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Lab Flashcards

1
Q

Why do we measure sodium levels

A

basic assessment of fluid status, and free water

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2
Q

Changes in sodium levels can cause

A

changes in mental status particularly in the elderly,
focal neuro déficits
seizures
a more rapid change in sodium level the greater the risk
this is due to fluid shifts in the skull

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3
Q

causes of hypernatremia

A

free water loss

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4
Q

sources of free water loss

A

urine, sweat, resp, GI

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5
Q

how to correct hypernatremia

A

given free water slowly, you can correct the na as quickly as it occurred

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6
Q

who gets hypernaremia

A

dementia patients, no thirst sense

ICU patients

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7
Q

Causes of hyponatremia

A

(pseudo-hyponatremia : high triglycerides, high blood sugars)

  • hypothyroidism, hypoaldosteronism (hypoadrenal)
  • Hypervolemic (CHF, cirrhosis) diuresis.. leave alone
  • Euvolemic (SIADH) (PNA, Lung CA).. restrict free water
  • Hypovolemic (The Brain prioritizes volume over Na and releases ADH in hypovolemic state) give fluids (NS)
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8
Q

What does aldosterone do?

A

Released by the kidneys in order to maintain NA and fluid.. retains NA and fluid and excretes potassium
Hypoaldosteronism: Addison’s disease, spironolactone, ACE, ARB—- high K and low sodium
Hyperaldoteronism: adrenal tumor.. high potassium

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9
Q

Causes of hyperkalemia

A

AKI
AKI
AKI soon to come
-hypoaldosterone state: Addison’s disease, spironolactone, ACE, ARB
- Hypoinsulin (K can not get into the cell.. once you give insulin K will drop)
- cellular injury, rhabdo, tumor lysis

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10
Q

treatment of hyperkalemia

A

Acutely: insulin and dextrose, beta agonist (albuterol)

sub-acute: kayexalte plus BM

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11
Q

Causes of Hypokalemia

A
  • decreased gut absorption (diarrhea not vomiting)
  • Increased loss through kidneys (diuretics: loop, HCTZ)
  • Hyperaldosterone
  • Hypomag (cannot hold onto K.. mostly seen in ETOH abuse)
  • increased cellular entry ( beta agonist, Alkalosis)
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12
Q

Low bicarb means…

A
  • decrease imply one of two types of metabolic acidosis, but always check the gap NA- (CL+Bicarb)
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13
Q

Main causes of Gap acidosis

A

if the gap is high there is extra acids.. there is often a life threatening process causing a gap
SAD
Shock/sepsis: lactate
AKI: kidneys can not get rid of acid (indication for dialysis)
DKA: ketones

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14
Q

Causes of Non gap acidosis and what does it look like

A
  • bicarb is low but the CL is high so there is no increase in the gap… LOSS OF BICARB
  • diarrhea- bicarb rich fluids from the pancreas
  • dehydration- especially after saline given
  • RTA (renal tubal acidosis)
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15
Q

Creatinine

A

it is a muscle breakdown product of creatine, its released from muscle into the plasma in a fairly steady state

  • roughly a marker for GFR marker of kidney function
  • it is related to muscle mass
  • 1.3 might be normal for a big muscle man, and 1.0 might be high for elderly women with low muscle mass
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16
Q

the relationship between Creatinine and GFR and how to use creatine

A

is curvilinear… a change from 1.0-1.2 implies a much bigger change in GRF than 6-7

  • convert to GFR using MDRD
  • tread over time
  • use in the context of the patient.. urine output and volume overload
17
Q

causes of creatinine

A

only AKI

18
Q

BUN

A

Not as good as creatinine, helps to suggest prerenal

  • byproduct of protein degradation
  • Low– not much.. maybe poor nutritional status
  • high– think AKI.. maybe GI bleed, TPN
19
Q

Mag.. why do we check it

A
  • when low can lead to hypocalcemia and hypokalemia
  • arrhythmias when mag low
  • check in patients at risk for arrhythmias and patients asa risk for hypomag.. ETOH abuse
20
Q

causes of hypomag

A
  • renal losses ( diuresis, loop)
  • ETOH abuse.. chronic.. mag wasting by the kidneys
  • Tacrolimis
21
Q

why is calcium important

A

stabilizes electrochemical gradients across cells
- allows cells that rely on action potentials to work
so critical for normal functioning of muscles cells ( heart, skeletal, smooth) and neurons

22
Q

calcium homeostasis

A

controlled by the parathyroid hormone which works on
- kidneys- to increase calcium absorption and excrete phos
- Gut- increased calcium absorption and excrete phos
- Bone- releases calcium and phos from the bone
high phos levels stimulate PTH
High calcium levels turn of PTH

23
Q

signs and symptoms of hypercalcemia

A
  • excessively stabilizes electrically active cells
  • slows smooth muscle cells and nerve cells
  • also leads to increase risks of stone formation
  • depressed
24
Q

primary hyperparathyroid

A
  • a single small adenoma on one of the four glands
  • secretes excess PTH
  • usually slight elevations in calcium
  • typically in middle aged women
  • usually not a problem but worry about osteoporosis fractures
25
Q

secondary hyperparathyroidism

A
  • kidney disease patients
  • kidneys can not remove excess phosphate
  • continued hyperphos stimulates PTH release
  • mild hypercalcemia with hyperphos
  • risk is severe damage to bone health
  • treatment: phos binders
26
Q

hypercalcemia of malignancy

A
  • extremely high calcium– 12-13
  • cancer cells secrete a hormone that looks like PTH
    – lung cancers in particular
    real PTH is actually low

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