U: Acid/base Ii

Front 1

When you're repleting pts with hypokalemia, why is it important to get serial measurements over time?

Back 1

The relationship b/t serum K and total body K isn't linear below ~3.2 meQ Serum.

Front 2

What is the key site of K secretion regulation in the renal sys? What hormone is the most relevant one for this process?

Back 2

Cortical Collecting Duct; aldosterone (acts in the CCD)

Front 3

Pts with too much aldosterone are prone to develop what re: K+ regulation? Explain concurrent metabolic alkalosis.

Back 3

Increased Na uptake in CCD --> urinary K loss --> hypokalemia
- more negative lumen --> increased H+ secretion from IC cells --> metabolic alkalosis

Front 4

What are the two mechanisms that can lead to hyperkalemia?

Back 4

redistribution (increased release from, or impaired entry into cells)
Decreased urinary excretion

Front 5

What are some of the things that can cause K+ redistribution?

Back 5

Acidosis (there is an H/K exchanger)
Low insulin
Digoxin
B-blocker (at high lvls)
cell injury (e.g. rhabdomyalsis, etc.)

Front 6

What are some factors that could impair urinary K+ excretion? (3)

Back 6

more + lumen i/ CT
decreased flow & Na delivery to CT
decreased aldo prod/actv.

Front 7

What is Amiloride?
- effect on +/- lumen?
- can it cause an acid/base disorder?

Back 7

K-sparing diuretic; blocks ENaC channel (inhib Na uptake)
- makes the lumen more +, inhib K secretion
- met acidosis

Front 8

What is often the first line tx for hyperkalemia?

1st line too: how do we "trick" potassium to go into cells?
- 2nd line: same principle, other drugs?

If the pt is in renal failure/has bad dysfunction, how can you get K out of the body?

Back 8

admin Ca++ to rase the threshold potential back above the resting membrane potential in myocytes.

Give insulin (fastest mechanism)
- B2 agonists, bicarb admin

Dialysis or Kayexalate admin.

Front 9

What kinds of problems can cause Hypokalemia via redistribution (ECF --> ICF)?

Back 9

too much insulin
B2 agonists
alkalosis
Barium poisoning

...notice the first two are essentially tx's for hyperkalemia.

Front 10

What is Bartter's syndrome?

Gitelman's syndrome?

How do these pts present?

Back 10

Defect in Loop that makes it look like they're on a loop diuretic. (Na/K/2Cl cotrans)

Defect in DT that makes it look like they're on a Thiazide diuretic. (Na/CL cotrans)

Pts present as hypokalemics.

Front 11

How can we differentiate b/t K depletion due to renal loss and that due to GI loss?

Back 11

GI: diarrhea + low urine potassium --> implies extrarenal K loss

Renal: high urine potassium (>30 on 24hr urine)

Front 12

What is the first branch of categorization we use on pts w/ metabolic alkalosis?

Back 12

Chloride sensitive = BP norm/low w/ low effective circ vol
- will respond to NaCl admin

Chloride insensitive = BP high w/ ^^ECF
- won't respond to NaCl admin

Front 13

What is going on during the Generation phase of metabolic alkalosis?
- signs?

Back 13

loss of gastric secretions (vomiting) --> generation of NaHCO3 --> reabs NaCl proximally in kidney b/c of starling forces
- low urine Chloride, high urine sodium
- NaHCO3 and KHCO3 are seen in urine

Front 14

What is happening int the maintainence phase of metabolic alkalosis?

In the most severe cases, what do you see re: acid/base of urine?

Back 14

volume depletion continues --> more reabs of Na, Cl in nephron
... there is eventually not enough Cl available to facilitate this reabs.... so the nephron starts to reabs NaBicarb --> metabolic alkalosis.

Paradoxical aciduria cause by the 2ndary increase in aldosterone, and the complete elim of nacl and bicarb from the urine.

Front 15

If pt presents with vomiting and one of the following two electrolyte profiles, give me the stage of alkalosis that they're in:

1) >15 Na, K, HCO3, <15 Cl, ph>6.5
2) <15 Na, Cl, HCO3; variable K, ph<5.5

Back 15

1. generation
2. maintainence

**try to understand why these values are the way they are**

Front 16

What can primary hyperaldosteronism cause re: metabolic acid/base dz?

What eventually helps us "escape" from the effects of aldosterone, so we don't end up like the Michelin man? (3)

Back 16

alkalosis:

Na retention --> volume expansion --> HTN, etc.
... eventually though, we'll excrete Na because of starling forces, so our total body NA will be elevated, but we will have reached a new steady state.

1. Starling forces in the PT (force of reabsorption is lower, we increasely excrete water and Na)
2. ANP is stimulated
3. Na/Cl cotrans in DCT is downreg (just like in a thiazide diuretic)

Front 17

What are U waves (little peaks post-T wave on EKG) indicative of?

Back 17

Hypokalemia

Front 18

Hyperkalemia is almost always due to...

Back 18

defect in renal excretion
- low flow
- decreased RAAS
- inhib of eNaC