Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
60 Cards in this Set
- Front
- Back
|
What is the ratio of intracellular to extracellular potassium?
|
30:1
|
|
|
What is external K balance?
|
Refers to balance between what we take in and what we excrete
|
|
|
What is internal K balance?
|
Refers to the distribution of L in the body.
Due to Na-K-ATPase, most K is intracellular. Many things cause shifts of K from intra to extracellular or reverse. |
|
|
What does insulin do to K?
|
It stimulates K uptake by both hepatic and skeletal muscle cells by stimulating Na-K-ATPase
|
|
|
What effect does giving somatostatin have on plasma potassium concentration?
|
presumably somatostatin suppresses insulin release and plasma [K+] rises
|
|
|
Stimulation of what aspects of sympathetic ns decrease and increase entry of K+ to cells?
|
1) β 2 stimulation INCREASES
2) α stimulation decreases/increases efflux |
|
|
What effect would phenylephrine have on plasma [K+]?
|
Phenylephrine is an α agonist, so it would increase plasma [K]
|
|
|
What effect would propranolol have on plasma [K+]?
|
Propranolol is a beta 2 blocker, so it would increase plasma [K]
|
|
|
What effect does epinephrine administration have on plasma [K?]
|
Causes decrease in plasma [K], indicating it's getting into cell (epinephrine preferentially stimulates Beta)
|
|
|
what happens to plasma [K] in
A) metabolic alkalosis B) metabolic acidosis |
A) H+ leaves cells, K+ comes in--> plasma [K] decreases
B) H+ enters cells, K leaves --> plasma [K] increases (This is a bigger effect than alkalosis) |
|
|
What happens in elevated anion gap metabolic acidosis?
|
H+ enters the cell with organic anion thus remaining electroneutral so a transcellular shift of K does not occur.
|
|
|
In the presence of a beta blocker, will plasma [K] increase more or less when KCl infusion given?
|
MORE. Beta blockers increase plasma [K] by making it harder for K to get into cell
|
|
|
Extracellular Hypertonicity : how does it affect plasma [K?]
|
Causes water to move out of cell, and K+ moves with water by solvent drag.
|
|
|
Cell breakdown from rhabdomyolysis, tumor lysis syndrome (eg from chemo tx) and ischemic necrosis cause what change to plasma [K]?
|
INCREASE it. It's due to the intracellular K getting released.
|
|
|
What happens in digoxin toxicity?
|
Na-K-ATPase inhibited, resulting in hyperkalemia
|
|
|
In normal or high K intake, where is the majority of K reabsorbed?
|
Proximal tubule (acutally this is the case in Low K too)
|
|
|
What is the difference in K reabsorption in the A) distal tubule and B) collecting duct in a low and high K diet?
|
A) In a low K diet, the distal tubule reabsorbs 3% of K.
In a high K diet, the distal tubule secretes 10-50% of filtered K. B) In the Low K diet, the collecting duct reabsorbs 10% of filtered K. In the high K diet, the collecting duct secrets 5-30% of filtered K. |
|
|
As urine flow rate increases, what happens to potassium secretion?
|
K secretion increases into the lumen in the collecting ducts.
|
|
|
What does it mean that Na reabsorption is load dependent in distal tubule?
|
The more you deliver to the distal tubule, the more it can reabsorb.
|
|
|
What happens to K as Na reabsorption increases?
|
Secretion of K increases to maintain electroneutrality.
|
|
|
What happens to K and Na in presence of aldosterone?
|
Na reabsorption increases, K secretion increases
|
|
|
How do the following affect K+ secretion?
A) Acidosis B) Alkalosis |
A) decreases bc intracellular [K] has decreased. More K is in plasma.
B) Increases because there is more intracellular K |
|
|
what does the presence of other luminal anions do to K secretion?
|
Increases K secretion
|
|
|
Which diuretics
A) Increase B) Decrease K secretion? |
A) Thiazide and loop
B) K sparing diuretics (spironolactone - aldosterone inhibitor) Basically they do the opposite to Na. |
|
|
In hypokalemia, what happens to Neuromuscular conduction?
|
Decreases excitability by increasing the negative potential of the cell.
|
|
|
Symptoms of hypokalemia
|
Generalized muscle weakness
Muscle Cramps Cardiac arrhythmias Renal Concentrating defects Rhabdomyolysis - localized Respiratory Failure |
|
|
Effects of hypokalemia on EKG
|
as [K] decreases, there is flattening of the T wave, appearance of U wave. As it decreases further, there is flat or inverted T wave and very prominent U wave
|
|
|
Flat or inverted T wave and prominent U wave is characteristic of what?
|
hypokalemia
|
|
|
When is torsade de pointe seen?
|
In hypomagnesemia or hypokalemia
|
|
|
What is torsade de pointe ?
|
pecific, rare variety of ventricular tachycardia that exhibits distinct characteristics on the electrocardiogram (ECG).
|
|
|
What is the net effect of hyperkalemia on nerve conduction?
|
Initially causes increase membrane excitability followed by state of decreased excitability and slowed conduction.
|
|
|
Effects of hyperkalemia on EKG?
|
Think of it as someone fishing for the T wave - hooking it and reeling it in. Then see prolongation of everything.
T wave peaks, then prolonged PR interval, then absent PR wave, then increasing spread of QRS and T, then a sine wave pattern. |
|
|
peaks of T wave followed by a sine wave pattern is characteristic of what?
|
hyperkalemia
|
|
|
What are causes of hypokalemia?
|
1) Decreased dietary intake (uncommon)
2) Increased entry into cells - transient hypokalemia 3) Increased GI losses of K - diarrhea mostly 4) Increased urinary losses - due to increased distal urine flow and hyperaldosteronism |
|
|
Adrenal adenomas (Conn Syndrome)
Bilateral Adrenal Hyperplasia Glucocorticoid Remedial Hyperaldosteronism Syndrome of Apparent Mineralocorticoid Excess Are all examples of what? |
primary hyperaldosteronism
|
|
|
How to determine etiology of hypokalemia
|
1) History - you can stop if there's diarrhea/vomiting
2) Urinary K to creatinine ratio |
|
|
medical condition that involves an accumulation of acid in the body due to a failure of the kidneys to appropriately acidify the urine
|
renal tubular acidosis
|
|
|
What is pseudohyperkalemia?
|
When a lab result or some other artifact causes false dx of hyperkalemia.
Examples are Ischemic blood draw, Hemolyzed blood sample, Thrombocytosis, Leukocytosis, Intravascular hemolysis. |
|
|
Causes of hyperkalemia
|
1) Increased intake - usually only a contributing cause, generally see it with renal dysfunction
2) Lethal injection/iatrogenic 3) Transcellular shifts/redistribution 4) Decreased renal excretion - ie, from decreased GFR 5) Hypoaldosteronism 6) Drug induced |
|
|
Tx of hyperkalemia
|
EMERGENCY.
Obtain EKG when suspected. 1) Calcium gluconate to antagonize effect of hyperkalemia on heart. 2) Redistribute potassium into cell - give glucose and insuline, bicarb, inhaled albuterol 3) Remove K from body with binding exchange resin - only works with defecation 4) Dialysis |
|
|
What is periodic paralysis?
|
group of rare genetic diseases that lead to weakness or paralysis (rarely death) from common triggers such as cold, heat, high carbohydrate meals, not eating, stress or excitement and physical activity of any kind. The underlying mechanism of these diseas es are malfunctions in the ion channels in skeletal muscle cell membranes that allow electrically charged ions to leak in or out of the muscle cell, causing the cell to depolarize and become unable to move (a channelopathy).
|
|
|
T/F Most serum calcium is bound to protein
|
T
|
|
|
2nd most abundant intracellular cation
|
Magnesium
|
|
|
What is the fractional excretion of Phosphorous?
|
20% - higher than Ca and Mg
|
|
|
Where does the majority of Mg reabsorption occur?
|
Unlike most substances, occurs in THICK ASCENDING LIMB and not prox tubule
|
|
|
T/F in the TAL, Mg and Ca compete for reabsorption
|
T
|
|
|
Hypercalcemia (increases, decreases) magnesium reabsorption and vice versa
|
Decreases
|
|
|
Where does hypermagnesemia come from?
|
(This is rare in the absence of impaired kidney function.)
1) Magnesium infusion or ingestion, or enemas 2) Tumor lysis syndrome 3) adrenal insufficiency 4) Diabetic ketoacidosis |
|
|
Symptoms of mild hypermagnesemia
|
nausea, flushing, HA, lethargy, drowsiness, diminished deep tendon reflexes
|
|
|
Symptoms of moderate - high hypermagnesemia
|
Somnolence, respiratory paralysis, bradycardia, ECG changes.
Muscle paralysis, heart block, cardiac arrest. |
|
|
What causes the neuromuscular toxicity seen in hypermagnesemia?
|
Decreased impulse transmission across NMJ
|
|
|
How does magnesium cause cardiac effects?
|
It's a CALCIUM CHANNEL BLOCKER. High intracellular Mg blocks K channels in heart.
|
|
|
T/F Hypermagnesemia can also cause hypocalcemia
|
T. This is due to competition for reabsorption in the distal tubule and inhibition of PTH.
|
|
|
Hypomagnesemia is seen in about __% of hospitalized patients
|
12
|
|
|
Cause of hypomagnesemia
|
1) Poor dietary intake
2) GI losses (diarrhea, bypass sx, PPIs, pancreatitis) |
|
|
Two mechanisms of renal losses of magnesium
|
1) Inhibition of sodium reabsorption - in prox tubule and distal tubule, Mg reabsorption follows sodium reabsorption
2) Primary defect in magnesium reabsorption |
|
|
Hypomagnesemia is frequently accompanied by what electrolyte problems?
|
Hypokalemia, hypocalcemia, metabolic alkalosis, partially because things such as diarrhea and diuretics can cause both.
|
|
|
What changes are seen in the ECG in hypomagnesemia?
|
1) Widening of QRS
2) Peaked T waves 3) Prolongation of PR interval 4) Increased risk of Torsades de Pointes |
|
|
How to distinguish between urinary Mg loss or GI Mg malabsorption?
|
Can distinguish from fractional excretion of Mg.
Normally if there is low mg in blood, the renal excretion is VERY low (below 2%). More than that is RENAL Mg wasting. |
|
|
Tx for hypomagnesemia
|
Replete Mg
If GI malabsorption –may need to give iv or IM If Renal wasting, will need to give large quantities, so may also need iv or IM as oral Mg causes diarrhea |
