Endocrine Flashcards
What is the structure of the Endocrine System
- 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
What is the function of the Endocrine System
Maintain homeostasis
How does the endocrine system maintain homeostasis?
- 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
What are the different types of dysfunction of the Endocrine System?
- Increaed function
- Decreased function
What are the types of increased function of the Endocrine System?
- Primary hyperfunction
- increasd hormone secretion by an abnormal gland
- Secondary hyperfunction
- Increased hormone secretion by a normal endocrine gland that is excessively stimulated
What are the types of decreased function of the Endocrine System?
- Primary hypofunction
- decreased hormone secretion by an abnormal glad
- Seconday hypofunction
- Decreased hormone secretion by a normal endocrine gland that is inadequately stimulated
What is the pattern of disease seen in the endocrine system?
- 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
What are the causes of disease in the Endocrine System?
- 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
What is the structure of the pituitary gland?
- Anterior lobe (adenohypophysis)
- Posterior lobe (Neurohypophysis)

What are the parts of the Adenohypophysis and what hormones do they produce?
- “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
- acidophils (somatotrophs and Gonadotrophs)
- Pars intermedia
- Melnotrophs
- Pars Tuberalis

What is the structure of the Neurohypophysis?
- “Posterior Lobe”
- Hypothalamic neurosecretory neurons
- Paraventricular and supraoptic nuclei
- ADH and Oxytocin
- Paraventricular and supraoptic nuclei
- Infundibular stalk
- Pars nervosa

What are the functions of the hormones from the Adenohypophysis
- 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
What are the functions of the hormones from the Neurohypophysis?
- Antidiuretic Hormone
- Regulates water exretion
- Oxytocin
- Stimulates smooth muscle contraction
What are the types of dysfunction of the Pituitary gland?
- Increased Hormone Activity
- Decreased Hormone Activity
What can cause increased hormone activity of the pituitary gland?
- Functional neoplasia
- Increased stimulation by hypothalamus
- Hormone-like substances
What can cause decreased hormone activity of the pituitary gland?
- Destructive lesions
- Non-responsive target cells
What are the pathology patterns seen in the pituitary gland?
- 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
What causes pathology of the pituitary gland?
- Genetic injury
- inherited or acquired
- Infectious agents
- Uncommon
- Nutritional
- Chemical
What is Chromophobe Adenoma in dogs?
- 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
-
Less likely to be functional and act as space-occupying mass
What is Pars intermedia adenoma?
- 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
- Can be functional or compressive, just like those from the pars distalis
- 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
What is pituitary pars intermedia dysfunction in horses?
- 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
What is somatotroph adenoma?
-
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)
-
Increased production of insulin-like growth factor 1 by the liver
- Non-functional adenoma can cause panhypopituitarism and hypothalamic compression
-
Basophil Adenoma
- Rare
What are Pituitary Cysts?
- 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
What are the types of pituitary cysts?
-
Craniopharyngeal duct cysts
- Diabetes insipidus, pituitary hypofunction
-
Pharyngeal hypophyseal cysts
- Respiratory distress
-
Oropharyngeal ectoderm cysts
- Panhypopituitarism
- Juvenile hypopituitarism in GS
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
What is Craniopharyngioma?
- Neoplastic remnants of Rathkes pouch oropharyngeal ectoderm
- Occurs in Young dogs, Rare
- Hypothalamic destruction and decreased hypothalamic trophic hormones
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
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
-
Blindness, depression, drooling, tongue prolapse
- Most common in Cattle
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
- Decreased ADH production or release
- Destruction of the neurohypophysis or supraoptic nuclei of the hypothalamus
- Nephrogenic diabetes insipidus
- Primary renal disease, ADH is normal
What is the structure of the Adrenal Gland?
-
Cortex (mesoderm origin)
- Zona glomerulosa
- Mineralocorticoids
- Zona fasciculata
- Glucocorticoids
- Zona reticularis
- Sex steroids
- Zona glomerulosa
-
Medulla (Neural crest origin)
- Catecholamines
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
-
Aldosterone:
-
Glucocorticoids
-
Cortisol and corticosterones
- Gluconeogenesis, protein and fat catablism, suppressive for inflammation and immunity
-
Cortisol and corticosterones
-
Sex Steroids
- Progesterone, estrogen and androgens
-
Catecholamines
- Epinephrine and norepinephrine
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
How can the Adrenal Gland dysfunction?
- Hyperfunction (Hyperadrenocorticism)
- Hypofunction (hypoadrenocorticism)
What is Hyperadrenocorticism?
- Primary or secondary adrenal involvement
- Polyuria, polydipsia, increased appetite, weakness, alopecia, increased infection
- “Cushing’s Disease”
What is Hypoadrenocorticism?
- Primary or secondary adrenal involvement
- Anorexia, weight loss, GI disturbances, dehydration
- “Addison’s Disease”
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
What causes pathology of the Adrenal Gland?
- Genetic predisposition
- pituitary neoplasia causing adrenal hyperplasia
- Chemical
- Exogenous administration of glucocorticosteroids
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
- Most arise from the zona fasciculata
- Can be multiple or single, unilateral or bilateral
- Contralateral adrenal gland atrophy occurs with functional unilateral neoplasms
What is functional adrenal cortical neoplasia?
- Result in hyperadrenocorticism
- PU/PD
- Increased appetite
- Muscle atrophy and weakness
- Alopecia (Endocrine dermatopathy)
- Increased incidence of infections
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
What are the Functions of glucocorticosteroids?
- Gluconeogenesis
- Lipogeness
- Protein Catabolic
- Anti-inflammatory
- Immunosuppression
- Inhibition of fibroplasia
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
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
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
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
- Malignant neoplasms often invade the great vessels
What is Adrenal Hypoplasia or agenesis?
- Rare condition of dogs
- Total agenesis is fatal
- Hypoplasia results in variable degrees of hypoadrenocorticism
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
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
- May also result from destruction (chronic inflammation) or non-functional neoplasia of the pituitary gland
- Results in hypoadrenocorticism
- Anorexia and weight loss
- Diarrhea and dehydration
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
- 15-30% of metastatic lesion may occur here
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
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
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 serum calcium concentration
-
Regulation of adrenal function
- Hypothalamic releasing factors
- Pituitary hormones
- TSH
how can the Thyroid gland Dysfunction?
- Hyperfunction (hyperthyroidism)
- Hypofunction (hypothyroidism)
What is Hyperthyroidism?
- Usually primary thyroid involvement
- Polyphagia, weight loss, weak, tachycardia
- Most common in cats
What is Hypothyroidism?
- Usually primary thyroid involvement
- Inactivity, alopecia, lethargy, weight gain, obesity
- Most common in dogs
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
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
- Goitrogenic compounds
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
- Most common in old cats (usually adenoma)
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
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
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
- These may arise due to long-term ingestion of high calcium rations
- Some can be functional
- Hypercalcitoninism
- Vertebral osteophytes and osteosclerosis
- Hypercalcitoninism
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
What are the types of Goiter?
- Diffuse:
- Excessive TSH stimulus due to decreased thyroid hormones
- Iodine deficiency is a common cause
- Excessive TSH stimulus due to decreased thyroid hormones
- 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
- Defective synthesis with normal iodine levels
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
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
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
What is the structure of Parathyroid Gland?
- Chief cells
- Comprise most of the gland
- Produce parathormone
- Oxyphil Cells
- Modified Chief cells
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
-
Parathyroid hormone (Parathormone)
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)
What is Hypoparathyroidism?
- Usually primary parathyroid involvement
- Variable signs, including anorexia, weakness, or tetany or convulsions
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
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
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
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
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
- In long-standing cases, hyperplasia becomes autonomous (no longer responsive to Ca2+ levels
- Clinical and pathological features are those of hyperthyroidism and renal failure
- Fibrous osteodystrophy
- Uremia and PU/PD
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
What is Calcinogenic plant toxicity?
- Grazing animals in areas with appropriate plants
- Plants with Vit D activity
- Cestrum diurnum
- Plants with Vit D activity
- Hypercalcemia is the result
- Increased bone density
- Soft tissue mineralization
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
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
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
- Hypocalcemia
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
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
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
- Na+ channels are activated with very little increase in membrane potential
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
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
-
Glucagon:
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
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
What causes pathogenesis of the pancreas?
- Nutritional
- Carb and fat excess or imbalance in the ration
- Genetic predisposition
- Neoplasia or autoimmunity
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
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
- acute pancreatic necrosis in dogs (chronic relapsing pancreatitis)
- 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
- Antagonism between insulin and other hormones
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
- Decreased uptake of glucose by insulin-sensitive cells
What are the clinical features of Diabetes Mellitus?
- Emaciation
- PU/PD
- Increased infections
- Hyperglycemia
- Glycosuria
- Ketoacidosis and ketonuria
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
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