Exam 8: L. 6: Pituitary/ADH; Parathyroid/Calcium Flashcards
Osmolality
Number of osmoles per kilogram of solvent
- biggest player = SODIUM
- osmoles draw water
Antidiuretic hormone
1) ADH = vasopressin
- released by posterior pituitary
- action: conserve water
Plasma osmolality
Most important stimulus for THIRST and ADH release
-1% increase in osmolality can cause ADH release
ADH actions
1) systemic effects/multiple organs
2) kidney
- increase permeability to water ==> allows reabsorption of solute free water
- urine production decreases/urine osmolality increases
- plasma osmolality decreases
Polyuria and polydipsia
1) polyuria: >50 ml/kg/day
(normal = 20-45 ml/kg/day)
2) polydipsia: >100 ml/kg/day
(normal: 20-70 ml/kg/day)
3) the vast majority of animals with PU/PD are polyuric* first
- polyuria leads to volume depletion ==> polydipsia develops to prevent dehydration (polydipsia is an appropriate body response)
PU/PD differential diagnoses
1) osmotic diuresis
2) diabetes insipidus
3) acquired (secondary) nephrogenic DI
- something is interfering with ADH receptor
4) iatrogenic
5) renal medullary solute washout
Osmotic diuresis
Increase in urinary solutes (i.e. glucose) pulls water = =>diuresis = =>hypovolemia = =>stimulates thirst = =>polydipsia
Example = diabetes mellitus, chronic renal failure
Diabetes insipidus
1) nothing to do with glucose or insulin!!
2) syndrome is related to ADH**
3) 2 manifestations: central and nephrogenic
- central: hypothalamus/pituitary not producing ADH (rare)
- nephrogenic: kidney not responding to ADH (usually it is acquired/secondary)
Acquired/secondary NDI
1) by far the largest category of DI
2) ADH and ADH receptors are present
3) problem: interference in normal interaction between ADH and the kidneys
4) PU/PD is typically severe
Causes of secondary NDI
Pyometra, hypercalcemia, hepatic disease, hyperadrenocortiscism, pyelonephritis, hyperthyroidism Addison’s disease, polycythemia, acromegaly, hyperaldosteronism, hypokalemia
Summarizing DI
1) most DI cases are acquired and nephrogenic
2) most are polyuric 1st, with polydipsia developing to prevent dehydration
3) usually limiting water is a BAD idea and may worsen the situation
4) do NOT limit water without knowing cause of PU/PD
Iatrogenic causes of PU/PD
1) anticonvulsants (phenobarbital)
2) glucocorticoids
3) diuretics
4) DOCP
5) synthetic thyroid hormone supplements
Renal medullary solute washout
1) loss of renal medullary solutes-sodium and urea
- loss of medullary hypertonicity
- impaired ability of nephron to concentrate urine
2) potential causes
- hepatic disease
- Addison’s disease
- chronic diuretic therapy
Water deprivation test
Bottom line: determine if animal has the ability to concentrate urine
1) used to differentiate between:
- psychogenic polydipsia (rare)
- central diabetes insipidus (rare)
- primary nephrogenic diabetes insipidus (rare)
ABSOLUTELY MUST RULE OUT ALL OTHER CAUSES OF PU/PD BEFORE DOING THIS TEST
Take several days to perform this test-do not abruptly deprive a PU/PD dog of water
Distribution of calcium
1) protein bound (primarily albumin) ~40%
2) complexed (with citrate, phosphate) ~10%
3) ionized ~50%
- biologically active form*
- most important form for feedback and maintenance!
Calcium flux
1) ionized calcium affected by acid-base:
- alkalosis = increases protein binding = DECREASES ionized calcium
- acidosis = decreases protein binding = increases ionized calcium
2) ionized calcium is UNAFFECTED by hypoalbuminemia
- total serum calcium and protein bound forms will decrease
- protein bound calcium acts as “pool” for ionized form
Actions of PTH
1) mobilizes calcium from bone
2) increases vitamin D conversion in kidney ==> increases INTESTINAL uptake of calcium
3) increases distal renal tubular resorption of calcium
4) increases renal phosphorus excretion
Etiologies of hypercalcemia
1) HARD IONS H = hyperparathyroidism A = Addison's disease R = renal disease D = hypervitaminosis D I = idiopathic (cats) O = Osteolysis (not common) N = neoplasia (VERY COMMON) S = systemic granulomatous disease
- **most significant levels of hypercalcemia are seen with:
- malignancy/neoplasia
- primary hyperparathyroidism
- vitamin D toxicity***
Clinical signs of hypercalcemia
1) PU/PD*
2) listlessness
3) urinary incontinence (secondary to PU/PD)
4) weakness
5) exercise intolerance
6) inappetence
Primary hyperparathyroidism
1) excessive secretion of PTH
2) etiologies
- parathyroid adenoma (most common)
3) signalment
- >7 years of age
4) clinical signs solely due to hypercalcemia!!
Remember
If a patient has hypercalcemia and the PTH level is at the upper end of normal, this is ABNORMAL!
Diagnosis of hyperparathyroidism
Elevated PTH (+/- normal range) in face of hypercalcemia!!
Therapy for hypercalcemia
1) IV fluid therapy
- saline diuresis at 2-3 times maintenance
2) diuretic therapy (furosemide)
- IF and ONLY IF fluid deficits have been replaced
3) glucocorticoid therapy (prednisone)
- IF and ONLY IF diagnosis has been made (if the hypercalcemia is due to lymphoma, the glucocorticoids may kill some of the lymphoma cells and make it hard to get diagnosis)
Hypercalcemia of malignancy
1) dog
- lymphoma**
- anal sac adenocarcinoma
2) cat
- lymphoma
- squamous cell carcinoma
3) malignancy = most common cause of pathologic hypercalcemia in dogs and cats!!
Clinical signs of hypocalcemia
1) seizure/tetany
2) hyperthermia (due to above)
3) tense abdomen, stiff gait, muscle fasciculations
4) cardiac arrhythmias
5) facial pruritus
- hypocalcemia
- methimazole treatment
most dogs present with acute signs, neurologic or neuromuscular
Specific diagnosis of hypoparathyroidism
1) High index of suspicion when:
- profound hypocalcemia
- hypomagnesemia
- hyperphosphatemia
- normal renal parameters!
2) LOW to undetectable PTH level in HYPOCALCEMIA animal
Emergency therapy: hypocalcemia
1) IV calcium administration
2) concurrent ECG monitoring
3) calcium gluconate
- 10% solution
- 1-1.5 ml/kg slowly
- infusion effects: 1-12 hours
4) monitor temperature
After emergency has passed, begin oral therapy: calcium, vitamin D
