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Physio II > Endocrine Diseases > Flashcards

Endocrine Diseases Flashcards

1
Q

Hyperadrenocorticism is also know by two other names

A
  • Cushing’s disease

- Cushing’s syndrome

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2
Q

Cushing’s disease is ______ to pituitary release of excess ACTH

A

secondary

C’s d AKA pituitary-dependent hyperadrenocorticism (PDH)

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3
Q

Cushing’s __________ in primary hyperadrenocorticism is d/t what?

A

syndrome; d/t adrenal tumor that increases cortisol

C’s s AKA adrenal-dependent dyperadrenocorticism (ADH)

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4
Q

___% of hyperadrenocorticism are due to anterior pituitary adenomas and are called PDH

A

80%

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5
Q

Classic signs of hyperadrenocorticism in dogs

A
  • PU/PD
  • Pendulous abdomen
  • bilateral alopecia
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6
Q

Thin skin is the hallmark sign of hyperadrenocorticism in what species?

A

cats

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7
Q

Signs of hyperadrenocorticism in horses

A
  • long hair coat out of season
  • broodmares with recent history of infertility
  • laminitis, weight loss, PD, inability to masticate properly
  • muscle wasting
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8
Q

Challenges of diagnosing Cushings in dogs (4)

A
  • incr serum enzymes
  • plasma [glucose] can be increased
  • plasma [total T4] can be decreased
  • hypercholesterolemia, decrease BUN
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9
Q

How is a low-dose dexamethasone suppression test used for Cushing’s testing?

A
  • should lead to a dec in plasma [cortisol] in NORMAL animals
  • No change = indicative of hyperadrenocorticism
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10
Q

How is a corticotropin stimulation test used for Cushing’s testing?

A
  • diagnostic for enlarged adrenal glands

- chronic pit. stimulation causes exaggerated corticotropin response

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11
Q

What can an abdominal ultrasound tell you for Cushing’s?

A

Both adrenals of same size = secondary locus

One adrenal enlarged relative to other = primary locus (the enlarged one is the diseased one)

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12
Q

4 common drugs in the medical management of ADH or PDH

A
  • mitotane
  • ketoconazole
  • L-deprenyl
  • trilostane
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13
Q

Beyond medical management, what else can be done for adrenal neoplasm?

A

surgery (adrenalectomy)

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14
Q

This disease is also called Addison’s-like syndrome

A

Hypoadrenocorticism

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15
Q

What is wrong endocrinologically with hypoadrenocorticism?

A
  • deficient glucocorticoid and mineralocorticoid synthesis

* increase in ACTH, renin, Angiotensin

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16
Q

Causes of Addison’s

A
  • usually primary, d/t lymphocytic infiltration of adrenal cortex
  • iatrogenic Addison’s = secondary to mitotane treatment for Cushing’s
  • autoimmune, opportunistic infections in AIDs destroy adrenal cortex
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17
Q

Common patients for Addison’s?

A

middle-aged dogs

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18
Q

Signs of Hypoadrenocorticism

A
  • hyperkalemia (arrhythmias)
  • hyponatremia (dec blood vol)
  • muscle atrophy, depression, weight loss
  • bradycardia/ widened QRS complex
  • hypotension
  • salt craving!
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19
Q

KEY sign of hypoadrenocorticism

A

bracycardia/widened QRS complex

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20
Q

Treatment of hypoadrenocoricism

A

Replacement therapy

  • mineralocorticoids
  • glucocorticoids
  • Deoxycorticosterone pivalate (DOCP) has both properties
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21
Q

Induced hyperadrenocorticism (Cushing’s syndrome)

A
  • iatrogenic

- overuse of glucocorticoids

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22
Q

Induced hypoadrenocorticism

A
  • iatrogenic

- adrenalectomy

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23
Q

Induced hypothroidism

A
  • iatrogenic

- treatment of goiter

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24
Q

What hormone is related to Diabetes Insipidus?

A

Vasopressin -specifically a loss of vasopressin action

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25
Q

DI can have two forms. What are they?

A
  • hypothalamic form - lesion in area where vasopressin is formed
  • nephrogenic insensitivity of vasopressin
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26
Q

Signs of DI

A
  • PU/PD
  • urine with a low specific gravity
  • dehydration
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27
Q

Differentials for DI

A
  • PD animals with overhydration

- dehydration via water restriction

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28
Q

Pathognomonic sign of DI

A

dilute urine

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29
Q

If the problem originates in the hypothalamus, what type of DI is it?

A

Central DI

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30
Q

If the problem is in the nephron, what type of DI is it?

A

Nephrogenic DI

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31
Q

Modified H2O deprivation test for DI

A
  • Determine if endogenous ADH release can occur = IF inc. ADH release and [ ] of urine, THEN NOT central DI
  • Confirm via response to exogenous ADH = IF response to exogenous ADH, THEN NOT nephrogenic
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32
Q

Why is it important to recognize renal failure prior to a water deprivation test?

A

failure may lead to incorrect/inconclusive diagnosis or morbidity in patients

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33
Q

Treatment for Hypothalamic DI

A

Rx vasopressin IM every 1-3 days

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34
Q

Treatment for Nephrogenic DI

A

-thiazide diurectics - have paradoxical effect on PU/PD

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35
Q

Pit. Dwarfism

A
  • fairly rare
  • deficiency in GH
  • commonly seen in German Shepherd 2-6 months old
    • autosomal defect in German Shepherds d/t cystic Rathke’s pouch
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36
Q

Clinical Signs of Pit. Dwarfism in young animals

A
  • proportional dwarfism
  • delayed dentition
  • delayed closure of growth plates
  • hair coat abnormalities (retention of puppy coat, no primary guard hairs)
  • Behavioral abnorms
  • reduced exercise performance
  • retain puppy-like behavior
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37
Q

Clinical Signs of Pit. Dwarfism in adult animals

A
  • abnorm. weight gain
  • reduced lean mass
  • reduced exercise performance
  • osteopenia
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38
Q

Differential Diagnosis for Pit. Dwarfism

A
  • hypothyroid dwarfism
  • portosystemic shunt
  • diabetes mellitus
  • hyperadrenocorticism
  • malnutrition
  • parasitism
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39
Q

Acromegaly (AKA hypersomatotropism)

A
  • excess GH, post-puberty

- d/t: pit. adenomas or pit. hyperplasia

40
Q

Clinical Signs of Acromegaly

A
  • KEY: net weight gain lean body mass in animals w/ Diabetes Mellitus
  • enlarged jaw, tongue, forehead, and extremities
  • striking hirsutism (excessive hair growth), failure to shed
41
Q

Diagnosis of Acromegaly

A

plasma [GH] and/or glucose suppression test

42
Q

Differential diagnosis for Acromegaly

A

-Cushing’s syndrome (hyperadrenocorticism

43
Q

Treatment of Acromegaly

A

radiation therapy

44
Q

Diabetes Mellitus

A
  • “sweet diuresis”

- absolute or relative deficiency of insulin

45
Q

Clinical Types of Diabetes Mellitus (3- this is not Type I/II)

A
  • nonketotic
  • ketoacidotic
  • nonketotic hyperosmolar syndrome
46
Q

Signs of DM

A
  • PU (and urinary tract infections)
  • PD
  • bacterial cystitis in females (glucose in urine)
  • cataracts
  • most patients are obese, but w/ recent weight loss and polyphagia
  • hepatomegaly (enlarged liver)
  • acetone breath (ketones)
47
Q

Why do cataracts form in relation to DM?

A

sorbitol or fructose trapped in lens

48
Q

Diagnosis of DM

A
  • persistent fasting hyperglycemia

- evidence of chronic hyperglycemia

49
Q

Control of DM

A

Goals

  • normal bodyweight
  • normal physical activity
  • normal water comsumption/urine output

Insulin therapy

50
Q

Type I DM

A
  • insulin-dependent diabetes

- inadequate insulin production in pancreas

51
Q

Type II DM

A
  • insulin-independent diabetes
  • more likely inherited
  • adequate/nearly adequate insulin production by pancreas
52
Q

As there is adeqaute/nearly adequate insulin production in Type II DM, why are there problems?

A
  • peripheral insulin resistance = dec GLUT4 transporters

- excessive glucose production by the liver

53
Q

Type ___ DM is also assoc. with obesity

A

II

54
Q

T/F: Insulin therapy is often part of treatment for both types of DM in companion animals

A

True

55
Q

T/F: Zinc complexes slow release of insulin

A

True

56
Q

Insulinoma

A
  • tumors of pancreas that secrete insulin
  • more common in ferrets than any other pet = ferrets older than 5 yrs are susceptible
  • can be small multiples or a single nodule
57
Q

Symptoms of Insulinoma

A
  • detached, unengaged mood, trance
  • lethargy, depression
  • weight loss
  • difficulty with rear legs
  • seizures, fainting (advanced cases)
58
Q

Diagnosis of Insulinoma

A

hypoglycemia after 4 hour fast

59
Q

Treatment of Insulinoma

A

best option = surgery

60
Q

What is the largest purely endocrine gland?

A

Thyroid

61
Q

Is the thymus normally palpable?

A

NO!

62
Q

What is a palpable enlargement of the thymus called?

A

goiter

63
Q

Job of follicular cells/ follicles of the thymus? (3)

A
  • collect and transport iodine
  • synthesize and secrete thyroglobulin
  • remove and secrete T3 and thyroxine (T4)
64
Q

Job of parafollicular cells of the thymus? (2)

A
  • secrete calcitonin

- calcium and phosphorus metabolism

65
Q

How do the parafollicular cells help with calcium metabolism?

A
  • decrease blood Ca2+

- increase urinary loss of Ca2+

66
Q

In regards to T3/T4, is the thymus pit. dependent or independent?

A

Pit. Dependent

67
Q

The thymus is pit. independent for parafollicular cells. What regulates their actions?

A

[Ca2+] in the blood

68
Q

T4 is a __________ for T3

A

prohormone

69
Q

Actions of calcitonin

A
  • lower blood Ca2+ and phosphorus

- antagonistic action to parathyroid hormone

70
Q

How does calcitonin lower blood Ca2+ and phosphorus? (2)

A
  • blocks osteoclasts action (inhibits bone resorption) = Ca2+ deposition
  • blocks renal reabsorption of calcium and phosphorus = Ca2+ excretion
71
Q

A non-neoplastic, non-inflammatory enlargement of the thyroid is a ____________

A

goiter

72
Q

Causes of Goiter (3)

A
  • iodine-deficient diet = 90%
  • goiterogenic compounds
  • genetic defects of thyroid hormone synthesis

There are other things as well.

73
Q

What can cause an excess of thyroid follicular hormone?

A
  • usually primary hyperthyroidism

- thyroid adenoma

74
Q

Clinical Signs/ Lab Findings of Hyperthyroidism

A
  • increased metabolic rate
  • goiter - 90%
  • weight loss
  • Polyphagia
  • PU/PD
  • hyperactivity, nernousness, insomnia
  • tachycardia
  • cardiac murur
  • diarrhe and increased fecal volume
  • serum enzymes may be elevated = stress leukogram
75
Q

Beyond clinical signs, what are some other things that might be seen with hyperthyroidism? (3)

A
  • heat insensitivity = feel hot, so will seek cold
  • unkempt coat
  • protuding eyes (more in human med)
76
Q

Diagnosis of hyperthyroidism

A
  • serum total T4 > 4 microgram/ decaliter
  • borderline cases differentiated by TSH stimulation test
  • thyroid scan - only necessary if no goiter
77
Q

Why are borderline cases of hyperthyroidism differentiated by TSH stimulation test?

A

tumors are not stimulated by TSH

78
Q

Treatment of Hyperthyroidism

A
  • antithyroid drugs
  • radioactive iodine
  • surgery = partial/complete thyroidectomy
  • propanolol for tachycardia and excess adrenergic effects
79
Q

Antithyroid drug can be used in the treatment of hyperthyroidism. Two examples methimazole and propylthiouracil. Why are they used?

A

methimazole = inhibits thyroperoxidase

propylthiouracil = goiterogenic compound

80
Q

Hypothroidism Signs (5)

A
  • cretinism
  • myxedema
  • lymphocytic thyroiditis
  • iodine deficiency
  • heat seeking
81
Q

How much of the thyroid may be non-functional before clinical hypothyroidism is apparent?

A

> 75%

82
Q

Additional signs of hypothyroidism

A
  • poor response to TSH stimulation
  • alopecia on dorsal proximal tail
  • lethargy
  • infertility
  • weight gain
  • hyperpigmentation of skin and thickening of skin
  • bracycardia, cardiac arrhythmias, hyperlipidemia
83
Q

Diagnosis of Hypothyroidism

A
  • hypercholesterolemia couple with other clinical signs
  • serum total T4 (and TSH)
  • biopsy of thyroid
84
Q

Treatment of Hypothroidism

A
  • Administer synthetic T4 (levothyroxine)

- Allow 6 weeks for improvement

85
Q

Hyperparathyroidism

A
  • excess PTH
  • results in disturbances of serum levels of Ca2+ (increases serum Ca2+)
  • affects metabolism of bone
86
Q

How is the metabolism of bone affected by hyperparathyroidism?

A
  • increased bone resorption
  • decreased radiographic density
  • incomplete fractures
87
Q

Signs of hyperparathyroidism

A
  • depressed mentation
  • muscular weakness
  • peptic ulcers
  • lethargy
  • renal failure
88
Q

Primary hyperparathyroidism

A
  • pit. independent
  • less common than secondary hyperparathyroidism
  • adenoma of chief cells
89
Q

Signs of primary hyperparathyroidism

A
  • calcification of soft tissues
  • loss of lamina dura of teeth
  • subperiosteal cortical resorption
  • mineralization of CT = relatedly, secondary renal probs
  • hypercalciuria, hypercalcemia
  • hyperphosphaturia, HYPOphosphatemia
90
Q

Secondary hyperparathyroidism (RENAL)

A
  • RENAL hyperparathyroidism (secondary) = caused by chronic renal failure
  • renal damage reduces 1,25-Vit. D synthesis

As [phosphate] increases, [Ca2+] decreases

  • hyperphosphatemia
  • NORMOcalcemia, HYPOcalciuria
  • rubber-jaw disease, loose teeth
91
Q

Secondary hyperparathyroidism (NUTRITIONAL)

A

-caused by nutritional deficiencies, mineral imbalances

ETIOLOGY

  • low calcium content of foods
  • excess phosphorus content of food
  • ratio: low Calcium, high phosphorus
  • inadequate Vit. D
  • hyperphosphaturia
  • mild hypocalcemia, hypocalciuria
  • vertebral fractures, lameness, reluctance to move
92
Q

Hypoparathyroidism

A

hyposecretion of PTH due to:

  • lymphocytic parathyroiditis
  • surgery for hyperthyroidism
93
Q

Clinical Signs of hypoparathyroidism

A

-serum calcium must be

94
Q

Lab findings/ diagnosis of hypoparathyroidism

A

-serum calcium 5.0 mg/dl

95
Q

Other causes of hypocalcemia

A
  • hypoalbuminemia

- hypercalcitonism

96
Q

Treatment of Hypoparathyroidism, acute hypocalcemia

A

IV calcium gluconate

97
Q

Treatment of Hypoparathyroidism, chronic hypocalcemia

A
  • oral calcium carbonate
  • oral Vit. D
  • low phosphorus diet

Physio II (8 decks)

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