Lecture 45+46 Flashcards

1
Q

equation for filter load?

A

GFR x plasma concentration

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2
Q

equation for excretion

A

Urine volume x urinary concentration

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3
Q

Net filtration rate equation

A

FL - ER

\+ = net reabsorption 
- = net secretion 
0 = no transport (net)
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4
Q

equation for renal blood flow?

A

RBF = RPF / (1 - HCT)

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5
Q

Proximal convoluted tubule and sodium uptake? how?

what enhances sodium intake?

A

2/3 of filtered sodium is reabsorbed here by
SGLT = sodium + glucose
NHE transporter = sodium in, H+ out

The basolateral Na/K pump creates the gradient for Na entry into the cell from the blood

catecholamines and Angiotension II stimulates Na uptake

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6
Q

PCT and water / electrolyte reabsorption?

A

the PCT has a high permeability to water

the water, K, and Cl follow Na (can occur through the tight junctions, paracellular, or go through the cell, transcellular

Cl goes into blood; anion goes out (formate)

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7
Q

BUN levels and kidney health?

A

Nitrogenous wastes are excreted from the body as urea, and, thus, plasma blood urea nitrogen (BUN) levels are a useful indicator of renal health and function

increased levels of BUN can lead to gout

moves paracellularly

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8
Q

PCT and glucose

A

All filtered glucose is reabsorbed in the PT via secondary active transport linked to sodium. Glucose
molecules are recovered from the early PCT by SGLT2 transporter and from the later PT by the SGLT1 transporter.

GLUT 1 and GLUT 2 transporters (facilitated diffusion) are also used

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9
Q

PCT and amino acids?

A

peptides enter the cell by the PepT1/T2 transporters
these transporters need H, as well. (H + AA)

these peptides are degraded in the cell by proteases and are transported in the blood as free AA

defects in this pathway lead to proteinuria

the concentration of glucose, AA should be zero leaving the PCT

can also go into cell by endocytosis and be released into blood by exocytosis

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10
Q

diabetes mellitus and the kidneys

A

reabsorption of glucose is proportional to plasma concentration until the Tm is meet

after the plasma glucose of 300mg is meet; glucose will be excreted due to saturation of transporters

will lead to polyuria + polydipsia

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11
Q

PCT- bicarbonate reabsorption

A

H+ is pumped into the tube by a Na/H exchanger
(H is out, Na in)

H+ combines with HCO3 to form H2CO3
Carbonic anhydrase converts H2CO3 to CO2 and H2O, then goes into cell

intracellular CA reforms H+ and HCO3

H+ is once again pumped out into tubule and HCO3 is returned to blood.

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12
Q

What stimulates the Na/H antiport in the PCT?

A

angiotensin II

In volume depleted states, the volume of HCO3 in the blood increases

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13
Q

what could happen due to defects in PCT?

A

metabolic acidosis
hypophosphatemia
osteopenia

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14
Q

How do diuretics work?

A

increase urine output by altering sodium handling

inhibit the reabsorption of Na, increase Na in the lumen, and thus more water remains in the lumen

more sodium excretion = more water excretion

used to reduce extracellular fluid volume (edema and hypertension)

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15
Q

Acetazolamide

A

This is a carbonic anhydrase inhibitor, thus a reduction in the reabsorption of HCO3 and reduction of activity of the Na/H antiport

sodium remains in lumen, thus more water in lumen

Used for altitude sickness

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16
Q

Loop of henle reabsorption?

A

Thin descending portion:
permeable to water
impermeable to solute

thin ascending portion:
impermeable to water

Thick ascending portion:
impermeable to water
solutes transported out of tubule

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17
Q

Loop of henle - thick ascending portion

A

Na/ K pump is very important because it leads to a deficiency of Na in the cell, thus allows for the action of the Na/Cl/K transporter

also allows for the Na/H antiporter to work (H out and Na in)

K will come into cell and then diffuse back into the lumen, thus the tubule is + in charge, thus this drives the movement of Mg and Ca into the blood via paracellular pathway

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18
Q

Loop diuretics?

A

Block the Na/K/Cl co-transporter

thus more Na/K/Cl in the urine, along with water and electrolytes!!

used for pulmonary edema

watch for hypocalcemia ( No K gradient)

19
Q

Early distal tubule reabsorption

A

reabsorbs Na, Cl, and Ca

Na/K pump creates a low intracellular concentration, thus NaCl crosses into cell by the Na/Cl symporter

Cl diffuses into blood

this segment is impermeable to water! Osmolarity decreases (lowest osmolarity)

20
Q

Ca reabsorption in the EDT?

A

Ca enters the cell passively by PTH

is put into the circulation by the 3Na/Ca antiporter

calbindin facilitates reabsorption of Ca

21
Q

Gitelman’s syndrome

A

mutation of the Na-Cl cotransporter

leads to ‘salt wasting’ due to excretion of Na and Cl

may lead to low blood Ca levels

22
Q

Thiazide diuretics

A

Inhibit the Na/Cl symporter of the DT

used to treat hypertension and heart failure

can lead to hypercalcemia!!
inhibiting Na leads to hyperpolarization which drives Ca into the blood

23
Q

Role of principle cells in the DT and collecting duct

role of aldosterone?

A

reabsorb sodium and secrete potassium

influenced by aldosterone

  1. increases ENaC channels
  2. increase ENaC opening time
  3. stimulates Na/K ATPase
24
Q

ADH and principle cells in the DT/CD?

A

principle cells express aquaporins that are regulated by ADH

ADH acts on the V2 receptors which increases water reabsorption

low ADH = low water reabsorption

25
Q

the syndrome of inappropriate antidiuretic hormone

A

Over secretion of ADH

high water reabsorption

26
Q

Intercalated cells in the DT/CD?

aldosterone?

A

contains H ATPase that pumps H+ into the lumen

H+ is eliminated from the body via buffers

aldosterone stimulates the H+ ATPase

excess aldosterone can lead to metabolic alkalosis

27
Q

Potassium sparing diuretics?

how do they work?

A

can be sodium channel blockers and/or aldosterone antagonists

reduce Na reabsorption, so K secretion is lowered

work?
blocking ENaC channels
block aldosterone receptors
block the production of aldosterone

28
Q

Conn’s syndrome?

A

the adrenal glands make to much aldosterone

seen:
hypertension (high Na)
hypokalemia
metabolic alkalosis (high HCO3)

treatment:
spironolactone

29
Q

1 kg = ? lbs

A

2.2 lbs

30
Q

1 kg = ? L

A

1 L

31
Q

equation for blood volume?

A

BV = PV / (1 - Hct)

32
Q

equation for ECF

A

ISF + PV

ECF = 1/3 or 33% of fluid (25% is plasma) 
ISF = 2/3 or 67% of fluid 
Males = 60% water 
female = 55% water
33
Q

what is helpful in measuring TBW

A
isotopic water (D2O) 
titrated water  (THO) 

goes to all body compartments

34
Q

what is helpful in measuring ECF?

A

sulfate
mannitol
inulin

these cannot cross membranes

35
Q

useful in measuring plasma volume?

A

radioactive albumin
evans blue

remains in plasma

36
Q

what compartments of fluid cannot be directly measured?

A

ICF and ISF

ICF = TBW - ECF
ISF = ECF - PV
37
Q

how to calculate compartment volume?

A

CV = amount injected - amount excreted/ concentration in plasma

38
Q

Darrow-Yannet diagram for isosmotic

A

Osmolarity does not change
ECF widens

ex. isotonic NaCl

39
Q

darrow-yannet diagram for hyperosmotic?

A

osmolarity increases in both ICF and ECF

ICF contracts, ECF widens

Ex. high intake of NaCl

40
Q

darrow-yannet diagram for hyposmotic

A

osmolarity in both decrease

both ICF and ECF widen

Ex: SIADH

41
Q

darrow-yannet; diarrhea

A

ECF thins

isosmotic

42
Q

darrow yannet; water deprivation

A

osmolarity of both increase

both get thinner

hyperosmotic

43
Q

both ICF and ECF have decreased osmolarity
ECF gets thinner, ICF gets wider?

what is it????

A

adrenal insufficiency