education education is learning what you didn’t even know you didn’t know. - daniel j. boorstin
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EDUCATIONEducation is learning what you didn’t
even know you didn’t know.-Daniel J. Boorstin
DISEASES OF THE PARATHYROID GLANDS
HYPERPARATHYROIDISM
HYPOPARATHYROIDISM
Thyroid/Parathyroid glands
1=normal thyroid gland2 and 3=parathyroid gland4=enlarged thyroid gland
2 glands for each thyroid lobe2 glands for each thyroid lobe
Parathyroid gland
• Secretion: Parathyroid hormone (PTH, Parathormone)
• Function: ↑ plasma Ca2+ concentration– 1. ↑ osteoclast activity– 2. ↑ Ca++ absorption from GI tract– 3. ↑ Ca++ reabsorption from kidney tubules
• Hyperparathyroidism → ________________• Hypoparathyroidism → __________________
Hyperparathyroidism
• Causes:– 1º hyperparathyroidism— ___________________________
– 2º hyperparathyroidism—poor diet; low Ca intake
• Clinical signs:– Many animals show __________________________
– signs occur as organ dysfunction occurs
• urinary/renal calculi (high plasma Ca++)
• cardiac arrhythmias, tremors (Ca++ necessary for normal muscle contraction)
• Anorexia, vomiting, constipation
• weakness
Signalment: 7-11 yrs; Keeshoondren
Hyperparathyroidism
Dx:• Routine chemistry panel
– ↑ blood Calcium (normal: ~ _____________ mg/dl))
– +/- ↓ blood Phosphorus (normal: ~2-6 mg/dl)
• PTH assay– normal PTH: dogs ~20 pg/ml, cats ~17 pg/ml– In a normal animal: if blood Ca++ is high, PTH is low (neg feedback)
– 1º Hyperparathyroidism: ______________________________
• Ultrasound of neck – enlarged glands, abdomen - uroliths
Dff: neoplasia (LSA), Addison’s, rodenticide toxicosis, ARF
Hyperparathyroidism
Tx:1. _________________________ of diseased parathyroid (generally 4 lobes are imbedded in thyroid gland)
Other options:2. Ultrasound-guided chemical (ethanol)
3. Ultrasound-guided heat (laser) ablation
Post-Op Care:1. Hospitalize for 1 wk; ↓PTH may predispose animal to hypocalcemia2. _____________________ (oral tabs, liquid)3. Vit D supplements (promotes Ca intestinal absorption)
Hyperparathyroidism
Client Info
1. Most hyperparathyroid animals show no signs when first diagnosed
2. Run _____________ chem panels on all normal, older animals
Hypercalcemia: Other causes
• Causes– Neoplasia (lymphoma, perianal gland
tumors)– Renal failure– Hypoadenocorticism– Vitamin D rodenticide– Drugs or artifacts (ex lipemia)
• Clinical signs vary with cause– PU/PD, anorexia, lethargy, vomiting,
weakness, stupor/coma (severe), uroliths
Hypercalcemia
• Tests– Elevated serum calcium levels
– Low to low-normal phosphorus concentrations
Hypercalcemia
• Treatment– Fluids: 0.9% NaCl
• No Ca2+ containing fluids
– Diuretics (furosemide): dilute urine
– Steroids
• Complications– Irreversible renal failure
– Soft tissue calcifications
Hypocalcemia
Causes:1. Parathyroid disease
a. Inadvertent removal of ____________________ during thyroidectomy (most common cause
b. 1º Hypoparathyroidism (uncommon in animals)
2. Chronic renal failure—a. may cause ↑ serum P, which can result in ↓ serum Ca (Ca:P __________________)b. Vit D normally activated in kidneyc. Protein-losing nephropathy results in loss of albumin-bound Ca
3. Puerperal Tetany (Eclampsia)—late gestation thru post-partum perioda. Improper prenatal ______________________________________b. Heavy lactationc. Inappropriate Ca++ supplementationd. Post-partum and late gestaion
http://www.thepetcenter.com/gen/eclampsia.html#The_video
Hypocalcemia
Clinical Signs:1. Restlessness, muscle tremors, tonic-clonic contractions,
seizures
2. ______________________ with excitement; __________________ in severe cases (Ca++ is necessary for proper muscle contractions)
3. Hyperthermia
4. Stiffness, ataxic
Hypocalcemia
Dx:Total serum < ______________ mg/dl
Tx:1. IV infusion of _______________________
solution (monitor HR and rhythm during infusion)2. ___________________ (IV) to control seizures3. Oral supplements of Ca (tabs, caps, syrup)4. Improve nutrition
Hypocalcemia
Client info:
1. Well-balanced diet; increase volume as pregnancy progresses
2. Signs in pregnant animal is _____________; call vet immediately
3. May recur with subsequent pregnancies
4. Early weaning is recommended
LIFE“Nobody can go back and start a new beginning, but anyone can start today
and make a new ending.”
-Maria Robinson
DISEASES OF THE PANCREAS
DIABETES MELLITUS (DM)INSULINOMA
EXOCRINE PANCREATIC INSUFFICIENCY (EPI)
Review of pancreas functions
• Long flat organ near _________________ and stomach
• Exocrine function (the majority of the pancreas):– ________________ enzymes
• Endocrine function – islets of Langerhans– Alpha cells => _______________– Beta cells => ___________________– Delta cells => ___________________
Pancreas
Pancreas: beta cells
Review
• Insulin – Moves glucose into ___________ to be used for energy
(glycolysis)
– _______________ blood glucose
• Glucagon– _________________ blood glucose
• Stimulates liver to release glucose
• Stimulates gluconeogenesis– Other hormones from other glands perform similar functions
(hyperglycemic effect)
• Growth hormone
• Glucocorticoids
Endocrine Pancreas
• Hyperglycemia– Definition: Excessively high blood glucose
levels• Normal in dogs: _________________ mg/dl
• Normal in cats: __________________ mg/dl
Diabetes Mellitus
• Definition: Disorder of carbohydrate, fat and protein metabolism caused by an absolute or relative ___________ deficiency
• Type I – Insulin Dependent DM – very low or absent insulin secretory ability
• Type II – Non insulin dependent DM (insulin insensitivity) – inadequate or delayed insulin secretion relative to the needs of the patient
Diabetes mellitusIncidence:
Dogs: ~100% Type I (Insulin dependent)Cats: ~ 50% Type I and 50% Type II
-non-insulin dependent catscan sometimes be managed withdiet and drug therapy
Causes: Chronic pancreatitis_______________________________ -beta cell destruction
Predisposing/risk factors:Cushing’s DiseaseAcromegalyObesityGenetic predispositionDrugs (steroids)
Diabetes mellitus
• Age/sex: – Dogs: 4-14 yrs, females 2x more likely to
be affected
– Cats: all ages, but 75% are 8-13yrs, neutered males most affected
• Breeds: Poodles, Schnauzers, Keeshonds, Cairn Terriers, Dachshunds, Cockers, Beagles
DM
• Pathophysiology– Insulin deficiency => impaired ability to use glucose from
______________, __________________ and _______________
– Impaired glucose utilization + gluconeogenesis => hyperglycemia
– Clinical signs develop when:• Exceeds capacity of renal tubular cells to reabsorb
• Dogs – BG > ________________ mg/dl
• Cats - BG > __________________mg/dl
– Glycosuria develops• Osmotic diuresis
• Polyuria/polydipsia
DM• SYSTEMS AFFECTED:
– Endocrine/metabolic: electrolyte depletion and metabolic _________________
– Hepatic: liver failure 2° to hepatic lipidosis (mobilization of free fatty acids to liver leads to hepatic lipidosis and ketogenesis)
– Ophthalmic: __________ (dogs) from glaucoma
– Renal/urologic: UTI, osmotic diuresis– Nervous: peripheral neuropathy in cats– Musculoskeletal: Compensatory weight
loss
Diabetes Mellitus
• Clinical Signs:– ____________________
– ____________________
– Weight loss (esp. cats)
– Dehydration
– Cataract formation-dogs
– Plantigrade stance-cats
Plantigrade postureDiabetic neuropathy
Diabetes in Cats:Plantigrade posture
Diabetes: Cataracts
Increase in sugar (sorbitol) in lens causes an influxof water, which breaks down the lens fibers
Diabetic Ketoacidosis
2 metabolic crises: ↑ lipolysis in adipose tissue → fatty acids →ketone bodies →ketoacidosis →coma (insulin normally _________________ lipolysis)↑ hepatic gluconeogenesis (in spite of high plasma glucose levels)
(insulin normally ____________________ gluconeogenesis)
Diabetic Ketoacidosis
• Definition: True medical _______________ secondary to absolute or relative insulin deficiency causing hyperglycemia, ketonemia, metabolic acidosis, dehydration and electrolyte depletion
• DM causes increased lipolysis => _________ production and _______________
Diabetic Ketoacidosis
• Diagnosed with ketones in urine or ketones in blood – Can use urine dip stick with serum.
• Clinical Signs– All of the DM signs
– Depression
– Weakness
– Tachypnea
– Vomiting
– Odor of acetone on breath
Diabetic Ketoacidosis
• IV fluids to rehydrate 0.9% NaCl – K (potassium) supplement
• Regular insulin to slowly decrease BG
• Monitor BG q 2-3 hrs
• When BG close to normal and patient stable switch to longer acting insulin
DM
• DIAGNOSIS:– CBC: normal– Biochemistry panel:
• Glucose > ________mg/dl (dogs), > _____________ (cats)
– UA• ____________________!!!!• ______________________• USG – low
– Electrolytes may be low due to osmotic diuresis– Blood gases (if ketoacidotic)– Fructosamine levels – mean glucose level for last 2-3 weeks
(dogs)• Ideal to test for regulation checks
DM Rx: INSULIN AND DIET!!!Table 1. Traditional insulin outline.
Duration/onset category
Insulin types Concentration
Rapid acting (emergency)
Regular (Humulin R) U-100 (100 units/ml)
Intermediate acting NPH (Humulin N) U-100
Lente (Vetsulin® by Intervet) NO LONGERAVAILABLE*
U-40 (40 units/ml)
Long acting PZI (Idexx) U-40
Ultralente NO LONGERAVAILABLE*
U-100
Glargine insulin analog U-100
Diabetes: Insulin therapy
DM: Insulin therapy
• INSULIN
– Beef-origin insulin is biologically similar to cat insulin
– Porcine-origin insulin is biologically similar to dog insulin
– Dogs and cats have responded well to human insulin products
• INSULIN ADMINISTRATION:
– ALWAYS USE THE ______________________ INSULIN SYRINGE! (U-40 vs. U-100)
• Insulin is given in units (insulin syringes are labeled in units, not mL)
DM: dietary management
• DIET– DOGS: high _____________-, complex carbohydrate diets
• Slows digestion, reduces the post-prandial glucose spike, promotes weight loss, reduces risk of pancreatitis
• Hill’s R/D or W/D– CATS: high _______________, low carbohydrate diets
• Cats use protein as their primary source of energy – blood glucose is maintained primarily through liver metabolism of fats and proteins
• Purina DM, Hill’s M/D• Often a diet change in cats can dramatically reduce or
eliminate the need for insulin– This is particularly true for type II
DM
• Oral hypoglycemics (cats NIDDM)o Sulfonylureas – Glipizide
oDirect stimulation of insulin secretion from the pancreas
oAlpha-Glucosidase Inhibitors – Acarbose (dogs)oDelays digestion of complex carbohydrates and delays
absorption of glucose from the intestinal tract.
Diabetes Mellitus: Monitoring
Find an ear vein Prick the ear to get Place drop of blood blood sample on green tip; readout in
a few seconds
Diabetes Rx: Urine glucose
Diabetes monitoring: Urine glucose
DM
• Client Education– ______________________ insulin replacement therapy– Insulin administered by _______________________________– _____________________ insulin, mix _____________ (no
bubbles), single use syringes– Cataracts common, permanent– Consistent diet and exercise– Recheck BG or curve regularly or fructosamine levels– Progressive– If animal _________________- NO INSULIN
Endocrine Pancreas
• Hypoglycemia– Definition: Low blood glucose levels– Causes
• Neonatal and juvenile• Septicemia• Neoplasia• Starvation• Iatrogenic – insulin overdose• Portosystemic shunt• Many others
Insulin Shock
Causes:
1. Insulin overdose (____________ syringe)
2. Too much exercise
3. Anorexia
Signs:
Weakness, incoordination,_______________, coma
Insulin Shock
Prevention
1. ________________ 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: ______________ of beta cells, secreting an excess of insulin
• SIGNS: prolonged ______________________ →weakness, ataxia, muscle fasciculations, posterior paresis, brain damage, seizures, coma, death,
Insulinoma: Dx
• Chem Panel– ↓blood glucose
– Simultaneous glucose and insulin tests
____________ glucose, __________________ insulin => insulinoma
• Observations– Symptoms occur after _______________ or _________________
– when symptomatic, blood glucose< ______________ mg/dl
– symptoms corrected with sugar administration
Insulinoma: RxSurgical Rx: removal of tumorMedical Rx: Acute, at home: administer glucose (Karo); keep animal quiet, seek vet careAcute, in Hosp adm. glucose (50% Dextrose)Chronic care feed 3-6 small meals/day (high protein, low fat)
limited exerciseglucocorticooid 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• 1. Usually, by the time insulinoma is diagnosed, metastasis has occurred
so prognosis is ______________________
• 2. With proper medical therapy, survival may be 12-24 mo
• 3. Always limit _____________ and _________________
• 4. Feed __________ , ________________meals throughout day; keep sugar source close during exercise
• 5. _________________________ 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
Exocrine Pancreas Insufficiency (EPI)
• Inability to process nutrients efficiently due to ____________ 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 ____________ % of pancreas is unable to secrete enzymes.– _________________ 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 ____________________ in dogs to be diagnostic • Canine 5.7-45.2
• Feline 12-82
• Treatment includes enzymatic supplement– ___________________ powder (Amylase, protase, lipase)
– 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.
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