolarity is 350
DCT and CD transporters
- 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
α cells
- 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
β cells
- 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
medullary CD transporters
- ADH-dependent water reabsorption via aquaporin-2
- ADH-dependent expression of UT-1 for urea reabsorption
ADH
- 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
V-2 receptors
- 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
aquaporin 4
found on hypothalamic glial cells - possible role as osmosensors
aquaporin-1 null
- normal in basal state
- cant maximally concentrate urine in water restriction
- main effect in dLOH, little effect on the proximal tubule
central vs. nephrogenic diabetes insipidus
- 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)
renal myogenic response
increase in transmural P -> increase in Ca conductance and release of endothelial factors -> vasoconstriction
tubuloglomerular feedback
- 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)
during increased Na+ intake ...
- 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
renal sensors
- 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
atrial natriuretic peptide (ANP)
- 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
renal sympathetic efferents
- if ECV decreased, increased firing and activity
- constricts the afferent arteriole, decreasing GFR
- Na+/H+ antiporters on apical PCT stimulated, which increases Na+ uptake
renin-angiotensin-aldosterone system
- 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
aldosterone
- 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
renal artery stenosis
- 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
glucocorticoid remediable aldosteronism
- 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
apparent mineralocorticoid excess
- 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
Liddle’s Syndrome
- 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
acetazolamide
- acts at the PCT
- inhibits carbonic anhydrase which decreases Na+/H+ activity
furosemide (Lasix)
- acts at the ascending loop of Henle
- inhibits activity of the Na+/K+/2Cl- transporter
thiazide (HCTZ)
- acts at the distal convoluted tubule
- inhibits the activity of the Na+/Cl- transporter
amiloride
- acts at the DCT and collecting ducts
- inhibits activity of ENaC channels
spirolactone
inhibits MR activity
VIP
- 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
chief cells
- in bottom of gastric glands (pyloric and oxyntic)
- release pepsinogen and gastric lipase
neck cells
secrete mucus for lubrication and buffering functions
parietal cells
- 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+)
HCl
- antibacterial
- denatures macromolecules
- catalyzes pepsinogen to pepsin
intrinsic factor
- helps absorption of B-12 in the large intestine - protects the vitamin from digestion
- deficiency results in pernicious anemia
enteroendocrine cells
- (<1%)secrete into interstitum
- gastrin (from pyloric glands only)
- somatostatin
- histamine
- ghrelin (only in oxyntic glands, does hunger)
stomach interdigestive phase
- 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
stomach cephalic phase
- 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
stomach gastric phase
- 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
early intestinal phase
- 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
late intestinal phase
- 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
HCl production by parietal cell
- 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
histamine
- 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
Zollinger-Ellison disease
- 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
ulcer medications
- 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)
Paneth cells
- <1% - found at crypt base
- protect against bacteria by secreting lysozyme and alpha defensins
M cells
- <1%, line lumenal surface of Peyer’s patches
- antigen-presenting cells
- most common in the ileum
columnar cells
- (~90%)
- have absorptive and secretory function, depending on location
goblet cells
- (6-10%)
- secrete mucus
acinar cells
- 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
pancreatic amylase
- first enzyme in starch breakdown
- starch -> disaccharides and trisaccharides
pancreatic lipases
break up phospholipids, cholesterol esters and triglycerides
pancreatic proteases
- enterokinase (a brush border enzyme) catalyzes conversion of trypsinogen into trypsin
- trypsin catalyzes the conversion of chymotrypsinogen into chymotrypsin and procarboxypeptidase into carboxypeptidase
central acinar cells
- 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
pancrease in interdigestive phase
- there is little action
- the sphincter of Oddi is closed
pancrease in cephalic phase
- vagal stimulation increases
- ACh released -> weak stim of release of pancreatic enzymes
- some contraction of the gall bladder, Oddi relaxation
pancrease in gastric phase
- vagal stim continues
- gastrin released in the stomach -> weakly stimulates CCK receptors in pancreas -> inc secretion of pancreatic enzymes gall B contraction
pancrease in early intestinal phase
- movement of food into SI -> release of gastrin and CCK
- CCK gets CCK receptors -> strong contraction of gall B and relaxation of Oddi
pancrease in late intestinal phase
low pH in duodenum -> release of secretin -> release of electrolyte solution from pancrease and bile duct to buffer
bile salt synthesis
- 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
enterohepatic circulation
- 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
phospholipids
- amphipathic - form mixed micelles with bile salts
- these are also solubilizers
cholestrerol
- 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
bile pigments
- 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
digestion of fats
- 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
difestion of carbs
- 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
SGLT-1
- sodium-dependent glucose transporter
- apical transporter that is able to transport glucose and galactose - high energy
GLUT-5
- transports fructose via energy-independent facilitated diffusion inside the cell
- fructose -> glucose immediatly the baso
GLUT-2
- on baso - transports glucose and galactose into systemic circulation
- huge gradiuent so via facilitated diffusion
pancreatitis
may result in a deficiency of amylase thus greatly interfering with the digestion of starches
lactose malabsorption syndrome
- 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
protein digestion
- 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
Hartnup’s disease
- defect in transporter that moves neutral aa's
- seldom nutritional def since neutral aa's can be transported by small peptide transporters
aquaporin 8
- found on both the basolateral and apical membranes of SI
crypt cell secretion
basolateral membrane
- 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
crypt cell secretion
apical membrane
- 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
movement of water into lumen
- 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
movement of water out of lumen
- 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
colon
- 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)
cholera
- 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
pancreatic cholera
- 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
cGMP pathway
- 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
ventromedial hypothalmus
– satiety center
- electrode stimulation suppresses food intake
- lesions lead to uncontrolled food intake
lateral hypothalmus
- lateral – hunger center
- electrode stimulation triggers food intake
- lesions cause anorexia
CCK and hunger
- 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
ghrelin and hunger
- 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
adipose tissue and hunger
- 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
leptin
- 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
estrogen and obesity
- female athletes have little adipose tissue so less leptin
- leptin has a stimulatory effect estrogen release, so thats decreased too
- amenorrhea in female athletes