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Exam 4 Pathology & Disease > Endocrine Disease > Flashcards

Endocrine Disease Flashcards

1
Q

The endocrine system is the collection of glands that

A

produce hormones that regulate metabolism, growth and development, tissue function, sexual function, reproduction, sleep and mood, among other things

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2
Q

What is hypothyroidism

A

impaired production and secretion of the thyroid hormones, resulting in a decreased metabolic rate

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3
Q

Clinical signs hypothyroidism

A

weight gain with no change in diet, PU/PD, tragic expression, leathery, recurrent skin and ear infections, bilaterally symmetric alopecia

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4
Q

Signalment for hypothyroidism

A

middle aged to older dogs; breeds: golden retriever’s, dobermans, cocker spaniels

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5
Q

Diagnosis of hypothyroidism

A

elevated CHOL, decreased thyroid hormones (T3/T4), increased TSH

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6
Q

Diagnosis of equine hypothyroidism

A

serum thyroid levels are not routinely done, typically response to Tx is done

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7
Q

Equine hypothyroidism clinical signs

A

Foals: weakness, incoordination, signs of dysmaturity, poor muscle development, enlarged gland

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8
Q

What is hyperthyroidism

A

a disorder resulting from excessive thyroid hormone; though functional benign enlargement (adenoma) is most common (98%), thyroid carcinoma (cancer) is another cause (2%)

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9
Q

Signalment for hyperthyroidism

A

middle aged to older cats

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10
Q

Clinical signs hyperthyroidism

A

weight loss, poor hair coat, rapid heart hate, voracious appetite or thirst, anxiety of nervousness, diarrhea or vomiting, and voacalizing

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11
Q

Diagnosis of hyperthyroidism

A

lump or mass in the neck detected during PE; elevated levels of thyroid hormone in the blood

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12
Q

Cure rate for radioactive iodide of hyperthyroidism

A

95-98% with one treatment

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13
Q

Goiter

A

an enlargement of the thyroid gland

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14
Q

Cause of goiter in small ruminants

A

iodine deficiency

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15
Q
A
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16
Q

Clinical signs for thyroid disease in small ruminants

A

poor wool/hair, dry skin, enlarged thyroid, tendon laxity, reproductive failure

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17
Q

Diabetes mellitus occurs when

A

the pancreas doesn’t produce enough insulin

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18
Q

Insulin is required for the body to

A

efficiently use sugars, fats and proteins

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19
Q

Etiology of diabetes mellitus

A

animals that are overweight or those with inflammation of the pancreas are predisposed to developing diabetes

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20
Q

Diagnosis of diabetes mellitus

A

serum chemistry reveals elevated BG, UA reveals glucosurla (+/- ketonuria)

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21
Q

Without insulin,

A

sugar accumulates in the blood and spills into the urine

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22
Q

Sugar in the urine causes the pet to

A

pass large amounts of urine and to drink lots of water

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23
Q

Two major forms of diabetes in the dog and cat

A

Uncomplicated diabetes and diabetes with ketoacidosis

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24
Q

Diabetic pets with ketoacidosis are very

A

ill and may be vomiting and depressed

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25
Q

Ketoacidotic diabetics are treated with

A

IV fluids and rapid acting insulin. Tx is continued until the pet is no longer vomiting and is eating, then the tx is the same as for uncomplicated diabetes

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26
Q

Tx of diabetes mellitus

A

insulin injections every 12 hours (with meals), dietary management, continuous glucose monitoring (CGM) e.g. Freestyle Libre

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27
Q

Insulin should always be given

A

simultaneously or just after a meal

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28
Q

When blood sugar level drops it can affect

A

neurological function. disorientation, tremors and coma may occur.

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29
Q

Signs of hypoglycemia

A

loss of appetite, extreme lethargy, lack of coordination, trembling, muscle twitching, weakness, seizures, and discoloration of skin and gums

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30
Q

Pets should have a blood glucose curve done _ _ after starting insulin then as recommended by DVM

A

2 weeks

31
Q

What is insulinoma

A

a functional tumor involving B-cells of the pancreas. This causes an over-secretion of insulin

32
Q

Clinical signs of insulinoma

A

sever hypoglycemia, low BG; abdominal u/s reveals pancreatic tumor

33
Q

Prognosis for insulinoma

A

extremely poor even with aggressive tx

34
Q

Disease of the adrenal glands

A

hypoadrenocorticism and hyperadrenocorticism

35
Q

Hypoadrenocorticism aka

A

Addison’s disease

36
Q

Addison’s disease is a deficiency in

A

the production of glucocorticoids and/or mineralocorticoids

37
Q

What are mineralocorticoids

A

hormones responsible for regulating the levels of electrolytes in the body

38
Q

Signalment for Addison’s disease

A

middle-aged dogs usually females; breeds: poodles, labradors

39
Q

Clinical signs of Addison’s disease

A

vague, ADR, PU/PD, vomiting, diarrhea, bradycardia, hypotension, dehydration

40
Q

Dx for Addison’s disease

A

Na:K <27:1, non regenerative anemia, elevated BUN/Crea/Ca, decreased BG/Albumin

41
Q

Definitive dx for Addison’s disease

A

ACTH stimulation test (low resting cortisol that remains unchanged after ACTH stimulation

42
Q

Tx of Addison’s disease

A

acute crisis management, glucocorticoids and mineralocorticoid replacement, monitor electrolytes, BUN/Crea, clinical signs

43
Q

Hyperadrenocorticism aka

A

Cushing’s disease

44
Q

What is Cushing’s disease

A

the overproduction of the hormone cortisol by the adrenal glands

45
Q

Etiology of hyperadrenocorticism

A

pituitary dependent, adrenal tumors, iatrogenic

46
Q

Signalment for Cushing’s disease

A

PDH: dogs < 20kg
Adrenal: dogs > 20kg

47
Q

Clinical signs of Cushing’s disease

A

PU/PD, bilateral flank alopecia, polyphasic, excessive panting, pendulous abdomen, calcinosis cutis, recurrent skin infections, lethargy

48
Q

Diagnosis of Cushing’s disease

A

elevated ALP/ALT, thrombocytosis, elevated BG, lipemia, elevated urine cortisol, low dose dexamethasone suppression test (LDDS), ACTH stimulation test

49
Q

Most common cause of Cushing’s disease is a tumor of the

A

pituitary gland

50
Q

Cushing’s disease may be the result of a benign of malignant tumor of the

A

adrenal glands

51
Q

Iatrogenic cushing;s disease

A

excessive cortisol from prolonged use of steroids

52
Q

Result of cushings disease

A

increased appetite, weight gain, PU/PD, excessive panting, bilaterally symmetrical flank alopecia, recurrent skin infections, chronic UTI’s, diabetes

53
Q

Specific testing to confirm cushings disease

A

low dose dexamethasone suppression test and ACTH stimulation test

54
Q

Low Dose Dexamethasone Suppression test usually takes _ _, if there is a pituitary tumor, the gland will

A

8 hours; not shut off its stimulatory message and ignores the dexamethasone. No drop in cortisol level is seen at the end of 8 hours

55
Q

ACTH stim test requires _ hours

A

1-2

56
Q

In ACTH test,

A

a dose of ACTH is given to the patient. If a larger than expected rise in cortisol levels is measured in 1-2 hours, we may diagnose Cushing’s syndrome

57
Q

When would we run the ACTH stimulation test?

A

it is the only test that can be used if the iatrogenic form of Cushing’s disease is suspected. This test is used to monitor tx of Cushing’s disease

58
Q

A screening test for Cushing’s disease; a positive test here does not confirm Cushing’s disease but a negative test DOES rule it out

A

Urine cortisol: Creatinine ratio

59
Q

Trilostane inhibits an enzyme that is needed in the production of

A

cortisol,

60
Q

Why must we perform ACTH stimulation test periodically when using Trilostane?

A

this drug along with Lysodren has the potential to cause a life-threatening Addisonian crisis if cortisol levels go too low

61
Q

Risk of not treating Cushing’s disease

A

euthanasia (due to urinating in house), problems regulating diabetes mellitus, thromboembolism, increased incidence of infections, systemic hypertension, glomerular nephropathy

62
Q

Pathology of equine cushing’s

A

hypertrophy of the pituitary resulting in an increased dopamine production and an increase in ACTH which increased the cortisol levels

63
Q

Clinical signs of equine cushings

A

long, shaggy coat, lethargy, sweating, PU/PD, recurrent laminitis, recurrent infections

64
Q

The parathyroid glands control

A

the calcium in our bodies- how much calcium in our bones and blood

65
Q

The most important element in our body

A

calcium

66
Q

Primary hyperparathyroidism

A

excessive production of PTH which results in the over production of calcium. Usually caused by the presence of a parathyroid adenoma or adenocarcinoma but may be caused by hyperplasia

67
Q

What causes nutritional (secondary_ hyperparathyroidism

A

problem with the Ca:P ratio in the feed; animals grazing pasture contain calcium oxalate pastures

68
Q

Clinical signs of nutritional (secondary) hyperparathyroidism

A

intermittent shifting leg lameness, loose teeth, spontaneous fractures, enlarged facial bones

69
Q

Eclampsia (puerperal tetany or postpartum hypocalcemia)

A

a secondary hypocalcemia

70
Q

Predisposing factors for eclampsia

A

improper perinatal nutrition, heavy lactation, inappropriate calcium supplementation

71
Q

Clinical signs of eclampsia

A

hyperthermia, salivation, muscle fasciculations, seizures

72
Q

Tx for eclampsia

A

slow IV infusion of calcium gluconate 10%, tx any seizures, diet change

73
Q

Prevention of eclampsia

A

do not supplement Ca++ during pregnancy but feed high quality diet after parturition (puppy food)

74
Q

Hypocalcemia (milk fever) in cattle

A

parturient paresis is an acute to parachute, afebrile, flaccid paralysis of mature dairy cows that occurs most commonly at or soon after parturition.

Exam 4 Pathology & Disease (5 decks)

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