Session 7

Front 1

what is the normal range of k

Back 1

3.5 -5

Front 2

what is hyperkalemia

Back 2

above 5

Front 3

what is hypokalemia

Back 3

below 3.5

Front 4

what is the effect of k on membrane potential

Back 4

it determines the resting membrane potential

Front 5

how does hypokalemia effect the resting membrane potential

Back 5

it makes it more difficult to depolarize

Front 6

what does hyperkalemia do to the resting membrane potential

Back 6

it makes it easier to reach threshold and therefore is hyperexcitable
more k's make you hyper

Front 7

what effects on the ecg does hyperkalemia have

Back 7

ventricular fibrillation
prolonged PR interval
depressed st segment
high t waves

Front 8

what effects on the ecg does hypokalemia have

Back 8

low t waves
high u waves
low st segment

Front 9

how is k filtered in the bowman's capsule

Back 9

it is freely filtered

Front 10

what happens to the k in the nephron

Back 10

it is 67% reabsorbed in proximal tubule
20% is reabsorbed in thick ascending limb of henle
and the physiological control occurs in the collecting duct

Front 11

what type of cells in the collecting duct work on the concentration of k

Back 11

principal cells - either reabsorb or secrete the k

Front 12

what are the 5 factors that affect k secretion

Back 12

extracellular k concentration
na concentration in tubular lumen
luminal flow rate
extracellular ph
aldosterone

Front 13

what happens to the urinary k when there is an increase in plasma k conc

Back 13

increases - you pee it out!

Front 14

what situations alter the k handling

Back 14

diuretics and a low sodium diet

Front 15

how does diuretics alter the k handling

Back 15

increase na volume delivery to late distal tubule and collecting duct and that increases K secretion

Front 16

how does a low sodium diet effect k

Back 16

hyperkalemia - less na delivery to the late distal tubule and collecting duct there is less k secretion and excretion

Front 17

what should a low sodium diet person also be doing

Back 17

eating less k

Front 18

how does the tubular flow rate affect k secretion

Back 18

more k secretion with higher tubular flow rates in the late distal and collecting duct

Front 19

how is the plasma k effected by plasma pH

Back 19

more alkaline pH more you secrete k
more acidic less secretion of k so acidemia favors hyperkalemia

Front 20

higher extracellular protons causes the h/k exchange which does what

Back 20

lowers the intracellular k concentration in the principal cells and therefore decreases k secretion

Front 21

what stimulates the secretion of k in the distal tubule and the collecting duct

Back 21

aldosterone

Front 22

what is the mechanism of aldosterone's stimulation of k secretion

Back 22

na/k atpase increase
and k channels

Front 23

as k increases in the serum plasma what happens to aldosterone

Back 23

it is stimulated

Front 24

what are 2 disorders of aldosterone secretion

Back 24

conn's disease and addison's

Front 25

what is conn's

Back 25

primary hyperaldosteronism
aldo secreting tumor
k secretion in collecting duct is in inappropriately stimulated

Front 26

what do you see with conn's disease in regards to k

Back 26

hypokalemia
think the "con-man" stole all the k away
also the person is alkylotic

Front 27

what is addison's

Back 27

destruction of the adrenals
aldo not secreted
decreased k secretion
hyperkalemia

Front 28

what is the concentration of k in addison's

Back 28

hyperkalemia

Front 29

what diuretics act at the proximal tubule

Back 29

osmotic and carbonic anhydrase inhibitors

Front 30

how does osmotic diuretics work

Back 30

they inhibit reabsorption of water and secondarily of na

Front 31

how does the carbonic anhydrase inhibitor work

Back 31

it inhibits the hco3 reabsorption and therefore is also good for the alkalotic pt

Front 32

how does furosimide work

Back 32

lasix inhibits the na, k, 2cl cotransporter in the loop
it lessens the water reabsorption and should be used under careful medical supervision;
remember if not used properly can cause a fury in the loop

Front 33

hydroclorothiazide

Back 33

works on the distal convoluted tubule
inhibits na cl cotransport

Front 34

triamterene

Back 34

potassium sparing diuretics
blocks na channels in collecting duct

Front 35

spironolactone

Back 35

aldosterone antagonist so is potassium sparing

Front 36

low extracellular ca will do what

Back 36

hypocalcemic tetany - this was definitely an old test question

Front 37

where is 45% of the free ca

Back 37

bound to albumin

Front 38

what effect does pH have on the free Ca concentration

Back 38

h competes with Ca for binding sites on plasma proteins
acidemia increases free ca
alkamemia decreases free ca

Front 39

what occurs with severe alkalemia

Back 39

pt develops hypocalcemic tetany

Front 40

what is the mechanism of proximal tubular ca reabsorption

Back 40

transcellular
3 na in exchange for one ca
and ca pump using atp

Front 41

where does paracellular ca reabsorption occur

Back 41

in the thick ascending loop of henle via channels in tight junctions driven by 6 mV transepithelial potential

Front 42

what hormones stimulate the ca reabsorption

Back 42

parathyroid
calcitrol
calcitonin

Front 43

decreased plasma ca does what to the parathyroid gland

Back 43

causes the pth secretion

Front 44

what does pth do

Back 44

increases ec ca

Front 45

where does 80% of the phosphate reabsorbed in the nephron

Back 45

proximal tubule

Front 46

what inhibits reabsorption of the phosphate in the proximal tubule

Back 46

parathyroid hormone

Front 47

where does the bulk of the mg handled in the nephron

Back 47

thick ascending limb of the loop of henle via the paracellular route due to 6 mV transepithelial potential