Midterm--Hyper, Hypo, Pathology Flashcards
The 5 S’s of endocrine organ function (what are the 5 functions)
sense synthesize store secrete signal
The only reliable indicator of malignancy?
Vascular invasion
4 potential causes for DIFFUSE atrophy of a gland?
excess circulating hormone
decreased stimulatory substance
autoimmune or toxic destruction
defective receptors
Which portion of the pituitary is responsible for most of the hormone secretion?
Pars distalis
Secondary lesions of stunted growth and retention of juvenial hair coat in a GSD might be related to?
Cystic Rathke’s pouch
A functional adenoma in the pars distalis would secrete which hormone?
Dogs
ACTH
this is PDH
Epidermal atrophy, flank alopecia, and calcinosis cutis would occur secondary to elevations in which hormone?
Cortisol
**Cortisol is high due to excessive ACTH secretion–>bilateral, diffuse, adrenal hypertrophy (HAC)
Adenomas of the pars INTERMEDIA are more common in which spp.? If functional, what do they secrete?
Horses secrete propiomelanocortin (POMC)
*can compress hypothalamus
How do adenomas of the pars distalis differ in cats?
they secrete GROWTH HORMONE
Excessive growth hormone in cats is related to?
3 features, 1 pathology
Features:
coarse facial features, increased bone growth, enlarged viscera
pathology:
insulin-resistant DM
Name the 3 layers of the adrenal glands and the main product of each
Glomerulosa–mineralocorticoids
Fasiculata–glucocorticoids
Reticularis–sex hormones
Salty, steroid, Sex
How can you know if a cortical adenoma is functional?
if the contralateral gland is atrophied
Functional pheochromocytomas secrete?
what two pathologic findings would be associated with it?
Catecholamines
1) cardiac hypertrophy
2) arteriosclerosis (related to hypertension)
Most common lesion in dogs diagnosed with Addison’s?
Idiopathic adrenal cortical atrophy
Due to ________ _______ tissue, follicular cell carcinomas can occur anywhere along the ventral neck (as well as in the heart)
ectopic thyroid tissue
*Associated with “cannonball” pulmonary mets
Which thyroid tumor is commonly associated with bulls fed high-calcium diets?
C-cell tumors
Finding infiltrates of lymphocytes and plasma cells in the thryoid could be indicative of?
Lymphocytic thyroiditis
**leads to hypothyroidism
Dermatologic changes and presence of atherosclerosis are pathologies associated with?
Hypothyroidism (no matter etiology)
If you find diffuse hyperplasia of the parathyroid gland, what abnormality would you expect on bloodwork?
low Ca levels
**ALL glands affected!!
Which pathologic finding is associated with hyperparathyroidism (regardless of etiology)?
Fibrous osteodystrophy
What are the 3 types of islet cell tumors that occur in the pancreas
insulinoma
gastrinoma
glucagonoma
Which pancreatic pathology is associated with uncontrolled vomiting and gastric ulceration?
Gastrinoma
Islet amyloidosis is commonly seen in which spp. with what type of disease?
Cats with type 2 diabetes
Which breed is predisposed to Chemodectomas (aortic body tumors)
Brachycephalics
What abnormality might you seen in a horse with periorbital paraganglioma?
Exopthalmos
How does the HPA axis differ in horses?
hypothalamus releases dopamine which acts on the pituitary’s INTERMEDIATE lobe to INHIBIT ACTH secretion
If you’re playing the odds with HAC (based on the 85, 15 rules):
1) where the tumor’s most likely location
2) likelihood it’s malignant
3) tumor’s likely size
1) anterior pituitary
2) unlikely (99% benign)
3) MICROadenoma
Typical signalment for a dog with HAC?
How does it differ with PDH vs. AT?
older (>7yr)
PDH= small dogs, both male and female
AT= large dogs; females slightly more likely
The 5 P’s (clinical signs) associated with HAC
PU, PD, polyphagia, potbelly appearance, panting
Which clinical sign of cushing’s is more severe in cats?
thin skin–can develop spontaneous tears
Though not commonly found, which dermatological manifestation of cushing’s would be pathognomonic?
Calcinosis cutis
Dogs with HAC are typically polyphagic, if the dog is anorexic, they most likely have which form?
pituitary MACROadenoma
also see neuro signs and blindness
More common labwork abnormality assoc. with dogs that have HAC?
elevated ALP
**corticosteroid induced ALP isoenzyme
What are the two broad categories of tests we using for diagnosing cushing’s and which specific tests fall under each category?
1) Screening tests
- -UUCR, LDDST, ACTH stim
2) Differentiation tests
- -HDDST, Endogenous ACTH, U/S
Concerning UCCR
1) what does it stand for
2) what is its primary use
3) what is its sensitivity and specificity
1) Urine cortisol : creatinine ratio
2) used to RULE OUT cushing’s (dog with a normal ratio is very unlikely to have HAC)
3) 75-95% sensitive; only 20% specific
What sample do you primarily use when interpreting LDDST? What are you looking for?
8hr sample
If > 30nmol/L at 8hr, consistent with HAC
Name 3 criteria that if present with LDDST would be consistent with PDH
1) suppression (< 30) at 4hr
2) 4hr < 50% baseline
3) 8hr < 50% baseline
*if none of these are present, still 50/50 chance btwn AT and PDH
Two advantages of ACTH stim
1) good test if the dog has a non-adrenal illness
2) only test to prove iatrogenic cushing’s
With ACTH stim, what type of response do we expect with:
1) AT or PDH
2) iatrogenic disease
1) expect a greater than normal response of cortisol secretion
2) expect cortisol to be low in the beginning and low on second sample
Concerning ACTH:
1) can you differentiate btwn PDH and AT
2) sensitivity and specificity
1) NO!!! Both show greater than normal release of cortisol
2) 85% for both
With HDDST, what responses would be consistent with PDH?
If none are met, what are chances it’s PDH?
1) complete suppression at 8hr
2) complete suppression at 4hr
3) <50% of baseline at 4hr
4) <50% baseline at 8hr
*If none present, 50/50 chance btwn AT & PDH
Though endogenous ACTH is great for differentiating, what is it’s major drawback?
requires intense special handling of sample
Treatment of choice for AT?
Surgery
What are our two drug options for tx of cushing’s?
Mitotane
Trilostane
MOA of:
1) Mitotane
2) Trilostane
1) destroys zona fasiculata and reticularis
2) competitively inhibits 3-beta-hydroxysteroid dehydrogenase (inhibits steroid synthesis)
How does dosing differ btwn Triolostane and Mitotane
Mitotane has both a loading and induction phase; loading is BID; maintenance is 2-3x per week
Triolostane is ALWAYS given BID
Both Mitotane and Trilostane are monitored with which test? How do they differ in timing?
ACTH stim
Trilostane—MUST be tested 4-6hr after pill is given
Mitotane can test any time
When treating PDH, where do we want cortisol levels to be?
30-150 pre AND post ACTH
**we want below normal to manage clinical signs
4 side effects of HAC treatment
1) cortisol deficiency (can see GI signs)
2) aldosterone deficiency (hypoNa/hyperK)
3) direct GI toxicity
4) Direct neurotoxicity (MITOTANE ONLY!!!)
L-deprenyl is specifically used to treat which type of HAC?
PDH with tumor in intermediate lobe
**prevents dopamine breakdown by inhibiting MAOB–>antagonizes ACTH secretion from IL
Hyperaldosteronism
1) most common in which spp.
2) predominantly benign or malignant
3) typical age of onset
1) CATS
2) malignant (75%)
3) avg. 11 (older cats)
What are the two main functions of aldosterone
1) regulation of Na & K (Saves Na, gets rid of K)
2) raises blood pressure
2 general types of clinical signs expected with aldosterone excess
1) polymyopathies (due to low K)
2) ocular signs (due to high BP)
Aldosterone excess can cause azotemia, so how would the labwork be different from renal failure?
phosphorous is normal
Two ways to raise K levels with hyperaldosteronism
K supplementation
Spironolactone (aldosterone antagonsit)
Hypoadrenocorticism is ALWAYS defined by _______ and SOMETIMES includes ________
cortisol deficiency (ALWAYS)
Aldosterone deficiency (Sometimes—typical)
What are the forms of Addison’s disease?
Primary–adrenals are issue
Secondary–pituitary is issue
Typical–aldosterone affected (HypoNa/hyperK)
Atypical–aldosterone normal
Typical signalment for Addison’s?
Younger to middle-aged (6m-9yr)
females slightly more likely
Name the 4 breeds that have a PROVEN genetic predisposition for Addion’s
Bearded collie
standard poodle
nova scotia DTR
Portuguese water dog
100% of Addisonian patients present with at least what type of signs?
GI signs (anorexia, V/D)
If you see which two clinical signs, you should always include addison’s on your list?
Sudden shock (for no apparent reason)
Severe GI hemorrhage
What physical exam finding would be a red flag & make you think addison’s?
Bradycardia (in the face of stress and dehydration)
If you see any of these 5 things, Addison’s should be on your differential list
Severe GI hemorrhage Megaesophagus Hypoalbuminemia Hypoglycemia "Renal failure"
EVEN if Na/K are NORMAL
Which test is required for diagnosis of hypoadrenocorticism?
ACTH stim
**dogs will have low pre and post samples
How is baseline cortisol used in diagnosing Addison’s?
Used to RULE OUT the disease
If baseline is >55 it’s not addison’s
How is endogenous ACTH test used? For which form of disease do we use it?
ONLY for Atypical disease
- if ACTH is high–primary dz
- if ACTH low–pituitary dz
Why do we care about the results of endogenous ACTH?
because if it’s primary atypical disease, it can progress to typical
Two treatment options to replace deficient mineralocorticoids?
Fludrocortisone (Florinef) Desoxycorticosterone pivalate (DOCP)
How do Florinef and DOCP differ in their GC content?
Florinef–has SOME GC activity; about 50% of patients will require additional prednisone
DOCP–has NO GC activity; ALL patients on this will also need prednisone
4 steps in addressing a hypoadrenal crisis
1) correct hypotension & hypovolemia (fluids)
2) provide glucocorticoids
3) correct electrolyte abnormalities
4) correct acidosis (not always necessary)
When providing glucocorticoids during a hypoadrenal crisis, which ones do you want to avoid and why?
Prednisone/prednisolone
will interfere with ACTH stim if you try to run it within 12hr
What are your 3 options for correcting electrolyte abnormalities with hypoadrenal crisis? Give brief MOA
1) Fluids
2) insulin & glucose (insulin drives K into cells; glucose prevents concurrent hypoglycemia)
3) Ca gluconate (protects heart from high K concentrations…doesn’t alter [K])
