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43 Cards in this Set
- Front
- Back
factors that can shift K+ into the cells
(decr extracellular K+) |
insulin
altosterone beta-adrenergic stimulation alkalosis |
|
factors that can shift K+ out of the cells
(incr extracellular K+) |
insulin defici (DM)
aldosterone defici (Addison's) beta-block acidosis cell lysis strenuous exercise incr ECF osmolarity |
|
Insulin increases? or decreases? potassium uptake into the cells
|
increases
(corrects hyperkalemia) |
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Conn's pts are prone to have
a) hyperkalemia b) hypokalemia |
b) hypokalemia
(K+ into cells) |
|
Addison's pts are prone to have
a) hyperkalemia b) hypokalemia |
a) hyperkalemia
(K+ out of cells) |
|
Excess aldosterone causes
a) hyperkalemia b) hypokalemia |
b) hypokalemia
(K+ into cells) |
|
Beta blocker treatment may cause
a) hyperkalemia b) hypokalemia |
a) hyperkalemia
(K+ out of cells) |
|
Increased epinephrin may cause
a) hyperkalemia b) hypokalemia |
b) hypokalemia
(K+ into cells) |
|
Metabolic acidosis may cause
a) hyperkalemia b) hypokalemia |
a) hyperkalemia
(K+ out of cells) |
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Metabolic alkalosis may cause
a) hyperkalemia b) hypokalemia |
b) hypokalemia
(K+ into cells) |
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What is the affect H+ ion conc in ECF on Na+K+ATPase pump?
|
slows it down
|
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What happens to a hypertensive, diabetic person on beta-blockers, who eats 6 bananas after exercising vigorously and causing trauma to his/her muscles.
|
hyperkalemia and possible secondary cardiac arrythmias and SCD.
|
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The most important sites for regulating potassium excretion are
|
the principal cells of the late distal tubules and cortical collecting tubules.
|
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90% of the epithelium of the late distal and cortical collecting tubules are _____ celss
|
principal
|
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Where does the energy for K+ secretion out of the principal cells come from?
|
Na+/K+ ATPase on the lasolateral sides of the principal cells
|
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Where does the energy come from for K+ reabsorption in the intercalated cells?
|
H+/K+ ATPase in the luminal membrane of the intercalated cells
|
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Acidosis promotes K+ movement out of the cells, thus increased K+ in the ECF (hyperkalemia).
Increased K+ in the ECF causes increased K+ secretion. Why does increased H+ concentration (acidosis) decrease K+ secretion? |
I'm asking. Why's that? There's a circle here or something.
|
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sodium depletion
a) increases b) reduces distal tubular flow rate |
b) reduces
|
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Decreased tubular flow rate
a) increases b) reduces potassium secretion |
b) reduces
|
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volume expansion,
high sodium intake, or diuretic drug treatment, These things a) increase b) decrease distal tubule flow rate |
increase
|
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A high sodium diet has 2 opposite effects on K+ excretion (they balance harmoniously).
What are they? |
Decreased aldosterone = decreased K+ secretion
Increased flow rate = increased K+ secretion |
|
what's the energy mechanism explaining why acidosis slows K+ secretion?
|
acidosis slows the Na+/K+ ATPase pump in the basolateral side of epithelium.
Thus, there is no energy to drive K+ secretion from the principals |
|
In chronic acidosis, up in the proximal tubule, NaCl and water reabsorption is slowed.
This leads to INCREASED FLOW in the distal tubule which dose WHAT to K+ secretion? |
increases it.
so, chronic acidosis causes MORE K+ secretion. the flow rate effect overides the ATPase pump effect. |
|
In the last question, chronic acidosis essentially caused al-K+loss-is. What's that cause?
|
alkalosis.
and the circle keeps turning. |
|
What causes tetany?
a) hypercalcemia b) hypocalcemia |
b) hypocalcemia
|
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What causes cardiac arrhythmia?
a) hypercalcemia b) hypocalcemia |
a) hypercalcemia
|
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What state is most prone to tetany?
a) acidosis b) alkalosis |
b) alkalosis
|
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Why does alkalosis cause hypocalcemia and tetany?
|
the plasma proteins suck up all the Ca++
|
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We haven't really concentrated on Ca++ action in the kidney. Why not?
|
Most (90%) of the Ca++ is excreted in the feces
|
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What condition causes PTH to be released with a normal total calcium level?
a) acidosis b) alkalosis |
b) alkalosis
(all the Ca++ is with the proteins) |
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At which part of the nephron is most Ca++ secreted?
|
Ca++ is not secreted in the nephron.
|
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Hyperphosphatemia
a) increases b) decreases PTH |
a) increases
|
|
It's easy to get confused...
Metabolic alkalosis increases Ca++ excretion. But alkalosis causes PTH to be produced, which a) increases b) decreases Ca++ excretion |
b) decreases
so, harmony is restored |
|
the primary site of Mg reabsorption
|
loop of Henle (65%)
prox (35%) dist ( 5%) |
|
Of all the ions in the ECF, which one has affects Mg++ excretion?
|
Ca++
Increased Ca++ in the ECF stimulates Mg++ excretion |
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Where in the nephron are Na+ and water secreted?
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Na+ and water are not secreted in the nephron
|
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1) a slight change in blood volume causes a MARKED change in cardiac output, (2) a slight change in cardiac output causes a LARGE change in blood pressure, and (3) a slight change in blood pressure causes a ______ change in urine output.
|
large
|
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Usually fluid spreads itself evenly in the ECF. What conditions cause more fluid to go to the interstitium rather than the plasma?
|
(1) increased capillary hydrostatic pressure,
(2) decreased plasma colloid osmotic pressure, (3) increased permeability of the capillaries, and (4) obstruction of lymphatic vessels. |
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What mechanism maintains the Na+ excretion of a Conn's pt
|
pressure natriuresis
|
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What mechanism maintains normal Na+ excretion in a pt with an Angiotensin II over-producing tumor?
|
pressure natriuresis
|
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In inappropriate ADH syndrome, pressure diuresis keeps the ECF from being ridiculous. However, Na+ levels in the ECF are not normal. why?
|
pressure natriuresis.
ECF Na+ levels become too low. |
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A pt has damage to his supraoptic nuclei. Why does this pt drink and pee so much?
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no ADH
|
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In the neprotic syndrome, plasma fluid volume decreases, b/c you lose fluid to the interstitium b/c of protein excretion. Why then, do the kidneys try to retain salt?
|
hypoperfusion --> RAAS, sympathetic
this further dilutes protein conc and adds to the edema |