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Clin Chem > Electrolytes > Flashcards

Electrolytes Flashcards

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1
Q

What is the INITIAL, REVERSABLE impact of HYPERcalcemia on renal fx?
-Clinical signs assoc.’d?

A
  • ↓ ADH response at tubules (and production of ADH) –> PU –> PD
    • NOTE: if animal becomes dehydrated –> azotemia w/ dilute USG –> Renal profile will LOOK LIKE Renal Azotemia
      • **BUT you should notice the HYPERcalcemia!
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2
Q

3 mechanisms assoc’d with renal failure that leads to HYPOcalcemia

??????

A
    • ↑ phos –> precipitation of Ca –> ↓ Ca (Mass Action)
  2. Phos inhibits 1-alpha-hydroxylase –> ↓ Vit D activation –> ↓ Ca absorption
  3. Chronic loss of renal mass –> ↓ 1-alpha-hydroxylase –> ↓ Vit D activation –> ↓ Ca absorption

???? - Protein losing nephropathy –> decreased albumin –> decreased Ca

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3
Q

Why is HYPERcalcemia more common in Horses with renal dz?

A
  • GI absorption is not regulated
  • Kidney regulates excretion
    therefore, renal azotemia –> inadequate excretion –> ↑Ca
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4
Q

Why is HYPOcalcemia more significant in ALKALEMIC animal.

A

Total Ca will NOT reflect Ionized!!

  • Primary ABNORMAL Ca Homeostasis (Lactation)
  • inability to mobilized Ca –> ↓ ionized Ca
  • w/ Concurrent alkalemia
  • Ca & H+ compete for binding sites on Albumin
    (( ↓ in H+ (alkalemia) –> more binding sites open for Ca –> ↓ IONIZED Ca (no change in total) ))
    -w/o Primary hypocalcemia, it would not be dramatic enough to cause clinical signs

Hypocalcemia + Alkalemia –> may show clinical signs ***Tx ASAP!!

-Milk fever, eclampsia

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5
Q

What is the clinical manifestation of HYPOcalcemia in Cow? vs Dog?
-why are they diff?

A

COW: flaccid paralysis

DOG: tonic paralysis

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6
Q

2 primary endocrine dz assoc’d w/ HYPERcalcemia

A
  • HHM (humoral hypercalcemia)

- Primary HyperParathyroidism

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7
Q

Why is HYPOmagnesemia assoc’d w/ hypocalcemia?

A
  • Decreased Mg –> Decreased ability to RELEASE PTH –> ↓ Ca

* *Grass Tetany

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8
Q

What RENAL parameter most commonly reflect alterations in Phos?

A
  • ↓ GFR
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9
Q

Major clinical consequence of SEVERE HYPOphosphatemia?

At what conc. should you be concerned?

A
  • Severe ↓ Phos –> ↓ ATP –> ↓ membrane integrity –> HEMOLYSIS!

*** Phos < 1 mg/dl

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10
Q

What is the role of HYPERphosphatemia in pathogenesis of Renal 2ndary HyperPTism

A

Hyperphos –>

  1. Mass action –> precipitation of Ca
  2. Inhibits 1-alpha-hydroxylase (Early) –> ↓ active Vit D –> Ca absorption from GI and Kidney

–> ↓ Ca –> hyperplasia of chief cells in Parathyroid gland –> hyperparathryoidism

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11
Q

What would cause Total Body Na+ to be low, while Serum Na+ is normal (with renal failure)?

A
  • Renal Na Loss (mild) + Dehydration (hemoconcentration)

** renal Na changes (↑/↓) are MILD

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12
Q

What is the significance of SEVERE HYPOnatremia in assoc w/ renal azotemia?

In what species would Severe hyponatremia + renal azotemia be a normal pathologic progression?

A
  • Na levels < 120’s –> lack of osmotic gradient
    = Medullary washout
    **Underlying causes w/ dehydration:
    1. Addisons
    2. 3rd space dz
    3. Diarrhea
  • Common to see a normal pathology in BOVINE
    - GI stasis –> sequestration
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13
Q

For total body K+, why is Serum K+ a poor indicator?

A
  • mostly INTRAcellular

Mechanisms for change:

  • excretion
  • intake
  • internal shifts/redistribution (pH/insulin)
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14
Q

2 mechanisms of HYPERkalemia (assoc’d w/ renal dz)

A
  1. Decreased GFR
  2. Decreased Secretion
    (3. Associated acidemia)
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15
Q

When is HYPOkalemia more significant (associated with acid-base balance)? Why?
What organ system will be affected?

A
  • HYPOkalemia + Acidemia
    = TOTAL BODY DEPLETION!!
  • -> Generalized weakness (disrupts membrane potentials)
  • -> eventually Rhabdomyolysis
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16
Q

Primary Hypercalcemia + Acidemia

A

–> underestimate degree of Ca ↑

NOT actuel life-treatining –> slow Soft tissue mineralization

17
Q

What effects does PTH have?

A
  1. Bone resorption -> ↑ Ca
  2. Renal reabsorption -> ↑ Ca
  3. ↑ Vitamin D production –> ↑ GI absorption
18
Q

What is the difference in Ca vs Mg ability to regulate ionized levels?

A 
Ca = Rapid alteration to correct
Mg = Slow
19
Q

What is the biologically active form of Ca?

What % of total Ca is it?

A

** Ionized Ca = 50% of total Ca

Protein bound & Complexed = unavailable

20
Q

What is the clinical presentation of an animal w/ HYPOcalcemia + HYPOalbuminemia?

A

No associated signs related to the hypocalcemia

- Bc doesn’t affect ionized pool

21
Q

DDx for severe hypercalcemia

A
  1. HHM
  2. Primary hyperparathyroidism
  3. Vit D toxicity (w/ ↑ Phos)
  4. Addison’s (other e-lyte abnormalities)
22
Q

DDx for mild hypercalcemia

A
  1. Renal failure
  2. Bony lesions
  3. +/- Alkalmeia (↑ protein bound)
23
Q

DDx for hypocalcemia (Lg animals)

A

Mild

  1. Hypomagnesemic (“Grass”) tetany
  2. Mercury tox – ↓ PTH release
  3. Equine colic

Severe

  1. Milk fever
  2. Blister Beetle toxicity (Cantharidin)
24
Q

DDx for hypocalcemia (Sm animals)

A

Mild

  1. Hypoproteinemia
  2. Renal failure
  3. Acute Pancreatitis –fat necrosis

Severe

  1. Eth Glycol tox
  2. Hypoparathyroidism
25
Q

How can Hypercalcemia –> primary renal azotemia?

A
  • underlying Ca disorder –> ↑ Ca interferes w/ ADH at tubules (D. insipidus)
  • -> PU –> PD
  • Vomiting is often assoc.’d –> Pre-renal azotemia
  • -> blood work LOOKS like Renal azotemia!

–> Metastatic calcification –> primary renal azotemia

26
Q

4 main mechanisms affecting Phos

A
  1. Renal – ↓ GFR
  2. Dietary – usually ↓
  3. Hormonal influence o
    • Young animal –active bone growth
    • Hypoparathyroidism (w/ ↓ Ca)
    • Vit D tox ( w/ ↑ Ca)
  4. Transcellular shifts (insulin)
27
Q

What should you check if you see LOW phos w/ azotemia?

A
  • Phos should be higher w/ azotemia
  • *Check CALCIUM
    • Primary disorder (HHM) –> increased calcium –> Mass action –> decreased Phos
28
Q

What species is most commonly associated with Hypomagnesemia?

A

Ruminants

  1. Milk Tetany
    • -all milk diet
  2. Grass tetany
    • -Lush pastures (high K)
    • -> interfere with Mg absorption
29
Q

DDx for Hypernatremia

A
  1. insensible loss –Fever, panting, water restriction
  2. GI loss *VOMITING
  3. Renal failure –> dehydration
  4. Diabetes insipidus
30
Q

What Na concentration –> medullary washout?

A

< 120’s

31
Q

Renal handling of K+

A
  • freely filtered
  • completely reabsorbed in PCT
  • Secreted in DCT = Primary route of excretion!
  • flow rate dependent
32
Q

DDx for Hyperkalemia

A
  1. Anuria / oliguria / Obstruction
  2. Hypoaldosteronism –> vomiting +bradycardia
  3. Acidemia
  4. Hemolysis in HORSES (RBC’s high K+)
33
Q

DDx for Hypokalemia

A
  1. Polyuria
  2. Anorexia -herbivores & cats
  3. Gastric vomiting
  4. insulin therapy
  5. Alkalemia
34
Q

Gastric content is low in K+, so why would you see HYPOkalemia w/ vomiting?

A

vomiting–> alkalosis –> transcellular shifts into cells & Kidneys SECRETE K+ in an attempt to retain H+ –> ↑ K in urine!

35
Q

What is the classic presentation of hypokalemic polymyopathy?

A

Generalized weakness + Cervical ventroflexion

36
Q

What gene is associated w/ HyPP?

What is the pathogenesis.

A

Point mutation = Skeletal muscle Na Channel gene
in Quarter horse, paint, appaloosas
–> increased membrane potential
–> uncontrolled firing
–> muscle fasiculations (non-clincal)

  • Episodes of transiently ↑ K+ –> Bradycardia
    • colic normal = tachycardia

Clin Chem (12 decks)

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