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Renal and Urinary 3 > Clinical Approach to Electrolyte Disorders > Flashcards

Clinical Approach to Electrolyte Disorders Flashcards

1
Q

Most potassium is where?

A

Muscle and IC

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2
Q

What increases and decreases serum K

A

HYpo - insulin, alpha antagonists and beta agonists alkalosis

Hyper - acidosis, hyperglycemia, beta 2 antagonist and alpha agonists, increase in osmolarity and exercise

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3
Q

Regulation of collecting duct K secretion

A

Distal tubule flow (dependent on upsteam Na reabsorption)…more Na reabsorption means more secretion bc more sodium coming into the cells

MC receptor (alosterone (serum K and RAAS) and GCs)

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4
Q

Hypokalemia levels

A

Under 3.5
Moderate under 3
Severe under 2.5

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5
Q

Causes of hypokalemia

A

First consider pseudo (K falls in test tube)

True - inadequate intake, shifts into cells, GI losses, renal losses)

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6
Q

Pseudohypokalemia

A

Cell K uptake in the test tube

Due to very high number of metabolically active cels (AML or CML)

Temp increases Na-KATPase and shifts K into cells

Often also associated with pseduohypoglycemia
Prevent by rapidly separating plasma and cells or store blood at 4C

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7
Q

Decreased oral postassium intake

A

Rarely sole

Causes more total body K depletion than hypokalemia

Contributing factor in other primary etiologies of hypokalemia

Urinary K losses can go as low as 10 mmol/day

Could be found in pts with eating disorders

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8
Q

IC shift causing hypokalemia

A

Alkalosis - small effect

INsulin

Increase B2-adrenergic (stress induced reelease, theophulline, albuterol)

Thyroid hormone (thyrotoxic periodic paralysis)

Anabolism (tx of pernicious anemia…rapidly expanding cell mass like leukemia or lymphoma)

Hypokalemia periodic paralyssis

Hypothermia

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9
Q

Renal loss

A

Primary hyperaldosteronism - adrenla hyperplasia or adenoma

Secondary hyperaldosteronism - diruetics, vomiting, salt wasting neprhopathies

Potassium wasting neprhopathies - hypermagnesemia, drug toxicity, polyuria, RTA

Mineralocorticooid excess - Cushing syndrome, licorice

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10
Q

Diuretic induced

A

INceased tubular flow

Increased sodium delivery so reabsorption through the ENaC

Enhanced tubule negative charge in tubule

Induce volume depletion and aldosterone secretion

All of this leads to increased K secretion

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11
Q

Hypokalmeia sx and signs

A

Due to hyperpolarization

PVCs, abnormal EKG (prolonged QT, U-wave), digitalis toxicity

Fatigue, weakness, paralysis and rhabdo

Rudced motility (constipation)

POlyuria and polydipsia due to renal concentring defect (mild nrphogenic DI)

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12
Q

Tx of hypokalemia

A

Oral KCl for mild to moderate

IV KCl for severe or sx…in slaine, NOT glucose to prevent insulin induced IC shift of insulin

Replace Mg if needed

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13
Q

Causes of hyperkalemia

A

Psuedo

True - increased intake

IC to EC shift

Decreased renal excretion

Over 5.4

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14
Q

Pseudohyperkalemia

A 
Hemolysis
Warm temp
Fragility
Severe leukocytosis or thrombocytosis
Fist clenching/tourniquet
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15
Q

Increased intake

A

Unusual cause of hyperkalemia if there is no renal failure

Enteral supplements, salt subs, blood transfusions, penicillin, dialysate

Take a good hx…highest content (dried figs, molasses, seaweed)

Very high - nuts, beans

High content - tomatoes, potetatoes, bananas, oranges

People who are on sodium restriciton often have risk factors for hyperkalemia

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16
Q

Hyperkalemia EC shift

A

Hyperosmolarity - DKA and hyperglycemia

Drugs - beta blockers, digoxin, succinylcholine

Acidemia

^all if membrane intact

If membane not intact - rhabdomyolysis, tumor lysis syndrome, hemolysis

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17
Q

Decreased renal excretion - hyperkalemia

A

Primary decrease in tubular flow and distal Na delivery

Primary decrease in MC activity

Abnormal cortical collecting duct

Loss of GFR will decrease sodium delivery (renal failure, ECF depletion and renal vasoconstrction)

Anything that blocks the ENaC channel (traimterene, amiloride, trimethoprim)

Hypoaldosteronsim (drugs, diabetes, type 4 RTA, adrenal insufficient, congential)

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18
Q

Consequences of hyperkalemia

A

Muscle weakness and paralysis

ECG changes and arrhythmias

Increase EC potassium reduces MC excitability

Increased potassium leads to suppression of trhe SA node and conduction by the AV node

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19
Q

Tx of hyperkalemia

A

Goal is to prevent arrhythmia

Based on the way the way that hyperkalemia occurred

Calcium stabilizes the cardiac membranes

Shift potassium into cells with insulin, bicarb, or beta2 agonist

Increase excretion with cation exchange resin/polymer or slaine, diuretics, dialysis

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20
Q

Forms of calcium and phosphate

A

Calcium - 45% is freely ionized…if albumin is low, more is ionized because amount bound to protein is lower….calcium corrected=measured+(.8(4-albumin))

Most of phosphate is in the bones…remainder is IC…small fraction in serum is phospholipids and inorganic phosphate…consides of HPO4 and H2PO4

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21
Q

PTH and calcitrol

A

PTH - from PT glands…increase calcium and decreased phosphorus

Calcitrol - from diet or cholestrol precursor with UV light…activated in liver and kidney…increease calcium and phosphorus

22
Q

What stimulates 1alpha hydroxylase

A

Low serum phosphate and PTH

Too much vitamin D and serum phosphate along with FGF 23 will suppress 1 alpha hydrozylase

23
Q

Calcium phosphate homeostasis

A

Bone formation inhibited by PTH

Bone resoprtion - activated by PTH and calcitrol and inhibited by calcitonin

Calcitriol increase reabsorption of Ca and phosphate in kidnyes…PTH blocks reasorption of phosphate but increases calcium…FGF23 blcoks phsophate uptake in kidneys

24
Q

Hypercalcemia clinically

A

Stones - neprholithiasis
Bones - bone pain
Groans - ab pain
Psychiatric overtones - confusion, depression, anxeity

Other sx could be constipation, weakenss, lethargy, anorexia

Renal insuffiency, distal RTA, NDI, dehydration

Short QT interval

25
Q

Causes of hypercalcemia

A

TPH excess

Excessive hormone indepednet bone resroption

Vit D excess

Excessive dietayr Ca

Increased renal Ca rebasorption

26
Q

PTH excess and horomone independent causes

A

PTH - hyperparathyroidism (adenoma), PTH secreting malignancy (squamous cell of the lung), lithium, familial hypocalcuric hypercalcemia

ID - osteolytic bone metastases, immobilization, Pagets, hyperthyroidism

27
Q

Vit D excess
Excessive Ca intake
INcreased renal Ca reabsorption

A

Ectopic calcitrol production…sarcoidosis

Milk alkali syndrome

Thiazides

28
Q

Dx eval of hypercalcemia

A

Measure PTH…if high, measure 24 hr urinary calcium excretion…high then priamary hyperPTH, low then familai hypocalcuric hyperclacemia

If low or normal, measure PTHrP, calcidiol, and calcitrol…PTHrP evelated - malignancy

Elevated calcidiol - excessive intake of calcium of Vit D

Elevated calcitrol with normal calcidiol - ectopic calcitriol production

None of 3 elevated - bone mets, consider rare cases

29
Q

Tx of hypercalcemia

A

IV hydration with saline solution

Loop diuretics (after volume normal) - inhibits renal Ca reabsortpion

Bisphos and calcitonin to inhibit bone resorption

Steroids in ectopic production of calcitrol - granulomatous dz and lymphoma

30
Q

Hypocalcemia clinical

A

NM irritability

Paresthesia, muscle twitching, largospasm, shortnes of breath

Cehck Chvostek’s sign and Trousseuas sign

Prolonged QT interval

31
Q

Causes of hypocalcemia

A

Decreased Ca intake
Vit D deficiency
PTH deficiency

32
Q

PTH def causes

A

Thyroidectomy or PTdectomy

AI hypoparathyroidism

Infiltration of PTH

Hypomagnesemia

PTH resistance

33
Q

Vit D def

A

Low clacidiol - low intake, inadequeate exposure, malapsorption

Decreased conversion of calcidiol to calcitrol - advanced chronic kidney dz

Calcitriol resist - Vit D resistant rickets

34
Q

Other hypocalc causes

A

Osteoblastic bone matasases, pancreatitis, hungry bones syndrome, multiple trnasfusion,s bisphosphonates, acute resp alkalosis, hyperphosphatemia (TLS, rhabdo)

35
Q

Dx of hypocalcemia

A

Assess serum phosphorus

Vit D def - low
Low PTH - high
Renal failure - High

36
Q

Hypocalcemia with increased PTH

A

Renal failure

Ca loss from circulation - pancreatits or tumor lysis

Vit D def or resistance

PTH resistance (dec Mg or sepsis)

37
Q

Hypocalcemia tx

A

Symp - IV calcium
Asym - oral calc

Correct vit D or Mg def

38
Q

Hyperphos clinical

A

Leads to hypocalcemia and stimulation of PTH

Manifestations related to hypocalcemia

Deposition of phosphate and calcium in soft tissues

Acute severe can cause neprhopathy or renal failure

39
Q

Causes of hyperphosphatemia

A

INcreased GI intake - laxatives

Dec urinary excretion - renal failure, familial tumoral calcinosis, hypoPTH, VIt D excess, acromegaly

Internal redistribution - TUmor lysis syndrome, rhabdo, lactic acidosis

40
Q

Dx of hyperphosphatemia

A

Work up the likely concurrent clacium disorders

If 1,25 D production decreased then decreased intestinal PO4 absorption

Will have high FGF 23 levels

41
Q

Tx of hyperphos

A

INtact renal function and acute - result on own…or saline with acetazolamide

IMapired renal function - dialysis

Intact chornic - tx underlying

Impaired - low phosphate diet and phosphate binders

42
Q

Hypophos clinical

A

Early - muscle weakness, dec MC contractility, encephalopathy, increased affinity of Hgb for O2
Dec bone mineralizaiton, bone pain

Late - rhabdo, resp failure, HF, seizures, hemolysis, osteomalacia

43
Q

Causes of hypophos

A

Dec GI absorption - dec intake, malabsorption, phosphate binderes

Inreased urinary excretion Vit D def, hyperparathyroidism, genetic dz, fanconi syndrome, tumor indcued osteomalacia

Internal reidstribtuon - refeeding, hungry bones syndrome, acute resp alkalaosis, durnig tx of DKA or HHS

44
Q

Hypophos dx evaluation

A

Check 24 hr phosphate xcretion

High - renal losses…check metabolic panel

Low calcidiol with normal or low calcium…vit D def

Elevated calcium and PTH - hyperpTH

Metabolic acisosis and glucosuria>hyperglycema - Fanconi syndrome

Low output - take a good hx…alcoholism, chronic diarrhea, severe GERN, PTectomy

45
Q

Tx of hypophos

A

Over 2 asx - no tx

Sx over 1 or ax 1-2 - oral phsphate repltion

under 1 and sx - IV phosphate, if asx - oral phsophate

46
Q

HyperMg clinical

A

CV - bradycardia, conduction block and hypotension

NM - decreased reflexes, muscle weakness, drowsiness, coma, PS blockade

47
Q

Cuase of hyperMg

A

Renal failure, acromegaly, familail hypocalcuric and hypercalcemia

Adrenal insuffiency

48
Q

Tx of hyperMg

A

Cessation of mag administraiton

Admin of calcium in sever esx hypermagnesemia

IV saline and furosemide

Dialysis

49
Q

Hypomag clinical

A

General weakness, NM hyperexcitability wit hyperrelxeia

CSpasm

Should have co-hypocalcemia and hypokalemia

Prolonged GT, ST depresison, ventriclular arrythimos, digoxin toxicty

50
Q

Causes of hypomagnesemia Dec GI uptake

A

Poor intkae, H+ pump inhibitors, primary intestinal hypomag

Excessive GI losses as well

51
Q

Renal losses and misc mechs for hypomag

A

Meds

Hypercal or hypokal

Osmotic diuresis

Transirent renal tubular dysfunction (alcohol)

Familai renal Mg wasting syndromes - Gitelman syndrome

Pancreatitis and hungry bones syndrome

52
Q

HypoMg tx

A

Oral if no sx

Iv is sx and arrhytmia

Cautious in renal fialure

Renal and Urinary 3 (22 decks)

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