Endocrine Flashcards

(94 cards)

1
Q

What is the structure of the Endocrine System

A
  • Derived from neural ectoderm
    • Strong association with vascular and neural tissue
  • Organs include:
    • Pituitary gland
    • Thyroid gland
    • Parathyroid gland
    • Adrenal gland
    • Gonads
    • Endocrine pancreas
    • Cemoreceptor organs
    • Pineal gland
    • Adipose tissue
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2
Q

What is the function of the Endocrine System

A

Maintain homeostasis

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3
Q

How does the endocrine system maintain homeostasis?

A
  • Hormone are the mediators of homeostasis
    • Polypptides
    • Steroids
    • Catecholamines and iodothyronines
  • Feedback systems regulate most hormone concentrations
    • Hypothalamus → pituitary → Target tissue axis
  • Some Hormonesrespond to plasma concentrations of vrious products or nervous stimuli
    • Thyroid C-cells, Parathyroid Cheif cells, adrenal medulla
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4
Q

What are the different types of dysfunction of the Endocrine System?

A
  • Increaed function
  • Decreased function
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5
Q

What are the types of increased function of the Endocrine System?

A
  • Primary hyperfunction
    • increasd hormone secretion by an abnormal gland
  • Secondary hyperfunction
    • Increased hormone secretion by a normal endocrine gland that is excessively stimulated
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6
Q

What are the types of decreased function of the Endocrine System?

A
  • Primary hypofunction
    • decreased hormone secretion by an abnormal glad
  • Seconday hypofunction
    • Decreased hormone secretion by a normal endocrine gland that is inadequately stimulated
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7
Q

What is the pattern of disease seen in the endocrine system?

A
  • Metabolic processes are altered with any enocrine abnormality
  • Neoplasia is the most common pathology pattern
  • Cell adaptation is fairly common; atrophy, hyperplasia
  • Immunopathology (autoimmunity) is relatively common as a pattern of endocrine disease
  • Developmental, cell injury, vascular disturbanes and inflammation are less common patterns associated with endocrine disease
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8
Q

What are the causes of disease in the Endocrine System?

A
  • Genetic alterations are important as predisposing factors for neoplasia, immunopathologic and developmental endocrine diseases
  • Nutritional factors can have significant impact on hormone-regulated homeostasis
  • Infectious, chemical and physical insults are less common causes of endocrine disease
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9
Q

What is the structure of the pituitary gland?

A
  • Anterior lobe (adenohypophysis)
  • Posterior lobe (Neurohypophysis)
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10
Q

What are the parts of the Adenohypophysis and what hormones do they produce?

A
  • “Anterior Lobe”
  • Pars dstalis
    • acidophils (somatotrophs and Gonadotrophs)
      • GH and LTH
    • Basophils (Gonadotrophs and Thyrotrophs)
      • LH, FSH, and TH
    • Chromophobes (Corticotrophs and melaotrophs)
      • ATCH and MSH
  • Pars intermedia
    • Melnotrophs
  • Pars Tuberalis
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11
Q

What is the structure of the Neurohypophysis?

A
  • “Posterior Lobe”
  • Hypothalamic neurosecretory neurons
    • Paraventricular and supraoptic nuclei
      • ADH and Oxytocin
  • Infundibular stalk
  • Pars nervosa
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12
Q

What are the functions of the hormones from the Adenohypophysis

A
  • Growth Hormone (somatotrophin)
    • regulates growth and metabolism
  • Luteotropic Hormone
    • Stimulates progesterone secretion
  • Luteinizing Hormone
    • Stimulates estrogen secretion
  • Follicle Stimulating Hormone
    • Stimulates ovarian follicle growth and spermatogenesis
  • Thyroid Stimulating Hormone (Thyrotrophinc, TSH)
    • Stimulats thyroid hormone secretion
  • Adrenocorticotrophic Hormone
    • Stimulates glucocorticoid secretion
  • Melanocyte Stimulating Hormone
    • stimulates melanocytes
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13
Q

What are the functions of the hormones from the Neurohypophysis?

A
  • Antidiuretic Hormone
    • Regulates water exretion
  • Oxytocin
    • Stimulates smooth muscle contraction
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14
Q

What are the types of dysfunction of the Pituitary gland?

A
  • Increased Hormone Activity
  • Decreased Hormone Activity
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15
Q

What can cause increased hormone activity of the pituitary gland?

A
  • Functional neoplasia
  • Increased stimulation by hypothalamus
  • Hormone-like substances
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16
Q

What can cause decreased hormone activity of the pituitary gland?

A
  • Destructive lesions
  • Non-responsive target cells
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17
Q

What are the pathology patterns seen in the pituitary gland?

A
  • Neoplasia
    • functional or non-functional
  • Cell adaptaion
    • Hyperplasia and atrophy
  • Developmental anomalies
    • Aplasia, hypoplasia or cysts
  • Immunopathology
    • Autoimmunity (lymphoplasmacytic hypophysitis)
  • Inflammation
    • Uncommon
  • Metabolic
    • All hormonal dysfunctions will result in metabolic alterations
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18
Q

What causes pathology of the pituitary gland?

A
  • Genetic injury
    • inherited or acquired
  • Infectious agents
    • Uncommon
  • Nutritional
  • Chemical
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19
Q

What is Chromophobe Adenoma in dogs?

A
  • Functional Adenoma
  • Neoplastic Chromophobes are unregulated and produce large amounts of ACTH
  • Excessive ACTH causes diffuse adrenocortical hyperplasia
    • “Hyperadrenocorticism” “Cushing’s Disease”
  • Approximately 80-90% of cases of canine hyperadrenocorticism are due to pituitary neoplasia
  • Most Common Pituitary tumor of dogs
    • Increased frequency in Boston Terriers, Beagles, Boxers, Dachshunds, and Miniature Poodles
  • May arise from hyperplastic nodules that mutate to become clonal
  • Microadenoma
    • More likely to be functional and produce excess ACTH
  • Macroadenoma
    • Less likely to be functional and act as space-occupying mass
      • Hypopituitarism or hypothalamic compression
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20
Q

What is Pars intermedia adenoma?

A
  • Pars intermedia is the second most common location for chromophobe adenoma in dogs
    • Can be functional or compressive, just like those from the pars distalis
      • Compressive = hypopituitarism or diabetes insipidus due to pressure on the hypothalamus or destruction of the neurohypophysis
  • Pars intermedia dysfunction is the most common endocrine abnormality of horses
    • most common in older horses
    • Possibly due to age-related oxidative injury of dopaminergic neurons
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21
Q

What is pituitary pars intermedia dysfunction in horses?

A
  • Decreased dopamine production results in increased activity of melanotrophs
    • Melanotrophs produce proopiomelanocortin (POMC)
    • POMC > ACTH > a-MSH + B-endorphin + corticotrophin-like intermediate peptide
  • Signs include increased hair growth (hypertrichosis/hirsutism), increased adipose tissue deposition, weight loss
  • Lesions range from diffuse hyperplasia to micro/macro adenoma
  • Hirsutism may be due to increased POMC activity or hypothalamic compression
    • Compression can interfere with thermoregulation and appetite centers
  • Melanotrophs are regulated by dopaminergic neurons and not the hypothalamic-pituitary-adrenal axis
    • Adrenal glands are usually normal
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22
Q

What is somatotroph adenoma?

A
  • Arise from somatotrophs (Acidophils)
    • Uncommon, mainly cats, dogs, sheep
    • Functional adenoma (increased growth hormone) in cats
      • Increased production of insulin-like growth factor 1 by the liver
        • Growth of soft tissue and bone (acromegaly, mainly facial bones)
        • Insulin-resistant diabetes mellitus (Type 2)
    • Non-functional adenoma can cause panhypopituitarism and hypothalamic compression
  • Basophil Adenoma
    • Rare
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23
Q

What are Pituitary Cysts?

A
  • Mainly in brachycephalic dogs
  • Abnomal development in or around the pituitary gland
    • Craniopharyngeal duct cyst
    • Pharyngeal hypophyseal cyst
    • Oropharyngeal ectoderm cyst
  • Can compress and damage surrounding structures
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24
Q

What are the types of pituitary cysts?

A
  • Craniopharyngeal duct cysts
    • Diabetes insipidus, pituitary hypofunction
  • Pharyngeal hypophyseal cysts
    • Respiratory distress
  • Oropharyngeal ectoderm cysts
    • Panhypopituitarism
    • Juvenile hypopituitarism in GS
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25
What is Pituitary dwarfism?
* Failure of Rathkes pouch ectoderm to differentiate into the adenohypophysis * **Autosomal recessive in GS** * Also occurs in Spitz, Toy Pinschers, and Karelian bear dogs * Generally normal until 2 months of age * **Manifestations due to decreased growth hormone** * Decreased insulin-like growth factor 1 * Decreased growth (retain infantile characteristics) * Retention of puppy hair progressing to alopecia
26
What is Craniopharyngioma?
* Neoplastic remnants of Rathkes pouch oropharyngeal ectoderm * Occurs in Young dogs, Rare * Hypothalamic destruction and decreased hypothalamic trophic hormones
27
What is a non-functional adenoma?
* Dogs, cats, and others * These can arise from any cell, but often of chromophobe origin * Hypopituitarism with endocrine gland atrophy and hypofunction
28
What causes Pituitary Gland Inflammation?
* Pituitary Abscesses * Most common in Cattle * Secondary to nasal septal infections * **Acts as a space occupying lesion** * **Blindness, depression, drooling, tongue prolapse** * Can mimic rabies
29
What are the Neurohypophysis diseases?
* Pituitary Diabetes Insipidus * Destruction of the neurohypophysis or supraoptic nuclei of the hypothalamus * Decreased ADH production or release * PU/PD, Dilute urine * Decreased Oxytocin * Nephrogenic diabetes insipidus * Primary renal disease, ADH is normal
30
What is the structure of the Adrenal Gland?
* **Cortex** (mesoderm origin) * Zona glomerulosa * Mineralocorticoids * Zona fasciculata * Glucocorticoids * Zona reticularis * Sex steroids * **Medulla** (Neural crest origin) * Catecholamines
31
What are the functions of Adrenal Gland?
* **Mineralocorticoids** * **Aldosterone**: * Regulates blood pressure * Promotes sodium retention and potassium excretion by renal tubules * Increases intracellular fluid volume and regulates extracellular fluid volume * **Glucocorticoids** * **Cortisol** and corticosterones * Gluconeogenesis, protein and fat catablism, suppressive for inflammation and immunity * **Sex Steroids** * Progesterone, estrogen and androgens * **Catecholamines** * Epinephrine and norepinephrine
32
What regulates the functions of the Adrenal Gland?
* **Pituitary hormones** * ACTH * **Renin-angiotensin system** * Renin (released from juxtaglomerular cell in response to low blood pressure) cleaves angiotensinogen * Angiotensin I and II contracts vascular smooth muscle and stimulates aldosterone secretion * **Neural Controls** * Catecholamine secretion
33
How can the Adrenal Gland dysfunction?
* Hyperfunction (Hyperadrenocorticism) * Hypofunction (hypoadrenocorticism)
34
What is Hyperadrenocorticism?
* Primary or secondary adrenal involvement * Polyuria, polydipsia, increased appetite, weakness, alopecia, increased infection * "Cushing's Disease"
35
What is Hypoadrenocorticism?
* Primary or secondary adrenal involvement * Anorexia, weight loss, GI disturbances, dehydration * "Addison's Disease"
36
What are the pathology patterns that affect the Adrenal Gland?
* **Metabolic** * Adrenal dysfunction will result in metabolic alterations * **Neoplasia** * Functional or non-functional * **Cell alteration and injury** * Secondary hyperplasia is common secondary to pituitary disease * Secondary atrophy due to hypopituitarism * **Developmental anomalies** * Aplasia, hypoplasia or cysts * **Immunopathology** * Autoimmunity
37
What causes pathology of the Adrenal Gland?
* Genetic predisposition * pituitary neoplasia causing adrenal hyperplasia * Chemical * Exogenous administration of glucocorticosteroids
38
What is adrenal cortical neoplasia?
* Adrenal cortical adenoma or carcinoma * Most arise from the zona fasciculata * Less commonly the zona glomerulosa in cats (hyperaldoteronism) or zona reticularis in ferrets (hyperestrogenism) * Adenomas are more common than carcinoma * old dogs mainly affected, also seen in old cattle * Can be multiple or single, unilateral or bilateral * Contralateral adrenal gland atrophy occurs with functional unilateral neoplasms
39
What is functional adrenal cortical neoplasia?
* Result in hyperadrenocorticism * PU/PD * Increased appetite * Muscle atrophy and weakness * Alopecia (Endocrine dermatopathy) * Increased incidence of infections
40
What is Hyperadrenocrticism?
* Clinical syndrome characterized by increased cortisol/glucocorticosteroids * Cushings disease * Most often due to ACTH-secreting pituitary adenoma * less often due to adrenal cortical adenoma or carcinoma * Lesions associated with hyperadrenocorticism * Hepatic lipidosis and glycogenosis * Epidermal and adnexal atrophy * Systemic mineralization * Skin, lung, muscle, stomach * Lymphoid tissue depletion
41
What are the Functions of glucocorticosteroids?
* Gluconeogenesis * Lipogeness * Protein Catabolic * Anti-inflammatory * Immunosuppression * Inhibition of fibroplasia
42
What is Diffuse Adrenal Cortical Hyperplasia?
* **Diffuse adrenal cortical hyperplasia** * Common in dogs * Occurs secondary to functional chromophobe adenoma of the pituitary gland * Excessive and unregulated secretion of ACTH * **Hyperadrenocorticism is the result** * Signs and lesions are the same as those of hyperadrenocorticism caused by primary adrenal neoplasia
43
What is Adrenal Cortical nodular hyperplasia?
* Common age-related change in dogs, cats and horses * Some of these are functional * Increased ACTH from pituitary hyperplasia or neoplasia * Some are non-functional and of minimal to no clinical significance
44
What are the types of Adrenal Medullary neoplasia?
* Phenochromocytoma * Arise in chromaffin cells of the medulla * Most common in dogs and cattle * Ganglioneuroma and neuroblastoma * Uncommon * Neuroectoderm origin
45
What is Pheochromocytoma?
* Most are non-functional * Functional neoplasia results in systemic hypertension due to norepinephrine secretion * They can be benign or malignant * Malignant neoplasms often invade the great vessels * Approximately 50% metastasize in dogs
46
What is Adrenal Hypoplasia or agenesis?
* Rare condition of dogs * Total agenesis is fatal * Hypoplasia results in variable degrees of hypoadrenocorticism
47
What is Diffuse (Iatrogenic) adrenal cortical atrophy?
* Most common in dogs on long-term glucocorticosteroids therapy * Exogenous glucocorticosteroids result in inhibition of adrenal cortical function and subsequent atrophy
48
What is Idiopathic Adrenal Cortical Atrophy?
* **Uncommon** conditions of dogs and cats * **Immune-mediated damage** and atrophy of the adrenal cortex * May also result from destruction (chronic inflammation) or non-functional neoplasia of the pituitary gland * **Signs usually occur only after 90% of the cortex is destroyed or atrophied** * Results in **hypoadrenocorticism** * **Anorexia and weight loss** * **Diarrhea and dehydration**
49
What Causes Adrenal Gland Destruction?
* A wide variety of processes periodically affect the adrenal gland * This is mainly **due to the rich vascular network a the cortico-medullary junction** * Ex: * Thrombosis due to DIC * Adrenalitis due to infectious emboli * Metastatic neoplasia * 15-30% of metastatic lesion may occur here * Melanotic neoplasia, hemangiosarcoma, Lymphosarcoma
50
What is Hypoadrenocorticism?
* Clinical syndrome characterized by **decreased adrenocortical hormones** * Addison's Disease * Mainly affects the **zona glomerulosa** * immune-mediated most common in Portuguese water dogs, Bearded Collie, Standard poodle * **Hypoaldosteronism** * Hyponatremia and hyperkalemia * Decreased cortisol is also present
51
What is the Structure of the Thyroid Gland?
* Two lobes with a narrow isthmus * Thyroid Epithelial cells * Arranged in follicles * Produce thyroid hormones * Thyroid C-cells * Small aggregates of cells between follicles * Produce calcitonin
52
What is the Function of the Thyroid Gland?
* **Thyroid** **hormones** (Triiodothyronine; T3 and Tetraiodothyronine; T4) * **increased metabolism** (protein synth, glycolysis, gluconeogenesis, lipolysis * **Stimulate heart and neural function** * **Calcitonin** * **Regulation of serum calcium concentration** * **Inhibition of osteoclasts** and bone resorption and synergistic with parathormone to decrease renal phosphorus absorption * **Regulation of adrenal function** * Hypothalamic releasing factors * Pituitary hormones * TSH
53
how can the Thyroid gland Dysfunction?
* Hyperfunction (hyperthyroidism) * Hypofunction (hypothyroidism)
54
What is Hyperthyroidism?
* Usually primary thyroid involvement * Polyphagia, weight loss, weak, tachycardia * Most common in cats
55
What is Hypothyroidism?
* Usually primary thyroid involvement * Inactivity, alopecia, lethargy, weight gain, obesity * Most common in dogs
56
What are the Patterns Pathogenesis of The Thyroid Gland follow?
* **Metabolic** * Thyroid dysfunction will result in metabolic alterations * **Neoplasia** * Usually functional, sometimes non-functional * **Cell alteration and injury** * Hyperplasia and atrophy are common * **Immunopathology** * Autoimmune destruction of the thyroid * **Developmental** * Ectopic thyroid tissue
57
What causes pathogenesis of the Thyroid Gland?
* **Genetic predisposition** * Thyroid neoplasia, hyperplasia or autoimmunity * **Nutritional** * Deficiency of iodine, tyrosine or other thyroglobulin components * **Chemical** * Goitrogenic compounds * Thiouracil, sulfonamides, cyanogenic plants
58
What are the types of Thyroid Gland Neoplasia?
* Thyroid follicular adenoma and carcinoma * Most common in old cats (usually adenoma) * These are often functional resulting in hyperthyroidism * There can be nodules in one or both lobes * Distinction between hyperplasia is sometimes difficult * Less Common in dogs (usually carcinoma) * These are often large, invasive, and metastatic to regional lymph nodes
59
What is Thyroid Follicular Nodular Hyperplasia?
* Most common as an age-related change in horses, dogs, and cats * Most are non-functional and of minimal significance * In cats, some of these may progress to adenoma
60
What is Hyperthyroidism?
* Functional neoplasms result in hyperthyroidism (increased basal metabolic rate) * Polyphagia with weight loss * Hyperactivity and nervousness * Weakness and heat intolerance * Tachycardia * May be due to mutation in the gene coding for the TSH receptor * This is different than Graves disease in humans since there are no auto-antibodies to the TSH receptor in cats
61
What is Parafollicular (C-cell) neoplasia?
* Most common in old bulls and horses * Often malignant in bulls, but incidental in horses * Bulls * These may arise due to long-term ingestion of high calcium rations * High calcium rations also induce hyperplasia initially * Pituitary or adrenal medulla neoplasia may occur concurrently * Some can be functional * Hypercalcitoninism * Vertebral osteophytes and osteosclerosis
62
What is Goiter?
* **Inhibition of thyroid hormone formation** * Nutritional deficiency of iodine or tyrosine * Goitrogenic compound ingestion * Cruciferous plants (Brassica sp.) * Drugs (phenobarbital, rifampin, among others) * Thyroid hyperplasia is the lesion * Cause varies * **Results in hypothyroidism** in postnatal animals * Stillbirth is most common when affected in utero * Neonates can also have signs of hypothyroidism * Myxedema
63
What are the types of Goiter?
* Diffuse: * Excessive TSH stimulus due to decreased thyroid hormones * Iodine deficiency is a common cause * Multinodular * Independent of TSH (autonomous) * Mainly in old cats * Dyshormonogenic * Defective synthesis with normal iodine levels * Due to genetic defect in thyroglobulin synthesis or thyroid peroxidase * Autosomal recessive in sheep and goats
64
What is Idiopathic follicular atrophy?
* Most common in dogs * **There is primary degeneration and atrophy of the thyroid gland** * Results in **hypothyroidism** * Accounts for approximately 50% of the cases of canine hypothyroidism
65
What is Lymphocytic thyroiditsi?
* Type of Thyroid Gland atrophy * Most common in dogs * Autoimmune destruction of the thyroid gland * There is fibrosis, atrophy, and lymphocytic infiltration of the gland * Results in hypothyroidism * Accounts for approximately 50% of these cases in dogs * Similar to Hashimoto's thyroiditis * Auto-antibodies to thyroglobulin
66
What is Hypothyroidism?
* Clinical syndrome characterized by decreased T3/T4 * Signs include: * Weight gain and inactivity * Alopecia (Endocrine dermatopathy) * Reproductive abnormalities * Hypercholesterolemia * Systemic Lesion associated with disease - The cause of ~50% of the cases of hypothyroidism in dogs * Hyperkeratosis and adnexal atrophy of the skin * Myxedema (facial edema) * Atherosclerosis * Hepatic lipidosis
67
What is the structure of Parathyroid Gland?
* Chief cells * Comprise most of the gland * Produce parathormone * Oxyphil Cells * Modified Chief cells
68
What is the function of the Parathyroid Gland
* Control nd maintenance of serum Calcium levels * **Parathyroid hormone (Parathormone)** * Released in response to low serum calcium * Stimulates GI absorption and resorption of Ca2+ from bone, increased renal retention of Ca2+ and inhibits phosphorus reabsorption * **Calcitonin** (From Thyroid C-Cells) * Released in response to high serum calcium * Decreases GI absorption and resorption from bone, decreased renal retention * **Vitamin D** (From skin or diet) * Conversion to calcitriol in the kidney * Synergistic with parathormone
69
What is Hyperparathyroidism?
* Primary or secondary parathyroid involvement * Usually secondary (primary renal or nutritional) * Increased lameness and fractures, facial bone enlargement and weakening (fibrous osteodystrophy)
70
What is Hypoparathyroidism?
* Usually primary parathyroid involvement * Variable signs, including anorexia, weakness, or tetany or convulsions
71
What is the Pattern of pathogenesis of the Parathyroid gland?
* Metabolic * Parathyroid dysfunction will result in abnormal calcium metabolism * Metabolic problems frequently causes parathyroid abnormalities * Cell alteration and injury * Hyperplasia is common secondary to renal or nutritional disease * Idiopathic hyperplasia * Development * Cyst formation; variable significance * Immunopathology * Autoimmunity * Neoplasia * Parathyroid involvement * Non-parathyroid neoplasm producing parathormone-like substances
72
What are the causes of pathology in the parathyroid gland?
* Nutritional * Deficiency or imbalance of calcium and phosphorus * Chemical * Plants with Vitamin-D-Like activity * Genetic Predisposition * Parathyroid neoplasia or autoimmunity
73
What is Hyperparathyroidism?
* A clinical syndrome characterized by excessive activity of parathormone * Features: * Hypercalcemia due to enhanced intestinal absorption and bone calcium mobilization * Fibrous osteodystrophy * Bone weakness and factures * Thickened facial bones * Gastrointestinal disturbances * Muscle weakness
74
What is Nutritional Secondary Hyperparathyroidism?
* Diets high in phosphorus and low in calcium * Grain with low quality roughage - Bran disease * Persistent hypocalcemia results in parathyroid hyperplasia and increased PTH secretion * Clinical and pathological features are those on hyperparathyroidism
75
What is Renal Secondary hyperparathyroidism?
* Dogs with chronic renal failure * Renal retention of phosphorus and loss of calcium * Decreased renal conversion of calcifediol to calcitriol also contributes to hypocalcemia * Persistent hypocalcemia results in parathyroid hyperplasia and increased PTH secretion * In long-standing cases, hyperplasia becomes autonomous (no longer responsive to Ca2+ levels * Tertiary parathyroid hyperplasia * Clinical and pathological features are those of hyperthyroidism and renal failure * Fibrous osteodystrophy * Uremia and PU/PD
76
What is Pseudohyperparathyroidism?
* Mainly dogs and sometimes cats * **Persistent hypercalcemia without increased PTH** * Hypercalcemia is due to production of parathormone hormone-related peptide (PHRP), osteolytic factors, Cytokines (TNF), among other substances by certain neoplasms * Adenocarcinoma of anal sac apocrine glands * Lymphosarcoma (canine) * Plasma cell tumors (multiple myeloma) * Unregulated hypercalcemia due to PTH-like activity * Neuromuscular and cardiovascular dysfunction * Soft tissue mineralization * Parathyroid gland atrophy
77
What is Calcinogenic plant toxicity?
* Grazing animals in areas with appropriate plants * Plants with Vit D activity * Cestrum diurnum * Hypercalcemia is the result * Increased bone density * Soft tissue mineralization
78
What are parathyroid cysts?
* Relatively common in dogs * Originate from embryonic duct between thyroid and parathyroid glands or other embryonic structures * Kursteiners usts * Minimal significance unless they are large and space-occupying
79
What is lymphocytic parathyroiditis?
* A type of parathyroid atrophy * Uncommon in adult dogs * increased incidence in miniature schnauzers * Most likely autoimmune origin * Lymphoid infiltrate, chief cell atrophy, fibrosis * Results in hypoparathyroidism * Increased neuromuscular excitability * Decreased bone reabsorption
80
What is Hypoparathyroidism?
* A clinical syndrome characterized by decreased activity or response to parathormone * Features: * Hypocalcemia * Decrease bone resorption of Ca2+ * Increased phosphorus retention by tubules * Altered neuromuscular excitability * Weakness, ataxia, tremors, tetany * Paresis
81
What is Parturient paresis / Puerperal tetany?
* Mainly in cattle and dogs * Cattle - parturient paresis “milk fever” * Dogs - puerperal tetany “eclampsia” * Profound hypocalcemia * Disease often due to acute need during parturition or lactation
82
How does Parturient paresis occur?
* PTH is produced, but there are reduced osteoclasts due to high Ca2+ ration * Mechanisms: * High threshold potential at neuromuscular junctions * Concurrent hypermagnesemia * Magnesium acts as a calcium channel antagonist * increased levels of VFA * Inhibitory at neuromuscular synapses
83
How does Puerperal tetany occur?
* Typically occurs at the peak of lactation * 2-3 weeks after whelping * More frequent in small breed dogs * Mechanisms * _Not due to inadequate PTH_ * Low threshold potential at neuromuscular junction * Na+ channels are activated with very little increase in membrane potential * Low Ca2+ in extracellular fluid lowers the threshold potential for activation of NA channels * **Repetitive firing of motor nerve fibers occurs**
84
What is the structure of the Endocrine Pancreas?
* **Alpha Cells** * Comprise 5-30% of the islet cell population * **Glucagon** is the major product * **Beta Cells** * 60-80% of the islet cell population * **Insulin** is the major product
85
What is the function of the Endocrine Pancreas?
* Control of glucose metabolism * **Glucagon**: * **Increases blood glucose** concentration * increased glycogenolysis (liver and other tissues) * Enhances hepatic gluconeogenesis and FA oxidation (lipolysis) * **Insulin**: * **Decreases blood glucose** concentration * Enhances glucose entry into cells and hepatic glycogen storage * Mainly hepatocytes, skeletal muscle, adipocytes * Increased glycogenesis and glucose oxidation, Increased lipogenesis
86
What results in Pancreas Dysfunction?
* Hyperfunction (Hyperinsulinism) * Primary islet cell neoplasia * Neurological signs and weakness * Hypofunction (Diabetes mellitus) * Beta cell destruction and deficiency * Emaciation, PU/PD, Dehydration, various organ and tissue abnormalities
87
What patterns of Pathogenesis occur in the Pancreas?
* **Metabolic**: * Endocrine pancreas dysfunction will result in abnormal carbohydrate metabolism * Metabolic problems (Amyloidosis) may cause islet cell abnormalities * **Cell alteration and injury** * Acute pancreatic necrosis of dogs will damage islets * **Developmental**: * Rare * Hypoplasia * **Immunopathology** * Autoimmunity
88
What causes pathogenesis of the pancreas?
* Nutritional * Carb and fat excess or imbalance in the ration * Genetic predisposition * Neoplasia or autoimmunity
89
What is Diabetes Mellitus?
* Most common in dogs, sometimes in cats * Often middle-age to older female dogs * more common in smaller breeds * The problem is **inadequate insulin activity** * **Type I** (insulin-dependent) form is due to decreased insulin secretion * **Type II** (non-insulin-dependent) form is due to inadequate insulin release or target cell response * more common in cats
90
What conditions can cause reduced insulin activity?
* **Islet cell hypoplasia** * **Destruction of Pancreatic islets** * acute pancreatic necrosis in dogs (chronic relapsing pancreatitis) * less often immune-mediated destruction * Islet amyloidosis in cats * **Failure of insulin release from islet cells** * **Failure of tissues to respond to insulin** * Antagonism between insulin and other hormones * Hyperadrenocorticism promotes hyperglycemia and insulin resistance * Growth hormone stimulates increased secretion of insulin-like growth factor
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How does Diabetes Mellitus occur in cats?
* More often **type II** * Predisposing factors: * Hyperadrenocorticism, excess GH activity, **Obesity** * **Islet amyloidosis** * **Co-secretion of** Islet amyloid Polypeptide (IAPP; **amylin**) with insulin * **Amylin fibrils can cause B-cell death** due to misfolding protein response * Insulin resistance * Decreased **uptake of glucose by insulin-sensitive cells** * Predominately hepatocytes, skeletal muscle, adipocytes
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What are the clinical features of Diabetes Mellitus?
* Emaciation * PU/PD * Increased infections * Hyperglycemia * Glycosuria * Ketoacidosis and ketonuria
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What are the pathological features of Diabetes mellitus?
* **Hepatic lipidosis/glycogenosis** * **Glomerulosclerosis and glycogen nephrosis** * **Microangiopathy** * Glomerulopathy retinopathy and gangrene * **Cataracts** (shift to sorbitol pathway) * Vascular lesions and necrosis are not as prominent as in humans * Other lesion associated with any predisposing factors * Adrenal cortical hyperplasia or pituitary adenoma
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What are Islet Cell Tumors?
* Rare, mainly dogs * **Insulinoma** is the most common type * a wide variety of hormones can be associated with functional islet cell neoplasia * May also see amyloidosis due to concurrent secretion of IAPP * **Neoplastic Bet cells produce excess insulin** * Hyperinsulinemia **resulting in hypoglycemia** * Neurological disease