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General Pathology > Endocrine > Flashcards

Endocrine Flashcards

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
Q

What is Pituitary dwarfism?

A
  • 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
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26
Q

What is Craniopharyngioma?

A
  • Neoplastic remnants of Rathkes pouch oropharyngeal ectoderm
    • Occurs in Young dogs, Rare
    • Hypothalamic destruction and decreased hypothalamic trophic hormones
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27
Q

What is a non-functional adenoma?

A
  • Dogs, cats, and others
  • These can arise from any cell, but often of chromophobe origin
  • Hypopituitarism with endocrine gland atrophy and hypofunction
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28
Q

What causes Pituitary Gland Inflammation?

A
  • 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
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29
Q

What are the Neurohypophysis diseases?

A
  • 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
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30
Q

What is the structure of the Adrenal Gland?

A
  • Cortex (mesoderm origin)
    • Zona glomerulosa
      • Mineralocorticoids
    • Zona fasciculata
      • Glucocorticoids
    • Zona reticularis
      • Sex steroids
  • Medulla (Neural crest origin)
    • Catecholamines
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31
Q

What are the functions of Adrenal Gland?

A
  • 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
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32
Q

What regulates the functions of the Adrenal Gland?

A
  • 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
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33
Q

How can the Adrenal Gland dysfunction?

A
  • Hyperfunction (Hyperadrenocorticism)
  • Hypofunction (hypoadrenocorticism)
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34
Q

What is Hyperadrenocorticism?

A
  • Primary or secondary adrenal involvement
  • Polyuria, polydipsia, increased appetite, weakness, alopecia, increased infection
  • “Cushing’s Disease”
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35
Q

What is Hypoadrenocorticism?

A
  • Primary or secondary adrenal involvement
  • Anorexia, weight loss, GI disturbances, dehydration
  • “Addison’s Disease”
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36
Q

What are the pathology patterns that affect the Adrenal Gland?

A
  • 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
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37
Q

What causes pathology of the Adrenal Gland?

A
  • Genetic predisposition
    • pituitary neoplasia causing adrenal hyperplasia
  • Chemical
    • Exogenous administration of glucocorticosteroids
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38
Q

What is adrenal cortical neoplasia?

A
  • 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
Q

What is functional adrenal cortical neoplasia?

A
  • Result in hyperadrenocorticism
    • PU/PD
    • Increased appetite
    • Muscle atrophy and weakness
    • Alopecia (Endocrine dermatopathy)
    • Increased incidence of infections
40
Q

What is Hyperadrenocrticism?

A
  • 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
Q

What are the Functions of glucocorticosteroids?

A
  • Gluconeogenesis
  • Lipogeness
  • Protein Catabolic
  • Anti-inflammatory
  • Immunosuppression
  • Inhibition of fibroplasia
42
Q

What is Diffuse Adrenal Cortical Hyperplasia?

A
  • 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
Q

What is Adrenal Cortical nodular hyperplasia?

A
  • 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
Q

What are the types of Adrenal Medullary neoplasia?

A
  • Phenochromocytoma
    • Arise in chromaffin cells of the medulla
    • Most common in dogs and cattle
  • Ganglioneuroma and neuroblastoma
    • Uncommon
    • Neuroectoderm origin
45
Q

What is Pheochromocytoma?

A
  • 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
Q

What is Adrenal Hypoplasia or agenesis?

A
  • Rare condition of dogs
  • Total agenesis is fatal
  • Hypoplasia results in variable degrees of hypoadrenocorticism
47
Q

What is Diffuse (Iatrogenic) adrenal cortical atrophy?

A
  • Most common in dogs on long-term glucocorticosteroids therapy
  • Exogenous glucocorticosteroids result in inhibition of adrenal cortical function and subsequent atrophy
48
Q

What is Idiopathic Adrenal Cortical Atrophy?

A
  • 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
Q

What Causes Adrenal Gland Destruction?

A
  • 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
Q

What is Hypoadrenocorticism?

A
  • 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
Q

What is the Structure of the Thyroid Gland?

A
  • 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
Q

What is the Function of the Thyroid Gland?

A
  • 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
Q

how can the Thyroid gland Dysfunction?

A
  • Hyperfunction (hyperthyroidism)
  • Hypofunction (hypothyroidism)
54
Q

What is Hyperthyroidism?

A
  • Usually primary thyroid involvement
  • Polyphagia, weight loss, weak, tachycardia
  • Most common in cats
55
Q

What is Hypothyroidism?

A
  • Usually primary thyroid involvement
  • Inactivity, alopecia, lethargy, weight gain, obesity
  • Most common in dogs
56
Q

What are the Patterns Pathogenesis of The Thyroid Gland follow?

A
  • 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
Q

What causes pathogenesis of the Thyroid Gland?

A
  • Genetic predisposition
    • Thyroid neoplasia, hyperplasia or autoimmunity
  • Nutritional
    • Deficiency of iodine, tyrosine or other thyroglobulin components
  • Chemical
    • Goitrogenic compounds
      • Thiouracil, sulfonamides, cyanogenic plants
58
Q

What are the types of Thyroid Gland Neoplasia?

A
  • 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
Q

What is Thyroid Follicular Nodular Hyperplasia?

A
  • 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
Q

What is Hyperthyroidism?

A
  • 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
Q

What is Parafollicular (C-cell) neoplasia?

A
  • 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
Q

What is Goiter?

A
  • 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
Q

What are the types of Goiter?

A
  • 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
Q

What is Idiopathic follicular atrophy?

A
  • 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
Q

What is Lymphocytic thyroiditsi?

A
  • 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
Q

What is Hypothyroidism?

A
  • 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
Q

What is the structure of Parathyroid Gland?

A
  • Chief cells
    • Comprise most of the gland
    • Produce parathormone
  • Oxyphil Cells
    • Modified Chief cells
68
Q

What is the function of the Parathyroid Gland

A
  • 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
Q

What is Hyperparathyroidism?

A
  • Primary or secondary parathyroid involvement
    • Usually secondary (primary renal or nutritional)
  • Increased lameness and fractures, facial bone enlargement and weakening (fibrous osteodystrophy)
70
Q

What is Hypoparathyroidism?

A
  • Usually primary parathyroid involvement
  • Variable signs, including anorexia, weakness, or tetany or convulsions
71
Q

What is the Pattern of pathogenesis of the Parathyroid gland?

A
  • 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
Q

What are the causes of pathology in the parathyroid gland?

A
  • Nutritional
    • Deficiency or imbalance of calcium and phosphorus
  • Chemical
    • Plants with Vitamin-D-Like activity
  • Genetic Predisposition
    • Parathyroid neoplasia or autoimmunity
73
Q

What is Hyperparathyroidism?

A
  • 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
Q

What is Nutritional Secondary Hyperparathyroidism?

A
  • 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
Q

What is Renal Secondary hyperparathyroidism?

A
  • 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
Q

What is Pseudohyperparathyroidism?

A
  • 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
Q

What is Calcinogenic plant toxicity?

A
  • 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
Q

What are parathyroid cysts?

A
  • 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
Q

What is lymphocytic parathyroiditis?

A
  • 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
Q

What is Hypoparathyroidism?

A
  • 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
Q

What is Parturient paresis / Puerperal tetany?

A
  • 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
Q

How does Parturient paresis occur?

A
  • 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
Q

How does Puerperal tetany occur?

A
  • 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
Q

What is the structure of the Endocrine Pancreas?

A
  • 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
Q

What is the function of the Endocrine Pancreas?

A
  • 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
Q

What results in Pancreas Dysfunction?

A
  • 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
Q

What patterns of Pathogenesis occur in the Pancreas?

A
  • 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
Q

What causes pathogenesis of the pancreas?

A
  • Nutritional
    • Carb and fat excess or imbalance in the ration
  • Genetic predisposition
    • Neoplasia or autoimmunity
89
Q

What is Diabetes Mellitus?

A
  • 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
Q

What conditions can cause reduced insulin activity?

A
  • 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
91
Q

How does Diabetes Mellitus occur in cats?

A
  • 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
92
Q

What are the clinical features of Diabetes Mellitus?

A
  • Emaciation
  • PU/PD
  • Increased infections
  • Hyperglycemia
  • Glycosuria
  • Ketoacidosis and ketonuria
93
Q

What are the pathological features of Diabetes mellitus?

A
  • 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
94
Q

What are Islet Cell Tumors?

A
  • 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

General Pathology (34 decks)

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