Test 3: endocrine Flashcards
pituitary will secrete ACTH which will cause the release of — from the adrenal glands which causes
cortisol
inhibitory to secretion of ACTH
feedback inhibition
give example of feedback inhibition
ACTH and cortisol
primary product will cause secondary organ to secrete a hormone which will turn off pathway
give example of feedback inhibition
ACTH and cortisol
primary product will cause secondary organ to secrete a hormone which will turn off pathway
anterior lobe of the pituitary is called
adenohypophysis
posterior lobe of the pituitary
neurohypohysis
three type of cells in the pars distalis
acidophils
basophils
chromophobes
acidophils secrete
somatotrophs→growth hormones
luteotrophs→ LTH and prolactine
basophils secrete
thyrotrophs- TSH
gonadotrophs- LH and FSH
chromophobes secrete
ACTH
melanocyte secreting hormone (MSH)
the posterior pituitary is made from — cells
modified glial cells (pituicytes) and axonal processess
cells in the posterior pituitary extend from the
supraoptic and paraventricular nuclei down the pituitary stalk to the posterior lobe (neurohypophysis)
posterior pituitary secretes
ADH and oxytocin
— cause contraction of smooth muscle in
uterus and myoepithelial cells surrounding
mammary gland ducts
oxytocin
corticotroph adenoma will cause
bilateral hyperplasia of the adrenal glands
and/or
CNS damage
pars distalis adenoma is most common in
dogs
pars intermedia adenoma are most common in
horses
less common in dogs
Equine Pituitary Pars Intermedia Dysfunction
unique form of cushings
caused by mass on pars intermedia
increased production of POMC peptides
loss of normal inhibitory control
what causes equine pituitary pars intermedia dysfuction
tumor in pars intermedia
decrease in dopamine
causes increased production of POMC peptides
from loss of inhibitory control
what controls the pars intermedia
dopamine
PPID is caused by a decrease in — which leads to —
dopamine → normally
inhibits cells (melanotrophs) in the pars
intermedia
loss of inhibition leading to hypertrophy and hyperplasia = mass
Equine Pituitary Pars Intermedia Dysfunction
POMC is turned into — in the pars distalis
ACTH, β-endorphin, β-
lipotropin
POMC is turned into — in the pars intermedia
ACTH → α-MSH,
corticotrophin-like intermediate lobe peptide (CLIP), β-MSH, β-endorphin
Plasma cortisol inhibits ACTH secretion by the — but has little effect on the —
pars distalis
pars intermedia
clinical signs of equine with mass in pars intermedia
PPID→ Equine Pituitary Pars Intermedia Dysfunction
fever, sweating, hypertrichosis/hirsutism
increased POMC
weight loss, muscle weakness
poor wound healing
PU/PD, increased appetite
hyperhidrosis
generalized sweating
hypertrichosis
hirsutism- too much hair- failure of seasonal shedding
what do acidophils produce
somatotrophs- growth hormones
luteotrophs- LTH and prolactin
acidophilic adenoma are seen in —
middle-aged to older, often male, cats
rare in dogs
acidophilic adenoma cause
acromegaly from too much growth hormone
cardiomegaly, enlargement of other organs
bone growth- broad facial structures
increased weight due to increased size of bone, muscle and organs
feline acromegaly can cause severe—- due to GH induced insulin resistance
insulin-resistant, diabetes mellitus
three causes of hypofunction of the pituitary glands
Compressive disease
Trauma
Congenital defects
pituitary carcinomas are usually nonfunctional, — and —
compressive and infiltrative
can expand and destroy the remaining pituitary and hypothalamus
ADH is released by the —
neurohypophysis (posterior lobe)
travels to the kidney and causes fluid retention
diabetes insipidus is a problem with —
ADH receptors
can be congenital- lack adenylate cyclase in the cytoplasm
can be secondary to a pyometra
what type of diabetes insipidus would improve with ADH supplement
hypophyseal form- brain form
nephrogenic form is issue with ADH receptor in the kidney
Hypofunction: Juvenile Panhypopituitarism (pituitary dwarfism)
due to lack of anterior pituitary - adenohypophysis
autosomal recessive trait in german shepherds
Panhypopituitarism clinical signs is due to
growth hormone
deficiency; +/- hypothyroidism and
hypoadrenocorticism
dwarfism
what part of the adrenal gland is NOT controlled by the pituitary?
Zona glomerulosa- makes mineralocorticoids (aldosterone)
what parts of the adrenal gland is controlled by the pituitary
Zona fasciculata- makes glucocorticoids
Zona reticularis- makes sex hormones
Mineralocorticoids (aldosterone) are produced where in the adrenal gland
zona glomerulosa
Glucocorticoids (principally cortisol) which are synthesized in the
zona fasiculata
Sex steroids are made where in the adrenal gland
zona reticularis
normal cortex:medulla ratio for most species
examined is approximately
1:1
Adrenal medulla is composed of chromaffin cells, which synthesize and secrete —
catecholamines-
mainly epinephrine
NOT controlled by the pituitary gland
Bilateral cortical hyperplasia of the adrenal gland
what makes this a carcinoma
invades the vena cava
primary adrenal hyperfunction is caused by
Adrenocortical adenoma/carcinoma
secondary adrenal hyperfunction is caused by
Corticotroph adenoma in Pituitary- aka “PDH”
What is the name given to syndrome of
adrenocortical hyperfunction?
cushings
What causes hyperfunction of the medulla of the adrenal gland?
Pheochromocytoma
too much epi or norepinephrine
cushings disease is caused by —
too much cortisol
cushing disease presents with
↑ALP
Pendulous abdomen “pot-belly”
PU/PD (dogs)
Increased appetite
Hepatomegaly
Panting!
primary pituitary tumor will cause what to happen to the adrenal gland
bilateral hyperplasia
high ACTH and high cortisol
one big adrenal gland with a tumor. is i functional?
yes
other adrenal gland has atrophied
high cortisol, low ACTH
addisons disease does what to the adrenal gland
bilateral adrenal cortical atrophy
immune mediated
caused by atrophy of all 3 cortical zones
leads to decreased cortisol and increased ACTH
what happens to ACTH and cortisol
high and high
low ACTH
high cortisol
non functional tumor
no change in ACTH and cortisol
pheochromocytoma
calcinosis cutis is —
mineralization of collagen of the dermis
can be caused by long term use of steroids
how to treat cushings
trilostane
enzyme blocker in the steroidogenesis pathway
block cortisol production in the adrenal gland
cats have what weird clinical sign with cushings
fragile skin
what happens when you remove the adrenal glands?
death
high Potassium
low sodium
volume of extracellular fluid and blood decrease
the heart begins to function poorly, cardiac output declines and shock ensues
need to supplement with salt and mineralocorticoids
primary hypoadrenocorticisim is also called
addison’s disease
addisons disease does what to the adrenal galnd
Idiopathic loss/atrophy of all 3 cortical zones
body can’t produce cortisol
clinical signs of addisons
Weakness/lethargy or collapse
Weak femoral pulse
Dehydration, bradycardia
Hypothermia
Abdominal pain, GI signs (e.g., diarrhea)
Hyponatremia and hyperkalemia with unconcentrated
urine. (low sodium, high potassium)
low aldosterone will cause
high potassium
hypovolemia, hypotension, reduced cardiac output;
hyperkalemia leads to decreased myocardial
excitability, increased refractory period, slowing of conduction.
low cortisol will cause what clinical signs
GI signs of
anorexia, vomiting, abdominal pain (unknown
mechanism); weight loss; diminished energy
metabolism; impaired tolerance of stress
secondary hypoadrenocorticism is caused by
long term steroid use
leads to decreased ACTH secretion, cause cortisol stops ACTH
how can treatment for cushings lead to addisons
treatment attacks cells that produce cortisol can eventually kill and atrophy area to cause addisons (too low cortisol and too low aldosterone)
What can cause hyperfunction of the adrenal medulla?
Tumor of medullary chromaffin cells.
pheochromocytoma
what kind of animals get pheochromocytoma
horse and dogs
horses- benign but functional
dogs- nonfunctional but malignant
not cats
clinical symptoms of pheochromocytoma
paroxysmal tachycardia, hypertension, hyperglycemia, vasoconstriction and diffuse sweating
what does pheochromocytoma do to ACTH and cortisol
nothing
active thyroid cells are —
cuboidal to columnarr
inactive thyroid cells are —
flattened and more colloid
C cells make
calcitonin
counters parathyroid hormone effects
iodine binds to — in the lumen to form thyroxine
(—) and triiodothyronine (—) via thyroid peroxidase
thyroglobulin
T4
T3
T3 and T4 are bound to —
plasma proteins
will form in the lumen then released into the blood stream
increased levels of T3 and T4 in the blood will cause
inhibition of TRH from the hypothalamus and TSH from the pituitary
hyperthyroidism is common in —
cats
hypothyroidism is common in —
dogs
—thyroidism
hypo
hyperthyroidism will do what to the thyroid?
will atrophy
small tumor (adenomatous hyperplasia) cause increased t4 and T3 will decreased TSH
what forms with feline hyperthyroidism
adenomatous hyperplasia
mass on thyroid that makes T3 and T4, normal thyroid gland will atrophy
clinical findings with hyperthyroidism in cats
Weight loss with
Ravenous appetite
Nervousness,
tachycardia
Heat intolerance,
weakness
Cardiomegaly →
arrythmias, saddle
thromboemboli and
death
two causes of hypothyroidism in dogs
Lymphocytic thyroiditis
Idiopathic atrophy
in lymphocytic thyroiditis the thyroid gland is invaded by —
lymphocytes, plasma cells
and macrophages
immune mediated canine hypothyroidism
when do you see signs of lymphocytic thyroiditis
75% of gland destroyed
genetic - beagles
dog hypothyroidism
what happens during idiopathic atrophy of the thyroid gland in a dog
Gland may be 1/10 size, replaced by adipose tissue
and fibrous connective tissue, may be end-stage of lymphocytic thryoiditis
hypothyroidism in a dog
clinical manifestation of hypothyroidism
slow metabolism
lethargic
exercise intolerance
Heat seeking, mental dullness, weight gain,
slow pulse
Neuromuscular and reproductive problems
Anemia
Hypercholesterolemia
dog hypothyroidism
what derm lesions will a dog with hypothyroidism have?
Scaling (bilateral alopecia- maybe but subtle), sometimes “rat” tail
Myxedema but only if severe → “tragic face”
Secondary infections →otitis, pyoderma
what is wrong?
hypothyroidism
myxedema →tragic face
scaling on tail
what blood test for hypothyroidism and what will it show
free T4
low T4
high TSH
goiters are bilateral enlargement of thyroid glands due to
— and — causes
nonneoplastic
noninflammatory
goiter will do what to thyroid
normal T4
or
hypothyroid
what causes goiter
Deficiency of iodine
Ingestion of goitrogenic substances
interfere with thyroid hormone synthesis
drugs, plants, Brassica
Excessive iodine- (rare)
genetic- defects in enzymes (or
thyroglobulin) for synthesis of thyroid hormones → increased TSH
old dogs will form what type of thyroid tumor
nonfunctional bilateral carcinoma
metastasize to the lungs
parathyroid gland is made of — cells that make —
chief cells
PTH
PTH does what
increases Calcium
Bone→activates bone resorption
Kidney →activates Vit D, reabsorbs calcium, gets rid of phorphorous
GI→ increases calcium absorption
what cell has the opposite effect of chief cells
chief cells- parathyroid- increase Calcium
C-cells in thyroid- make calcitonin that decrease Calcium
why is vit D needed for calcium
can get vit D from diet or the sun
turned into Vit D3 (cholecalciferol)
activated in the liver (25-
hydroxy D3) and kidney (1,25 -vitamin D3)
allows for increased absorption of Ca:P, needed for mineralization and ossification
What is the cause of primary hyperparathyroidism?
Functional parathyroid adenoma (dogs)
What happens to blood calcium with primary hyperparathyroidism
Does not respond to negative feedback
High
What clinical signs would you expect to see with hyperparathyroidism
Anorexia, muscle weakness, PU/PD, stiff gait, +/- pathologic fractures (rare), thickened mandible (rare) or loose teeth (rare)
elevated serum PTH and Ca
what causes secondary hyperparathyroidism?
Chronic renal disease
how does Chronic renal disease cause secondary hyperparathyroidism?
↓ P excretion by kidneys (hyperphosphatemia)
↓ active Vit D3 → ↓ intestinal absorption of Ca
High P lowers serum Ca → PTH secretion → Parathyroid hyperplasia → osteocyte release of calicum
What are the clinical signs of secondary hyperparathyroidism?
Chronic renal disease (vomiting, PU/PD, dehydration, breath
odor of ammonia) and fibrous osteodystrophy (FOD) “rubber jaw”
FOD is uncommon and usually affects young animals
what two tumors cause Pseudohyperparathyroidism
anal sac adenocarcinoma
Lymphosarcoma
will produce Parathyroid hormone related protein (PTHrP)
will cause high Calcium
blood test of animals with Pseudohyperparathyroidism will show?
high calcium
low PTH
tumors will produce Parathyroid hormone related protein (PTHrP)
primary hyperparathyroidism effects what animals?
dogs
beta cells in the pancreas make
insulin
alpha cells in the pancreas make
glucagon
delta cells in the pancreas make
somatostatin
F cells in the pancreas make
Pancreatic polypeptide
what does insulin do
increases cell uptake & storage of glucose, amino
acids, FA, secreted in response to hyperglycemia
causes protein synthesis in muscle
increases glycogen synthesis in the liver
What causes hyperfunction of the endocrine pancreas?
Most common cause is iatrogenic insulin
overdose (low BG)
Functional tumor of islet cells
what animals get beta cell tumors /insulinomas
Uncommon in dog- malignant to lymph nodes and liver
rare in cat
common in ferrets- benign
dog or ferret will have a malignant insulinoma?
dog- less common to have a beta cell tumor but malignant
beta cell tumor common in ferret but usually benign
What are clinical signs of beta cell hyperfunction?
insulinoma →low BG
incoordination, ataxia,weakness, syncope, muscle twitching, blindness, polyphagia, seizures
Ferret: weakness but seizures are uncommon
common benign in ferret
malignant uncommon in dogs
DM is caused by
pancreas beta cells not making insulin
or
insulin receptors not working
type 1 DM
skinny DM
lose beta cells that make insulin
need to be given insulin
type 2 DM
fat people DM
insulin resistance- receptors not working
clinical signs of DM
high BG
glucose in urine
PU/PD
weight loss
ketoacidosis
cataracts
fatty liver
what causes the fatty liver in animals with DM
lack of insulin means body breaks down lipids and muscle for energy
leads to ketoacidosis
liver will try to filter but excess fat will be stores in the liver