Endocrinology - ADH and Calcium

Question 1

What is polyuria?

Answer 1

Increased urine production - 50 ml/kg/day

Question 2

What is the normal urine production of a small animal?

Answer 2

20-45 ml/kg/day

Question 3

What is polydipsia?

Answer 3

Increased thirst - 100 ml/kg/day

Question 4

What is the normal water intake of a small animals?

Answer 4

20-70 ml/kg/day

Question 5

True or false: The vast majority of animals are polydipsic first.

Answer 5

false - they are polyuric first

Question 6

How does polyuria lead to polydipsia?

Answer 6

Polyuria leads to volume depletion which leads to polydipsia to prevent dehydration

Question 7

True or False: Water restriction is not the answer to treat PU/PD.

Answer 7

TRUE

Question 8

What are the major differential diagnoses for PU/PD?

Answer 8

Osmotic diuresis, diabetes insipidus, renal medullary solute washout, drug-induced, and primary polydipsia

Question 9

What is osmotic diuresis?

Answer 9

It is when there is an increase in urine solutes resulting in water pulled into the tubule and thus increased water loss through the urine

Question 10

What are some disease processes that can cause osmotic diuresis?

Answer 10

Diabetes mellitus/DKA, Fanconi syndrome or primary renal glucosuria, CKD/AKI, and post-obstructive diuresis

Question 11

What is diabetes insipidus?

Answer 11

A disorder characterized by the production of a large amount of dilute urine that occurs when water is not able to be reabsorbed from the renal tubule (action of ADH)

Question 12

What are the two manifestations of diabetes insipidus?

Answer 12

central and nephrogenic

Question 13

What is central diabetes insipidus also known as?

Answer 13

primary pituitary DI

Question 14

What is central diabetes insipidus caused by?

Answer 14

A lack of ADH production - there is some issue with the pituitary gland

Question 15

What is nephrogenic diabetes insipidus?

Answer 15

There is partial or complete lack of renal response to ADH

Question 16

What are the two forms of nephrogenic diabetes insipidus?

Answer 16

Primary and secondary/acquired

Question 17

What is primary nephrogenic diabetes insipidus?

Answer 17

Congenital lack of ADH receptors or lack of response to ADH- it has not been described in small animals

Question 18

What can cause acquired NDI?

Answer 18

bacterual endotoxins, hypercalcemia, hyperadrenocorticism, hypokalemia, and others

Question 19

What is renal medullary solute washout?

Answer 19

The loss of renal medullary solutes due to an impaired ability of the nephron to concentrate urine

Question 20

What are the potential causes of renal medullary solute washout?

Answer 20

Hepatic disease, chronic diuretic use, and many other causes of PU/PD

Question 21

What drugs are the ‘common offenders’ of causing PU/PD?

Answer 21

Anticonvulsants, glucocorticoids, and diuretics

Question 22

What is primary polydipsia?

Answer 22

It is polydipsia that cannot be explained as a compensatory response to excessive whater loss

Question 23

What is psychogenic polydipsia?

Answer 23

Behavioral compulsive water consumption - diagnosis of absolute exclusion

Question 24

Why does polyuria develop in cases of psychogenic polydipsia?

Answer 24

to prevent overhydration

Question 25

What is the clinical approach to PU/PD?

Answer 25

Get a history to verify, do a thorough PE, do a minimum database to rule out easy causes, use a UA to look for hyposthenuria or concentrated urine, and do additional diagnostics

Question 26

What additional diagnostics can be done to diagnose the underlying cause of PU/PD?

Answer 26

UCCR, LDDST, T4, imaging, urine culture, leptospirosis testing, bile acids

Question 27

What is a Desmopressin (DDAVP) trial?

Answer 27

It is a synthetic ADH analog that is used to tread CDI - if given and there is a positive response it is suggestive of CDI

Question 28

What is a water deprivation test used for?

Answer 28

To determine if the patient has the ability to concentrate urine

Question 29

What is the water deprivation test used to differentiate between?

Answer 29

Primary/psychogenic polydipsia and diabetes insipidus

Question 30

When should the water deprivation test only be performed?

Answer 30

If all other causes of PU/PD have been ruled out

Question 31

What is the biologically active form of calcium?

Answer 31

ionized calcium

Question 32

What does the maintenance of normal calcium depend on the interaction of?

Answer 32

parathyroid hormone, vitamin D, and Calcitonin

Question 33

What is PTH secreted by?

Answer 33

chief cells of the parathyroid gland

Question 34

What does PTH do in the bone?

Answer 34

Increase calcium mobilization

Question 35

What does PTH do in the kidney?

Answer 35

Increases renal tubular calcium reabsorption, increase vitamin D conversion to the active form, and increases phosphorus excretion

Question 36

What is the net effect of PTH action?

Answer 36

Increase Ca and decrease P

Question 37

What does vitamin D do in the intestine?

Answer 37

Increaes phosphorus absorption and increases calcium absorption

Question 38

What is the net effect of Vitamin D action?

Answer 38

Increases calcium and phosphorus

Question 39

What is calcitonin secreted by?

Answer 39

C cells of the thyroid gland

Question 40

Where is the primary site of action of calcitonin?

Answer 40

the bone

Question 41

What is hypercalcemia?

Answer 41

When blood inionized calcium levels increase - PTH falls, vitamin D conversion stops, there is decreased Ca absorption from GI tract, increased renal calcium excretion, and calcium is deposited in bones

Question 42

What are the etiologies of hypercalcemia?

Answer 42

HARDIONS G - Hyperparathyroidism, Addison's, Renal disease, Hypervitaminosis D, Idiopathic, Osteolysis, Neoplasia, Spurious, Granulomatous disease, and Growth

Question 43

What etiologies are the highest calcium levels seen with?

Answer 43

Primary hyperparathyroidism, neoplasia, and vitamin D toxicity

Question 44

What clinical signs are associated with hypercalcemia?

Answer 44

PU/PD, weakness, lethargy, exercise intolerance, and inappetance

Question 45

What is the clinical approach to hypercalcemia?

Answer 45

Complete history, physical exam, minimum data base, imaging, lymph node aspiration, bone marrow evaluation, and PTH panel/malignancy panel/vitamin D panel

Question 46

What is primary hyperparathyroidism?

Answer 46

Excessive secretion of PTH by autonomously functioning parathyroid gland

Question 47

What is the etiology of primary hyperparathyroidism?

Answer 47

parathyroid adenoma

Question 48

What is the signlament for primary hyperparathyroidism?

Answer 48

Older dogs, Keenshond is overrepresented

Question 49

What clinical signs are associated with primary hyperparathyroidism?

Answer 49

PU/PD, can present with lower urinary tract signs, clinical signs can be subtle

Question 50

What will you find on diagnostic evaluation of primary hyperparathyroidism

Answer 50

PE is often normal and there is an elevated or inappropriately normal PTH level in the face of high ionized calcium

Question 51

How is primary hyperparathyroidism treated?

Answer 51

Surgery, percutaneous ablation, and monitor/treat for hypocalcemia following definitive therapy

Question 52

What causes hypercalcemia of malignancy in dogs?

Answer 52

Lymphoma, anal sac adenocarcinoma, and multiple myeloma

Question 53

What causes hypercalcemia of malignancy in cats?

Answer 53

lymphoma and squamous cell carcinoma

Question 54

What is hypercalcemia of malignancy often mediated by?

Answer 54

parathyroid hormone

Question 55

What causes vitamin D toxicosis?

Answer 55

Cholecalciferol rodenticides, psoriasis medications, some plants, and iatrogenic

Question 56

What are the clinical effects of vitamin D toxicosis?

Answer 56

Severe hypercalcemia and severe hyperphosphatemia

Question 57

How is vitamin D toxicosis diagnosed?

Answer 57

history of exposure or vitamin D assay

Question 58

How is vitamin D toxicosis treated?

Answer 58

non-specific treatment of hypercalcemia + salmon calcitonin

Question 59

What are some non-specific treatments for hypercalcemia?

Answer 59

IV fluids, furosemide, biphosphonates, and glucocorticoids

Question 60

What is hypocalcemia?

Answer 60

When blood ionized calcium levels decrease - PTH rises, Vitamin D conversion occurs, increased GI calcium absorption, decreased renal calcium excretion, and calcium mobilized from bones

Question 61

What are the etiologies for hypocalcemia?

Answer 61

LEANCHAP - Lack of PTH, Eclampsia, Acute renal failure, Renal, Chronic kidney disease, Hypoalbuminemia, Acute pancreatitis, and phosphate enemas Also - Sepsis, malabsorption, and blood transfusions

Question 62

What clinical signs are associated with hypocalcemia?

Answer 62

Seizure/tetany, stiff gait, muscle fasciculations, hyperthermia, cardiac arrhythmias, facial pruritus, and chewing on paws

Question 63

What is hypoparathyroidism?

Answer 63

Lack of PTH due to loss of functional parathyroid tissue

Question 64

What are the causes of hypoparathyroidism?

Answer 64

Iatrogenic with thyroidectomy, parathyroidectomy, and primary immune-mediated destruction

Question 65

When should you have a high index of suspicion in hypoparathyroidism cases?

Answer 65

Profound hypocalcemia, hypomagnesemia, hyperphosphatemia, normal renal parameters, and low to undetectable PTH levels in the face of hypocalcemia

Question 66

What is the goal of hypoparathyroidism treatment?

Answer 66

To increase calcium level to a point that eliminates clinical signs

Question 67

What is the emergency treatment for hypocalcemia?

Answer 67

IV calcium administration very slowly to avoid causing arrhythmias

Question 68

What is the chronic therapy for hyothyroidism?

Answer 68

oral calcium, vitamin D (calcitriol), and to treat the clinical signs

Question 69

What is eclampsia?

Answer 69

Hypocalcemia resulting from lactation and calcium loss into milk