Urinary Pathophys: Review Of Renal Phys And Acid/base

Front 1

Where are all glomeruli located?

Back 1

Cortex!

Front 2

What advantage do animals with a higher juxtamedullary/cortical nephron ratio have?

Back 2

Greater concentrating ability!

Front 3

What part of the kidney is most metabolically active?

Back 3

Cortex and outer medulla

Front 4

What part of the kidney is anaerobic?

Back 4

Inner medulla

Front 5

What part of the kidney is poorly perfused?

Back 5

medulla

Front 6

What are the main kidney functions?

Back 6

-maintain composition of body's internal environment (filter, reabsorb, secrete, excrete)
-regulate osmolarity, fluid volume, electrolytes, acid/base balance
-gluconeogenesis
-Vit D activation
-EPO production
-hormone excretion

Front 7

How is excretion measured?

Back 7

mg/min (urine flow x urine conc)

Front 8

How is secretion measured?

Back 8

mg/min (PAH exc.- PAH filtered)

Front 9

How is GFR measured?

Back 9

ml/min (creatinine clearance=CR exc/Pl conc)

Front 10

How is filtration (i.e. filtered load) measured?

Back 10

mg/min (GFR x Pl. Conc.)

Front 11

What governs filtration of plasma across the barrier in glomeruli?

Back 11

Hydrostatic and osmotic forces

Front 12

PF = PG - PB - piG?

Back 12

-Pf=net filtration pressure across glomerulus
-Pg=mean hydrostatic pressure in glomerular capillaries
-Pb=mean hydrostatic pressure in Bowmans' space
-piG=plasma oncotic pressure in glomerular capillaries
-piB=oncotic pressure in Bowman's space

Front 13

Which one of the osmotic/hydrostatic forces is most variable?

Back 13

Plasma oncotic pressure in glomerular capillaries

Front 14

How does it vary and why?

Back 14

It increases across the capillary because bluid is lost from the capillary

Front 15

What is the effect of afferent arteriole constriction?

Back 15

Decreased RPF and GFR

Front 16

What is the effect of efferent arteriole constriction?

Back 16

Decreased RPF but increased GFR (back pressure)

Front 17

What factors are most likely to affect GFR? (8)

Back 17

-changes in RBF
-changes in glomerular capillary hydrostatic pressure
-changes in mean hydrostatic pressure of Bowman's space
-changes in concentration of plasma proteins
-increased permeability of the glomerular filter
-decrease in total area of glomerular capillary bed
-tubuloglomerular feedback
-ageing

Front 18

How will glomerular capillary hydrostatic pressure change?

Back 18

-changes in systemic blood pressure (prerenal azotemia)
-afferent or efferent arteriolar constriction

Front 19

How will mean hydrostatic pressure of Bowman's capsule change?

Back 19

-ureteral obstruction (crystals)
-extratubular compression secondary to interstitial edema or inflammation
-dz of the tubular epithelium that restrict movement of glomerular filtrate through the nephron

Front 20

How will concentration of plasma proteins change?

Back 20

-dehydration
-hypoproteinemia
-precipitation of heme proteins during a hemolytic crisis

Front 21

How are GFR and RPF autoregulated?

Back 21

-afferent arteriolar constriction: response to a sudden increase in BP
-angiotensin II (efferent arteriolar constriction): response to decrease in BP

Front 22

What is most energy expended on in the kidney?

Back 22

Na+ reabsorption

Front 23

Where is Na+ reabsorbed along the nephron?

Back 23

- 67% in prox tubule
- 25% in thick ascending limb
- 3-5% in distal tubule (aldosterone stimulated)
- 3-5% in collecting ducts
- less than 1% excreted

Front 24

What is Na+ reabsorption in the prox nephron coupled to?

Back 24

H+ secretion and indirectly to HCO3- reabsorption

Front 25

How is K+ handled across the nephron?

Back 25

-65% reabsorbed in prox nehpron
-25% reabsorbed in thick ascending limb
-5-9% reabsorbed in distal nephron if ther eis a low K+ diet
-there can be 0-110% secretion in distal nephron depending on diet, aldosterone, acid/base, flow rate, luminal anions

Front 26

Do the kidneys normally
excrete more K+ than
the digestive tract ?

Back 26

Yes

Front 27

In general, what is the
relationship between
Ca++ and the kidneys ?

Back 27

Free ionized plasma Ca++ and thus Ca++ filtered load increase in acidemia because H+ dissociates Ca++ from plasma proteins

Front 28

How is Mg++ handled across the nephron?

Back 28

-30% reabsorbed in PT
-65% in thick ascending limb (loop diuretics reallllly decrease its reabsorption)
-1% in DT and CD
-3% excreted

Front 29

How is PO4 handled across the nephron?

Back 29

-80% reabsorbed in PT
-10% reabsorbed in DT
-10% excreted

Front 30

What does PTH do to prox tubular phosphate reabsorption?

Back 30

reduces it

Front 31

What part of the nephron is a countercurrent multiplier and how does this work?

Back 31

-Thick ascending limb
-electrolyted reabsorption here is largely electroneutral
-loop diuretics reduce the reabsorption, creating an osmotic diuresis

Front 32

Where does the transepithlial PD become negative?

Back 32

in the early distal tubule because this is where Cl- lags behind Na+ reabsorption

Front 33

How do thiazide diuretics affect the transepithelial PD?

Back 33

it does not allow the negative transepithelial PD to occur at the distal tubule and thus keeps it positive which favors Ca++ reabsorption

Front 34

What happens to transepithelial PD in the late distal tubule and collecting duct?

Back 34

-it becomes more negative (-50) which favors K+ and H+ secretion
-K+-sparing diuretics (i.e., aldosterone antagonists) that inhibit this reabsorption lead to acidemia

Front 35

What is aldosterone secretion stimulated by?

Back 35

-Increase in plasma K+
-angiotensin II and III

Front 36

What does ADH do?

Back 36

Increase H2O and urea permeability and the urea goes on to contribute to medullary interstitial fluid osmolarity

Front 37

How much of the cardiac output do the kidneys receive?

Back 37

23%

Front 38

How much of the plasma perfusing the glomerulus is filtered?

Back 38

20%

Front 39

Why do you need high renal blood flow?

Back 39

-supplying O2 and metabolic substrates to kidney
-ensure an adequate GFR necessary for excretion of metabolic waste products (urea, uric acid, creatinine)

Front 40

What is renal tubular acidosis?

Back 40

Damage to the proximal renal tubular cells that contributes to acid/base imbalanes seen in some patients with renal dz

Front 41

What are functions of prox tubule?

Back 41

-isotoic reduction of glomerular filtrate
-Na+/H+ exchange
-lots of reabsorption of stuff
-gluconeogenesis
-serction of NH3, salicylate, oxalates, some antibiotics

Front 42

What part of the nephron is freely permeable to H2O but not to electrolytes?

Back 42

descending limb

Front 43

What part of the nephron is impermeable to water?

Back 43

thick, ascending limb

Front 44

What are the 3 cell types in the collecting duct?

Back 44

-primary cells: aldosterone sensitive and important in reabsorption of Na+ and secretion of K+
-alpha-intercalated cells: actively pump H+ into lumen
-beta-intercalated cells: secrete HCO3- in exchange for Cl- and reabsorb H+

Front 45

What is urodilatin?

Back 45

-peptide hormone secreted by the distal tubule and collecting ducts that inhibits Na+, H2O and urea reabsorption in teh medullary region fo the collecting ducts
-not found in systemic blood

Front 46

What is the vasa recta??

Back 46

- receives 1-2% of total renal blood flow
-maintains medullary interstitial concentration gradient

Front 47

What is important about the juxtaglomerular apparatus?

Back 47

-where afferent arteriole and distal tubule come into close contact with each other
-JG cellspecialized myoepithlial cells that synthesize and secrete renin

Front 48

What happens as a result of diarrhea in terms of acid/base?

Back 48

-metabolic acidosis because fecal HCO3- concentration is higher than the plasma concentration

Front 49

Who are the primary buffers?

Back 49

- Hb
- protein
- HCO3
- NH3
- HPO4
- CaHPO4

Front 50

anion gap

Back 50

kill me

Front 51

Which way does the buffer equation shift during metabolic acidosis?

Back 51

LEFT

Front 52

What are 6 important items that influence plasma K+ balance?

Back 52

-hyperosmolarity: moves into ECF
-exercise: moves into ECF
-cell lysis: moves into ECF
-insluin: moves into ICF
-Beta antagonists: move into ICF
-acid base balance: moves into or out of cell in exchange for H+

Front 53

What happens to K+ in chronic acidemia?

Back 53

Increase in its excretion

Front 54

What are examples of conditions associated with a metabolic alkalosis?

Back 54

-excessive H+ loss from vomiting, K+ wasting diuretics, aldosterone excess
-excess alkali intake
-increasing seating (Cl- loss
)
-severe K+ depletion
-free water deficit
- hypoproteinemia

Front 55

Which way does the buffer equation shift in metabolic alkalosis?

Back 55

RIGHT

Front 56

How does the kidney compensate for metabolic alkalosis?

Back 56

-Increase HCO3= filtered load
-decrease HCO3- reabsorption
-increase HCO3- excretion

Front 57

Does clelular K+ gain occur with alkalemia

Back 57

yes, it goes into cells in exchange for H+

Front 58

Why is their tissue K+ gain and enhanced renal K+ excretion in metabolic alkalosis?

Back 58

-there is more K_ uptake by cells so that there is an icnreased intracellular K+
-there is more H+ and thus a lower pH and increased perm. of luminal membranes to K+

Front 59

Which way does the buffer equation shift in resp acidosis?

Back 59

right

Front 60

What are the kidneys doing during resp acidosis?

Back 60

generating lots of bicarb to put in blood

Front 61

Which way does the buffer equation shift in resp alkalosis?

Back 61

Left

Front 62

What is the renal compensation for resp alkalosis?

Back 62

Dump HCO3- into the urine