Exam2 Michelsintro Flashcards
what percentage of body is water? intracell portion? extra cell?
60% body is water
40% intracell
20% extracell
Where is sodium higher?
extra cell
where is K higher?
inside cell
Where is Cl higher
extracell
What controls fluid movement primarily between ECF and ICF
Na, so NaK ATPase
what controls fluid within ECF i.e. plasma and interstilium
the oncotic and hydrostatic pressures
what is non-pitting edema
swollen cell sdue to increased ICF volume
what is pitting edema
increased interstitial fluid volume
which type of edema does not respond to diuretics
non pitting edema
What is isoosmotic volume contraction. give examples
osmolarity is same
change in volume of ECF only
diarrhea, vomiting, hemorrhage
give example of isometric expansion
giving saline
What is hyperosmotic volume expansion and give examples
osmolarity and volume of ECF increases
ICF volume decreases to keep equilibrium(water)
excess NaCl intake, mannitol infusion
what is hyoosmotic volume expansion and give examples
addition of pure water will decreased ECF osmolarity and the water increases in both ECF and ICF
SIADH, psychogenic polydipsia
what is the renal response to volume expansion
decreased SAN causes nephron to vasodilate, increasing GFR Heart increases BNP and ANP brain decreases ADH release dec renin. dec Ang I II and aldosteron leads to water loss overall
What is a hypoosmotic volume contraction and give example
osmolarity of ECF decreases and volume
ICF volume increases
examples
hypoaldosteronism and adrenal insufficiency
what is hyperosmotic volume contraction
lost water
osmolarity of ECF increases and volume
ICF volume decreases and water shiffts from ICF to ECF to equilibrate
dehydration and diabetes inspidus
what are the bodies response to volume contraction
increased SAN vasoconstriction of renal vasc (afferent and efferent) GFR decreases Heart dec ANP and BNP increase in ADH increase renin, ANG I II and aldosterone to decrease Na and water secretion
what happens to a cell in a hypotonic(hypoosmotic) environment
the cell swells
what happens to the cell in a hypertonic solution
cell shrinks
where is the cortex and medulla of kidney? where are the nephrons
cortex is the outside
medulla inside
nephrons–> juxtamedullary loop of henle extend into medulla
cortical nephron stays in Cx
Which type of nephron is important in concentrating urine
juxtamedullary
osmolarity of renal medulla increases during the center
which cells release renin
juxtaglomerular cells
what cells autoregulate vasculature of renal system
macula densa cells
describe glomerular capillaries
high hydrostatic pressure filter into bowmans capsule
describe peritubular capillaries
low hydrostatic pressure so water and solute are reabsorbed here
what inn affects renal blood flow, GFR and filtration fraction
symapthetic system
what stimulates renin release
signals from sympathetic cells working on glomerular cells
what are the layers of the glomerulus
fenestrated endothelium
glomerular BM has negative charge( prevent proteins)
Podocyte epithelium slit pores between podocytes(prevent large molecules)
what is normal GFR
125 ml/min or 180L/day
What are the 3 physical factors of GFR
hydraulic conductivity
SA for filtration
capillary ultrafiltration pressure
high oncotic pressure does what
pulls water towards it
where does fluid enter after glomerular capillaries
peritubular capillaries
What is the filtration fraction
part of renal plasma flkow that is diverted into proximal convoluted tubule
how do we calculate FF
GFR/RPF renal plasma flow
what dictates FF
ultrafiltration pressure
What happens with and increased FF
oncotic pressure of efferent arteriole increases leading to greater reabsorption
what is normal FF
20%
what happens to oncotic P and hydrostatic pressure of capillary during volume contraction
dec hydrostatic
increased oncotic
to increases absorption
what changes the hydrostatic pressure of glomerular capillaries
renal arteriole BP
afferent arteriole R
efferent arteriolar R
what happens to GFR when mesangial cells contract
shorten loops and decrease GFR
what happens with afferent arteriole constriction
pressure drop so decreased GFR
renal blood flow falls because increased R
what happens with efferent arteriolar constriction
pooling of blood in glomerular capillaries
icnreased hydrostatic of glomerular capillaries increases GFR
renal blood flow dec
What happens in the arterioles with increased systemic BP
increased GFR, increased RBF
what happens with moderate efferent arterole constriction
dec RBF renal blood flow
increased GFR and increased P built up in the hydrostatic glomerular capillary
What affects of SAN has on efferent and afferent arterioles
constrict afferent
less constriction efferent
dec RBF and dec GFR
What effects of SAN on renin system
increased renin by grnaular cells
so Ang II helps BP
how does ANG II work on renal system
contricts efferents more so the BP will increase and stabilize GFR
What effect on Na does the SAN do
stimulates reabsorption in proximal tubules, Thick ascending lopps, distal convoluted and collectin duct
Where is ACE located
endothelial cells in lung
does ADH go up or down in hypotension
increase because want to conserve water. increase blood volume
What do PGI2 and PGE2 do on renal system
increase renal blood flow, vasodilatory
What is Clearance
volume of plasma from which substance is completely removed by kidneys in given period of time
ml/min or L/hr
what does clearance of kidneys tell you
how effectively kidneys are removing substance from blood
how do you calculate clearance
concentration of substance in urine times the volume
all over the concentration of substance in plasma
the plasma clearance of creatnine is used for what
Inverse indicator of GFR
inulin too
if GFR has fallen 25% what will Pcreatnine look like
increased 4X
what is P creatnine used for clinically
chronic long term monitoring of GFR
what is glomerular filtration
filtration of plasma from gc into bowmans
what is tubular reabsorption
transferral of substances from tubular lumen to peritubular capillaries
what is tubular secretion
transferral of substances from peritubular capillaries to tubular lumen
organic cations and anions
breakdowns from drugs
what is kidney excretion
voiding of substances in urine
how do you calculate tubular reabsorption
glomerular filtration - urinary excretion
if excretion is less then filtration what was net result
net reabsorption
how do you calculate urinary excretion rate
the concentration in urine and the volume or urine
what are types of secondary active transport
co and counter transport
what is reabsorbed in proximal tubule
most filtered substances: Na K Cl Ca HCO3 and PO4
all glucose and aa
what are secreted in proximal tubule
organic anions and cations (drug metabolites, cretnin and irate)
What controls moevement in proximal tubule
the ATPase on the basolateral membrane
Na co transports what molecules into cell from tubule lumen
glucose and K and Cl
what is Na exchanged for on luminal membrane in proximal tubule
H+
countertransporter
Where do loop diuretics work
co transport of Na K 2Cl in the thick ascending limb
where is there Na Cl co transport
early distal convoluted tubule
what exchange d occurs in proximal tubule
co transport glucose aa and PO4
countertransport of Na H
what channels are present in the late distal convoluted tubule/collecting duct
luminal membrane channels
How does water move between cells
transcell and paracell
What is PAH
para-amino-hippurate acid
if the tubular lumen has lower pH what happens
favors reabsorption of organic acids
traps organic bases in lumen
how do you help a patient who overdosed on aspirin
decrease acidity of lumen
give bicarb
Increase pH(traps acid in lumen)
why does inulin increase as you move down proximal tubule
as you go through tube more water reabsorption is taking lpace. concentratin the inulin
how do [ ] Na and K change in proximal tubule
no change
what substances are reabsorbed in proximal tubule more than water
HCO3, aa and glucose
which part of the loop of henle is impermeable to water
ascending limb
If K levels are messed up, what other ion may have issues in thick ascending limb
Mg
where is the major site of physiological control of Na water balance
late DCT and collecting duct
What does ANP do
inhibits Na reabsorption and medullary collecting duct
majority of K is reabsorbed wehre
in proximal tubule mostly
then TAL of loop
what cells in collecting duct secrete K
principal cells
What are the 5 factors that affect K secretion in collecting duct
extracell K cocnentration Na reabsorption, negative luminal voltage, attracts K luminal fluid flow rate extracell pH aldosterone
what does aldosterone do
stimulate K secretion in collectin gduct
how does extracell pH affect K
K and H exchange across cell membranes
how does luminal fluid flow rate affect K lvels
dilution of secreted K
how does Na reabsorption affect K levels
negative luminal voltage, attracts K
how can a low Na diet lead to hyperkalemia
less Na delivery to date distal tubule and collecting duct causing less K secretion/excretion
How is hyperkalemia treated
increasing downstream delivery Na to distal tubule and collecting ducts
what is the countercurrent multiplier mechanisms
increased osmolarity in medulla that concentrates urine
recycling of Na and K in region to keep high osmolarity
increased blood flow affects countercurrent how?
decreases the concentration
what are the levels of ADH in dehydrated individuals
high because want to save water
how does ADH help reabsorb water
second messengers leading to increase aquaporins on tubular side of cell
What is free water Clearance
amount of water excreted by kidneys without solute
if the urine osm is less than the P osm or Clearance of water then?
pure water is cleared. hypotonic urine
How does ADH affect clearance water
changing permeability of collecting duct
What are the effects of ANP on Na and water excretion
increase GFR via efferent constriction afferent dilation
inhibits Na reabsorption in medullary collecting duct
suppress renin
suppress aldosterone
systemic vasodilator
suprresses ADH secretion and actions
what is normal blood pH
7.4
what are the kidneys defense for pH changes
chemical buffers, intracell(proteins) and respiration(CO2)
kidneys(urinary buffers)
what factors control renal H secretion
intracell pH, plasma PCO2, carbonic anhydrase, Na reabsorption, ECF K levels, aldosterone
What is anion gap informative for
metabolic acidosis Dx
What is chronic reparatory acidosis and alkalosis
changes in repiration in the presence of renal compensation
takes 2-3 days for kidneys to compensate for initial disturbance
what can cause metabolic acidosis
gain of fixed acid
loss HCO3
(HCO3 falls)
how do we measure anion gap
cations(Na)- anions (Cl and HCO3)
what is normal anion gap range
8-11 mEg/L
if there is metabolic acidosis what happens to anion gap
increased
by is Anion gap unchanged with hyperchloremic acidosis
loss of HCO3 matched by Cl
know anion gap equation
cations Na minus anions Cl and HCO3
what are causes of high anion gap acidosis
Mudpiles
methanol, uremia, diabetic ketoacidosis, propylene glycol, isoniazid lactic acidosis, ethylene glycol, salicylates
what is metabolit alkalosis
gain of strong base
loss of fixed acid
review extra slides of graphs with lots of detail
second half of ppt and video has most
