Electrolytes Flashcards
What is the INITIAL, REVERSABLE impact of HYPERcalcemia on renal fx?
-Clinical signs assoc.’d?
- ↓ 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!
- NOTE: if animal becomes dehydrated –> azotemia w/ dilute USG –> Renal profile will LOOK LIKE Renal Azotemia
3 mechanisms assoc’d with renal failure that leads to HYPOcalcemia
??????
- ↑ phos –> precipitation of Ca –> ↓ Ca (Mass Action)
- Phos inhibits 1-alpha-hydroxylase –> ↓ Vit D activation –> ↓ Ca absorption
- Chronic loss of renal mass –> ↓ 1-alpha-hydroxylase –> ↓ Vit D activation –> ↓ Ca absorption
???? - Protein losing nephropathy –> decreased albumin –> decreased Ca
Why is HYPERcalcemia more common in Horses with renal dz?
- GI absorption is not regulated
- Kidney regulates excretion
therefore, renal azotemia –> inadequate excretion –> ↑Ca
Why is HYPOcalcemia more significant in ALKALEMIC animal.
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
What is the clinical manifestation of HYPOcalcemia in Cow? vs Dog?
-why are they diff?
COW: flaccid paralysis
DOG: tonic paralysis
2 primary endocrine dz assoc’d w/ HYPERcalcemia
- HHM (humoral hypercalcemia)
- Primary HyperParathyroidism
Why is HYPOmagnesemia assoc’d w/ hypocalcemia?
- Decreased Mg –> Decreased ability to RELEASE PTH –> ↓ Ca
* *Grass Tetany
What RENAL parameter most commonly reflect alterations in Phos?
- ↓ GFR
Major clinical consequence of SEVERE HYPOphosphatemia?
At what conc. should you be concerned?
- Severe ↓ Phos –> ↓ ATP –> ↓ membrane integrity –> HEMOLYSIS!
*** Phos < 1 mg/dl
What is the role of HYPERphosphatemia in pathogenesis of Renal 2ndary HyperPTism
Hyperphos –>
- Mass action –> precipitation of Ca
- Inhibits 1-alpha-hydroxylase (Early) –> ↓ active Vit D –> Ca absorption from GI and Kidney
–> ↓ Ca –> hyperplasia of chief cells in Parathyroid gland –> hyperparathryoidism
What would cause Total Body Na+ to be low, while Serum Na+ is normal (with renal failure)?
- Renal Na Loss (mild) + Dehydration (hemoconcentration)
** renal Na changes (↑/↓) are MILD
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?
- 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
For total body K+, why is Serum K+ a poor indicator?
- mostly INTRAcellular
Mechanisms for change:
- excretion
- intake
- internal shifts/redistribution (pH/insulin)
2 mechanisms of HYPERkalemia (assoc’d w/ renal dz)
- Decreased GFR
- Decreased Secretion
(3. Associated acidemia)
When is HYPOkalemia more significant (associated with acid-base balance)? Why?
What organ system will be affected?
- HYPOkalemia + Acidemia
= TOTAL BODY DEPLETION!! - -> Generalized weakness (disrupts membrane potentials)
- -> eventually Rhabdomyolysis
Primary Hypercalcemia + Acidemia
–> underestimate degree of Ca ↑
NOT actuel life-treatining –> slow Soft tissue mineralization
What effects does PTH have?
- Bone resorption -> ↑ Ca
- Renal reabsorption -> ↑ Ca
- ↑ Vitamin D production –> ↑ GI absorption
What is the difference in Ca vs Mg ability to regulate ionized levels?
Ca = Rapid alteration to correct Mg = Slow
What is the biologically active form of Ca?
What % of total Ca is it?
** Ionized Ca = 50% of total Ca
Protein bound & Complexed = unavailable
What is the clinical presentation of an animal w/ HYPOcalcemia + HYPOalbuminemia?
No associated signs related to the hypocalcemia
- Bc doesn’t affect ionized pool
DDx for severe hypercalcemia
- HHM
- Primary hyperparathyroidism
- Vit D toxicity (w/ ↑ Phos)
- Addison’s (other e-lyte abnormalities)
DDx for mild hypercalcemia
- Renal failure
- Bony lesions
- +/- Alkalmeia (↑ protein bound)
DDx for hypocalcemia (Lg animals)
Mild
- Hypomagnesemic (“Grass”) tetany
- Mercury tox – ↓ PTH release
- Equine colic
Severe
- Milk fever
- Blister Beetle toxicity (Cantharidin)
DDx for hypocalcemia (Sm animals)
Mild
- Hypoproteinemia
- Renal failure
- Acute Pancreatitis –fat necrosis
Severe
- Eth Glycol tox
- Hypoparathyroidism
How can Hypercalcemia –> primary renal azotemia?
- 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
4 main mechanisms affecting Phos
- Renal – ↓ GFR
- Dietary – usually ↓
- Hormonal influence o
- Young animal –active bone growth
- Hypoparathyroidism (w/ ↓ Ca)
- Vit D tox ( w/ ↑ Ca)
- Transcellular shifts (insulin)
What should you check if you see LOW phos w/ azotemia?
- Phos should be higher w/ azotemia
- *Check CALCIUM
- Primary disorder (HHM) –> increased calcium –> Mass action –> decreased Phos
What species is most commonly associated with Hypomagnesemia?
Ruminants
- Milk Tetany
- -all milk diet
- Grass tetany
- -Lush pastures (high K)
- -> interfere with Mg absorption
DDx for Hypernatremia
- insensible loss –Fever, panting, water restriction
- GI loss *VOMITING
- Renal failure –> dehydration
- Diabetes insipidus
What Na concentration –> medullary washout?
< 120’s
Renal handling of K+
- freely filtered
- completely reabsorbed in PCT
- Secreted in DCT = Primary route of excretion!
- flow rate dependent
DDx for Hyperkalemia
- Anuria / oliguria / Obstruction
- Hypoaldosteronism –> vomiting +bradycardia
- Acidemia
- Hemolysis in HORSES (RBC’s high K+)
DDx for Hypokalemia
- Polyuria
- Anorexia -herbivores & cats
- Gastric vomiting
- insulin therapy
- Alkalemia
Gastric content is low in K+, so why would you see HYPOkalemia w/ vomiting?
vomiting–> alkalosis –> transcellular shifts into cells & Kidneys SECRETE K+ in an attempt to retain H+ –> ↑ K in urine!
What is the classic presentation of hypokalemic polymyopathy?
Generalized weakness + Cervical ventroflexion
What gene is associated w/ HyPP?
What is the pathogenesis.
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
