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Pathology > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Hormones secreted by acidphils of anterior pituitary

A

Growth hormone/somatotrophin (by somatotropes)
Prolactin/lueteotrophic hormone (by luteotrophs)

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2
Q

Hormones secreted by basophils of anterior pituitary

A

Thyroid stimulating hormone (thyrotrophs)
LH/FSH (gonadotrophs)

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3
Q

Hormones secreted by chromophobes of anterior pituitary

A

Adrenocorticotropic hormone
Melanocyte secreting hormone

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4
Q

Most likely cause of hyperfunction of pituitary gland

A

Neoplasm!

(Functional corticotroph adenoma - over production of ATCH by anterior pituitary)

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5
Q

Impact of excess cortisol

A

Changes due to:
Gluconeogenic, lipolytic, protein catabolic, anti-inflammatory action of glucocorticoids

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6
Q

Sequeale of corticorph adenoma

A

Compression, hemorrhage —> CNS damage

Cortical hyperplasia (by action of ACTH on adrenal glands)

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7
Q

Types of corticotroph adenoma / species predilection

A

Pars distalis adenoma (dogs)

Pars intermedia adenoma (horses, less commonly in dogs)

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8
Q

Equine pituitary pars intermedia dysfunction (PPID)

A

Adenoma of pars intermedia
Similar to Cushing’s of other animals

Autonomous production of POMC (pro-opiomelanocortin) peptides (inc in ACTH activity), loss of normal inhibitory control

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9
Q

Pathogenesis of PPID

A

Dec in dopamine which normally inhibits cells in pars intermediate

Loss of inhibition —> increased peptide synthesis

Hypertrophy + hyperplasia —> adenoma formation

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10
Q

Actions of POMC in PPID

A

In pars distalis —> ATCH, b=endorphin, b-lipotropin

In pars intermediate —> ACTH —> a-MSH, corticotrophin-like intermediate lobe peptide, b-MSH, b-endorphin

Plasma cortisol inhibits ATCH secretion by pars distalis (but little effect on pars intermedia)

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11
Q

Sequelae of adenoma of pars intermedia

A

Compression of hypothalamus —> deranged function

Compression —> fever, sweating, hirsutism

POMC —> inc ACTH activity —> Cushings-like disease

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12
Q

Clinical syndromes of PPID

A

Weight loss muscle weakness, atrophy
Increased susceptibility to infection / poor would healing
PU/PD, increase appetite, somnolence, intermittent fever

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13
Q

Hypertrichosis

A

(Hirsutism), long hair/hair overgrowth due to failure of seasonal shedding

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14
Q

Hyperhidrosis

A

Generalized sweating, excess sweating

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15
Q

Equine Cushings

A

Hypertrichosis/hirsutism
Hyperhidrosis
Laminitis

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16
Q

Functional acidophilus adenoma

A

Tumor of pituitary overproducing GH —> over production of tissue —> acromegaly

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17
Q

Feline acromegaly

A

Cardiomegaly+ enlargement of various organs (liver, kidney)
New bone deposition
Increased weight due to inc muscle/organ/bone mass

Respiratory stridor (due to thickening airy MM)
Severe, insulin-resistant DM due to GH-induced IR

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18
Q

Hypofunction of pituitary due to

A

Compressive disease (tumor, can cause neuro signs)
Trauma
Congenital defects

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19
Q

Nonfunctional pituitary tumors

A

Clinical signs due to compression, decrease in secretion of tropic hormones

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20
Q

Pituitary carcinoma

A

Usually nonfunctional, compressive, infiltrative

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21
Q

Diabetes insipidus

A

Hypophyseal form, hypofunction of pituitary gland

ADH in low levels from compression/destruction of neurohypophysis —> can not trigger increased water absorption in kidneys

Clinical manifestation: increased urine production

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22
Q

Nephrogenic DI

A

Target cells in kidney not responding to ADH
- congenital or acquired in animals with pyometra

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23
Q

Juvenile panhypopituitarism

A

Failure of differentiation of pharyngeal ectoderm —> undifferentiated cells produce fluid —> cysts in sella tursica —> absence of adnohypophysis

Pituitary dwarfism

Autosomal recessive in German Shepard (occasionallly in other dogs)

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24
Q

Clinical signs of panhypopituitarism

A

Slow growth, small stature
Failure to gain adult coat, delayed eruption of permanent teeth, delayed epiphyseal closure, infantile external genitalia

Due to growth hormone deficiency

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25
Q

Pituitary cysts

A

Relatively common finding in dogs

Often incidental

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26
Q

Cause of primary adrenal gland hyperfunction

A

Adrenocortical adenoma / carcinoma

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27
Q

Cause of secondary adrenal gland hyperfunction

A

Corticotroph adenoma in pituitary (PDH)
(Cushing’s syndrome)

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28
Q

Cause of hyperfunction of adrenal medulla

A

Pheochromocytoma

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29
Q

Causes of Cushing’s syndrome

A

Anterior pituitary tumor (inc in ACTH —> inc cortisol)

Adenocortical tumor (inc in cortisol)

Exogenous steroids (also produces adrenal atrophy)

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30
Q

Predilection based on cause of Cushing disease

A

PDH (pituitary tumor) - middle aged to older, Poodles, Dachshunds, German Shepard, boxers

AT (adrenocortical) - older female dogs

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31
Q

Signs of Cushings

A

Inc ALP
Pendulous abdomen, pot-belly
PU/PD (IN DOGS!)
Increased appetite
Hepatomegaly (steroid hepatopathy?)
Panting

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32
Q

Clinical manifestations of Cushings

A

Muscle atrophy
Alopecia, thin skin
Calcinosis cutis (mineralization of collagen in dermis)
Increased susceptibility to pathogens
Diabetes mellitus

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33
Q

Treatment of Cushings

A

Lysodren (mitotane) - controlled destruction of cortex (inhibits adrenal steroidogenesis, direct cytotoxic effect on adrenal cortex)

Trilostane - newer drug, blocks enzyme in steroidogenesis pathway

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34
Q

Cushings in cats

A

Rare
Concurrent with DM
No steroid hepatopathy
May have fragile skin (dermal atrophy)

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35
Q

Sequelae of loss of mineralcorticoid activity

A

Potassium elevated in extracellular fluid
Sodium decreased in extracellular fluid
Volume of extracellular fluid/blood decreases

—> heart poorly function —> cardiac output declines —> shock

36
Q

Adrenocortical insufficiency (hypoadrenocorticism)

A

Idiopathic loss/atrophy of all 3 cortical zones
Cortex:medullary ratio < 1
Gradual process, exacerbated by stress

aka Addison’s disease

Thought to be autoimmune disease in dogs

37
Q

Clinical signs of Addison’s

A

Weakness/lethargy
Weak femoral pulse
Dehydration, bradycardia
Hypothermia
Abdominal pain, GI signs
Hyponatremia, hyperkalemia, unconcetrated urine

38
Q

Hormonal response to Addison’s

A

Decreased aldosterone (hypovolemia, hypotension, reduced CO, hyperkalemia —> cardiac dysfunction)
Decreased cortisol (GI signs, dminished energy metabolism, impaired stress tolerance)

39
Q

Most common cause of secondary hypoadrenocorticism

A

Long-term exposure to exogenous corticosteroids —> negative feedback to hypothalamus/pituitary —> dec ACTH secretion

(Treatment of PDH with mitotane can destroy glomerulosa - use with care)

40
Q

“Atypical Addison’s”

A

Incorrectly named secondary hypoadrenocorticism

Clinical signs due to decreased glucocorticoids (not loss of all three cortical zones of adrenal gland)

41
Q

Discoid lupus

A

Disease in some dogs
Only affects nose —> erosions of nose

42
Q

Steroid withdrawal

A

Decrease in cortisol —> anorexia, vomiting, abdominal pain, weight loss, diminished energy metabolism, impaired stress tolerance

43
Q

Treatment of steroid withdrawal (with associated adrenal atrophy)

A

Physiologic prednisone

44
Q

Pheochromocytoma

A

Tumor of medullary chromatin cells of adrenal medulla —> medullary hyperfunction

Benign is more common (most incidental findings at necropsy)

Malginant tumors will metastasize widely, may invade vena cava

45
Q

Clinical signs of medullary hyperfunction

A

Tachycardia, hypertension, hyperglycemia, vasoconstriction, diffuse sweating

Difficult to document in animals

May invade vena cava

46
Q

Which cells produce thyroid stimulating hormone?

A

Basophils of anterior pituitary

47
Q

Which part of the pituitary can cause thyroid disease if dysfunctional?

A

Basophils of anterior pituitary

48
Q

Thyroid disorders - species predilection

A

Feline —> hyperthyroidism

Canine —> hypothyroidism

49
Q

Feline hyperthyroidism

A

Common in aged cats

Multifocal, firm, brown nodules compromised of well-differentiated thyroid tissue

Often bilateral

Elevated T4 and T3

50
Q

Clinical and pathologic findings of feline hyperthyroidism

A

Weight loss with ravenous appetite
Nervousness, tachycardia
Heat intolerance, weakness

Cardiomegaly —> arrhythmia, saddle thromboemboli, death

51
Q

Causes of canine hypothyroidism

A

Lymphocytic thyroiditis (immune-mediated)

Idiopathic atrophy

52
Q

Lymphocytic thyroiditis

A

Immune-mediated hypothyroidism

Infiltration of thyroid glands by lymphocytes, plasma cells, macrophages

75% of gland destroyed before clinical signs

Genetic component

Release of antigens into circulation by thyroid gland damage; circulating autoantibodies to thyroglobulin

53
Q

Clinical manifestation of canine hypothyroidism

A

Slowing of metabolism —> lethargy, exercise intolerance, heat speaking, mental dullness, weight gain, slow pulse

Neuromusclar, repro problems

Anemia and hypercholesteremia *** (can cause atherosclerosis)

54
Q

Potential dermatological lesions associated with canine hypothyroidism

A

Scaling (dandruff)

“Rat” tail

Myxedema (mucus deposits in skin) —> “tragic face”

Secondary infections —> otitis/pyoderma

55
Q

Diagnosis of hyper/hypothyroidism

A

Measurement of FREE T4 (total T4 not accurate)

56
Q

Iodine deficiency

A

Fetal development problems - mental retardation, deaf-mutism, spasticity

Goiter - bilateral enlargement of thyroid glands (due to impaired synthesis of thyroid hormone)

57
Q

Goiter

A

Bilateral enlargement of thyroid glands due to non neoplastic + non inflammatory causes

Reflects impaired thyroid hormone synthesis

—> Euthyroid or hypothyroid state

58
Q

Dietary causes of goiter

A

Deficiency of iodine

Ingestion of goitrogenic substances (interfere with hormone synthesis; drugs, plants, Brassica - pants in cabbage/mustard/cruciferous family)

Excessive iodine (rare)

59
Q

non-dietary causes of goiter

A

Hereditary defects in enzymes for synthesis of thyroid hormones

60
Q

Other thyroid diseases

A

Cysts in thyroid gland (common, fairly incidental)
Thyroid carcinoma (dogs)

61
Q

Glandular cells involved in Ca homeostasis

A

Chief cells (parathyroid gland) —> increase Ca in blood

Thyroid C-cells (calcitonin) —> decrease Ca in blood

62
Q

Actions of Parathyroid hormone

A

Increases bone resorption

Promotes reabsorption of Ca by kidney; dumping of P

Increases intestinal absorption of Ca

63
Q

Actions of calcitonin

A

Counters the action of parathyroid hormone in bone/kidney

Inhibits bone resorption

64
Q

Action of vitamin D (cholecalciferol)

A

Increases absorption of Ca and phosphorus from intestines
Required for mineralization of bone matrix/endochondral ossification in young animals

Modified in liver, then kidneys (sites regulated by PTH)

65
Q

Hyperparathyroidism

A

Too much parathyroid hormone

66
Q

Cause of primary hyperparathyroidism

A

Functional parathyroid adenoma (dogs)

67
Q

What happens to blood calcium in hyperparathyroidism

A

Ca levels high because do not respond to negative feedback

68
Q

Clinical signs of hyperparathyroidism

A

Anorexia, muscle weakness, PU/PD, stiff gait +/- fractures, thickened mandible or loose teeth (rare)

Elevated serum PTH + Ca

69
Q

Most common cause of secondary hyperparathyroidism

A

Chronic renal disease

70
Q

Mechanism of secondary renal hyperparathyroidism

A

Dec in P excretion (hyperphosphatemia)
Dec active vit D3 —> dec intestinal absorption of Ca

High P lowers serum calcium (precipitation) —> PTH secretion —> parathyroid hyperplasia —> osteocyte release of Ca

71
Q

Clinical signs of secondary hyperparathyroidism

A

Chronic renal disease - vomiting, PU/PD, dehydration, breath odor of ammonia
Fibrous osteodystrophy “rubber jaw” - uncommon, usually in young animals

72
Q

Pseudohyperparathyroidism

A

Parathyroid related protein / related substances secreted from certain tumors

Humoral hypercalcemia of malignancy (adenocarcinoma of apocrine glands of the anal sac; lymphosarcoma)

PTH is low, parathyroid glands are ATROPHIED

73
Q

Tumors causing pseudohyperparathyroidism

A

Anal gland sac carcinoma

Lymphosarcoma

Malignant tumors growing within bone

Malignant neoplasms which metastasize to bone

74
Q

Hypoparathyroidism causes

A

Iatrogenic (inadvertent removal of parathyroid glands - i.e. removal of thyroid nodules in cats)

Idiopathic hypoparathyroidism - rare, in dogs (lymphocytic parathyroiditis —> dec Ca —> nervousness, ataxia w muscle tremor —> tetany and seizures)

75
Q

Actions of insulin

A

Increases cell uptake / storage of glucose

Adipose tissue: promote storage, prevent fat breakdown
Muscle: promote protein synthesis
Liver: increase glycogen synthesis

76
Q

Actions of glucagon

A

Maintains serum glucose levels, antagonist to insulin

Adipose tissue: increase lipolysis

Increase glycogenolysis, increases gluconeogenesis

77
Q

Causes of hyperfunction of the endocrine pancrease

A

Iatrogenic insulin overdose

Functional tumor of islet cells

78
Q

Insulinoma

A

a Beta cell tumor

Common in ferrets, uncommon in dogs, rare in cats

Malignant in dogs; benign in ferrets

79
Q

Clincial signs of beta cell hyperfunction

A

In coordination, ataxia, weakness, syncope, muscle twitching, blindness, polyphasic, seizures

**in ferrets, weakness is seen but seizures uncommon

80
Q

Glucagonoma

A

Very rare tumor, may be seen in dogs

81
Q

Diabetes mellitus

A

Relative or absolute insulin deficiency; prevents target cell utilization of glucose

Hyperglycemia, glucosuria

82
Q

Type I DM

A

Genetic susceptibility
Immunologic destruction of beta cells —> insulin insufficiency
CIRCULATING AUTOANTIBODIES to islet components precedes hyperglycemia

Typically DM presents in dogs

83
Q

Type II DM

A

Characterized by insulin resistance and “dysfunctional” beta cells

Genetic susceptibility with long lag phase before hyperglycemia

Diet, exercise, hypoglycemic drugs

Cats often Type II DM

84
Q

Manifestations of DM

A

Hyperglycemia —> glycosuria —> osmotic diuresis leading to PU/PD
Polyphagia
Weight loss (cell “starvation”
Increased lipolysis —> ketoacidosis
Glucose enters lens —> cataracts
Fatty liver —> lack of insulin breakdown of lipids/protein, inc lipids in hepatocytes

85
Q

Histologic changes in DM

A

Typically none

Can see islet Amyloidosis in cats

Pathology (21 decks)

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