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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
Pituitary cysts
Relatively common finding in dogs Often incidental
26
Cause of primary adrenal gland hyperfunction
Adrenocortical adenoma / carcinoma
27
Cause of secondary adrenal gland hyperfunction
Corticotroph adenoma in pituitary (PDH) (Cushing’s syndrome)
28
Cause of hyperfunction of adrenal medulla
Pheochromocytoma
29
Causes of Cushing’s syndrome
Anterior pituitary tumor (inc in ACTH —> inc cortisol) Adenocortical tumor (inc in cortisol) Exogenous steroids (also produces adrenal atrophy)
30
Predilection based on cause of Cushing disease
PDH (pituitary tumor) - middle aged to older, Poodles, Dachshunds, German Shepard, boxers AT (adrenocortical) - older female dogs
31
Signs of Cushings
Inc ALP Pendulous abdomen, pot-belly PU/PD (IN DOGS!) Increased appetite Hepatomegaly (steroid hepatopathy?) Panting
32
Clinical manifestations of Cushings
Muscle atrophy Alopecia, thin skin Calcinosis cutis (mineralization of collagen in dermis) Increased susceptibility to pathogens Diabetes mellitus
33
Treatment of Cushings
Lysodren (mitotane) - controlled destruction of cortex (inhibits adrenal steroidogenesis, direct cytotoxic effect on adrenal cortex) Trilostane - newer drug, blocks enzyme in steroidogenesis pathway
34
Cushings in cats
Rare Concurrent with DM No steroid hepatopathy May have fragile skin (dermal atrophy)
35
Sequelae of loss of mineralcorticoid activity
Potassium elevated in extracellular fluid Sodium decreased in extracellular fluid Volume of extracellular fluid/blood decreases —> heart poorly function —> cardiac output declines —> shock
36
Adrenocortical insufficiency (hypoadrenocorticism)
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
Clinical signs of Addison’s
Weakness/lethargy Weak femoral pulse Dehydration, bradycardia Hypothermia Abdominal pain, GI signs Hyponatremia, hyperkalemia, unconcetrated urine
38
Hormonal response to Addison’s
Decreased aldosterone (hypovolemia, hypotension, reduced CO, hyperkalemia —> cardiac dysfunction) Decreased cortisol (GI signs, dminished energy metabolism, impaired stress tolerance)
39
Most common cause of secondary hypoadrenocorticism
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
“Atypical Addison’s”
Incorrectly named secondary hypoadrenocorticism Clinical signs due to decreased glucocorticoids (not loss of all three cortical zones of adrenal gland)
41
Discoid lupus
Disease in some dogs Only affects nose —> erosions of nose
42
Steroid withdrawal
Decrease in cortisol —> anorexia, vomiting, abdominal pain, weight loss, diminished energy metabolism, impaired stress tolerance
43
Treatment of steroid withdrawal (with associated adrenal atrophy)
Physiologic prednisone
44
Pheochromocytoma
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
Clinical signs of medullary hyperfunction
Tachycardia, hypertension, hyperglycemia, vasoconstriction, diffuse sweating Difficult to document in animals May invade vena cava
46
Which cells produce thyroid stimulating hormone?
Basophils of anterior pituitary
47
Which part of the pituitary can cause thyroid disease if dysfunctional?
Basophils of anterior pituitary
48
Thyroid disorders - species predilection
Feline —> hyperthyroidism Canine —> hypothyroidism
49
Feline hyperthyroidism
Common in aged cats Multifocal, firm, brown nodules compromised of well-differentiated thyroid tissue Often bilateral Elevated T4 and T3
50
Clinical and pathologic findings of feline hyperthyroidism
Weight loss with ravenous appetite Nervousness, tachycardia Heat intolerance, weakness Cardiomegaly —> arrhythmia, saddle thromboemboli, death
51
Causes of canine hypothyroidism
Lymphocytic thyroiditis (immune-mediated) Idiopathic atrophy
52
Lymphocytic thyroiditis
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
Clinical manifestation of canine hypothyroidism
Slowing of metabolism —> lethargy, exercise intolerance, heat speaking, mental dullness, weight gain, slow pulse Neuromusclar, repro problems Anemia and hypercholesteremia *** (can cause atherosclerosis)
54
Potential dermatological lesions associated with canine hypothyroidism
Scaling (dandruff) “Rat” tail Myxedema (mucus deposits in skin) —> “tragic face” Secondary infections —> otitis/pyoderma
55
Diagnosis of hyper/hypothyroidism
Measurement of FREE T4 (total T4 not accurate)
56
Iodine deficiency
Fetal development problems - mental retardation, deaf-mutism, spasticity Goiter - bilateral enlargement of thyroid glands (due to impaired synthesis of thyroid hormone)
57
Goiter
Bilateral enlargement of thyroid glands due to non neoplastic + non inflammatory causes Reflects impaired thyroid hormone synthesis —> Euthyroid or hypothyroid state
58
Dietary causes of goiter
Deficiency of iodine Ingestion of goitrogenic substances (interfere with hormone synthesis; drugs, plants, Brassica - pants in cabbage/mustard/cruciferous family) Excessive iodine (rare)
59
non-dietary causes of goiter
Hereditary defects in enzymes for synthesis of thyroid hormones
60
Other thyroid diseases
Cysts in thyroid gland (common, fairly incidental) Thyroid carcinoma (dogs)
61
Glandular cells involved in Ca homeostasis
Chief cells (parathyroid gland) —> increase Ca in blood Thyroid C-cells (calcitonin) —> decrease Ca in blood
62
Actions of Parathyroid hormone
Increases bone resorption Promotes reabsorption of Ca by kidney; dumping of P Increases intestinal absorption of Ca
63
Actions of calcitonin
Counters the action of parathyroid hormone in bone/kidney Inhibits bone resorption
64
Action of vitamin D (cholecalciferol)
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
Hyperparathyroidism
Too much parathyroid hormone
66
Cause of primary hyperparathyroidism
Functional parathyroid adenoma (dogs)
67
What happens to blood calcium in hyperparathyroidism
Ca levels high because do not respond to negative feedback
68
Clinical signs of hyperparathyroidism
Anorexia, muscle weakness, PU/PD, stiff gait +/- fractures, thickened mandible or loose teeth (rare) Elevated serum PTH + Ca
69
Most common cause of secondary hyperparathyroidism
Chronic renal disease
70
Mechanism of secondary renal hyperparathyroidism
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
Clinical signs of secondary hyperparathyroidism
Chronic renal disease - vomiting, PU/PD, dehydration, breath odor of ammonia Fibrous osteodystrophy “rubber jaw” - uncommon, usually in young animals
72
Pseudohyperparathyroidism
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
Tumors causing pseudohyperparathyroidism
Anal gland sac carcinoma Lymphosarcoma Malignant tumors growing within bone Malignant neoplasms which metastasize to bone
74
Hypoparathyroidism causes
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
Actions of insulin
Increases cell uptake / storage of glucose Adipose tissue: promote storage, prevent fat breakdown Muscle: promote protein synthesis Liver: increase glycogen synthesis
76
Actions of glucagon
Maintains serum glucose levels, antagonist to insulin Adipose tissue: increase lipolysis Increase glycogenolysis, increases gluconeogenesis
77
Causes of hyperfunction of the endocrine pancrease
Iatrogenic insulin overdose Functional tumor of islet cells
78
Insulinoma
a Beta cell tumor Common in ferrets, uncommon in dogs, rare in cats Malignant in dogs; benign in ferrets
79
Clincial signs of beta cell hyperfunction
In coordination, ataxia, weakness, syncope, muscle twitching, blindness, polyphasic, seizures **in ferrets, weakness is seen but seizures uncommon
80
Glucagonoma
Very rare tumor, may be seen in dogs
81
Diabetes mellitus
Relative or absolute insulin deficiency; prevents target cell utilization of glucose Hyperglycemia, glucosuria
82
Type I DM
Genetic susceptibility Immunologic destruction of beta cells —> insulin insufficiency CIRCULATING AUTOANTIBODIES to islet components precedes hyperglycemia Typically DM presents in dogs
83
Type II DM
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
Manifestations of DM
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
Histologic changes in DM
Typically none Can see islet Amyloidosis in cats

Pathology (21 decks)

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