.renal: Potassium And Divalent Cations

Front 1

Internal balance refers to the distribution of patoassium in the body. Due to Na-K ATPase, most potassium is where?

Back 1

Intracellular

Front 2

Insulin stimulates K uptake by...

Back 2

both hepatic nad skeletal muscle cells by stimulating the Na-K ATPase (indirectly) to transfer K+ into cells!

Front 3

True or False:
Regarding internal K+ balance, Beta-2 stimulation increases entry of K+ into cells.

Back 3

TRUE

Beta-2 agonists are epinephrine and albuterol. These increase intracellular K+ / decreases extracellular K+

Front 4

Regarding internal K+ balance, what do the following do to K+ movement into cells?

A. Epinephrine
B. Albuterol
C. Propranolol,
sotalol
D. alpha-adrenergic stimulation
E. Beta-2 stimulation

Back 4

A. Epinephrine : is a beta-2 agonist, decreases plasma K+ / increases intracellular K+
B. Albuterol: same as Epi
C. Propranolol: is a beta-2 antagonist thus increases plasma K+
D. alpha-adrenergic stimulation: increases plasma K+
E. Beta-2 stimulation: decreases plasma K+ / increases intracellular K+

Front 5

Regarding internal K+ balance, of the following options (elevated anion gap metabolic acidosis, normal anion gap metabolic acidosis, metabolic alkalosis), which results in:
1. Low plasma K
2. Elevated plasma K
3. lack of transcellular shift of K

Back 5

1. Low plasma K: metabolic alkalosis
2. Elevated plasma K: normal anion gap metabolic acidosis
3. lack of transcellular shift of K: elevated anion gap metabolic acidosis

Hint 5

1. Low plasma K: metabolic alkalosis --> H+ leaves cells to buffer extracellular pH and K+ shifts intracellularly to maintain electroneutrality.
2. Elevated plasma K: normal anion gap metabolic acidosis --> excess H+ moves inside the cell adn K+ ecits to maintain neutrality
3. lack of transcellular shift of K: elevated anion gap metabolic acidosis --> H+ enters the cell with organic anion thus remaining electroneutral so transcellular shift of K does not occur see syllabus p. 105 for your drawing

Front 6

True of False:
Regarding internal K+ balance, if you give too much digoxin for, say CHF, you could potentially inhibit the Na-K ATPase

Back 6

True

Front 7

Regarding internal K+ balance, name things that shift K+
A. out of the cell (3)
B. into the cell (2)

Back 7

A. Shifting K+ out of the cell: Hyperosmolarity (via solvent drag), exercise, cell lysis
B. Shift K+ into the cell: Insulin, beta-agonists

Front 8

Regarding external (renal) K+ balance, what do the following do to K+ secretion?
A. acidosis
B. alkalosis
C. presence of other luminal anions
D. Thiazide diuretics
E. Loop diuretics
F. K sparing diuretics

Back 8

A. acidosis: decreases K+ secretion because H+ enters the cell, K leaves the cell, decreased intracellular K concentration and thus decreasing secretion
B. alkalosis: stimulates K+ secretion b/c opposite of above
C. presence of other luminal anions: increased K+ secretion
D. Thiazide diuretics: increased
E. Loop diuretics: increased
F. K sparing diuretics: decreased

Front 9

What are the clinical symptoms for
A. hypokalemia
B. hyperkalemia

Back 9

for BOTH hypo and hyper,
- generalized muscle weakness,
- muscle cramps
- cardiac ectopy / arrhythmias

Front 10

What are the effects of hypokalemia on the EKG?

Back 10

Front 11

Hypokalemia is often associated with a prominent ___ -wave.

Back 11

Prominent U0wave.

Front 12

What are the hyperkalmia readings on an EKG?

Back 12

Front 13

How do you determine the cause of hypokalemia?

Back 13

1. History
2. Urinary potassium to creatinine ratio. If > 22 mEq of K per gram creatinine, then it is urinary potassium wasting. Otherwise, poor intake, excess GI loss or tranascellular shift prob.

Front 14

Which of the following is/are not cause(s) of hyperkalemia?

A. strenuous exercise
B. metabolic acidosis
C. primary hyperaldosteronism
D. excess insulin
E. beta adrenergic antagonist

Back 14

C. primary hyperaldosteronism
D. excess insulin

are causes of HYPOkalemia, the rest are causes of hyperkalemia

Front 15

When hyperkalemia is reported, what is the first thing to do?

Back 15

Obtain an EKG to check for changes.

Front 16

What drugs cause hypokalemia? (3)

Back 16

Diuretics, Amphotericin B, Aminoglycosides

Front 17

Which types of Renal Tubular Acidosis cause hypokalemia?

Back 17

RTA Type 1 and RTA Type 2

Front 18

What is the treatment for hyperkalemia?

Back 18

1. Calcium to stabilize heart membrane!
2. redistribution of patssium into the cell (glucose and insulin bolus, beta-2 agonist like albuterol, or if they are acidic sodium bicarbonate
3. Removal of potassium from the body: kayexalate, sodium polystyrene, diuretics or dialysis

Front 19

True or False:
If you are hypomagnesemic, can't reabsorb K+ and thus lose K+ in urine.

Back 19

True

Front 20

What is NOT reabsorbed primarily in the proximal tubule portion of the nephron?

A. Na+
B. K+
C. Ca++
D. Mg++
E. P

Back 20

D. Mg++

It is primarily reabsorbed in the thick ascending limb of the loop of henle!

Front 21

In the thick ascending limb of the loop of henle, what two cations compete for reabsorption?

Back 21

Mg++ and Ca++

Thus, hypercalcemia decreases Mg reabsorption;
hypermagnasemia decreases Ca reabsorption

Front 22

What are possible causes of hypermagnasemia?

Back 22

Magnesium infusion (to treat preeclampsia), magnesium ingestion (laxatives, Epsom salts), near drowning in the Dead Sea, DKA, Lithium ingestion

Front 23

What are possible causes of hypomagnesemia?

Back 23

*Poor dietary intake

*GI losses like
1. diseases assoc with generalized malabsorption like diarrhea, steatorrhea, small bowel bypass surgery
2. Congenital defect in Mg reabs
3. Acute pancreatitis
4. Proton Pump Inhibitors (anything that prevents Na+ reabs prevents Mg++ reabs too since Mg++ pretty much follows Na+ around)

*Renal losses
1. inhibition of sodium reabs
2. primary defect in Mg reabs

Front 24

What are the symptoms of hypomanesemia?

Back 24

Very similar to effects of hypocalcemia and hypokalemia which frequently accompany it.... Tetany, numbness and tingling, positive Chevostek's and Trousseau's sign.

Front 25

What are the cardiac effects of hypomagnesemia?

Back 25

Widening of the QRS, Peaked T waves, Prolongation of the PR interval, Increased risk of toursade de pointes

Front 26

Magnesium is a calcium channel blocke and high intracellular magnesium blocks potassium channels in the heart. Thus, milkd hypermagnesemia yields ______ and _______ while severe hypermagnesemia yields _______ and ________.

Back 26

Mild hypermagnesemia yields bradycardia and hypotension;
severe hypermagnesemia yields complete heart block and cardiac arrest

Front 27

What is the treatment for hypermagnesemia?

Back 27

Depends on the renal function. If normal or improving renal function, then stop Mg ingestion adn simply observe and Mg should come down on its own. BUT if pt has renal failure, then dialysis is treatment. Calcium chloride IV can antagonized some of the actions of hypermagnesemia.

Front 28

Hypomagnesemia is frequently accompanied by what three other conditions?

Back 28

Hypokalemia, hypocalcemia, and metabolic alkalosis.

Front 29

What are symptoms of hypermagnesemia?

Back 29

Nausea and vomiting, hyporeflexia, hypotension, somnolence, heart block, paralysis

Front 30

When can you use Winter's formula to calculate renal rules for compensation?

Back 30

For metabolic acidosis!

Winter's formula:
Expected pCO2 = (HCO3 X 1.5) + 8

Front 31

What are the 7 causes of respiratory alkalosis Dr.D wants you to know?

Back 31

Sepsis
Anxiety
Aspirin toxicity
Pneumonia
Asthma
Prengancy
Cirrhosis

Front 32

What are the differential diagnosis for respiratory alkalosis that you need to know? (8)

Back 32

Hysteria/Anxiety
Salicylate Toxicity
Pneumonia
High Altitude
Pregnancy
Cirrhosis
Asthma

(v. similar list to the 7 causes of respiratory alkalosis Dr.D wants us to know: Sepsis, Anxiety, Aspirin toxicity, Pneumonia, Asthma, Prengancy, Cirrhosis

Front 33

The following are differential diagnoses for which acid base condition:

COPD, narcotics

Back 33

respiratory acidosis

Front 34

The following are differential diagnoses for which acid base condition:

hysteria/anxiety, salicylate toxicity, pneumonia, high altitude, pregnancy, cirrhosis, asthma

Back 34

respiratory alkalosis

Front 35

The following are differential diagnoses for which acid base condition:

salicylate toxicity, pneumonia, high altitude, pregnancy, cirrhosis, asthma

Back 35

respiratory alkalosis

also hysteria and anxiety

Front 36

The following are differential diagnoses for which acid base condition:

pneumonia, high altitude, pregnancy, cirrhosis, asthma

Back 36

respiratory alkalosis

also hysteria and anxiety, as well as salycilate toxicity

Front 37

The following are differential diagnoses for which acid base condition:

Saline responsive:
vomiting, volume contraction, diuretics

Saline unresponsive:
primary hyperaldosteronism
bilateral hyperplasia, adenoma, renal vascular disease

Back 37

metabolic alkalosis

Front 38

What are possible differential diagnoses for:

A. normal anion gap metabolic acidosis
B. elevated anion gap metabolic acidosis

Back 38

A. normal anion gap MA: diarrhea, RTA (Type 1: Distal –acidifcation defect ; Type 2: Proximal –defective bicarbonate reabsorption ; Type 4 –Hyperkalemia causing inhibition of ammonia synthesis and too little buffer found in the urine) , Renal failure

Elevated anion gap MA:
MUDPILES (methanol, Uremia, DKA, propylene glycol, isoniazid, lactic acidosis, ehtylene glycol, ethanol. salicylates)

Front 39

Regarding MUDPILES, methanol is metabolized by alcohol dehydrogenase to _________ and ________.

Back 39

methanol is metabolized to formaldehyde and formic acid. It is the formic acid which is toxic and causes blindness and basal ganglion infarcts.

Front 40

Regarding MUDPILES, ehtylene glycol is metabolized by alcohol dehydrogenase to _______ and ______.

Back 40

glycolic and oxalic acids, which can injure the kidney

Front 41

Renal tubular acidosis is a group of disorders in which the kidney is unable to maintain acid-base balance despite normal or near normal glomerular filtration rate. Match the defect to the type of RTA.

1. defect is in hydrogen ion secretion or inability to acidify the urine
2. defect is ammonia excretion
3. defect is in deficient bicarbonate reabsorption from the filtrate.

Back 41

1. Type 1 RTA (distal)
2. Type 4 RTA: primary problem is hyperkalemia which turns off ammonia synthesis
3. Type 2 RTA (proximal)

Front 42

What is the "delta-delta" calculation?

Back 42

It compares the anion gap value to the bicarbonate value. If your anion gap is increased, there should be an equal number decrease of bicarbonate since that bicarb buffers the additional anions. If the two are not matched, then it tells you what additional acid base disorder is present.