1. Diseases of the exocrine pancreas
Exocrine Pancreatic Insufficiency

2. Exocrine Pancreas Insufficiency (EPI)
Inability to process nutrients efficiently due to lack of production of enzymes from pancreas.
Pancreatic acinar atrophy
Found most commonly in German Shepherds and Rough Collies through a recessive gene.
In cats, EPI is primarily the result of chronic pancreatitis

3. Diagnosis of EPI
Not usually evident until 85-90% of pancreas is unable to secrete enzymes.
Weight loss although no change in diet or appetite (appetite often increases)
Persistent tarry diarrhea.
Flatulence
Poor haircoat

4. Testing and treatment for EPI
TLI (trypsin-like immunoreactivity)
Detects trypsin and trypsinogen
Usually want below 2.5 in dogs to be diagnostic
Canine
Feline 12-82
Treatment includes enzymatic supplement
Viokase powder
Raw ox or pig pancreas

5. Client considerations
Usually life long treatment.
Can be very expensive.
Can be well controlled.
Should not breed animal that has EPI.

6. DISEASES OF THE ADRENAL GLANDS
CUSHING’S DISEASE
(Hyperadrenocorticism)
ADDISON’S DISEASE
(Hypoadrenocorticism)

7. Adrenal Glands

8. ADRENAL GLANDS mineralocorticoids Glucocorticoids Androgens
epinephrine

9. Physiology
Hypothalamus – Corticotropin realeasing factor (CRF) >>> Anterior Pituitary Gland – Adrenocorticotropic hormone (ACTH)
>>> ADRENAL CORTEX
Glucocorticoid hormone
Mineralocorticoid hormone
Sex hormones (Androgens)
SNS >>> ADRENAL MEDULLA >>> Epinehrine and norepinephrine
Increase HR, Inc. BP, Dilated air passages – lungs, dec. GI function, vasoconstriction

10. Hormone Functions Mineralocorticoids – Aldosterone
Regulates electrolyte and H2O balance
Hypoadrenocorticism/ Addison’s
Primarily Dogs
Life threatening
Glucocorticoids
Promote gluconeogenesis
Suppress inflammation
Suppress immune system
Inhibit cartilage growth and development
Hyperadrenocorticism / Cushing’s

11. Hyperadrenocorticism (Cushing’s Disease)
Definition: Disorder caused by deleterious effects of high circulating cortisol concentrations on multiple organ systems
Systems affected:
Renal
Skin
Cardiovascular
Respiratory
Endocrine/metabolic
Musculoskeletal
Nervous
Reproductive

12. Cushing’s Disease Effects of excess glucocorticoids:
suppress inflammation
suppress immune system
inhibit cartilage growth, development,
and repair
Causes:
Anterior pituitary lesion (pituitary-dependent disease) – 85% of cases
Adrenal tumor (excess cortisol secretion independent of pituitary control) – 15-20% of cases
Overmedication with glucocorticoids - Iatrogenic

13. Cushing’s Disease

14. Cushing’s Disease
Bilaterally symmetrical alopecia, pot-belly, pyoderma

15. Cushing’s Disease
Pot bellied
PU/PD
Muscle wasting
Thin coat

16. Cushing’s Disease Clinical Signs: Some are similar to hypothyroidism
signs are slow to develop and usually go unnoticed by owner
Clinical Signs:
Some are similar to hypothyroidism
Dog >6 yr old (most are female)
PU/PD/PP
Pot bellied; obese
Muscle atrophy and weakness, lethargy, excess panting
Bilateral symmetric alopecia; pruritis; pyoderma (↓ immune response)
Calcinosis cutis (firm plaques of Ca++ under skin)
Abnormal gonadal function (lack of estrus; soft, small testicles)

17. Cushing’s Disease: Calcinosis cutis
Commonly seen on the dorsal midline, ventral abdomen and inguinal region.
Skin is usually thin and atrophic

18. Cushing’s Disease: Dx Chemistry Panel
↑ ALP, ALT, cholesterol, blood glucose
↓ BUN
Lipemia
Low USG < 1.015, proteinuria, hematuria, pyuria, bactiuria
Urine cortisol/creatinine ratios (sample collected at home)
Normal ratio=no Cushing’s
Elevated ratio=may be Cushing’s
ACTH Stimulation test
Normal patients show an increase of plasma cortisol
Pituitary dependent disease (excess ACTH release) and Adrenal tumors: 60-85% show EXAGGERATED cortisol response
Does not differentiate between Pit disease and Adrenal tumor

19. ACTH Stimulation for Hyperadrenocorticism
Take a pre blood sample.
Inject ACTH stimulation gel or liquid
Verify amounts with lab as there is difference between amount to be injected with gel and liquid.
Wait two hours and take a post sample

20. Cushing’s Disease: Dx Low-Dose Dexamethasone Suppression Test
Inject low dose of steroid (should suppress ant. pit [ACTH])
Measure plasma cortisol at 0, 4, 8 h
Interpretation:
Normal dogs will show decrease in plasma cortisol
Pituitary tumor and adrenal tumor will not show any effect at 8 h (cortisol will still be high)

21. Cushing’s Disease: Dx
High-Dose Dexamethasone Suppression Test (used to differentiate between Pit Dis and Adrenal tumor)
Dosing: 0.1 mg/kg IV
Collect plasma cortisol at 0, 4, and 8 h
Interpretation:
Pituitary dependent disease—70-75% will show decrease at 4 or 8 h
Adrenal tumor—no change in plasma cortisol level (tumor is autonomous)

22. Cushing’s Disease: Rx Surgical removal— Medical treatment
FAT - Specialized surgery; most vets would refer surgery
Pituitary tumors are not surgically removed
Medical treatment
Lysodren (o,p,DDD)—necrosis of z fasiculata (middle), z reticularis (deep)
-repeat ACTH stimulation q 7-10 d until cortisol normal
-like chemotherapy
-excess dose affects z glomerulus (Addison’s Dis)

23. Cushing’s Disease: Rx
2. trilostane (Vetoryl®)—less side-effects than o,p,DDD -interfers with cortisol production (doesn’t kill cells) -FDA approved

24. Cushing’s Disease: Client info
Serious disease; life-long treatment
Periodic monitoring required
Addison’s disease may result
Prognosis: average life expectancy is mo on therapy with frequent recurrence of clinical symptoms – varies with cause (pit vs adrenal, tumors)

25. Hyperadrenocortism

26. Addison’s Disease (Hypoadrenocorticism)
Definition: Disorder caused by deficient production of glucocorticoids (cortisol) or mineralocorticoids (aldosterone) or both
Secondary disease caused by chronic administration of corticosteroids

27. Addison’s Disease (Hypoadrenocorticism)
Not as common as Cushing’s Disease; rarely seen in cats
Deficiency of Glucocorticoids and Mineralocordicoids
Clinical signs due to Mineralocorticoid (Aldosterone) deficiency
Clinical Signs:
lethargy, weakness, anorexia, wt loss
Vomiting/Diarrhea
PU/PD, dehydration
Bradycardia

28. Addison’s Disease Pathophysiology
Decreased aldosterone => Increased K and decreased Na
=> decreased volume => azotemia, hypotension, dehydration, weakness, depression
Hyper K => heart (bradycardia)
Glucocorticoid deficiency => vomiting, diarrhea, melena, lethargy, wt loss, hypoglycemia (less common than expected)

29. Addison’s Disease: Dx
Chem Panel Na:K ratio <25:1 !!!(normal=27:1 to 40:1) ↑ BUN, Creatinine, Ca++ ↓ blood glucose, albumin (less common ACTH Stimulation test (definitive test) normal dog= ↑ cortisol hypoadrenocorticism dog= low, unchanged cortisol level Endogenous ACTH will be increased (1º hypoadrenocorticism; lack of neg feedback)

30. What is your Dx? Chem Panel (What is not normal?)
Parameter Value Normal value
BUN 81 mg/dl mg/dl
Creatinine 2.1 mg/dl mg/dl
Sodium 131 meq/L meq/L
Potassium 6.5 meq/L meq/L
Na:K ratio

31. What is your Dx? ACTH Stimulation Test Results Value Normal
Plasma Cortisol
Pre-ACTH
Post-ACTH

32. Addison’s Disease: Rx Acute Crisis (may be life-threatening situation)
Normal saline IV (low Na+ is hallmark finding of Addison’s)
Glucorticoid replacement(cortisol will also be low)
Dexamethasone or Prednisone (IV or IM)
Mineralocorcorticoid replacement
Florinef® (fludrocortisone acetate)—po
Percortin-V (desoxycorticosterone pivalate) injection
Chronic Management
Glucocorticoid replacement
Prednisone
Prenisolone
Florinef® (fludrocortisone acetate)—po daily (not cheap; 50¢/tab)
Percortin-V (desoxycorticosterone pivalate)—inj ~monthly (expensive)
Monitor electrolytes, BUN/Creatinine, clinical signs

33. Addison’s disease: Client info
Mineralocorticoid deficiency is life-threatening
Animal requires periodic blood tests
Glucocorticoids needed in times of stress
Always remind attending vet of pet’s condition
Hormone replacement therapy continued for life of pet
Prognosis: Good to excellent after stabilization and treatment

34. Hypoadrenocorticism
Addison’s in crisis

35. References Alleice Summers, Common Diseases of Companion Animals