Lecture 1: Endocrine Flashcards
What are endocrine glands
Specialized secretory epithelial cells arranged in cords, packets, or follicles (thyroid) supported by fine fibrovascular stroma
What is the function of endocrine glands
Synthesis, store and secrete products into bloodstream—> produce signals with distant physiological effects
What does endocrine mean
Cell secretes a product that acts on distant cells (systemic effects)
What is autocrine
Cells secrete a product that acts on itself
What is paracrine
Cells secrete a product that acts on a neighbor cell
What is primary hypofunction
Endocrine organ not making hormone because of direct damage
What are some examples of primary hypofunction
- Organ destroyed (ex: abscess)
- Organ not developed (aplasia)
- Organ defect (goiter)
What is secondary hypofunction
Endocrine organ not making hormone because lack of stimulation by hormones from another endocrine organ
What is the mechanism of endocrine disease on adrenal gland: pituitary gland is destroyed and now the adrenal gland is not stimulated
Secondary hypofunction
What is primary hyperfunction
Endocrine organ is making too much hormone because of functional tumor/ hyperplasia
What are some examples of primary hyperfunction
- Functional cortical adenoma of adrenal gland
- Functional thyroid gland adenoma
What is a secondary hyperfunction
Endocrine organ making too much hormone because overstimulated by hormones
What are the mechanisms of endocrine disease: pituitary gland dependent Cushing overstimulating the adrenal gland by tumor in pituitary
Pituitary: primary hyperfunction
Adrenal: secondary hyperfunction
What is hyper secretion of hormones or hormone like factors by nonendocrine neoplasms
Non- endocrine organs make substances that are new hormones or are hormones that resemble existing hormones produced by normal endocrine organs
What is the mechanism of endocrine disease: humoral hypercalcemia of malignancy due to PTHrP. PTHp is produced by tumor cells and resembles normal PTH and will function similarly (increase Ca2+)
Hyper secretion of hormones or hormone like factors by non-endocrine neoplasms
What is the mechanism of endocrine disease: secondary hyperparathyroidism due to chronic renal disease or nutritional imbalance
Endocrine hyperactivity due to disease of other organs
Is a functional endocrine neoplasm more likely to be benign or malignant
Benign
Hyperplasia/adenoma or carcinoma: regional invasion and destruction, metastasis
Carcinoma
What type of tissue is this? Identify green, blue and yellow outlined areas
tissue: pituitary gland
Green: pars distalis
Blue: pars intermedia
Yellow: pars nervosa
What do somatotrophs make
Growth hormone
What do lactotrophs make
Prolactin
What do corticotrophs make
ACTH
What do thyrotrophs make
TSH
What do gonadotrophs make
FSH and LH
The pars nervosa is responsible for releasing what hormones
Vasopressin (ADH)
Oxytocin
Images from old female goat, what is wrong and what is the mechanism of endocrine disease
Brain: pituitary tumor
Mammary gland: increased size due to increased prolactin being released by pituitary
Diagnosis: functional lactotroph adenoma with hyper secretion of prolactin
Mechanism: primary hyperfunction of pituitary gland
Describe the HPA axis
- Hypothalamus releases CRH
- Pituitary gland releases ACTH (pars distalis)
- Adrenal gland releases cortisol
- Negative feedback to hypothalamus to decrease release of CRH
What mechanism of endocrine disease would occur with if the pituitary gland was destroyed by inflammation and non-functional tumors
Primary hypofunction
What mechanism of endocrine disease would occur with a congenital/hereditary maldevelopment of pituitary
Primary hypofunction
What mechanism of endocrine disease would occur with functional pituitary tumors
Primary hyperfunction
What produces ADH and what is the function
Produced by pituitary gland pars nervosa and acts on kidneys to reabsorb water
Patient presents with PU/PD to determine type of diabetes insipidus you add exogenous ADH, if the patient is able to concentrate their urine, what type of DI do they have? What structure is likely destroyed and what is the host level of ADH
Central DI
Pars nervosa destroyed
ADH is low
Patient presents with PU/PD to determine type of diabetes insipidus you add exogenous ADH, if the patient is not able to concentrate their urine, what type of DI do they have? What structure is likely intact and what is the host level of ADH
Nephrogenic DI
Pars nervosa intact
ADH high-kidney not responsive
What are some reasons an animal might have central DI
Pituitary tumor or abscess
What species commonly gets somatotroph adenoma
Cats
What hormone is affected with somatotroph adenoma and what are some clinical signs of this
- GH increased
- Acromegaly and adult onset DM
What hormone is affected in cortciotroph adenoma. What two organs does that hormone affect and what is the mechanism of endocrine disease for each organ
- Increase ACTH- primary hyperfunction
- Bilateral symmetric adrenal gland cortical hyperplasia of ZF and ZR- secondary hyperfunction
What are some gross findings of the pituitary gland and adrenal glands in patients with pituitary dependent cushings
- Big pituitary gland
- Bilateral symmetric, big cortices of adrenal glands
Based on these findings what is top differential
Corticotroph adenoma- pituitary dependent cushings
What is the mechanism of endocrine disease for a pituitary gland carcinoma
Primary Hypofunction
What part of the pituitary is affected in horses with PPID
Pars intermedia
What is the pathogenesis/outcome from PPID causing compression of hypothalamus
- Hypothalamic or neurohypophyseal dysfunction
- Intermittent hyperpyrexia, polyphasic, hirsutism
What is the pathogenesis/outcome of PPID being endocrinologically active
- Excess POMC
- Increase CLIP, MSH, beta-endorphin
- Increase ACTH
- Adrenal gland cortical hyperplasia (secondary hyperfunction)
Why is pituitary hypofunction/ aplasia in fetuses a problem in pregnant animals
- Fetal hormones needed for final growth/ development
- Parturition not activated—> prolonged gestation
What is the pathogenesis of pituitary cysts and pituitary dwarfism
- Failure of pars distalis to develop
- Cysts replace portion or all of adenohypohysis
- Juvenile panhypopituitarism
- Hyposomatotrophism- no growth hormone- no patient growth
What pituitary hormone is most affected in pituitary dwarfism
Somatrophs- don’t produce enough GH
Brain from an abnormally small “adult” German shepherd. What is wrong
Cyst on pars distalis causing decreased production of GH
Pars nervosa is okay
What does the zona glomerulosa produce
Mineralcorticoids/ aldosterone
What does the zona fasisculata produce
Glucocorticoids/ cortisol
What does the zona reticularis produce
Sex hormones
Which layer of the adrenal gland cortex is not under ACTH control
Zona glomerulosa
What does the adrenal medulla produce
Epinephrine and norepinephrine
What is the cause of Addison disease
Immune mediated
How is Na+ and K+ affected in Addison disease and why
Na+ decreases and K+ decreases because Addisons disease destroys all cortical layers of adrenal gland, including ZG which produces aldosterone which normally retains Na+ and removes K+
Based on these images- what is top differential
addisons disease
What is the cause of secondary hypoadrenocorticism
Iatrogenic or pituitary gland damage
How is Na+ and K+ affected in secondary hypoadrenocortisim and why
Normal, because secondary hypoadrenocortisim only affects ZF and ZR, not ZG which produces aldosterone
Based on this image and the fact that electrolytes were normal, what is likely dx
Secondary hypoadrenocortisim
Adrenal gland- in general, what is wrong
hypoadrenocortisim- cortex much smaller than medulla
Describe the HPA axis when there is a pituitary dependent hyperadrenocorticism
- Increase ACTH release
- Adrenal cortical hyperplasia and increase cortisol
- No feedback loop because tumor will continue to release ACTH
Describe the HPA axis with adrenal gland dependent hyperadrenocorticism due to cortical adenoma in right adrenal gland
1.normal ACTH released from pituitary
2. Lots of cortisol released from right adrenal gland, decreased cortisol release from left adrenal gland (atrophy of left adrenal cortex and some atrophy on right side of affected areas)
3. Negative feedback loop decrease ACTH (results in atrophy of the unaffected adrenal glands)
What are some signs of Cushings disease
- Polyphagia
- Distended abdomen
- Hepatomegaly
- Calcinosis cutis
- Immunosuppression- UTI’s and pneumonia
These findings are consistent with what dz
hyperadrenocorticism/ cushings
What is Conn’s syndrome in cats/ pathogenesis
- Functional tumor of the ZG or hyperplasia of ZG
- Increase aldosterone
- Increase Na+ and decrease K+
- Hypertension and polymyopathy
How does the electrolyte balance differ in Conn’s syndrome vs primary hypoadrenocorticism (Addisons)
Conn’s syndrome: increase aldosterone—> increase Na+ and decrease K+
Addisons: decrease aldosterone—> decrease Na+ and increase K+
What is the pathogenesis/ outcome of phreochromocytoma
- Increase production of catecholamines
- Hypertension, tachycardia, left sided concentric ventricular hypertrophy, cardiomyopathy
What is the #1 adrenal gland medullary tumor
Pheochromocytoma
Which one is malignant
A
What to components are needed to form T3/T4
Iodine and thyroglobulin
What do C cells produce and what is the effect
Calcitonin- decrease Ca2+ (released when hypercalcemia)
What can cause acquired goiter
Iodine deficient or excess, goitrogenic compounds
What can cause inherited goiter
Congenital dyshormonogenetic
Does goiter cause hypo or hyperthyroidism
Hypo
What tissue is this, which is normal vs abnormal (what wrong)
Left: C-cell hyperplasia
Right: normal
What wrong
Lymphocytic thyroiditis
How is T3/T4 and TSH affected in hypothyroidism
Decrease T3/T4 and increase TSH
What are some signs of hypothyroidism
Weight gain, alopecia, atherosclerosis, hepatomegaly
What are 3 examples that cause thyroid tissue loss and therefore hypothyroidism
- Idiopathic follicular atrophy/ collapse
- Lymphocytic thyroiditis
- Destroyed by non-functional tumor
What is the pathogenesis for congenital dyshormonogentic/ inherited goiter
- Inherited autosomal recessive mutation
- Abnormal pathway
- Decrease T3/T4 due to mutations preventing iodothyronine production
- Increase TRH and TSH
- Thyroid gland hyperplasia and colloid endocytosis
- Goiter and hypothyroidism
How does a functional adenoma or thyroid hyperplasia affect T3/T4 and what does it cause
Increase T3/T4–> hyperthyroidism
What are some signs of hyperthyroidism
Weight loss, triangular shaped face, nervousness, tachycardia, dysrythmia, ventricular hypertrophy
Dog presents with thyroid gland mass, what is it most likely
Carcinoma
Cats with thyroid gland mass what is it most likely
Hyperplasia or adenoma
How does PTH affect Ca2+ and phosphorus
Increase Ca2+ and decrease phosphorus
How does vitamin D affect Ca2+ and phosphorus
Increase both
How does calcitonin affect phosphorus and Ca2+
Decrease both
What cells produce PTH and why
Chief cells in response to hypocalcemia
What is the pathogenesis of parathyroid gland insufficiency
- Decrease PTH
- Progressive decrease of blood Ca2+ and increase phosphorus
- Hypokalemia and hyperphosphatemia
- Neuromuscular tetany and excitability
What does primary hyperparathyroidms look like
Functional tumor, asymmetrically enlarged glands
What does secondary hyperparathyroidism look like
Hyperplasia, symmetrically enlarged glands
What are some causes of secondary hyperparathyroidism
Nutritional imbalance
Chronic renal failure
How does primary hyperparathyroidism affect Ca2+ and phosphorus
Hypercalcemia and low to normal phosphorus
How can nutrition cause secondary hyperparathyroidism
- Low calcium, high phosphorus
- PTH increase activity via chief cell hyperplasia
- Bone resorption and fibrous osteodystrophy
How can chronic renal failure cause secondary hyperparathyroidism
- Decrease vitamin D3 and chronic increase phosphorus
- Decrease Ca2+
- PTH increases via chief cell hyperplasia
- Bone resorption
What are some causes of pseudohyperparathyroidism
- Carcinoma
- Lymphoma
- Anal sac apocrine gland adenocarcinoma
- Plasma cell myeloma
What happens during pseudohyperparathyroidism
- Secrete biologically active PTHrP
- Action mimics normal PTH
- Hypercalcemia and low to normal phosphate is
