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INPATIENT > Nephrology, mineral, fluid, electrolyte, acid-base disorders > Flashcards

Nephrology, mineral, fluid, electrolyte, acid-base disorders Flashcards

1
Q

Hypocalcemia:

5 etiologies

A
  1. hypoparathyroidism e.g. postthyroidectomy
  2. vitamin D deficiency
  3. chronic renal failure
  4. accelerated net bone formation e.g. postparathyroidectomy
  5. calcium sequestration e.g. pancreatitis
    * purple book 7-12*
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2
Q

Hypocalcemia:

Clinical manifestations

A
  1. Neuromuscular irritability:
  • –Chvostek sign (tapping facial nerve -> contraction of facial muscles)
  • –Trousseau sign (inflation of BP cuff -> carpal spasm)
  • –Irritability, depression, psychosis
  • –Long QT
  1. Osteomalacia

purple book 7-12

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3
Q

Hypocalcemia:

Diagnostic studies

A
  1. Ca, ionized Ca
  2. albumin
  3. PTH
  4. 25(OH)D, 1,25(OH)2 D
  5. Cr, Mg, PO4
  6. Urine calcium

purple book 7-12

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4
Q

Hypocalcemia:

Treatment

A
  1. Treat concomitant vit D deficiency
  2. Symptomatic: IV Ca gluconate + calcitriol, +/- Mg
  3. Asymptomatic: oral Ca
  4. In chronic renal failure: phosphate binder, oral Ca, calcitriol
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5
Q

Hypercalcemia:

5 etiologies

A
  1. Hyperparathyroidism
  2. Malignancy (PTH-related peptides, or cytokines -> increased osteoclast activity, or incr vit D, or local osteolysis)
  3. Vitamin D excess, e.g. granulomas, which increase 1,25(OH2 D
  4. Increased bone turnover, e.g. hyperthyroidism, Paget disease
  5. Thiazides

purple book 7-11

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6
Q

Hypercalcemia:

Clinical manifestations

A
  1. Hypercalcemic crisis:
  • polyuria
  • dehydration
  • AMS
  1. Osteopenia
  2. Nephrolithiasis
  3. Abd pain, N/V, constipation, anorexia, pancreatitis
  4. Calciphylaxis: calcification of small-med blood vessels of dermis and subq fat -> ischemia & skin necrosis
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7
Q

What 2 causes account for over 90% of cases of hypercalcemia?

A
  1. hyperparathyroidism
  2. malignancy
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8
Q

Hypercalcemia:

Diagnostic studies

A
  1. Ca, ionized Ca
  2. albumin
  3. PTH
  4. PO4
  5. Urine calcium

purple book 7-11

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9
Q

Hypercalcemia:

Acute treatment

A
  1. Normal saline
  2. Furosemide
  3. Bisphosphanates
  4. Calcitonin

purple book 7-12

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10
Q

Hypokalemia:

3 main etiologies

A
  1. Transcellular shifts: alkalemia, insulin, etc.
  2. GI potassium losses: diarrhea, laxative abuse, etc.
  3. Renal potassium losses:

–Hypertensive: hyperaldosteronism

–Hypotensive or normotensive:

—-acidosis: DKA

—-alkalosis: diuretics, vomiting, Gitelman syndrome

purple book 4-10

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11
Q

Hypokalemia:

Clinical manifestations

A
  1. N/V, ileus, weakness, muscle cramps, rhabdomyolysis, polyuria
  2. EKG: U waves, flattened T waves

purple book 4-10

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12
Q

Hypokalemia:

Workup

A
  1. Rule out transcellular shifts
  2. Get 24 hr urine potassium, compare urine and plasma osm and K -> transtubular potassium gradient (TTKG), which is (Urine K / Plasma K) / (Urine osm / Plasma osm)
  3. HIgh TTKG = renal loss, Low TTKG = extrarenal loss
  4. If renal, check BP, acid-base status, Urine Cl

purple book 4-10

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13
Q

Hypokalemia: Treatment

A
  1. Potassium supplementation
  2. Treat underlying cause
  3. Supplement Mg (can’t fix hypokalemia if there’s hypomag)

purple book 4-10

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14
Q

Hyperkalemia: 3 main etiologies

A
  1. Transcellular shifts
  2. Decreased GFR, e.g. AKI, ESRD
  3. Normal GFR with decreased renal K excretion, e.g. CHF, hypoaldosteronism

purple book 4-11

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15
Q

Hyperkalemia: Clinical manifestations

A
  1. Weakness, nausea, paresthesias, palpitations
  2. EKG: peaked T waves, increased PR interval, widening of QRS, loss of P wave

purple book 4-11

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16
Q

Hyperkalemia: Workup

A
  1. Rule out pseudohyperkalemia
  2. Rule out transcellular shift
  3. Assess GFR
  4. If GFR normal, check TTKG - (Urine K / Plasma K) / (U osm / P osm); if < 6, consider hypoaldosteronism

purple book 4-11

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17
Q

Hyperkalemia: Treatment

A
  1. Calcium supplementation
  2. Insulin
  3. Bicarb
  4. B agonists e.g. albuterol
  5. Kayexalate
  6. Diuretics
  7. Hemodialysis

purple book 4-11

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18
Q

Hypomagnesemia: 3 main etiologies

A
  1. Diminished absorption or intake

–Malabsorption, chronic diarrhea, ALCOHOLISM

–Proton pump inhibitors

  1. Increased renal loss

–Diuretics

–Hyperaldosteronism, Gitelman syndrome

–Hyperparathyroidism, hyperthyroidism

–Hypercalcemia

–Drugs (aminoglycoside, cetuximab, cisplatin, amphotericin B, pentamidine)

  1. Miscellaneous

–Diabetes mellitus

–Post-parathyroidectomy (hungry bone syndrome)

–Respiratory alkalosis

–Pregnancy

CURRENT

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19
Q

Hypomagnesemia: s/s

A

–Causes neurologic symptoms and arrhythmias (like hypokalemia & hypocalcemia).

–Impairs release of PTH.

CURRENT

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20
Q

–Hypermagnesemia is almost always the result of ______.

–______ and ______ are underrecognized sources of magnesium.

–Pregnant patients may have severe hypermagnesemia from intravenous magnesium for ______.

A

–Hypermagnesemia is almost always the result of advanced CKD and the impaired magnesium excretion.

–Antacids and laxatives are underrecognized sources of magnesium.

–Pregnant patients may have severe hypermagnesemia from intravenous magnesium for preeclampsia and eclampsia.

CURRENT

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21
Q

Hypermagnesemia: s/s

A

–Muscle weakness

–Decreased deep tendon reflexes

–Mental obtundation, and confusion

–Weakness, flaccid paralysis, ileus, urinary retention, and hypotension

–Serious findings include respiratory muscle paralysis and cardiac arrest

CURRENT

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22
Q

Hypermagnesemia: Treatment

A
  1. Calcium chloride
  2. Hemodialysis
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23
Q

Hyperphosphatemia: Most common cause

A

Advanced CKD

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24
Q

Hyperphosphatemia: Treatment

A

Calcium carbonate (binds phosphate)

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25
Q

Hypophosphatemia: Causes

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26
Q

Hypophosphatemia: s/s

A

rhabdomyolysis, paresthesias, and encephalopathy

27
Q

Hyponatremia, hypernatremia

A

Self - go read about hyponatremia and hypernatremia in the purple book, 4-6

28
Q

Approach to interpreting an arterial blood gas

A
  1. Anticipate the disorder (what is the clinical picture?)
  2. Acidemic or alkalemic? (pH < 7.40 or > 7.40?)
  3. Metabolic or respiratory?

–acidosis with HCO3/PCO2 down = Metabolic

–alkalosis with HCO3/PCO2 up = Metabolic

–acidosis with PCO2/HCO3 up = Respiratory

–alkalosis with PCO2/HCO3 down = Respiratory

  1. If metabolic acidosis, is there an anion gap?

– [Na - (Cl + HCO3)]

  1. Is compensation appropriate? (use formulas)
  2. Is there more than one disorder present? (use formulas)

Dr. Anderson handout

29
Q

Acid-base disturbance of: PE

A

respiratory alkalosis

30
Q

Acid-base disturbance of: Hypotension/decreased perfusion

A

metabolic acidosis

31
Q

Acid-base disturbance of: Vomiting

A

metabolic alkalosis

32
Q

Acid-base disturbance of: Severe diarrhea

A

metabolic acidosis (non-gap)

33
Q

Acid-base disturbance of: Cirrhosis

A

respiratory alkalosis

34
Q

Acid-base disturbance of: Renal failure

A

metabolic acidosis

35
Q

Acid-base disturbance of: Sepsis

A

resp. alk/metab. acid

36
Q

Acid-base disturbance of: Pregnancy

A

respiratory alkalosis

37
Q

Acid-base disturbance of: Diuretic use

A

metabolic alkalosis

38
Q

Acid-base disturbance of: COPD

A

respiratory acidosis

39
Q

Causes of Anion Gap Metabolic Acidosis

A

G - glycols (ethylene and propylene)

O - oxoproline

L - L-lactate

D - D-lactate

M - methanol

A - aspirin

R - renal failure

K - ketoacidosis (diabetic, alcoholic, starvation)

40
Q

Causes of Normal anion gap (hyperchloremic) Metabolic Acidosis

A

H - hyperalimentation

A - acetazolamide, amphotericin

R - renal tubular acidosis

D - diarrhea

U - ureteral diversion

P - pancreatic fistula

S - spironolactone, saline resuscitation

41
Q

Causes of metabolic alkalosis

A

C - contraction alkalosis

L - licorice

E - endocrine (Cushing, etc.)

V - vomiting

E - excess alkali ingestion

R - refeeding

P - post-hypercapnia

D - diuretics

42
Q

Causes of respiratory acidosis

A

LOW/SLOW BREATHING/OXYGEN EXCHANGE

–drugs

–disorders of respiratory muscles or chest wall

–upper airway obstruction

–disorders affecting gas exchange across pulmonary capillaries

–mechanical ventilation

43
Q

Causes of respiratory alkalosis

A

FAST/DEEP BREATHING/OXYGEN EXCHANGE

C - CNS disease

H - hypoxia

A - anxiety

M - mechanical ventilation

P - progesterone

S - salycylates, sepsis

44
Q

Fluids of choice for RESUSCITATION?

A

NS or LR

45
Q

Fluids of choice for MAINTENANCE?

A

D5 1/2 NS

46
Q

Indications for PLATELETS?

A

aplastic anemia, cancer, ITP

47
Q

Indications for PRBCs?

A

to raise hematocrit; chronic and/or acute blood loss

48
Q

Acute Kidney Injury: 3 main etiologies

A
  1. Prerenal

–decreased effective arterial volume

–renal vasoconstriction

  1. Intrinsic

–acute tubular necrosis (drugs, toxins, contrast)

–acute interstitial nephritis (sulfa drugs, NSAIDs, PPIs, infection, leukemia/lymphoma, autoimmune)

–glomerulonephritis

  1. Postrenal

–obstructions/blockages: BPH, prostate cancer, anticholinergic meds, bilateral nephrolithiasis

49
Q

What is the definition of AKI?

A

Abrupt ( < 48 hrs) increase in creatinine > 0.3 mg/dL

OR

increase in creatinine > 50%

OR

urine output < 0.5 mL/kg/h for > 6 hrs

50
Q

What is the workup for AKI?

A
  1. H&P: recent procedures, meds, thirst, volume status, s/s of obstruction
  2. Urine eval: output, sediment
  3. Fractional excretion of sodium: > 2% -> acute tubular necrosis
  4. Maybe renal u/s, bx
51
Q

What are the casts found in prerenal AKI?

A

transparent hyaline casts

52
Q

What are the casts found in acute tubular necrosis?

A

muddy brown casts

53
Q

What are the casts found in acute interstitial nephritis?

A

WBC casts

54
Q

What are the casts found in glomerulonephritis?

A

RBC casts

55
Q

What are the indications for urgent dialysis?

A

A - acidemia

E - electrolyte disorder, usually hyperkalemia

I - intoxication/ingestion: methanol, ethylene glycol, lithium, salicylates

O - overload of volume (CHF)

U - uremia

56
Q

Clinical assessment of volume overload:

symptoms?

physical exam?

A

Symptoms:

  • Paroxysmal nocturnal dyspnea
  • Orthopnea
  • Edema
  • DOE
  • Weight gain
  • Cough

Physical Exam:

  • Third heart sound
  • Abdominal jugular reflux
  • JVD
  • Crackles
  • Lower extremity edema
  • SBP < 100 mm Hg
57
Q

What are the stages of CKD?

A

1 - kidney damage with normal or incr GFR; GFR > 90

2 - kidney damage with mild decr GFR; GFR 60-90

3 - moderate decr GFR; GFR 30-59

4 - severe decr GFR; GFR 15-29

5 - kidney failure; GFR < 15; dialysis

*kidney damage = pathologic abnormalities or markers of damage in blood, urine, or imaging studies

NKF KDOQI Clinical Practice Guidelines for Chronic Kidney Disease: Evaluation, Classification, and Stratification

58
Q

What are the dietary restrictions for CKD?

A
  1. Restrict Na
  2. Restrict K
  3. Restrict PO4
  4. Strict BG control if diabetic
  5. Consider protein restriction
59
Q

What is the JNC8 guideline regarding HTN in CKD patients?

A

Goal: < 140/90

Drugs: ACEi/ARB

60
Q

What is the Cockroft-Gault equation for estimating creatinine clearance?

A

(140-age) * (Wt in kg) * (0.85 if female) / (72 * Cr)

61
Q

What is the most common cause of sudden death in patients with ESRD?

A

Hyperkalemia

Due to missed dialysis or dietary indiscretion

Medscape

62
Q

What are 5 etiologies of SIADH?

A
  1. malignancy, esp. lung or brain
  2. pulmonary - pneumonia, TB, COPD
  3. intracranial - trauma, stroke, hemorrhage, infection
  4. drugs - antipsychotics, antidepressants
  5. pain, nausea

purple book 4-7

63
Q

What electrolyte imbalance does SIADH cause and how is it treated?

A

Euvolemic hypotonic hyponatremia

Free water restriction

+

hypertonic saline

+

conivaptan/tolvaptan

purple book 4-7

INPATIENT (11 decks)

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