Endocrinology Flashcards
What is the pathogenesis of hypersomatotropism in cats?
pituitary tumor producing GH–>increased IGF-1–>tissue proliferation and insulin resistance
What is the pathogenesis of hypersomatotropism in dogs?
mammary tissue producing GH, usually as a result of hyperprogesteronemia
will still get insulin resistance same as cats but in dogs this doesn’t result in diabetes mellitus
What is the typical signalment of a dog with hypersomatotropism?
intact female or history of progestin use
usually associated with dysmenorrhea
What is the typical signalment of a cat with hypersomatotropism?
Cat with difficult to manage diabetes mellitus/insulin resistance, PU/PD/polyphagia, may have prognathism/increased body size/organomegaly, if measured have high IGF-1 levels
What is the recommended treatment option for a cat with hypersomatotropism and what does post-treatment care include?
Hypophysectomy- will need supplementation of thyroxine, cortisol, and synthetic ADH post-op
**Pasireotide works as well for treatment of HST but is very expensive
What causes central diabetes insipidus?
primary pituitary problem- absolute ADH deficiency
Usually due to a space-occupying lesion in the pituitary gland
True or false: nephrogenic diabetes insipidus is caused by a primary renal problem?
False- usually caused by a metabolic problem causing renal dysfunction–>ADH “resistance”
Rarely a primary renal disorder
What clinical signs will you see with central diabetes insipidus?
Marked and unrelenting polydipsia and secondary polyuria, usually nothing else wrong with animal
What are the clinical signs you’d see with hyposomatotropism?
smaller animal but PROPORTIONAL
might have puppy fur
gonadotropin abnormalities- persistent estrus or infertility in males
What is the pathogenesis of hyposomatotropism?
adenohypophyseal malformation +/- maturation defect
GH deficiency, gonadotropin deficiency, and thyrotropin deficiency
Someone brings in two puppies that are siblings and 3 weeks old, one of them is noticeably smaller than the other but still has a proportional body. If the smaller puppy happened to have an endocrine disorder, is it more likely to be pituitary dwarfism or congenital hypothyroidism?
Congenital hypothyroidism- affected puppies show signs really early on (3-4 weeks of age)
Pituitary dwarfism puppies also have thyrotrophin deficiency but it’s usually not sufficient enough to affect them this early on in life
Name some processes Calcium is involved in
Nerve conduction and neuromuscular transmission
Muscle contraction
Intracellular messenger involved in cell signaling pathways
Coagulation
List the 3 main regulators of Calcium in the body
- PTH- increases Ca and decreases phosphate
- Active form of Vit D (calcitriol)- increases Ca AND phosphate
- Calcitonin (not much clinical significance)
What forms of Calcium make up total serum Calcium and which form do we care most about?
Ionized, complexed, and protein-bound
IONIZED (~50% of total) because active form
If you’re going to measure serum Calcium, what other things on the biochemistry do you need to look at and why?
- Albumin- will impact the protein-bound portion of total serum Calcium
* *If low albumin, total calcium may be low
* *If high albumin, total calcium may be high - Phosphate- checking calcium phosphate product that could cause irreversible soft tissue calcification
What is a consequence of prolonged, untreated hypercalcemia?
Irreversible damage to many organs, especially kidneys
True or false- if an animal has hypercalcemia on routine bloodwork but no clinical signs and appears normal on exam you should re-check in a year or if/when they develop clinical signs
False- should re-check right away and repeatable hypercalcemia should never be ignored, even if no clinical signs
If an animal has clinical signs associated with hypercalcemia, what would they be?
PU/PD, weakness/lethargy/depression, GIT signs, facial pruritus and oral discomfort, muscle twitching/fasciculations, cardiac tachydysrhythmias (rare), sudden death
Hypercalcemia can cause PU/PD and azotemia, what is the mechanism of each?
Interferes with ADH action in collecting duct, impairs NaCl resorption from LOH decreasing medullary hypertonicity
Causes vasoconstriction of afferent arterioles decreasing GFR, if phosphate high as well can cause nephron destruction by calcium phosphate deposits
True or false- it can be normal to have hypercalcemia in a rapidly growing, young dog
TRUE- considered non-pathological
What is the pathogenesis of primary hyperparathyroidism?
Adenoma of one of the parathyroid glands–>up-regulation of PTH
What are some neoplasms that cause increased PTH-like activity?
anal sac adenocarcinoma, lymphosarcoma, multiple myeloma, thymoma
**aka humoral hypercalcemia of malignancy
What will the levels of calcium and phosphate be if you have increased PTH or PTH-like activity?
Ionized hypercalcemia and low or low-normal phosphate
**Also PTH likely to be “inappropriately not suppressed” even if still in normal reference range or may have elevation in serum PTHrP
What are some causes of hypercalcemia that ARE NOT related to PTH or PTH-like activity AND what will their phosphate level be?
Vit D toxicity, granulomatous inflammation, hypoadrenocorticism, CKD, idiopathic in middle-aged cats, significant osteolysis, Mesothelioma
HIGH phosphate
A Keeshund comes in with primary hyperparathyroidism. Why have they developed this AND what will you see on ultrasound of their neck?
Genetically predisposed- will see one large adenomatous parathyroid gland and the other 3 have atrophied
A Nova Scotia Duck Tolling Retriever comes in for pollakiuria, you run bloods along with the urinalysis and find hypercalcemia. What is one of the first things you should check for when looking for the reason for the hypercalcemia?
Primary hyperparathyroidism- check PTH and check if phosphate is low and maybe ultrasound neck
These dogs often seem normal but may develop urolithiasis and present with lower urinary tract signs
If an animal has hypercalcemia secondary to CKD, what will their phosphate level be?
HIGH
If kidney problems with hypercalcemia but low phosphate, the hypercalcemia cannot be due to the kidney disease (might actually be causing the kidney problems)
Hypercalcemia in cats is most often caused by:
CKD, idiopathic hypercalcemia
Hypercalcemia in dogs is most often caused by:
neoplasia, primary hyperparathyroidism
What are some treatments to reduce hypercalcemia?
fluid therapy, furosemide, bisphosphonates (pamidronate or alendronate)
What are some conditions that cause hypocalcemia and why does it need immediate treatment if causing clinical signs?
Anything that lowers albumin, pancreatitis
SEIZURES!!
What is the acute treatment for hypocalcemia?
IV 10% calcium gluconate
What is the subacute treatment for hypocalcemia?
Calcitriol or AT-10 orally
Where is the embryological defect that causes pituitary dwarfism?
Rathke’s pouch
What is the main cause of goiter?
Iodine deficiency
If you have an iodine deficiency, you can’t iodinate the thyroid hormones –> decreased T4 –> increased TSH –> thyroid hyperplasia
What immune cells cause destruction leading to hypothyroid?
T cells
What can we measure to help confirm a case of hypothyroid?
TGAA - thyroglobulin auto antibodies
What are some common clinical signs of hypothryoid?
Lethargy, weight gain Bilateral symmetrical alopecia Hyperpigmentation "scurfy" coat = dandruff * Mostly seen in dogs*
Why would ALP/ALT be raised with diabetes mellitus?
Because of fat deposition within the hepatocytes
What does alkalotic urine indicate?
UTI! Urease producing bacteria are presenting, therefore making the pH more alkaline
Can commonly be seen alongside DM
What are causes of hyperthyroid?
Hormone producing tumor (adenoma/adenocarcinoma) - RARE
OR
Mutations in the TSH receptors/G proteins/or exposure to dietary/environmental goitrogens
When would you see calcification of soft tissues?
When levels of calcium and phosphate multiplied together > 5.5
Ex: Calcium - 3.1
Phosphate - 3.4
3.1 x 3.4 = 10.54 > 5.5
What are the potential causes of diabetes mellitus?
Obesity Medications/steroids Pregnancy/Diestrous Endocrinopathies - Cushing's, acromegaly, hyper/hypothyroid Neoplasia
What are the types of DM?
Type 1 - ABSOLUTE INSULIN DEFICIENCY - due to Beta-cell destruction - usually seen in DOGS and thought to be an immune mediated disease
Type 2 - Insulin resistance with Beta-cell dysfunction –> relative insulin deficiency - usually seen in CATS
Type 3 - “Other specific types of DM” - Pancreatic disease, hypersomatotropism, secondary to drugs- glucocorticoids
Type 4 - GESTATIONAL - diestrus/pregnancy associated
What are some clinical signs associated with DM?
Weight loss with increased appetite
PU/PD
Lethargy
Can get diabetic neuropathy - usually in cats
Can get diabetic cataracts - usually in dogs
DKA –> vomiting/inappetence
Hepatomegaly
What are some signs of DM on bloodwork?
Fasting hyperglycemia
Elevated ALP - fat deposition in hepatocytes
Fasting hyperlipemia
Elevated fructosamine
The tendency towards metabolic acidosis - elevation in serum ketones
What is fructosamine?
The compound created when glucose binds to albumin
What insulin is best for dogs? Cats?
Currently in the UK only 2 insulins licensed for use in dogs and cats
Dogs = Lente insulin (caninsulin) - TWICE DAILY
Cats = Protamine Zinc (ProZinc) - TWICE DAILY
Once given - suggest re-assessment in 3-5 days
When is the best time to administer insulin?
45min before meal
We want to match the opposing effects of the insulin and the meal to minimize malutilization and achieve stable blood glucose levels over the 12 hour period (BID meds)
True or false: if we have a new diagnosis of DM, we should also test for hyperthyroid in cats.
TRUE - Especially when testing with fructosamine - If we have low fructosamine levels - could be a FAKE LOW
Increased T4 –> increased protein turnover so you will get low albumin levels, thus creating a fake low fructosamine
What is an ideal diet for a diabetic patient?
LOW CARBS
Increased water intake - consider wet food (Diabetic wet foods by Royal Canin/Hills)
What is the best treatment for DKA?
IVFT
Electrolytes - K/PO4/Na
Insulin CRI
Dextrose
What is the best way to monitor DM?
LOOKING AT CLINICAL SIGNS - Weight, BCS, consumption/appetite
Can also look at BG curves, fructosamine, urine dipstik
Freestyle Libre interstitial glucose reader
What signs are included in the diabetic clinical score?
Weight loss
PU/PD
Increased appetite
Attitute/acitivty
What are signs of remission for DM?
Resolution of signs Normal or decreased fructosamine Persistent normal BG Persistent normal urine glucose Hypoglycemia
True or false: Lipemia will falsely increase serum protein levels.
TRUE - total protein levels are influenced by lipemia and artificially elevates them
On bloodwork, what else can appear similar to DM? How can we differentiate?
PANCREATITIS
Because islets producing insulin are in the middle of the pancreas during an inflammatory process going on –> many animals can have elevation in BG - for a period of time they will stop producing insulin
Look at ketones in urine - DKA would also look like pancreatitis because of vomiting/inappetence
LOOK AT AMYLASE - is it 3x the upper reference limit?
What are signs of DKA?
Need 3/4 components to ensure DKA - (HAVE TO BE SICK) Dehydration GI signs - inappetence, V/D Preceded by PU/PD Metabolic disturbances - acidosis
- MORE COMMON IN ANIMALS WITH SEVERE INSULIN DEFICIENCY
Why is potassium low with DKA?
How would you treat this?
If there is an acidosis, the serum potassium should increase
Potassium is usually intracellular
With acidosis - H ions move down the concentration gradient into the cell - now have + charge inside cell
Cell has to maintain neutrality so + charge now has to move out - SO potassium is the cation most permeable to the cell membrane and will go into extracellular space
BUT WITH DIABETES/DKA
Will be vomiting and losing potassium in vomit
Will have PU/PD - will lose potassium in the urine
TMT - do not want to rush K influx = extremely dangerous –> electrical instability
Use 0.45% sodium chloride (not LRS)
Do not add bicarbonate because it will correct potassium too quickly
Because insulin decreases blood glucose before ketones, what would be the proper treatment for DKA? How do we continue to suppress ketone production while avoiding hypoglycemia?
REDUCE INSULIN
START DEXTROSE INFUSION
If we overdose Addisonian patients with glucocorticoids, what is a possible side effect?
PSEUDOMYOTONIA - walk around stiff
Start stiff and warm out of it
Opposite of myasthenia gravis a bit
What are the 2 biomarkers for too much cortisol?
- Increased ALP
2. Stress leukogram
What is the normal adrenal production of cortisol in the dog per day?
0.2 mg/kg/day
True or false: prednisone has 5x the glucocorticoid activity of cortisol.
TRUE
What is the first thing that should come to mind with a cat with increased ALP?
HYPERTHYROID
How would you diagnose hyperthyroid?
Basal total T4
T3 suppression test - admin T3 orally, measure T4, if T4>0 then you have hyperthyroid
T3 –> negative feedback to TSH so should–> decreased T4
Thyroid scintigraphy
Why would you get azotemia after treating hyperthyroid?
Hyperthyroid increases GFR
Correcting hyperthyroid –> decreased GFR –> increased creatinine
If hyperthyroid is bad enough, how can it lead to azotemia?
Hyperthyroid increases GFR
Hyperfiltration –> glomerular sclerosis –> decreased GFR –> azotemia
What are treatment options for hyperthyroid?
- Medical - Methimazole, Carbimazole
- Unilateral thyroidectomy - if 1 gland if larger than other
- Bilateral thyroidectomy
- Thyroid irradiation - radioactive iodine
- Dietary tmt - lower iodine
What are clinical signs of hypothyroid?
Lethargy Overweight - possible exercise intolerant Muscle/joint pain Dermal changes = alopecia, hyperpigmentation, thickened skin Infertility
How can you tell if congenital hypothyroid is present?
RADS - epiphyses do not mature normally/calcify
Why would you see non-regenerative anemia with hypothyroid?
Decreased EPO production
Decreased BM depression
What are the 2 best things to test for to take with suspected hypothyroid?
BASAL TOTAL T4 and CANINE TSH - 95% specificity when in combination
What is the treatment for hypothyroid?
Thyroxine tablets! DUH!!!
What would cause a primary negative energy balance in a cow?
Usually decreased feed intake - not enough energy in feed or just not enough feed
When does ketosis complex usually occur?
POSTPARTUM! 2-10 weeks after calving - happens in about 5% of cows
Can be primary (not enough feed intake) or secondary to hypocalcemia, RFM, LDA, mastitis (anything that makes cow lose appetite)
What is the best test to diagnose ketosis in a cow? How is it treated?
BHBA - Beta hydroxybutrate levels
IV dextrose, propylene glycol
Appetite stimulants
What are the 2 forms of ketosis?
- Wasting Form - gradual decrease in appetite, weight loss, dry feces
- Neurological Form - sudden onset of abnormal behavior, walk in circles, head pushing, apparent blindness, licking of skin/objects, chewing, hyperesthesia
How would we prevent fatty liver syndrome?
Prevent overly fat or poor condition at calving/lambing
high energy-dense ration
quality forage - maize silage
Force walking - to food/water
supplements
Ensure mothers of twins/triplets - get more feed
What is the pathophysiology of PPID?
The loss of normal inhibition from dopamine from the hypothalamus –> overproduction of hormones - ACTH, alpha -MSH (melanocyte-stimulating hormone), CLIP (corticotropin like intermediate peptide), Beta endorphin
What is the signalment of PPID?
Older horses
Ponies more likely affected
No sex predilection
What are common signs of PPID?
Hypertrichosis Hyperhydrosis Laminitis Weight loss PU/PD Bulging suborbital fat pad Lethargy
What does PPID cause laminitis?
CLIP produced in PPID antagonizes insulin so pancreas increases the concentration of insulin, predisposing them to laminitis
We think that the laminae have insulin or insulin-like receptors increasing the risk for laminitis
How would we diagnose PPID in early stages vs. advanced?
Early - TRH stim test - give TRH and measure ACTH response
Advanced - Resting ACTH concentration - BASAL
Both - assess insulin status since CLIP antagonizes
How would we treat PPID?
Dopamine agonist - Pergolide/Prascend
5HT antagonist (since 5HT stimulated in PPID)
Diet and exercise
Monitor clinical signs - attitude, activity, PU/PD, sweating
Look at the initial response for the first 30 days then long term response for 1-12 months
What are the 3 ways in which EMS can ~manifest~? And how can we test each of them?
- Hyperinsulinemia - high concentrations all the damn time - TEST WITH - resting insulin concentrations
- Excessive insulin response to oral carbohydrates - peaks throughout day when they’re eating
TEST WITH - oral glucose test/oral sugar test - fast, given glucose, measure insulin levels - Tissue insulin resistance - tissues not responding
TEST WITH - insulin tolerance test - not fasted, insulin, take blood at 0 and 30 minutes
How do we treat/manage EMS?
Diet - no grain or pasture
Ideal - feed only hay, soak hay to decrease calories
Exercise
Metformin - increase insulin sensitivty
Thyroxine - increases metabolic rate resulting in weight loss
What are 2 signs NOT associated with Cushing’s?
Inappetence
Pruritis
What are common signs seen with Cushing’s?
PU/PD PANTING!! - cortisol in body Poor hair coat Inactive "Old for their age" Epaxial muscle wasting - spine
When a cat has diabetes that is hard to manage, what are the 2 likely reasons?
Has Cushing’s or has hypersomatotrophism
Feline Cushing’s get skin tears/lesions
What would we see on a blood test for an animal with Cushing’s?
Stress leukogram
ALP»_space; ALT (1000 - 250)
Hypercholesterolemia
What is the best test to diagnose Cushing’s and how does it work?
Low Dose Dexamethasone Suppression Test (LDDST)
Measure cortisol at 0, 4, 8 hours after giving Dex at 0.01 mg/kg IV
Normal cortisol should DECREASE for 8 hours
If not suppressed at 4 hours or 8 hours - adrenal depedent - adrenals making a shit ton of cortisol
If suppresses at 4 hours and rebounds at 8 hours = PITUITARY DPDT - adrenals will not suppress at all
How can we tell on the US if Cushing’s is pituitary-dependent or adrenal dependent?
If adrenal dependent - usually will only see a unilateral enlargement of the adrenal gland
If pituitary-dependent - will see a bilateral enlargement of adrenal glands
What is the treatment for Cushing’s?
TRILOSTANE BABY! - suppresses cortisol production
Trilostane increases ACTH –> increased blood flow to adrenals –> destruction of the gland
ADH - surgery to remove offending adrenal gland
PDH - could do hypophysectomy
What is seen in an Addisonian crisis?
Acute collapse
Hypovolemia signs
Poor circulation
Tachy/bradycardia
What are some symptoms of Addison’s?
Called the great pretender - a lot of non-specific signs GI abnormalities - V/D Lethargy Inappetence Melena
What are two specific things on blood work you would see with Addison’s?
Decreased serum Na - not retaining it with aldosterone and Increased serum K
Opposite of stress leukogram=
- decreased neutrophils, monocytes
- increased lymphocytes, eosinohils
What test do you use to diagnose Addison’s? How does it work?
ACTH Stim test
Take basal cortisol levels
Give ACTH analog
1 hour later take another cortisol level (blood)
With Addison’s will not increase AT ALL
Should have subnormal levels of cortisol before and after ACTH
What is the treatment for Addisonian crisis/Addison’s?
Crisis - IVFT, Hormone supplementation, mineralo/glucocorticoids, hydrocortisone sodium succinate
Addison’s - treat with oral meds - Pred/Florinef
What small mammal is most susceptible to DM?
DEGUS!!! - get type 2 insulin resistance
What endocrine disorder is most common in guinea pigs?
Thyroid disorders - hyperthyroid
Weight loss, thyroid palpation, bilateral alopecia, hyperactive, polyphagia
TMT = surgery to remove thyroid or methimazole/radioactive iodine
What is the difference with Cushing’s in ferrets?
SEX HORMONE DEPENDENT
With lack of mating –> increased estrogen (since only ovulate when mating)
Adrenals have sex hormone receptors
Leads to HAC signs but caused by sex hormones
(sorry I’m trying to make this simple af because I dont have time to learn about a mf ferret)
