Endocrine 2 Flashcards
Why are e-lytes affected w/ Addison’s, not Cushings?
Addisons =GC + MC’s
Cushings =GC only
3 forms of Cushings
1 - Pituitary dependent
• ↑ ACTH production (dog)
2- Adrenal dependent
•adrenocortical adenoma
3 - Iatrogenic
• Adrenal atrophySignalment of Cushing’s dog
- Middle aged / older dog
- PU / PD / PP
- bilateral alopecia
- pot-belly
- thin-skinned
- Calcinosis cutis
- Weak/lethargic
- “old dog”
Signalment of Cushing’s cat
- Extra thin Skin –> tearing
- STRONG assoc w/ DM (75% of cushiness = DM)
• Mostly Pituitary origin
Signalment of Cushing’s horse
not the same pathogenesis (Adenoma of Pituitary Pars intermedia)
• Hirsutism
Erythron of Cushing’s patient
↑ androgens –> Stimulate polycythemia
• high Hct (may seem like dehydration, w/o other evidence)
• inappropriate polychromasia w/ nRBCs
Clin Chem changes assoc’d w/ Cushings
• ↑ ALP (cALP)
- mild ↑ ALT/GGT
• ↑ glucose (no glucouria)
• ↑ cholesterol / lipemia
• USG -- GC block ADH at kidney/centralWhat are atypical changes in liver enzymes for Cushings
Lg’er elevations in ALT / GGT / Bc
• more than drug induction
• indicate hepatopathy
- hydropic change (glycogen) –> swelling –> block canuliculi
What might you see in a Equine cushing’s patient that is diff than other species
Glucosuria
- due to higher levels of circulating glucose
Pathogenesis of Cushings to DM
GC anatagonist to insulin –> burn out –> DM
Why do you see ↑ cholesterol/ lipemia?
Antagonize insulin –> ↑ lipoprotein lipase activity –> ↓ lipoprotein breakdown –> prolong cholesterol +/- TG 1/2 life
Signalment & presenting signs of Addison’s
- Young / middle aged dog (cat = rare)
- Female
- GI signs (vomiting)
- Bradycardia (from ↑ K)
- Addisonian crisis - cardiovascular collapse & shock
CBC/chem of Addison’s
- Lack of stress response (w/ ill dog)
- lymphs / eosins (maybe elevated)
• ↓ glucose (37%) - lack of basal GC
• ↑ K
• ↓ Na
• < 23:1 Na:K ratio (strongly suggestive)
• ↑ Ca possible
• Pre-renal azotemia (vomiting)
- ↓ Na –> 2° renal azotemia (medullary washout)
If you see ↑ K/ ↓ Na (ratio < 23:1) what are the possible ddx?
• Addisons!!
• Consider parameters individually
- GI sequestration + acidosis – could cause this too
Describe Thyroid hormone
• 80-90% secreted as T4
• 99% is protein bound
- free T3 = 3-5x’s»_space; free T4 activity
What is ↓ protein’s affect on thyroid?
↓ total thyroid measure – in euthyroid animal
Signalment of hyperthyroid
- older cat
- hyperactive
- thin
- PP
( hyperplasia / adenoma )
CBC/chem assoc’d w/ hyperthyroid
- polycythemia (50%)
- ↑ Heinz bodies
• ↑ ALT, ALP
- 2/3 cases show enzyme ↑ -- reasons unclear - DON'T think these ONLY mean liver!
Dz assoc’d w/ heinz bodies in cats
1 - Hyperthyroid
2- DM
3- Lymphosarcoma
4- Exogenous oxidants - acetaminophen, onion tox
• New methylene blue stain
Signalment for Hypothyroid
- Doberman / Dachshund / cocker
- middle aged
- Mid-sized
- Heat-seeker & hypothermic W/O shivering
- Obesity
- Bilateral alopecia w/ dry skin
Glandular atrophy / lymphocytic thyroiditis
What are clinical signs that are assoc’d w/ Critical condition hypothyroid?
- Weakness
- NON-pitting edema
- Serous cavity effusion
• Myxedema w/ stupor = rare life-threatening
CBC assoc’d w/ Hypothyroid
• Mild non-regenerative anemia
- ↓ oxidative metabolism – body is good at ↓ Hct
• usually no stress leukogram
– differentiated it from cushings!
Chemistry assoc’d w/ hypothyroidism
• ↑ cholesterol
- > 500 = strongly suggests hypothyroid
Ddx for ↑ cholesterol
1 - Hypothyroid ( >500) 2- Pancreatitis 3- Cholestasis 4- DM 5- Renal failure (nephrotic syndrome)
What is “Sick Euthyroid Syndrome”?
Should you supplement T4?
Degree of ↓ correlated w/ degree of sickness (ICU patients)
- protective mechanism to ↓ metabolism during Negative nitrogen balance
- Do not give T4 – will correct itself
Dz / Drugs assoc’d w/ Sick Euthyroid Syndrome
Dz • Cushings / Addisons • DM • Chronic renal failure • Liver dz • Pyoderma
Drug • Anesthetics • Glucocorticoids • NSAIDs • Furosemide • Anti-convulsants
- resolve 1° condition
Hormones that regulate Ca++
PTH
- ↑ Ca ↓ P
Calcitonin
- ↓ Ca ↓ P
Vitamin D
- ↑ Ca ↑ P
Ddx of hypercalcemia
- 1° hyperparathyroidism
- Humoral hypercalciemia of malignancy
- Hypervitaminosis D
- addisons
- granulomatous dz involving bone
Horse
• Renal dz
Classic pattern of 1° hyperparathyroidism
↑ Ca / ↓ P
↑ Ca –> deposits in tubules –> renal failure
• Phos may be normal if renal failure (due to ↑ retention)
Most common cause of significant hypercalcemia
Humoral hypercalcemia of Malignancy
• Lymphosarcoma
• Anal sac adenoma
Classic pattern hypervitaminosis D
↑ Ca / normal to ↑ Phos (even w/o azotemia)
• if there is azotemia –> you may want to interpret it as ↑ Phos due to azotemia, but should be thinking about ↑ Vit D too!
Differentiate btwn 1° renal failure & hypercalcemia-induced renal failure, using ↑ Ca
1° renal failure
–> mild ↑ in Ca
Hypercalcemia induced renal failure
• ↑ ↑ ↑ Ca –> renal failure
1 cause for Hypocalcemia
Hypoalbuminemia
- mild change
Causes for hypocalcemia
1 - hypoalbuminemia
2- Renal failure (non-equine)
- esp. Ethylene glycol tox
3- Hypoparathyroidism
4- Pancreatitis
5- Parturient paresis
6- Hypomagnesemia
7- Blister beetles
8- Mercurial skin compound (horse)Hypoparathyroid
↓ Ca ↑ Phos
• measure PTH during hypocalcemia
- if low during this time = hypocalcemia
Parturient paresis
Milk fever = cow
↓ Ca –> ↓ Ach release –> flaccid paralysis
Eclampsia = Bitch & mare
↓ Ca –> ↓ membrane stability –> ↑ firing –> Puerperal tetany
Hypomagnesemia
- Grass tetany
- Seasonal/winter tetany
- calves on whole milk for extended time
Clinical signs of hypomagnesemia
- hyper-excitability
- Twitching
- staggering
- paresis
- tetany
- convulsion
what ion is assoc’d with Mg? What does it do with hypomagnesemia?
Ca
• Mg required for PTH release
• may contribute to clinical signs
Phos
• mild ↓
What is the toxin assoc’d w/ blister beetles?
What are the assoc’d lesions?
Cantharidin
• often find them in alfalfa
** Combined GI symptoms, Renal dysfunction, ↓ Ca
