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Small Animal Medicine > Endocrinology - ADH and Calcium > Flashcards

Endocrinology - ADH and Calcium Flashcards

1
Q

What is polyuria?

A

Increased urine production - 50 ml/kg/day

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2
Q

What is the normal urine production of a small animal?

A

20-45 ml/kg/day

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3
Q

What is polydipsia?

A

Increased thirst - 100 ml/kg/day

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4
Q

What is the normal water intake of a small animals?

A

20-70 ml/kg/day

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5
Q

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

A

false - they are polyuric first

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6
Q

How does polyuria lead to polydipsia?

A

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

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7
Q

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

A

TRUE

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8
Q

What are the major differential diagnoses for PU/PD?

A

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

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9
Q

What is osmotic diuresis?

A

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

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10
Q

What are some disease processes that can cause osmotic diuresis?

A

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

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11
Q

What is diabetes insipidus?

A

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)

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12
Q

What are the two manifestations of diabetes insipidus?

A

central and nephrogenic

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13
Q

What is central diabetes insipidus also known as?

A

primary pituitary DI

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14
Q

What is central diabetes insipidus caused by?

A

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

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15
Q

What is nephrogenic diabetes insipidus?

A

There is partial or complete lack of renal response to ADH

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16
Q

What are the two forms of nephrogenic diabetes insipidus?

A

Primary and secondary/acquired

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17
Q

What is primary nephrogenic diabetes insipidus?

A

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

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18
Q

What can cause acquired NDI?

A

bacterual endotoxins, hypercalcemia, hyperadrenocorticism, hypokalemia, and others

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19
Q

What is renal medullary solute washout?

A

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

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20
Q

What are the potential causes of renal medullary solute washout?

A

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

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21
Q

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

A

Anticonvulsants, glucocorticoids, and diuretics

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22
Q

What is primary polydipsia?

A

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

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23
Q

What is psychogenic polydipsia?

A

Behavioral compulsive water consumption - diagnosis of absolute exclusion

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24
Q

Why does polyuria develop in cases of psychogenic polydipsia?

A

to prevent overhydration

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25
Q

What is the clinical approach to PU/PD?

A

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

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26
Q

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

A

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

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27
Q

What is a Desmopressin (DDAVP) trial?

A

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

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28
Q

What is a water deprivation test used for?

A

To determine if the patient has the ability to concentrate urine

29
Q

What is the water deprivation test used to differentiate between?

A

Primary/psychogenic polydipsia and diabetes insipidus

30
Q

When should the water deprivation test only be performed?

A

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

31
Q

What is the biologically active form of calcium?

A

ionized calcium

32
Q

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

A

parathyroid hormone, vitamin D, and Calcitonin

33
Q

What is PTH secreted by?

A

chief cells of the parathyroid gland

34
Q

What does PTH do in the bone?

A

Increase calcium mobilization

35
Q

What does PTH do in the kidney?

A

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

36
Q

What is the net effect of PTH action?

A

Increase Ca and decrease P

37
Q

What does vitamin D do in the intestine?

A

Increaes phosphorus absorption and increases calcium absorption

38
Q

What is the net effect of Vitamin D action?

A

Increases calcium and phosphorus

39
Q

What is calcitonin secreted by?

A

C cells of the thyroid gland

40
Q

Where is the primary site of action of calcitonin?

A

the bone

41
Q

What is hypercalcemia?

A

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

42
Q

What are the etiologies of hypercalcemia?

A

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

43
Q

What etiologies are the highest calcium levels seen with?

A

Primary hyperparathyroidism, neoplasia, and vitamin D toxicity

44
Q

What clinical signs are associated with hypercalcemia?

A

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

45
Q

What is the clinical approach to hypercalcemia?

A

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

46
Q

What is primary hyperparathyroidism?

A

Excessive secretion of PTH by autonomously functioning parathyroid gland

47
Q

What is the etiology of primary hyperparathyroidism?

A

parathyroid adenoma

48
Q

What is the signlament for primary hyperparathyroidism?

A

Older dogs, Keenshond is overrepresented

49
Q

What clinical signs are associated with primary hyperparathyroidism?

A

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

50
Q

What will you find on diagnostic evaluation of primary hyperparathyroidism

A

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

51
Q

How is primary hyperparathyroidism treated?

A

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

52
Q

What causes hypercalcemia of malignancy in dogs?

A

Lymphoma, anal sac adenocarcinoma, and multiple myeloma

53
Q

What causes hypercalcemia of malignancy in cats?

A

lymphoma and squamous cell carcinoma

54
Q

What is hypercalcemia of malignancy often mediated by?

A

parathyroid hormone

55
Q

What causes vitamin D toxicosis?

A

Cholecalciferol rodenticides, psoriasis medications, some plants, and iatrogenic

56
Q

What are the clinical effects of vitamin D toxicosis?

A

Severe hypercalcemia and severe hyperphosphatemia

57
Q

How is vitamin D toxicosis diagnosed?

A

history of exposure or vitamin D assay

58
Q

How is vitamin D toxicosis treated?

A

non-specific treatment of hypercalcemia + salmon calcitonin

59
Q

What are some non-specific treatments for hypercalcemia?

A

IV fluids, furosemide, biphosphonates, and glucocorticoids

60
Q

What is hypocalcemia?

A

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

61
Q

What are the etiologies for hypocalcemia?

A

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

62
Q

What clinical signs are associated with hypocalcemia?

A

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

63
Q

What is hypoparathyroidism?

A

Lack of PTH due to loss of functional parathyroid tissue

64
Q

What are the causes of hypoparathyroidism?

A

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

65
Q

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

A

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

66
Q

What is the goal of hypoparathyroidism treatment?

A

To increase calcium level to a point that eliminates clinical signs

67
Q

What is the emergency treatment for hypocalcemia?

A

IV calcium administration very slowly to avoid causing arrhythmias

68
Q

What is the chronic therapy for hyothyroidism?

A

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

69
Q

What is eclampsia?

A

Hypocalcemia resulting from lactation and calcium loss into milk

Small Animal Medicine (100 decks)

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