Endocrinology Flashcards
receptors occur on a different type of target cell located near the cells secreting the signaling molecules
paracrine signaling
(i.e fibroblast growth factor family0
receptors occur on the nuclear envelope of the cells that synthesized or internalized the signaling molecules
intracrine signaling
(i.e steroid hormone)
signaling molecule in vesicle (hormone of chemical messenger)
receptors occur on a different type of target cell located distant from the cells secreting the signaling molecules
endocrine signaling
(ie. thyroid stimulating hormone)
receptors occur on the plasma membrane of the same type of cell that secretes the signaling molecules
autocrine signaling (interleukin-1 in monocytes)
disruption in hormone causes___________
dysregulation in the controlled substance
Insulin/glucagon- glucose
Parathyroid/calcitonin - calcium
Aldosterone - Potassium
What is produced by the neurohypophysis
-Antidiuretic hormone (ADH) : acts on kidney tubules
-Oxytocin: acts on uterus smooth muscles and mammary glands
What are the 2 hormones produced by the acidophils in the pars distalis
-Prolactin
-Growth hormone
What is the only hormone without a recognized negative feedback from its target organ
Prolactin
anabolic through indirect effects leading to hepatic production of insulin growth like factor and cellular proliferation
Increased protein synthesis, mobilization of FA, decreased utilization of glucose are combination of both direct and indirect effects
Growth hormone
What is an example of a major counterregulatory hormone to insulin
Growth hormone
Glucocorticoids
Growth hormone results in:
Increased protein synthesis, mobilization of FA, decreased utilization of glucose
cellular proliferation
Acidophil or Basophil?
Prolactin
Acidophil
Acidophil or Basophil?
Growth hormone
Acidophil
Acidophil or Basophil?
FSH
Basophil
Acidophil or Basophil?
LH
Basophil
Acidophil or Basophil?
ACTH
Basophil
Acidophil or Basophil?
TSH
Basophil
contain no secretoy contents. May respresent stem cells or degranulated cells
in the pars distalis
Chromophobes
What serves as a substrate for every hormone produced in adrenal glands
Cholesterol
What are the layers of the adrenal cortex
Outer to inner
1) Glomerulosa- aldosterone
2) fasciculata- cortisol
3) reticularis - androgens
What is produced in the zona glomerulosa
aldosterone
What is produced in the zona fasciculata
cortisol
What is produced in the zona reticularis
androgens
When is renin produced
when the macula densa sense sense that there is a decrease in blood flow/cardiac output/perfusion to the kidneys
that converts angiotensin I to Angiotensin II to cause vasoconstriction and tells cortex to produce aldosterone
What converts renin from the macula densa cells to angiotensin I
angiotensinogen from the liver
What converts angiotensin I to angiotensin II
Angiotensin converting enzyme (ACE) from the lungs
What stimulates the release of vasopressin/ADH
1) Hyperosmolarity
2) Hypovolemia/ Hypotension
pituitary releases it to vasoconstrict (Increased arterial pressure) and increase renal fluid reabsorption (increase blood volume and arterial pressure)
What are the effects of vasporession/ADH
pituitary releases it to vasoconstrict (Increased arterial pressure) and increase renal fluid reabsorption (increase blood volume and arterial pressure)
How might you get diabetes insipidus
1) Defect in the hypothalamus or posterior pituitary leading to inadequate ADH
2) Defect in the kidneys, insensitive to ADH, adequate ADH (nephrogenic )
Aldosterone has its action at the
distal renal tubule
-promote retention of Na+ and wasting of K+
-forms osmotic gradient that allows water to be saved
Aldosterone allows for the retention of ______ and the wasting of ______
retention of Na+ and wasting of K+
What are the effects of glucocorticoids
1) Promotes hepatic gluconeogenesis
2) Inhibits glucose uptake and metabolism in peripheral tissues (insulin counter-regulatory)
3) Directly increases lipolysis and redistributes fat via circulation
4) Promotes protein catabolism, impairs extracellular matrix
5) Promotes diuresis- inhibits vasopressin, increases GFR
6) Prevents arachidonic acid metabolism by phospholipase A2
7) Suppresses lymphocyte and macrophage function via lipid mediators and changes in growth factors IL-2
What effect does glucocorticoids have on lymphocytes and macrophages
suppresses them and changes IL-2 growth factors
What effect does glucocorticoids have on vasopressin
It inhibits vasopressin
-promotes diuresis and increases GFR
How can you tell what the acidophils and basophils secrete in the pars distalis
need to do IHC
what produces catecholamines such as epinephrine and norepinephrine
the medulla of the adrenal gland- chromaffin cells
What is the thickest layer of the adrenal cortex
zona fasciculata (produces glucocorticoids)
What is the appropriate ratio of medulla to cortex in the adrenal gland
1:1 medulla to cortex
what color does the adrenal medulla stain
purple
What is an example of primary hyperfunction
androgen-producing tumors of the adrenal cortex
what is an example of primary hypofunction
immune-mediated destruction of the thyroid or adrenal cortex
What is an example of secondary hyperfunction
hypercortisolism due to ACTH-productng tumor
What is an example of secondary hypofunction
uncommon- target tissue dysfunction: insulin resistance
What can cause endocrine hyperfunction
1) Functional neoplasia / Abnormal feedback (ex: tumor)
2) Exogenous hormone administration
3) Hormone like substances (PHrp)
What can cause endocrine hypofunction
1) Non-functional neoplasia (pituitary)
2) Inflammatory destruction (usually autoimmune)
3) Congenital defects
4) Defects in hormone production or release
5) Idiopathic atrophy
6) Failure of tropic hormone secretion
7) Insensitivity of target organ
Since hormones often have multiple functions,_______________ are common
secondary lesions in distant organ systems are common
What is the signalment of dogs with hyperadrenocortism
Older dogs
polyphagia and weight gain
PU/PD
Pustular “skin disease” +/- hard bone like plates
occasionally acute respiratory distress (thrombosis)
What CBC findings will you see in a dog with Cushings
Lymphopenia
Mild neutrophilia - Stress leukogram
Mild thrombocytosis
What Chemistry findings will you see in a dog with cushings
-Modest hyperglycemia - 170 mg/dl
-Hypercholesterolemia
-Marked and disproportionate elevation in ALP
What UA findings will you see in a dog with Cushings
Specific gravity of 1.013
What is seen clinically with dogs with Cushings
Clinical: Older dogs, polyphagia and weight gain, PU/PD
Pustular “skin disease” +/- hard bone like plates,
occasionally acute respiratory distress (thrombosis), pendulous abdomen, hepatomegaly, muscle atrophy, alopecia (no growth)
CBC: Lymphopenia, Mild neutrophilia - Stressleukogram
Mild thrombocytosis
Chem: -Modest hyperglycemia - 170 mg/dl, Hypercholesterolemia, Marked and disproportionate elevation in ALP
UA: Specific gravity of 1.013
What might you see on necropsy of a dog with pituitary Cushings
-Bilateral Adrenalocortical hyperplasia (pituitary)
-adenoma/carcinoma on pituitary
-Enlargement of the Adrenal Cortex (no longer 1:1 to the medulla)
-Acute/Chronic renal infarct (thrombi) - tissue dies from coagulative necrosis
How do you find the adrenal glands
find the phrenicoabdominal vein
T/F: Cushing dogs hypercoagulable
True
How might an animal die from cushings disease acutely?
Hyercoagulability
-Deep vein thrombosis and pulmonary thromboembolism as a result of both increased coagulation factors and decreased anti-thrombin III
-Pulmonary thromboemoblism- high V/Q mismatch
Why do we see glycogen being stored in the liver with cushings disease
cortisol promotes glucagon and inhibits insulin function
stores instead of being properly being used
What occurs during dermal mineralization in cushing dogs
collagen is broken down and replaced with mineral
85% of dogs with hyperadrenocorticism are
pituitary caused
Adenoma in the pars distalis leading to excessive primary secretion of ACTH -> Cortisol is secreted with no sensitivity to negative feedback
Bilateral adrenal cortical hyperplasia
What effects on the adrenal glands will you see with pituitary dependent HA
bilateral cortical hyperplasia
With adrenal dependent HA, there is
contralateral cortical atrophy
excessive cortisol production
Inhibition of ACTH secretion
What might be a non-neoplastic, age related pituitary form of Cushings
older dogs have increased monoamine-oxidase leading to increased degradation of dopamine in CNS leading to decreased negative feedback of pituitary corticotrophs
Persistent secretion of ACTH
The hypercoagulable state seen with hyperadrenocorticism causes:
1) Deep vein thrombosis
2) Pulmonary thromboembolism
*From increased coagulation factors and decrease anti-thrombin III
Hypercoagulable state seen in hyperadrencorticism is a result of and increase in _________ and a decrease in _______
Increased coagulation factors
Decrease anti-thrombin III
Pulmonary thromboembolism from a hypercoagulable state of hyperadrenocortism results in a
High V/Q mismatch
What enzyme is increased in non-neoplastic, age-related, pituitary dependent hyperadrenocorticism
Increased monoamine-oxidase
Increases dopamine degradation in CNS, decrease negative feedback on piuitary corticotrophs
persistent secretion of ACTH
What is a result of increased monoamine-oxidase
Increases dopamine degradation in CNS, decrease negative feedback on pituitary corticotrophs
persistent secretion of ACTH
What is the signalment of dogs with hypoadrenocorticism
Younger dogs (age 2-5 years)
Clinical history of intermittent hemorrhagic diarrhea
Acute-onset bradycardia
Cardiac arrest
What is seen clinically of dogs with hypoadrenocorticism
Signs: younger dogs (2-5yr), intermittent hemorrhagic diarrhea, acute-onset bradycardia, cardiac arrest
CBC: Normal lymphocyte and neutrophil counts, mild non-regenerative anemia
Chemistry: hypoglycemia, hyperkalemia, hyponatremia, hypoand hypochloridemia, Azotemia with minimally concentrated urine (Na:K ratio of <25:1)
What CBC findings are seen in dogs with hypoadrenocorticism
Normal lymphocyte and neutrophil counts, mild non-regenerative anemia
What chemistry findings are seen in dogs with hypoadrenocorticism
hypoglycemia
hyperkalemia
hyponatremia
hypochloridemia
Azotemia with minimally concentrated urine (Na:K ratio of <25:1)
What Na:K ratio is typically seen in dogs with hypoadrenocorticism
<25:1
What do the adrenal glands look like on necropsy of a dog with hypoadrenocorticism
Diffuse atrophy of the adrenal cortex
*Large medullary region comparatively
What cell type is in the adrenal glands of hypoadrencorticism
lymphocytic adenolitis - autoimmune process
*hard to tell from this because it will be destroyed by the time the dog presents
What is lost with canine hypoadrenocorticism
Adren cortical atrophy- loss of aldosteroen and cortisol, possibly hyperplastic pars distalis from elevated ACTH production
Loss of Na+ and retention of K+
Glucocorticoid: hypoglycemia and skin pigmentation-spill over of excess ACTH
Why might an animal with Hypoadrenocorticism have a non-regenerative anemia
cortisol promote erythropoiesis
anemia may be compounded by gastrointestinal hemorrhage from the loss of mucosal integrity
Hypoadrenocorticism result in (Hypo/hyperglycemia)
Hypoglycemia
What is the signalment of PPID
Older horse- age >20years
Persistent lameness with radiographic evidence of chronic laminitis
Mild muscular atrophy
Unkempt and long hair coat, inconsistent with season
Overly docile mentality- changes in neurotransmitters
Moderate hyperglycemia
What are some clinical signs of PPID
-Chronic laminitis
-Hypertrichosis-overproducing hair
-Hyperhidrosis
-Pendulous abdomen
-Epaxial muscle wastage
What is the reason for overly docile mentality in horses with PPID
pituitary compressing on the brain above leading to impaired function of the hypothalamus
beta-endorphin
How do you diagnose laminitis in horses on necropsy
take a saggital section of the hoof . if the coffin bone does not parallel the hoof wall and you have bulging of the tissue
T/F laminitis is an inflammation issue
F: it is more of an architectural issue, mechanical issue and separation from the basement membrane
diagnose with PAS stain
How do you diagnose laminitis on histology
PAS stain to look for architecture and disconnect from basement membrane
What provides negative inhibition of the melanocytes in the pars intermedia
Dopamine
Lack of ______ leads to increased POMC peptides- ACTH, MSH, b-END, and CLIP being produced
dopaminergic inhibition
Where does the increased ACTH of PPID come from and what causes it
Increased ACTH from the pars intermedia due to decreased dopamine inhibition of the pars intermedia
Normally when doing a TRH test, shows that when you give TRH, __________ but abnormally when TRH is given __________
Normal: MSH increases
Abnormal: ACTH increases
Some clinical signs of PPID can be attributed to hypothalamic derangement from pressure of enlarging pituitary, such as
-Muscle wasting and PU/PD manifested because of elevated glucocorticoids + nervosa compression with impaired ADH secretion
-Elevated b-endorphin causes altered mentality
PPID-associated laminitis
50% of PPID have laminitis
2/3 of laminitis is associated with hyperinsulinemia
Hyperglycemia and peripheral insulin resistance at the root of laminitis
Pathogenesis is poorly understood
-Glucose deprivation to laminae that may be driven by ACTH
-Results in insulin resistance and hyperinsulinemia similar to type 2 diabetes mellitus
-Hyperphagia?
-Pain relief from endogenous b-endorphin
What is the typical signalment for feline acromegaly
Typically older cats, age >10 years
mentally dull and non-responsive upon presentation
Severe hyperglycemia >250mg/dl
stress leukogram and mild erythrocytosis
Elevated liver enzymes
Hyperphosphatemia without renal azotemia, mild proteinuria present
UA shows marked glucosuria
Is feline acromegaly congenital or acquired
acquired
What age of cats are typically impacted by acromegaly
typically older cats, age>10 years
What facial differences are seen with feline acromegaly
Broadened maxilla
Protruded mandible
Ears pushed back
*oppositional bone growth
Growth hormone induces
IGF-1
25% of cats with diabetes have
unbeknownst acromegaly
What causes acromegaly
an acquire excess of growth hormone secretion due to acidophil adenoma of the pars distalis
What changes in the pancreas will you see with acromegaly
*Swollen (degeneration) and vacuolated B cells overporducing insulin to counteract the insulin resistance
alpha and delta and epsilon cells are pushed in the middle
islet amyloidosis
How do cats with acromegaly typically present
with renal failure - proliferative glomerular nephropathy
with uncontrolled diabetes (Type 2 diabetes mellitus due to growth hormone mediated resistance- down regulation of insulin receptors on the target cells)
Prolonged insulin secretion and beta cell exhaustion
What is a congenital excess of growth hormone called
gigantism
What is the pathogenesis of acromegaly
1) Excess production of growth hormone due to acidophil adenoma of pars distalis
2) Excess production of IGF-1 leading to appositional bone growth, visceral organomegaly, nodular proliferative changes in pancreas, kidney and glomerular disease with proteinuria
3) GH induced reabsorption of phosphate
4) True erythrocytosis due to IGF-1 effects on bone marrow
5) Lack of ketosis due to altered fat metabolism
6) Likely associated with cardiomyopathy
What effects does IGF-1 have on the bone marrow
causes a true erythrocytosis
How do you diagnose acromegaly
1) measure IGF-1 in blood
2) follow up with a CT
What portion of the adrenal gland do tumors typically develop in ferrets
Zona reticularis- androgens producing
What is the signalment for ferrets with androgen-producing tumors of the adrenal cortex
middle aged ferret 5-7 years
What clinical signs do ferrets get if they have androgen-producing tumor of adrenal cortex
Alopecia (total body) and dermatopathy
Palpable+painful abdominal mass
Pale mucus membranes, petechiae
Females: vulvar swelling
Males: prostatic hyperplasia
Non-regenerative anemia, thrombocytopenia, leukopenia (from estrogen immunosuppression)
What do male ferrets with androgen-producing tumor of adrenal cortex typically get
Prostatic hyperplasia
What do female ferrets with androgen-producing tumor of adrenal cortex typically get
Vulvar swelling
Are androgen-producing tumor of adrenal cortex in ferrets metastatic
Yes but dont really tend to
What is the main detriment to ferrets with androgen-producing tumor of adrenal cortex
effects of estrogen on the bone marrow
should have around 50-75% hematopoietic cells for their age and they have around 20%
What might be the cause of androgen-producing tumor of adrenal cortex in ferrets
-Photoperiod being altered
-Chronic stimulation of zona reticularis by LH results in proliferative lesions
Why is pancytopenia seen as a result of bone marrow aplasia in ferrets with androgen-producing tumor of adrenal cortex
poorly understood
myelopoiesis-inhibitory factor
androgen-producing tumor of adrenal cortex in the ferret is caused by what two things
1) Bilateral cortical hyperplasia (45%)
2) Neoplasia of the zona reticularis (55%): carcinoma > adenoma
What can cause prostatic squamous metaplasia in male ferrets
High levels of secreted estrogen compounds from androgen-producing tumor of adrenal cortex
Rupture of prostatic cysts can lead to
prostatis are keratin is being released
What might result from an enlarge prostate due to androgen-producing tumor of adrenal cortex
Rupture of prostatic cyst leading to keratin release and suppurative prostatis
Dysuria from enlargement
What is a tumor of the adrenal tumor
pheochromocytoma
-may or may not release catecholamines
What is the signalment for pheochromocytoma
multiple species but most frequently older dogs and aged cattle
What are the clinical signs of canine pheochromocytoma
acute onset blindness (hypertension- retinal detachment)
bilateral mydriasis
tachyarrythmias
dyspnea
unremarkable clinpath - mild hyperglycemia
Are pheochromocytomas malignant?
Yes very much so, very high unlike other adrenal processes
Where to pheochromocytomas typically spread to
invasion into the vena cava, obstruct blood flow, can cause infarction
tumor emboli
T/F pheochromocytomas cause retinal deteachment
True: from hypertension
What is implicated in the development of pheochromocytoma
calcium homeostasis
-hypercalcemia and excess vitamin D result in chromaffin cell proliferation
What can result due to a pheochromocytoma?
-Catecholamine induce cardiomyopathy (beta adrenergic stim leading to vasoconstriction and coronary vasospasm leading to myocardial infarction
-Retinal detachment
-paroxysmal hypertension
Thyroperoxidase
oxidizes iodide (I-) to iodine (I2) in the colloid
Describe the process of generating T3 and T4
Iodide (I-) from the blood moves through the cell to the lumen and is oxidized to iodine (I2) in the colloid by thyroperoxidase
CHO modification on Tyr occurs to make thyroglobulin and is released into the colloid
Thyroglobulin binds I2 on Tyr to become iodinated thyroglobulin
Endocytosis of colloid -> digestion of iodinated thyroglobulin to generate T3 and T4 which diffuse out of the cell into adjacent capillaries
What are the effects of thyroid hormone
-Increased metabolism of fats and carbs, protein synthesis
-Cardiovascular- increases HR, contractility, and CO
-Nervous System- enhance sympathetic nervous system and mental activity
-Nearly every cell in body some effect
-Developmental biology
What are the mechanisms of thyroid destruction
1) Atrophy- lack of trophic stimulation (pituitary neoplasia/destruction)
2) Inflammatory- autoimmune thyroiditis
3) Neoplasia (Non functional thyroid tumors- usually carcinoma and nonthyroid neoplasia- lymphoma)
Non-functional thyroid tumors leading to thyroid destruction is normally caused by
carcinoma
What are the mechanisms of thyroid proliferation
1) functional neoplasia- usually adenoma
2) adenomatous hyperplasia
functional neoplasias leading to proliferation of thyroid is usually cased by
adenoma
What is the cause of canine hypothyroidism
Primary is most common
Destruction/loss of the follicles
a) idiopathic follicular atrophy
b) lymphocytic thyroiditis
c) non-functional tumor, amyloidosis
Defect of thyroid hormone production
Is hypothyroidism in dog caused by atrophy of the thyroid gland?
not technically
not a concern with the thyroid stimulating hormone
pituitary is still functional and the destruction of the thyroid isnt producing T3/T4. TSH will be high
What is the most likely cause of hypothyroidism in livestock
nutritional from iodine deficiency- defect of thyroid hormone production
-goiter
What are the lesions seen with hypothyroidism
-obesity with normal to decreased eppetite
-Changes in mentation,activity level
-skin changes: alopecia, pigmentation, myxedema
-heat seeking behaviors
Hypercholesterolemia seen in hypothyroidism leads to
artherosclerosis
what is the only time you see artherosclerosis in domestic species
hypothyroidism
where do you normally see artherosclerosis in hypothyroid dogs
coronary arteries on heart
cerebral arteries going to brain
hepatmegaly, lipidosis
Glomerular, Corneal lipidosis
What is the pathogenesis of atherosclerosis
decreased thyroid hormone
Decreased lipid metabolism/utilization
Hypercholesterolemia
endothelial damage
increased permeability
mobilization of macrophages
atherosclerosis
*Thrombosis is a major concern
What is seen in the skin lesions of hypothyroidism
-Symmetrical alopecia
-Hyperpigmentation
-Epidermal/Dermal atrophy
-Myxedema
What is the pathogenesis of alopecia in hypothyroidism
Hypothyroidism
No stimulation of follicular epithelial cells
Increased number of follicles in telogen (resting state)
progressive alopecia
What are the causes of secondary hypothyroidism
-atrophy: T3/T4 synthesis is intact but stimulation of TSH is lost (Destructive pituitary lesion)
-goiter: inadequate thyroxine synthesis (low T3/T4) - iodine deficient diets (lambs, pigs, foals), goitrogenic compounds, genetic defect in enzymes or thyroglobulin
hypothyroid but proliferative lesion
You get an excessive colloid appearance
and atrophic thyroid cells
True thyroid atrophy
-Secondary Hypothyroidism
no TSH production
What is the pathogenesis of goiter
Follicular cells cant make T3/T4 -> pituitary increase release of TSH -> thyroid hyperplasia/hypertrophy
How might you get inadequate thyroxine synthesis (low T3/T4)
1) Iodine deficient diets (lambs, pigs, foals)
2) genetic defect in enzymes or thyroglobulin
3) goitrogenic compounds
What cells make T3/T4
follicular cells
How do goitrogenic compounds interfere with thyroxine synthesis
-Interfere with iodine transport by trapping it
-Iodine cant be added onto surface of the thyroglobulin molecule
-processing into active hormone
What are the clinical signs seen in cats with hyperthyroidism
-Increased basal metabolism (Weight loss with increased appetite)
-Renal: PU/PD, Increased GFR
-Cardiovascular system: tachycardia, hypertension, cardiac hypertrophy, detached retina
-GI: vomiting, diarrhea/bulky stool
Increased liver enzymes (ALT, ALP, AST)
70% also have signs of hyperparathyroidism
+/- azotemia
High T3/T4
How do cats end up with hyperthyroidism
Primary Hyperfunction
Functional proliferative lesion
-unilateral or bilateral
-nodular hyperplasia (multinodular adenomatous hyperplasia
-Adenoma
-Adenocarcinoma (uncommon)
What is the most common cause of death in cats with hyperthyroidism
cardiac hypertrophy
-narrowing of lumen and increased heart wall width
-endocardial fibrosis- can lead to a a thrombus
saddle thrombus
a thrombus lodged in the iliac artery- causes tissue necrosis to both of the back legs
How does hyperthyroidism result in a saddle thrombus
hyperthyroid
cardiomyocyte hypertrophy
turbulent flow
LA/LV thrombosis
Thromboembolism
Saddle thrombus
Do cats normally get thyroid adenomas or carcinomas
are they functional?
follicular adenoma - functional
Do dogs normally get thyroid adenomas or carcinomas?
are they functional?
Follicular carcinoma
non functional
but aggressive
Do bulls normally get thyroid adenomas or carcinomas
are they functional?
Parafollicular adenoma or carcinoma- functional
Do horses normally get thyroid adenomas or carcinomas
are they functional?
follicular adenoma < parafollicular cell adenoma
follicular cell carcinoma
more common than adenomas in dogs
fixed, locally invasive
unilateral> bilateral
high metastatic potential
lungs and distant organ > lymph nodes
What cells make parathyroid hormone
chief cells of parathyroid
PTH is secreted in response to
hypocalcemia (low ionized Ca2+)
What do parafollicular cells make
calcitonin
(decreases calcium levels)
What does parathyroid secretion result in
1) Osteoclasts- liberate Ca2+
2) Kidney reabsorption
3) active Vitamin D activation to function to increase absorption of Ca and P in the GI
What are the target organs of PTH
1) Bone: Ca2+ and PO4 out of the bone into the blood
2) Kidney: increased Ca2+ absorption in distal convoluted tubule, decreased PO4 absorption in proximal tubule
Ca2+ increase in the blood, decrease in urine
PO4 decrease in bloodm increase in urine, increased VitD conversion
3) Increased absorption of vitD and both Ca2++ and PO4 -> increase both in blood
Primary hyperPTH
proliferative
-hyperplasia (multifocal/nodular)
-functional neoplasms: parathyroid adenoma > carcinoma (unilateral)
Is functional parathyroid adenoma or carcinoma more common
adenoma
Secondary hyperPTH to target organ dysfunction
Hyperplasia (diffuse, bilateral)
-renal or nutritional secondary hyperPTH
Pseudohyperparathyroidism
Hypersecretion of hormone analog PTHrP seen in lymphoma, anal sac apocrine gland adenocarcinoma, multiple myeloma
bilateral atrophy of parathyroid gland
What conditions if PTHrP seen in
lymphoma, anal sac apocrine gland adenocarcinoma, multiple myeloma
What do parathyroid adenomas look like
large mass encompassing the entire parathyroid gland
defined margin
What effect does increased PTH have on intestine
increased intestinal Ca2+ and PO4 absorption
What effect does increased PTH have on kidney
Decreased Ca2_ excretion
Increased PO4 excretion
Increased Vit D activation
What effect does increased PTH have on bone
Increased bone resorption
What effect does increased PTH have on blood
Increased Ca2+ : PO4 ratio
How can you get secondary hyperparathyroidism
1) Nutritional - too little calcium, too much phospohrus, too little vitamin D
2) renal disease: impaired nephron function leading to P retention, loss of Ca -> hyperparathyroidism
How do you get nutritional secondary hyperparathyroidism
Diet with either
too little calcium
too much phsophorus
Too little Vitamin D
If an animal has secondary hyperparathyroidism from either nutritional deficiencies or kidney disease, how does this appear on necropsy
Hyperplastic parathyroid
-increased signaling from too little calcium, too much phosphorus or too little vitamin D
How do you get secondary hyperparathyroidism from kidney disease
impaired nephron function leading to P retention, loss of Ca, decreased vit D, and metabolic acidosis
leads to increased ionized Ca2+, decreased intestinal Ca2+ and PO4 absorption, and increased Ca2+ and PO4 binding
-Decreased serum Ca2+
-IIncreased PTH and bone resportion
If Ca * PO4 is 60-70 what begins occuring
tissue mineralization all over body-> destruction of function and tissue death
Fibrous osteodystrophy
increased osteoclastic bone resorption
replacement with fibrous connective tissue
attempts at osteoblastic production of immature woven bone (poorly mineralized)
more common in reptiles
increased osteoclastic bone resorption
replacement with fibrous connective tissue
attempts at osteoblastic production of immature woven bone (poorly mineralized)
Fibrous osteodystrophy
Rickets
vitamin D deficiency
hypoparathyroidism
primary: autoimmune parathyroiditis
Secondary: chemical/toxic injury- parathyroid gland removal
C-peptide
surrogate of beta cell function
For every ___ molecule of there is _____ C-peptide
1 insulin molecule to 1 C=peptide
direct indicator of how much insulin an animal can make
C-peptide
Is insulin anabolic or catabolic
anabolic -> energy used to build big molecules and store sugars and fat
-blood glucose levels decrease
Is glucagon anabolic or catabolic
catabolic -> energy released from big molecules as they are broken down
-Blood glucose levels increase
Is metformin beneficial
only when the cat has levels of detectable insulin. measure c-peptide
