l11 Flashcards

1
Q

what is the total body content potassium

A

50 meq/kg of body weight or 3500 meq for 70 kg person

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2
Q

intracellular concentration potassium

A

150 mEq/L (98%)

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3
Q

how much potassium is in muscle cells, rbc, liver, and bones?

A

muscle- 2600 mEq

RBC, liver, bones- 300 mEq

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4
Q

how much potassium in ECF

A

65 mEq (@% body weight)

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5
Q

normal range plasma K+

A

3.5-5 mEq/l

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6
Q

value of ecf for hyperkalemia and hypokalemia

A

hyperkalemia- above 5 meq/L

hypokalemia- below 3.5 mEq/L

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7
Q

what 2 hormones are upregulated after a meal and help Na-K ATPase, and which is the most important

A

epinephrine and insulin. insulin is the most important

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8
Q

what is th eplasma K in patients with B blocker (propanolol)

A

elevated longer because K not uptoo

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9
Q

one way to treat hyperkalemia with glucose

A

give glucose to release insulin, which will regulate K hyperkalemia by increasing Na-K ATPase

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10
Q

A drop in 0.1 pH results in how much change in K

A

increase 0.6 mEq/L plasma K results

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11
Q

acidosis causes what change in plasma k

A

Variable
acidosis causes hyperkalemia- inhibits K/H exchanger and inhibition of Na-K ATPase on basso lateral membrane on distal nephron
-inhibition of Na K ATPase in pt cells by low pH decreases na/water reabsorption, increases tubular flow, enhancing k secretion
-chronic acidosis-ecf can decreases and inorganic acids can rise and aldosterone is secreted

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12
Q

metabolic or respiratory acidosis causes K changes

A

metabolic acidosis (HCL, NaHCO3) causes shift in plasma K, but respiratory or organic acids (lactic acids, ketones) do not cause a shift in K

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13
Q

how does increases in osmolality (hyperglycemia) change K

A

hyperosmolality- h2o moves out first to ecf then [K] inside cell increase, so K moves to ecf- results in hyperkalemia

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14
Q

how much K excreted per ady

A

90 mEq

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15
Q

how is K reabsorbed in kidney

A

mostly in proximal tubule (80%) and TAL (10%); by intercellular diffusion through junctions and positive potential favors paracellular reabsorption; in TAL by NaK2CL transporter

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16
Q

where does K secretion and reabsorption take place

A

mostly secretion by principal cell distal tubule (uptake by basolateral Na-K ATPase, higher conductance of apical channels so K diffuses into lumen); reabsorption by intercalated a type MCD (H secreted out, K in)

17
Q

what 3 factors control K secretion

A

1) Na K ATPase
2) electrochemical gradient for K movement across apical membrane
3) apical permeability to K

18
Q

how does hyperkalemia regulate K secretion

A

hyperkalemia increases NaK ATPase on basolateral membrane and increases permeability of K on apical membrane- both in distal nephron; independent of aldosterone because in adrenalectomized animals see same results

19
Q

how does aldosterone (and nagiotensin 2) regulate K secretion

A

upregulates Na K atpase, k and Na channels in principal cells in distal nephrons. also increased Na into cell depolarizes lumenal membrane and K secreted

20
Q

how does adrenal tumor or addisons disease effct plasma k

A

adrenal tumor- hypokalemia becuase too much aldosterone leads to K secretion
-aldosterone deficiency in addison’s disease- hyperkalemia because not secreting K

21
Q

ANP and plasma K

A

ANP inhibits aldosterne, so K not secreted

22
Q

what 3 factors cause high flow to increase K secretion

A

1- high flow rate deforms mechano-sensitive channels that causes opening of Ca-K channels
2- maintains high chemical gradient by diluting and washing away secreted K
3- more Na delivered to distal nephron, so more Na reabsorbed and K secreted and depolarizes lumenal membrane

23
Q

what is the effect of diurectics on plasma K

A

increases flow rate, which increases K secretion. so K needs to be administered to prevent hypokalemia. or use spironolactones as competitive inhibitors of aldosterone as a diurectic to inhibit K secretion

24
Q

what is the effect of acidosis on plasma K

A

variable-
inhibits Na-K ATPase at distal nephrone so K secretion reduced
-also inhibits Na-K ATPase at proximal tube and decreases salt and water reabsorption, which increases flow, which would increase K secretion
-chronic metabolic acidosis, ECF volume decrease stimulating RAA system which would increase K secreation

25
Q

Hyper polarization of principal cell membrane would cause what change to K secretion

A

Hyperpolarization would decrease driving force for K secretion

26
Q

Deformation of principal cells does what to k secretion

A

Deformation leads to influx of Ca which activate K channel

27
Q

How does ADH effect U/P for inulin?

A

It increases u/p for inulin because more water reabsorbed

28
Q

Loop diuretic and tubular osmolar clearance

A

Loop diuretic inhibits sodium and water reabsorption, so there would be a higher osmolar clearance

29
Q

Loss of blood volume and free water clearance

A

For a big loss in blood volume, baroreceptor sand cardiopulmonary receptors stop firing, ADH activated, increases urine concentration and therefore negative free water clearance

30
Q

Diabetic ketoqcidosis and H and titratable acid concentration

A

Diabetic ketoqcidosis causes increase formation of HCO3- and increased secretion of H and therefore increases TA