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Endocrinopathies - Coggle Diagram
Endocrinopathies
Pathological processes
DoG
Developmental
Aplasia, hypoplasia
Eg. anterior pituitary gland - Rathke's pouch mal-development
Primary hypofunction
Proliferative lesions
Functional
Unresponsive to negative feedback
Hyperfunctional tumours
Eg. Hyperadrenocorticism "Cushing's Syndrome"
Pituitary dependent
Non-functional
Eg. Hypoadrenocorticism "Addison's Disease"
Pituitary neoplasm
2^ Hypofunction
Inflammation and repair
Auto-immune
Hypothyroidism
Auto-immune thyroiditis
Adrenal TB - granulomatous
Deposits and pigmentation
Diabetes mellitus
Hyperpigementation - HypoA
Mechanisms
Hyperfunction
Primary hyperfunction
Eg. Phaeochromocytoma - adrenal medulla
Over-secretion of hormone
Neoplasia, hyperplasia - target organ
Eg. Hyperthyrodism (cats)
Enlarged thyroid gland - adenoma
Excessive production of T3 and T4
Secondary hyperfunction
Excessive secretion of trophic hormone
Mediates hypersecretion of hormone by target organ
Eg. Hyperadrenocorticism "Cushing's Syndrome"
Pituitary-dependent (80%)
ACTH secreting tumour
Adrenocortical-dependent (20%)
Adrenocortical tumour
Iatrogenic
Excessive GCS administration
Secondary to diseases of other organs
Secondary hyperparathyroidism
Nutritional
Decreased dietary Ca
Meat only diet in kittens / puppies
Increased dietary Ca binding agents
Eg. oxalates in buffel grass
Renal
Chronic renal failure
PCT epithelium destruction
Phosphorous retention
Disrupted Vitamin D metabolic activity
Decreased intestinal absorption of Ca
Effects
Increased osteoclast activity
Increased bone resorption
Bone fragility - fractures
Metabolic bone disease - fibrous osteodystrophies
Decreased renal excretion of Ca
Active vitamin D synthesis
Kidneys
Increased GIT Ca absorption
Hypersecretion by non-endocrine tumours
Para-neoplastic effects
Eg. adenocarcinoma of anal sacs; lymphoma
Iatrogenic syndromes - hormone excess
GCS administration
Directly causes hyperA
Progestagen administration
Indirect Acromegaly (GH effect)
Abnormal hormone breakdown
Decreased breakdown
Effective hypersecretion
Eg. hepatic cirrhosis
Decreased hepatic degradation of oestrogen
Hyperoestrogenism + feminisation
Hypofunction [ malignancy]
Primary hypofunction
Immune-mediated injury
Auto-immune thyroiditis (dogs)
Hypothyroidism
Eg. Adrenal-dependent HypoA
Mineralcorticoid deficiency
Electrolyte imbalance
Glucocorticoid deficiency
Moderate hypoglycaemia
Insufficient gluconeogenesis
Destructive lesion
Eg. Neurohypophysis destruction --> Diabetes insipidus
Eg. Neurogenic Diabetes Insipidus
Biochemical defect
Vitamin-dependent rickets in pigs
Congenital dyshormongenetic goitre in ruminants
Non-functional thyroid hyperplasia response
Decreased T3 and T4 production
Hypoplasia/ aplasia
Secondary hypofunction
Pituitary dependent HypoA / Hypothyroidism
Destructive lesion in one organ
Decreased trophic hormone secretion
Target organ hypoplasia / atrophy
Endocrine dysfunction -
failure of target cell response
Eg. Nephrogenic Diabetes insipidus
Renal tubular epithelial cells unresponsive
Antidiuretic hormone (ADH)
Inadequate urine concentration
Dilute urine
Eg. Insulin resistance - Diabetes mellitus
Failure to uptake glucose
Abnormal hormone breakdown
Increased breakdown
Eg. Induction of hepatic microsomal enzymes
Increased thyroxin breakdown
Hypothyroidism
Effective hyposecretion