Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CRRAB II- Week 1 > Popham- Kalemic > Flashcards

Popham- Kalemic Flashcards

1
Q

How much K is normally stored in an adult?

A

3000-4000 mEq

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the daily intake and excretion of K?

A

4-120 mEq

Excretion min= 15-25 mEq

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What percent of K is intracellular?

A

98%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How much K is extracellular?

A

4-5 mEq/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How much K is normally in the serum?

A

4-5 mEq/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What defines a body deficit vs. excess of K?

A

Deficet: decrease by 1 mEq/L = 200-400 mEq

Excess: increase by 1 mEq/L = 100-200 mEq

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the functions of K?

A

Prot and glycogen synthesis
Maintains RMP via Na/K ATPase
Determines membrane excitability
Allows AP generation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are sxs of LOW or HIGH K?

A

Unable to get an AP in muscles
Cramps
Muscle weakness/paralysis
EKG changes and arrythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How does hypercalcemia affect AP?

A

increases threshold potential and protects against hyperkalemia, which has decreased resting potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What exacerbates hyperkalemia?

A

Metabolic acidosis

Causes K to be released form cells as HCl is buffered into cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What drug potentiates risk of hypokalemia?

A

Digoxin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What can potentiate the risk of hyperkalemia?

A

Hyponatremia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What effects K distribution into cells and ECF?

A
  1. concentration dependent

2. Acid-base dependent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What happens if you drink 40 meq of OJ?

A

40 meq> 17 ECF > increase K by 2.4 meq/l

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What increases K distribution into cells?

A
  1. Catecholamines and insulin increase Na/KATPase activity> uptake K into skeletal muscle and liver
  2. HIGH CONC causes passive movement of K into cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What happens to K in acidemia vs alkalosis?

A

Acidemia: K+ moves OUT of cells as H+ is buffered into cells

Alkalosis: K+ moves INTO cells as H+ is buffered into the extracellular fluid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What determines excretion of K by the kidney?

A
  • Plasma K+ concentration
  • Urine flow in distal tubule (permissive)
  • Aldosterone: causes K+ secretion by principal cells of collecting tubule
  • Outer medulla, cortical & inner medulla
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What influences K handling in the renal tubule?

A
  • K is filtered at glomerulus
  • Reabsorbed proximal tubule, following water and sodium
  • Reabsorbed loop of Henle (thick ascending limb), via NaK2Cl carrier in luminal membrane
  • Secreted distally: distal tubule, collecting tubule via principal cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Where can K be reabsorbed in cases of severe hypokalemia?

A

Collecting duct by intercalated cells

20
Q

How is K secreted in the distal tubule?

A

Principal cells
• Luminal membrane: Na+ & K+ channels
• Basolateral membrane: Na-K ATPase

Aldosterone
• Released in response to 0.1 meq/l increase in K+
• Increases # of open Na+ & K+ channels
• Increases activity of Na-K ATPase

K concentration in blood: gradient

Distal flow is permissive

21
Q

What usually causes hypo/hyperkalemia?

A

adrenal glands or kidneys

NOT diet

22
Q

What shifts K from extracellular to intracellular?

A

– Insulin
– Catecholamines
– Concentration gradient
– Acid-base status

23
Q

What are the major determinants of K excretion by the kidney?

A

– K concentration
– Aldosterone
– Distal tubular urine flow (permissive)

24
Q

What is a MAJOR toxicity of both hypo and hyperkalemia?

A

cardiac arrythmias

25
Q

What causes hypokalemia?

A
  1. Decreased intake (rare)
  2. Increased entry into cells – met alk, hyperinsulinemia,
  3. catechol/β-agonists
  4. Increased GI losses
  5. Increased urinary losses – impaired H20/salt reabsorp, hypercalcemia, mineralcorticoid excess (aldosterone), hypomagnesemia
  6. Increased sweat losses
  7. Dialysis
26
Q

How do you evaluate hypokalemia?

A
  1. Determine if loss is GI or renal
  2. GI losses should be obvious, except in cases of anorexia/bulemia/laxative abuse
  3. 24 hour urine K+ when hypokalemic
    a. Kidney can decrease urine excretion of K+ to 25-30 meq in 24 hours
    b. If urine K is low, then loss is not from kidney
  4. Acid/base status: acidosis or alkalosis
27
Q

What can cause LOW urinary K and acidosis?

A

LOWER GI losses

from laxatives/villous adenoma

28
Q

What can cause low urinary K and Alkalosis?

A

Upper GI loss

vomiting

29
Q

What causes high urinary K and acidosis?

A

Ketoacidosis, type I or II RTA

30
Q

What causes high urinary K and alkalosis?

A

Normotensive: vomiting (GI loss, but high urinary K due to urinary bicarb excretion with metabolic alkalosis) diuretics (early), Bartter’s syndrome (Inherited)

Hypertension

  1. High renin: diuretics,renovascular disease, reninoma, Cushings
  2. Low renin: measure aldosterone
31
Q

What does low vs high aldosterone indicate in situations when there is low renin?

A

low- exogenous mineralcorticoid

high- adrenal adenoma or hyperplasia

32
Q

What complications can occur with hypokalemia?

A
  1. Muscle weakness, cramps, cardiac arrhythmias
  2. Rhadomyolysis (K+ < 2.5 meq/l)
  3. Renal dysfunction:
    a. loss of urinary concentrating ability
    b. Increase in urinary NH3 and NH4+ production/excretion
    c. Hypokalemic nephropathy/Interstitial fibrosis
  4. Hypertension: low K+ diet causes uptake of Na+
33
Q

How do you treat hypokalemia?

A
  1. Replace to get patient out of danger initially, then more gradually replace entire K deficit
  2. K+ deficit can only be approximated:
    a. Roughtly 200-400 meq for each 1 meq/l drop in K+
    b. Below 2, K+ deficit can be much greater due to shifts out of cells to compensate
  3. Treat underlying cause of low potassium
  4. Potassium replaced orally or intravenously
34
Q

What causes hyperkalemia?

A
  1. Increased Intake: oral or IV
  2. Shift: Movement from cells into extracellular fluid – muscle/tissue breakdown, insulin deficiency w/ hyperglycemia, met acidosis
  3. Decreased urinary excretion – MCC = renal failure, hypoaldosteronism
35
Q

What causes hypoaldosteronism?

A
  1. Secondary decrease in aldosterone due to decreased activity of renin-angiotensin system
  2. Primary decrease in adrenal synthesis of aldosterone
  3. Aldosterone resistance
36
Q

What causes secondary decreases in aldosterone?

A

i. Hyporeninemic hypoaldosteronism (diabetics with CKD)
ii. Drugs: ACEi, NSAID’s, cyclosporine
iii. HIV disease/clinical AIDS

37
Q

What causes aldosterone resistance?

A

Drugs: K+ sparing diuretics, Trimethoprim

Pseudohypoaldosteronism

38
Q

How do you diagnose hyperkalemia?

A

DX = Transtubular K Gradient (TTKG) <7

39
Q

How do you calculate TTKG?

A

[Urine K+ / (Uosm/Posm]

/Plasma K+

40
Q

What should you do if K is 6.5-7 meq/l and there are no EKG changes?

A

check for pseudohyperkalemia

41
Q

What should you do if there are EKG changes and you suspect hyperkalemia?

A

Start treatment immediately

*Monitor on telemetry

42
Q

What can potentiate K toxicity?

A

Concomitant acidemia or hyponatremia

43
Q

How do you treat hyperkalemia?

A

Antagonize K+ effects (seconds/minutes)
a. Calcium IV

Shift K+ into cells (minutes)

a. Glucose & insulin
b. NaHCO3
c. Beta-agonists: albuterol nebs
d. 3% NaCl if hyponatremia present

Remove excess K+ (hours)

a. Loop diuretics if patient makes urine
b. Cation-exchange resins (kayexalate): avoid rectal use
c. Hemodialysis/peritoneal dialysis

44
Q

What EKG changes are associated with hypokalemia?

A
  1. PR interval prolongation
  2. ST depression
  3. Flattened/ inverted T waves
  4. U-waves
  5. QRS widening
45
Q

What ST changes are associated with hyperkalemia?

A
  1. PR interval prolongation
  2. Elevated T waves
  3. Widened QRS
46
Q

How should you treat EKG changes seen with hypokalemia?

A
  • Concomitant digoxin use increases risk
  • Treat to get out of danger, replace losses, and prevent further losses
  • Check for hypomagnesemia
47
Q

How should you treat EKG changes seen with hyperkalemia?

A
  • Antagonize membrane effects: Calcium IV
  • Shift K+: insulin/glucose/NaHCO3
  • Remove K+: diuretics, Kayexylate, dialysis

CRRAB II- Week 1 (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions