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Insulin shock

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Title: Insulin shock


1
DISEASES OF THE PANCREAS
  • Insulin shock

2
Insulin Shock
  • Causes
  • Insulin overdose (misread syringe)
  • Too much exercise
  • Anorexia
  • Signs
  • Weakness, incoordination, seizures, coma

3
Insulin Shock
  • Prevention
  • Consistent diet (type and amount)/consistent
    exercise (less insulin with exercise)
  • Monitor urine/blood glucose at same time each day
  • Feed 1/3 with insulin the rest 8-10 h later (at
    insulin peak)
  • Have sugar supply handy

4
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,

5
Insulinoma Dx
  • Chem Panel
  • ?blood glucose
  • Simultaneous glucose and insulin tests
  • Low glucose, High insulin gt insulinoma
  • Observations of Whipples Triad
  • Symptoms occur after fasting or exercise
  • when symptomatic, blood glucoselt50 mg/dl
  • symptoms corrected with sugar administration

6
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) injectionsinhibits
    synthesis and release of insulin by both normal
    and neoplastic beta cells

7
Insulinoma Client info
  • 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 dogs mouth during
    seizure to avoid being bitten

8
Diseases of the exocrine pancreas
  • Exocrine Pancreatic Insufficiency

9
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

10
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

11
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

12
Client considerations
  • Usually life long treatment.
  • Can be very expensive.
  • Can be well controlled.
  • Should not breed animal that has EPI.

13
DISEASES OF THE ADRENAL GLANDS
  • CUSHINGS DISEASE
  • (Hyperadrenocorticism)
  • ADDISONS DISEASE
  • (Hypoadrenocorticism)

14
Adrenal Glands
15
ADRENAL GLANDS
mineralocorticoids Glucocorticoids Androgens
epinephrine
16
Physiology
  • Hypothalamus Corticotropin realeasing factor
    (CRF) gt Anterior Pituitary Gland
    Adrenocorticotropic hormone (ACTH)
  • gt ADRENAL CORTEX
  • Glucocorticoid hormone
  • Mineralocorticoid hormone
  • Sex hormones (Androgens)
  • Sympathetic Nerv Sys gt ADRENAL MEDULLA gt
    Epinehrine and norepinephrine
  • Increase HR, Inc. BP, Dilated air passages
    lungs, dec. GI function, vasoconstriction

17
Hormone Functions
18
Hyperadrenocorticism (Cushings 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

19
Cushings 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

20
Cushings Disease
21
Cushings Disease
Bilaterally symmetrical alopecia, pot-belly,
pyoderma
22
Cushings Disease
Pot bellied PU/PD Muscle wasting Thin coat
23
Cushings Disease
signs are slow to develop and usually go
unnoticed by owner
  • Clinical Signs
  • Some are similar to hypothyroidism
  • Dog gt6 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)

24
Cushings Disease Calcinosis cutis
Commonly seen on the dorsal midline, ventral
abdomen and inguinal region. Skin is usually
thin and atrophic
25
Cushings Disease Dx
  • Chemistry Panel
  • ? ALP, ALT, cholesterol, blood glucose
  • ? BUN
  • Lipemia
  • Low USG lt 1.015, proteinuria, hematuria, pyuria,
    bactiuria
  • Urine cortisol/creatinine ratios (sample
    collected at home)
  • Normal rationo Cushings
  • Elevated ratiomay be Cushings
  • 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

26
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

27
Cushings 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)

28
Cushings Disease Dx
  • High-Dose Dexamethasone Suppression Test (used to
    differentiate between Pit Dis and Adrenal tumor)
  • Collect plasma cortisol at 0, 4, and 8 h
  • Interpretation
  • Pituitary dependent disease70-75 will show
    decrease at 4 or 8 h
  • Adrenal tumorno change in plasma cortisol level
    (tumor is autonomous)

29
Cushings Disease Rx
  • Surgical removal
  • 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 (Addisons Dis)

30
Cushings Disease Rx
  • 2. trilostane (Vetoryl)less side-effects than
    o,p,DDD
  • -interfers with cortisol production (doesnt
    kill cells)
  • -FDA approved

31
Cushings Disease Client info
  • Serious disease life-long treatment
  • Periodic monitoring required
  • Addisons disease may result
  • Prognosis average life expectancy is 20-30 mo on
    therapy with frequent recurrence of clinical
    symptoms varies with cause (pit vs adrenal,
    tumors)

32
Addisons 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

33
Addisons Disease (Hypoadrenocorticism)
  • Clinical Signs
  • lethargy, weakness, anorexia, wt loss
  • Vomiting/Diarrhea
  • PU/PD, dehydration
  • Bradycardia

34
Addisons Disease
  • Pathophysiology
  • Decreased aldosterone gt Increased K and
    decreased Nagt decreased volume gt azotemia,
    hypotension, dehydration, weakness, depression
  • Hyper K gt heart (bradycardia)
  • Glucocorticoid deficiency gt vomiting, diarrhea,
    melena, lethargy, wt loss, hypoglycemia (less
    common than expected)

35
Addisons Disease Dx
  • Chem Panel
  • NaK ratio lt251!(normal271 to 401)
  • ? 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)

36
What is your Dx?
  • Chem Panel (What is not normal?)
  • Parameter Value Normal value
  • BUN 81 mg/dl 7-27 mg/dl
  • Creatinine 2.1 mg/dl 0.4-1.8 mg/dl
  • Sodium 131 meq/L 141-156 meq/L
  • Potassium 6.5 meq/L 4.0-5.6 meq/L
  • NaK ratio 20 27-40

37
What is your Dx?
  • ACTH Stimulation Test Results
  • Value Normal
  • Plasma Cortisol
  • Pre-ACTH 0.2 2-6
  • Post-ACTH 0.3 6-18

38
Addisons Disease Tx
  • Acute Crisis (may be life-threatening situation)
  • Normal saline IV (low Na is hallmark finding of
    Addisons)
  • Glucorticoid replacement(cortisol will also be
    low)
  • Dexamethasone or Prednisone (IV or IM)
  • Mineralocorcorticoid replacement
  • Florinef (fludrocortisone acetate)po
  • Percortin-V (desoxycorticosterone pivalate)
    injection

39
Addisons disease TX
  • Chronic Management
  • Glucocorticoid replacement
  • Prednisone
  • Prenisolone
  • Mineralocorcorticoid replacement
  • Florinef (fludrocortisone acetate)po daily (not
    cheap 50/tab)
  • Percortin-V (desoxycorticosterone pivalate)inj
    monthly (expensive)
  • Monitor electrolytes, BUN/Creatinine, clinical
    signs

40
Addisons disease Client info
  1. Mineralocorticoid deficiency is life-threatening
  2. Animal requires periodic blood tests
  3. Glucocorticoids needed in times of stress
  4. Always remind attending vet of pets condition
  5. Hormone replacement therapy continued for life of
    pet
  6. Prognosis Good to excellent after
    stabilization and treatment

41
References
  • Alleice Summers, Common Diseases of Companion
    Animals
  • http//www.aahanet.org/PublicDocuments/AAHADiabete
    sGuidelines.pdf
  • http//www.vetmed.wsu.edu/cliented/diabetes.aspx
  • http//www.sciencedirect.com/science/article/pii/S
    0378427408001732
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