Transcript DISEASES OF THE PANCREAS

DISEASES OF THE
PANCREAS
INSULIN SHOCK
Insulin Shock
Causes:
1. Insulin overdose (misread syringe)
2. Too much exercise
3. Anorexia
Signs:
Weakness, incoordination, seizures, coma
Insulin Shock
Prevention
1. Consistent diet (type and amount)/consistent
exercise (less insulin with exercise)
2. Monitor urine/blood glucose at same time each day
3. Feed 1/3 with insulin; the rest 8-10 h later (at
insulin peak)
4. Have sugar supply handy
Insulinoma
 CAUSE: tumor of beta cells, secreting an excess of
insulin
 SIGNS: prolonged hypoglycemia→weakness, ataxia,
muscle fasciculations, posterior paresis, brain damage,
seizures, coma, death,
Insulinoma: Dx
 Chem Panel
 ↓blood glucose
 Simultaneous glucose and insulin tests
Low glucose, High insulin => insulinoma
 Observations of Whipple’s Triad:
 Symptoms occur after fasting or exercise
 when symptomatic, blood glucose<50 mg/dl
 symptoms corrected with sugar administration
Insulinoma: Rx
Surgical Rx: removal of tumor
Medical Rx:
Acute, at home:
administer glucose (Karo); keep animal quiet, seek vet care
Acute, in Hosp
adm. glucose (50% Dextrose)
Chronic care
feed 3-6 small meals/day (high protein, low fat)
limited exercise
glucocorticooid therapy (antagonizes insulin effect at cellular
level)
Diazoxide (↓insulin secretion, tissue use of glucose, ↑blood
glucose)
Octreotide (Sandostatin) injections—inhibits synthesis and
release of insulin by both normal and neoplastic beta cells
Insulinoma: Client info
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1. Usually, by the time insulinoma is diagnosed,
metastasis has occurred so prognosis is poor
2. With proper medical therapy, survival may be
12-24 mo
3. Always limit exercise and excitement
4. Feed multiple, small meals throughout day; keep
sugar source close during exercise
5. Karo syrup on mm provides for rapid absorption
of glucose into blood stream
6. Avoid placing hand into dog’s mouth during
seizure to avoid being bitten
Diseases of the exocrine
pancreas
EXOCRINE PANCREATIC
INSUFFICIENCY
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
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
Testing and treatment for EPI
 TLI (trypsin-like immunoreactivity)
 Detects trypsin and trypsinogen
 Usually want below 2.5 in dogs to be diagnostic
 Canine 5.7-45.2
 Feline 12-82
 Treatment includes enzymatic supplement
 Viokase powder
 Raw ox or pig pancreas
Client considerations
 Usually life long treatment.
 Can be very expensive.
 Can be well controlled.
 Should not breed animal that has EPI.
DISEASES OF THE ADRENAL GLANDS
CUSHING’S DISEASE
( H YP ER A DR EN O C O R TI C I SM )
ADDISON’S DISEASE
( H YP O A DR EN O C O R TI C I SM )
Adrenal Glands
ADRENAL GLANDS
mineralocorticoids
Glucocorticoids
Androgens
epinephrine
Physiology
 Hypothalamus – Corticotropin realeasing factor
(CRF) > Anterior Pituitary Gland –
Adrenocorticotropic hormone (ACTH)
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> ADRENAL CORTEX
Glucocorticoid hormone
 Mineralocorticoid hormone
 Sex hormones (Androgens)
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 Sympathetic Nerv Sys > ADRENAL MEDULLA >
Epinehrine and norepinephrine

Increase HR, Inc. BP, Dilated air passages – lungs, dec. GI
function, vasoconstriction
Hormone Functions
Mineralocorticoids – Aldosterone
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Regulates electrolyte and H2O balance
Hypoadrenocorticism/ Addison’s
Primarily Dogs
Life threatening
Glucocorticoids
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Promote gluconeogenesis
Suppress inflammation
Suppress immune system
Inhibit cartilage growth and development
Hyperadrenocorticism / Cushing’s
Hyperadrenocorticism (Cushing’s Disease)
 Definition: Disorder caused by deleterious
effects of high circulating cortisol concentrations
on multiple organ systems
 Systems affected:
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Renal
Skin
Cardiovascular
Respiratory
Endocrine/metabolic
Musculoskeletal
Nervous
Reproductive
Cushing’s Disease
Effects of excess glucocorticoids:
suppress inflammation
2.
suppress immune system
3.
inhibit cartilage growth, development,
and repair
Causes:
1.
1.
2.
3.
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
Cushing’s Disease
Cushing’s Disease
Bilaterally symmetrical alopecia, pot-belly, pyoderma
Cushing’s Disease
Pot bellied
PU/PD
Muscle wasting
Thin coat
Cushing’s Disease
signs are slow to develop and usually go unnoticed by owner
Clinical Signs:
1.
Some are similar to hypothyroidism
2.
Dog >6 yr old (most are female)
3.
PU/PD/PP
4.
Pot bellied; obese
5.
Muscle atrophy and weakness, lethargy, excess
panting
6.
Bilateral symmetric alopecia; pruritis; pyoderma
(↓ immune response)
7.
Calcinosis cutis (firm plaques of Ca++ under
skin)
8.
Abnormal gonadal function (lack of estrus; soft,
small testicles)
Cushing’s Disease: Calcinosis cutis
Commonly seen on the dorsal midline, ventral abdomen and inguinal region.
Skin is usually thin and atrophic
Cushing’s Disease: Dx
Chemistry Panel
1.
2.
3.
4.
↑ ALP, ALT, cholesterol, blood glucose
↓ BUN
Lipemia
Low USG < 1.015, proteinuria, hematuria, pyuria, bactiuria
Urine cortisol/creatinine ratios (sample collected at home)
1.
2.
Normal ratio=no Cushing’s
Elevated ratio=may be Cushing’s
ACTH Stimulation test
1.
2.
3.
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
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
Cushing’s Disease: Dx
Low-Dose Dexamethasone Suppression Test
1.
2.
Inject low dose of steroid (should suppress ant. pit [ACTH])
Measure plasma cortisol at 0, 4, 8 h
Interpretation:
1.
2.
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)
Cushing’s Disease: Dx
High-Dose Dexamethasone Suppression Test (used to
differentiate between Pit Dis and Adrenal tumor)
1.
Collect plasma cortisol at 0, 4, and 8 h
Interpretation:
1.
2.
Pituitary dependent disease—70-75% will show decrease
at 4 or 8 h
Adrenal tumor—no change in plasma cortisol level (tumor
is autonomous)
Cushing’s Disease: Rx
Surgical removal—
1.
2.
FAT - Specialized surgery; most vets would refer surgery
Pituitary tumors are not surgically removed
Medical treatment
1.
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)
Cushing’s Disease: Rx
2. trilostane (Vetoryl®)—less side-effects than
o,p,DDD
-interfers with cortisol production (doesn’t
kill cells)
-FDA approved
Cushing’s Disease: Client info
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Serious disease; life-long treatment
Periodic monitoring required
Addison’s disease may result
Prognosis: average life expectancy is 2030 mo on therapy with frequent
recurrence of clinical symptoms – varies
with cause (pit vs adrenal, tumors)
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 followed by
sudden cessation
Addison’s Disease (Hypoadrenocorticism)
Clinical Signs:
1.
2.
3.
4.
lethargy, weakness, anorexia, wt loss
Vomiting/Diarrhea
PU/PD, dehydration
Bradycardia
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)
Addison’s Disease: Dx
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Chem Panel
Na:K ratio <25:1!(normal=27:1 to 40:1)
↑ BUN, Creatinine, Ca++
↓ blood glucose, albumin (less common
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ACTH Stimulation test (definitive test)
normal dog= ↑ cortisol
hypoadrenocorticism dog= low, unchanged cortisol level
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Endogenous ACTH will be increased (1º
hypoadrenocorticism; lack of neg feedback)
What is your Dx?
Chem Panel
Parameter
BUN
Creatinine
Sodium
Potassium
Na:K ratio
(What is not normal?)
Value
81 mg/dl
2.1 mg/dl
131 meq/L
6.5 meq/L
20
Normal value
7-27 mg/dl
0.4-1.8 mg/dl
141-156 meq/L
4.0-5.6 meq/L
27-40
What is your Dx?
ACTH Stimulation Test Results
Value Normal
Plasma Cortisol
Pre-ACTH
Post-ACTH
0.2
0.3
2-6
6-18
Addison’s Disease Tx
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)
1.
2.
a.
Dexamethasone or Prednisone (IV or IM)
Mineralocorcorticoid replacement
3.
a.
b.
Florinef® (fludrocortisone acetate)—po
Percortin-V (desoxycorticosterone pivalate) injection
Addison’s disease TX
Chronic Management
Glucocorticoid replacement
1.
a.
b.
Mineralocorcorticoid replacement
2.
a.
b.
3.
Prednisone
Prenisolone
Florinef® (fludrocortisone acetate)—po daily (not cheap;
50¢/tab)
Percortin-V (desoxycorticosterone pivalate)—inj ~monthly
(expensive)
Monitor electrolytes, BUN/Creatinine, clinical signs
Addison’s disease: Client info
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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
References
 Alleice Summers, Common Diseases of Companion
Animals
 http://www.aahanet.org/PublicDocuments/AAHADi
abetesGuidelines.pdf
 http://www.vetmed.wsu.edu/cliented/diabetes.aspx
 http://www.sciencedirect.com/science/article/pii/S
0378427408001732