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249 Cards in this Set

  • Front
  • Back
Generally what are the two main types of hormones
Those made up of amino acids and do not enter the cells (attach to receptors i.e. ADH)

Those that enter the cell and have their effect inside the cell (thyroxine)
What are some organs involved in hormone production
Pituitary
Thyroid
Pancreas
Parathyroid
Adrenals
Ovaries
Placenta etc...
What hormones are produced by the anterior pituitary gland
TSH
GH
ACTH
FSH
LH
MSH (melanocyte stimulating hormone)
What hormone controls sodium and potasium regulation
Aldosterone
What does cortisol do
Regulates cell membrane integrity
What hormone is responsible for glucose regulation
Insulin
What hormone is responsible for growth regulation
Growth hormone
What hormone is responsible for water conservation
ADH
What is responsible for the release of hormones from the anterior pituitary gland
Releasing factors produced in the hypothalmus
True or False most hormones function on a positive feedback system
False most hormones function on a negative feedback system
What hormones are released by the posterior pituitary
Oxytocin
ADH
Where are ther hormones released from the posterior pituitary produced
Produced in the hypothalmus and transported via neurons to the posterior pituitary gland
True or False the pituitary is an extension of the hypothalmus
TRUE
What are the characteristics of diabetes insipidous
Large volumes of dilute urine

Insipid = tasteless
What are the two forms of diabetes insipidous
Central diabetes insipidous
Primary renal diabetes insipidous
Which form of diabetes insipidous is rare
Primary renal form of diabetes insipidous is very rare
True or False many times it is impossible to differentiate between central and primary renal diabetes insipidous
TRUE
What happens with central diabtetes insipidous
1. Lack of ability to produce ADH
2. Lack of appropiate response to increased osmolality
What is the normal trigger for ADH release
Increased serum osmolality
When is there maximal release of ADH
Maximal release of ADH occurs at 320 mOsm
True of False ADH release is increased by hypovolemia
TRUE why would I trick you
What is meant by nephrogenic diabetes insipidous
Secondary diabetes insipidous
True or False excess calcium concentration will block or partially block ADH's effect
TRUE
Where is the thirst center located
Hypothalmus
What stimulates thirst
Increased serum osmolality

sodium is the major substance that stimulates thirst
What is the most significant clinical sign of diabetes insipidous
Polyuria/polydipsia
True or False CBC abd biochem profiles are usually normal and urine specific gravity is > 1.008 with central diabetes insipidous
FALSE blood is normal, specific gravity is < 1.008
True or Fasle central diabetes insipidous is a common disease but partial or subtle presentations of diabetes insipidous can be challengiing to treat
FALSE central diabetes insipidous is not a common disease
What is the specific test for diabetes insipidous
Water deprivation test
How is the water deprivation test performed
Patient values are collected for body weight, serum psmolality, urine spec. grav, serum urea concentrations.
Animal is deprived of water and the same measurments are taken every two hours
How long is a water deprivation test conducted
Until concentration exceeds 1.020 - 1.025
Animal loses more then 5% of its body weight
BUN goes above the normal range
Serum osmolality exceeds 305 mOsm
What does it mean if patients are able to concentrate urine during a water deprivation test
They don't have diabetic insipidous
If an animal loses 5% bwt, with no concentration what is the problem
Problem is with ADH
Not producing ADH or it is not functioning properly
What level of kidney loss is required for BUN to increase
75% kidney loss required for BUN to increase
At what point do you get a loss of concentrating ability with the kidney
2/3
What is the risk of performing a water deprivation test
Medullary washout
What is the best test for profound PU/PD
Modified water deprivation test
What is the modified water deprivation test
Animals water intake is slowly decreased over several days
What is DDAVP
Endogenous
What is the ADH response test
Give ADH to see if the concentrat
What are the lab findings with central diabetes insipidous
Normal CBC biochem
Specific garvity < 1.008
What are the differential for a urine specific gravity <1.008
Central diabetes insipidous
Psychogenic polydipsia
Nephrogenic diabetes insipidous
How is a water deprivation test performed
Measure baseline bodyweight, serum osmolality, urine specific gravity and serum urea concentration
When is a water deprivation test stopped
Urine concentration reaches 1.020-1.025
Animal loses 5% of its body weight
BUN goes above normal range
Serum osmolality >305 mOsm
What does it mean if they can concentrate urine on a water deprivation test
It means they do NOT have diabetes insipidous
What can you cay about the water deprivation test when an animal loses 5% of its body weight without concentrating its urine
There is something wrong with ADH
Either its not producing ADH or the ADH is not functioning
How much kidney loss is required to get an increase in BUN
75%
How much kidney loss is required to get a loss of concentrating ability
2/3 of kidney function lost = loss of ability to concentrate urine
What are the risks od a water deprivation test
If animal is PU/PD you can get medually washout

If PU/PD use a modified test
What should you do next when you reach the end point of a water deprivation test and still have no concentrated urine
Administer ADH and see if the animal responds

may take several days with medually washout
What does it mean if there is a negative water deprivation test followed by a positive ADH test
Central diabetes insipidous
When do you see psychogenic polydipsia
Young excitable dogs
May be associated with primary brain disease
May be associated with the PU/PD of cushings
True or False animals with psychogenic polydipsia will have a serum osmolality of < 285 mOsm
True because they are overhydrated
What can cause nephrogenic diabetes insipidous
Normal ADH release but unable to exert its effects via receptor sites in the kidney
May be due to increased serum calcium and possible Cushings
WHere is growth hormone released from
Anterior pituitary from GHRH

Mammary tissue from progesterone
What inhibits the release of growth hormone
somatostatin
Why is GH release due to progesterone important in dogs
Because dogs keep their CL even if they are not pregnant and it releases progesterone this stimulates the release of growth hormone
What is the main catabolic effect of growth hormone
Insulin antagonism
Causes lipolysis and gluconeogenisis
Decrease glucose transport across cell membranes
Net effect is hyperglycemia
What are the slow effects of growth hormone
stimulates growth, chondrogenesis and protein synthesis
What causes acromegaly in dogs
Middle aged intact female dogs post estrus
Dogs given progesterone to prevent estrus
What causes acromegaly in cats
Pituitary tumor
What happens with acromegaly
Excessive growth hormone results in excessive soft tissue and bony growth

Also leads to insulin resistance
What are clinical signs of acromegaly in dogs
Soft tissue proliferation esp with the head
Wide spaces between the teeth, increased pharyngeal tissue
Increased and thickened skin folds especially of the neck
usually not diabetic but polyuria and polyphagia
what are the clinical signs of acromegaly in the cat
Not as pronounced as in the dog
Most common sign is severe insulin resistance -> manifests as difficult to control diabetes melitus
How can you diagnose acromegaly
Measure basal GH concentration
Measure IGF-1 concentration
What is the treatment for dogs with acromegaly
Spay intact females

Discontinue progesterone administration
What is the treatment for cats with acromegaly
Tratement of the pituitary tumor - surgery, radiation therapy, possibly synthetic somatostatin
Who gets pituitary dwarfism
German Shepherd dogs
What causes pituitary dwarfism
Congenital pituiatary disfunction
Lask of TSH production
What are the clinical signs of piituitary dwarfism
Failure to grow
Normal conformation
Retained puppy haircoat
Possible kidney problems
How can you diagnose pituitary dwarfism
Stimulation test with GHRH to measure post treatment GH is the most accurate method
True or False pituitary dwarfism can be treated with canine GH
FALSE canine GH is not available
True or False pituitary dwarfism can be treated with human GH
FALSE the dog will produce antibodies to human (or synthetic) GH
True or False pituitary dwarfism can be treated with porcine GH
TRUE porcine GH is the same as canine GH
How does the adrenal look on ultrasound
Kind of a penut shape
What are all steroidal compounds formed from
Cholesterol
Where does the catabolism of most steroids occur
In the liver
What causes the release of cortisol
ACTH
(Adrenocorticotropic hormone)
What causes the release of ACTH
(Adrenocorticotropic hormone)
CRH (corticotropic releasing hormone) from the hypothalmus
What causes an increase in CRH
CRH stimulated by

Decresed serum cortisol
Arginine vasopressin (humans)
Angiotensin II (humans)
Where is ACTH released from
Pituitary
What decreases CRH release
Increased serum cortisol (also has an effect on the pituitary)
ACTH
Oxytocin (humans)
What causes aldosterone release
Renin from the kidney via serum angiotensin II
Decreased serum sodium
What is Cushing's disease
Hyperadrenocorticism

Excess production of cortisol by the adrenal cortex
What are the types of hyperadrenocorticism
** Excess production of ACTH by pituitary (PDH - pituitary dependant hyperadrenocorticism)
** Primary adrenal tumor (ADH - Adrenal dependant hyperadrenocorticism)

Ectopic ACTH syndrome
Ectopic CRH syndrome
True or False Cushing's is rare in cats
TRUE
What is the typical signalment for Cushings
Middle aged to older dogs

Females slightly more then males
What has a better prognosis pituitary dependant or adrenal dependant hyperadrenocorticism
PDH has a better prognosis
What are common clinical signs of Cushing's
Bilaterally symetrical truncal alopecia
PU/PD
Polyphagia
Abdominal enlargement
Muscle weakness
Lethargy
Secondary skin problems (seborrhea, pyoderma, hyperpigmentation, calcinosis cutis)
Blood vessel fragility
Weight gain
Panting
Signs of lower urinary tract dz (secondary UTI)
What is the most important clinpath abnormality
Increased ALP if there is no increased ALP it is not likely Cushing's
What are the screening tests for hyperadrenocorticism
ACTH stimulation test
Low dose dexamethazone suppression test
Urine cortisol/creatinine ratio UCCR
How does concurrent disease affect hyperadrenocorticism testing
Concurrent disease is a chronic stressor which makes the results of testing more difficult to interpret
What is atypical hyperadrenocorticism
Dogs have clincal signs and typical hematological and biochemical findings consistant with hyperadrenocorticism but normal ACTH and LDDS results
What are disxcriminatory tests used for with Cushing's
To determine where the disorder is
Pituitary dependant hyperadrenocorticism or adrenal tumor
What are the dicriminatory tests for Cushing's
High dose dexamethasone suppression test
Endogenous Acth concentration
Abdominal ultrasound
Radioisotope imaging
CT or MRI
True or False if an animal doesn't supress with a high dose dexamethosone test you can rule out Cushing's
FALSE even if they do not suppress you still can not rule out Cushings with a HDDS test
What does it mean if you get suppression with a HDDS test
you have PDH
What are good discriminatory results for an endogenoud ACTH test
If you get high or low levels of suppression you will have PDH or ADH respectively
What is radioisotope testing useful for with hyperadrenocorticism
Good for distinguishing a unilateral adrenal tumor from PDH
(limited availability)
True or False for hyperadrenocorticism CT/MRI cannot differentiate between bilateral hyperplasia or bilateral neoplasia of adrenals
TRUE
What is CT/MRI useful for with hyperadrenocorticism
For differentating unilateral neoplasia from PDH
True or False most often we treat medically for PDH
TRUE
What drugs are used to treat hyperadrenocorticism
o'p'DDD (mitotane)
Ketoconazole
Selegiline
Trilostane
Melatonin
Flaxseed oil with lignans
What is the main drug used for Cushing'
o'p'DDD
(Mitotane)
Why are people scared of using Mitotane
Can make the dog Addisonian

Needs good monitoring
How does Mitotane work
Causes selective destruction of zona fasiculata and reticularis

Dogs with PDH show an exaggerqated response to Mitotane may get clinical remission
What is the goal when treating with Mitotane
ACTH stimulation tests consistent with hypoadrenocorticism
or
ACTH test results in the low normal range
How does ketoconazole work for treating Cushing's
Inhibits production of cortisol by the adrenal cortex

Less serious side effects then Mitotane
What are the disadvantages of treating Cushing's with ketoconazole
Must treat multiple times a day
Side effects include vomiting and hepatopathy
How does Selegiline (Deprenyl) work for Cushing's
Irreversible inhibitor of monamine oxidase type B

Normalizes (increases) dopamine concentrations
What do you need to consider when treating Cushing's with Trilostane
Could lead to full blown Addison's need to send home prednisilone just in case cortisol goes too low
How does Trilostane work for treating Cushing's
Trilostane is a steroid analogue that is a competitive inhibitor of 3-beta hydroxysteroid dehydrogenase system

exactly what I was thinking !!!!
What are the surgical options for treating hyperadrenocorticism
Adrenalectomy
Unilateral for primary adrenal tumor
Bilateral for PDH
How can you get iatrogenic hyperadrenocorticism
Exogenous glucocorticoid administration
How do you treat iatrogenic Cushing's
Gradual withdrawl of exogenous glucocorticoids
True or False small dogs can absorb enough glucocorticoids from topical treatments to display iatrogenic Cushing's
TRUE
Why do you want to do a gradual withdrawl with iatrogenic Cushing's
Because the adrenals have been suppressed you want to give them a chance to regain normal adrenal function
Which is more common Addison's or Cushing's
Cushing's
How does the animal preent with the acute form of Addison's disease
Really sick

Addisonian crisis ?
What is Addison's disease
Deficient glucocorticoid production (cortisol) and mineralcorticoid (aldosterone) production by the adrenal cortex
What are the etiologies for Addison's
Immune mediated destruction
Granulomatous destruction
Iatrogenic
Waterhouse Fredrichsen syndrome (associated with sepsis and multi-orgqn failure)
What are etiologies for cortisol only deficiencies
Pituitary lack of ACTH
Iatrogenic
Early adrenal destruction
What is the pathophysiology of iatrogenic Addison's
Glucocorticoids are given for a prolonged period of time then acutely stopped
What are the clinical signs of Addison's
Mainly GI - vomiting and diarrhea
How long does it take to recover from iatrogenic Addison's
Weeks to months to have cortisol production back uo to normal levels
True or False hypoadrenocorticism can present as just a deficiency in cortisol but not in aldosterone
TRUE
How gets Addison's typically
Young adults (males?)
Standard poodles may be at an increased risk
What do you see clinically with cortisol deficiencies
GI signs and lethargy
What do you see clinically with aldosterone deficiency
Depressions
Cardiac arrythmias
What is unique with the acute form of Addison's
You get bradycardia and shock (a mismatch)
True or False you will see a stress response and variable PCV on a CBC with Addison's
FALSE you will not see a stress response with Addison's
What should you think if you sodium is low and your potassium is high
Addison's
What Na/K ratio is suggestive of Addison's
< 25:1
Suggesstive of Addison's but also GI, renal and hepatic diseases
How can you diagnose Addison's
ACTH stimulation test
What would you expect to see on an ACTH stimulation test with Addison's
No increase in glucocorticoids when ACTH is administered
What is seen on radiographs with Addison's
Microcardia
Small caudal vena cave
What is seen on ECG with Addison's
Tented T waves with increased amplitude
Lack of P waves
Bradycardia
Widened QRS complexes
What is the acute treatment for Addison's
IV fluids (may require shock doses)
Glucocorticoids
If severe hyperkalemia give crystalline insulin and dextrose or calcium gluconate or sodium bicarb
Why would you give crystalline insulin and dextrose or calcium gluconate or sodium bicarb with sever hyperkalemia from acute Addison's
Because Insulin drives glucose into cell with K
Glucose goes into cell with K
and Bicarb swapd H for K in the cell so they will all reduce serum potassium levels


Check the accuracy of this statement with others
Why would you chose to treat Addisons with dexamethasone over prednisone
Because prednisone shows up on cortisol assay (inaccurate test results)
True or False if you are giving insulin for Addison's you should always give dextrose
TRUE
What do you use for chronic treatment of Addison's
Fludrocortisone +/- prednisone
Deoxycortiosterone pivilate (lasts a month) + prednisone
Prednisone alone if it is jsut a cortisol deficiency
What treatments are given in order for hyperkalemia from Addison's
1. Ca gluconate
2. Insulin and dextrose
3. Sodium bicarb (could be problematic)
What can stress do to the cortisol requirement
May increase it by 10X or more
What is the typical presentation of hypothyroidism
Middle aged dogs no sex predilection
True or False spontaneous hypothyroidism is common in the cat
False it is rare
What are clinical signs of hypothyroidism
Decreased metabolic rate
Dermatopathies
Reproductive dysfunction
Neuromuscular dysfunction
What conditions are associated with decreased metabolic rate with hypothyroidism
Mild weight gain
Heat seeking
Lethargy
What conditionas are associated with reproductive dysfunction with hypothyroidism
Prolonged inestrus interval or anestrus
What are the neuromuscular dysfunctions associated with hypothyroidism
Facial nerve paralysis
Constipation
What are the clinical signs of hypothyroidism in cats
NOT A TRICK QUESTION
Lethargy
Poor hair growth, seborrhea
Puffy face
Hair loss
What are the clinicopathologic abnormalities associated with hypothyroidism
Anemia
Hypecholesteremia
Mildly increased liver enzymes
Mild hyponatremia
What is the etiology of hypothyroidism
Lymphocytic-plasmacytic thyroiditis
Thyroid atrophy
Thyroid neoplasia
TSH or TRH deficiency
Congenital
Iodine deficiency
What test would you run to diagnose hypothyroidism
Minimum database
Tests of thyroid function
Others based on clinical signs
What are the tests of thyroid function
Resting T4
Resting FT4
Endogenous TSH concentration
TSH or TRH stimulation test
Response to therapy
Thyroid hormone antibody concentrations
Thyroglobulin antibody concentrations
Thyroid biopsy
Radioisotope uptake
True or False if the TT4 is normal the dog is likely euthyroid
TRUE
What are the advantages and disadvantages of testing the resting total T4 concentrations
Advantage: Easy
Disadvantage: Measures both free and protein bound hormone, influenced by non-thyroidal factors, may get false increase with anti T4 antibodies
What are the advantages and disadvantages of testing the resting free T4 concentrations
Advantages: easy, measures just the free/active portion of the hormone
Disadvantages: still influenced by non-thyroidal factors (less then TT4)
What are some influencing factors on thyroid hormone concentrations
Age
Breed
Temperature
Time of day
Nutrition
Surgery
Concurrent illness
Drugs
What are the advantages and disadvantages of testing the endogenous canine TSH concentrations
Advantages: Easy
Disadvantages: Influenced by non-thyroidal factors

can be used in conjunction with TT4 or FT4
What do you need to condsider when test to see if there is a response to treatment for hypothyroidism
Clinical signs respond at different rates
If signs resolve you need to stop treatment to see if they recurr
If signs do not fully resolve measure TT4 if low up the dose, if normal look for other causes
What is the treatment for hypothyroidism
Levothyroxine (synthroid?)
Who get hyperthyroidism
Middle aged to older cats
No sex predilection
Usually bilateral thyroid involvement
Thyroid changes rarely malignant
What is the etiology of hyperthyroidism
Genetic?
Environmental, nutritional, other? (canned food or cat liiter?)\Decreased inhibitory protein
What are the clinical signs of hyperthyroidism
PU/PD
Polyphagia
Weight loss
Vomiting. diarrhea
Oily or matted haircoat
Behaviour change
What are the signs of apathetic hyperparathyroidism
anorexia
weight loss
lethargy
What would you expect to see on physical exam with hyperthyroidism
Thin/emaciated
OIly/matted haircoat
Hyperactivity or aggression
Tachycardia
Palpable thyroid enlargment
Dyspnea
Cardiac murmur or gallop rythym
What are the clinicopathologic abnormalities for hyperpthyroidism
Stress leuogram
Mile erythrocytosis or anemia
Mild hyperphosphatemia
Possible azotemia
How can you diagnose hyperthyroidism
Minimum data base
Thoracic rads, ECG
Resting TT4, FT4
T3 suppression test
TRH stimulation test
What can you say about the results of a TT4 and hyperthyroidism
If increased it is diagnostic for hyperthyroidism
If normal (esp with concuurrent illness) you can not rule out hyperthyroidism
True or False FT4 is incresed in hyperthyroid and some cats with non-thyroidal illness
TRUE

Should not be used as the primary diagnostic test for hyperthyroidism
what can you say with a high normal TT4 and a normal FT4
Probably not hyperthyroid
What can you say with a normal TT4 and increased FT4
Likely hyperthyroid
What would you expect to happen in a normal and a hyperthyroid cat with a T3 supression test
Normal cat -> suppression of T4

Hyperthyroid cat -> no suppression of T4
What are the biggest drawbacks to performing a T3 suppression test
Owner has to pill the cat as scheduled and it require two blood samples
What would you expect with a TRH stimulation test in a normal cat
Increased T4
What would you expect with a TRH stimulation test in a hyperthyroid cat
Little or no increase in T4
What are the advantages and disadvantages of performing a TRH stimulation test
Advantages: Done in hospital one day
Disadvantages: Some cats have transient side effects and it is not 100% diagnostic (for thyroid or non-thyroid causes)
What are the advantages and disadvantages to a technesium scan
Advantages: useful before a thyroidectomy
Disadvantages: limited availability, may require sedation, Accuracy?
What is the mediacal treatment for hyperthyroidism
Methimazole
Propylthiouracil (PTU)
What are the non-mediacal treatment options for hyperthyroid
Thyroidectomy
Radioactive iodine
Percutaneous ethanol injection for solitary nodule or radiofrequency abalation
True or false hyperthyroidism may mask renal failure
TRUE cause increased renal blood flow and GFR
What are the side effects to medical treatment of hyperthyroidism
Anorexia, vomiting
Facial excoriations/pruritis
hepatopathy
Granulocytopenia
Bleeding tendencies
What are the risks of thyroidectomy
Requires anesthesia
risk of post op hypocalcemia with bilateral thyroidectomy (from removal of parathyroid gland anyone?)
Other surgical complications
What are the advantages of a thyroidectomy for hyperthyroidism
Usually curative
What are the advantages of radioactive iodine treatment for hyperthyroidism
Safe
Usually curative
Works for ectopic thyroid tissue as well
What are the disadvantages of radioactive iodine therapy
Limited availability
Prolonged hospital stay (requires isolation 5-10 days post treatment)
May need repeat treatments
What hormones are produced in the pancreatic islet cells
Glucagon (alpha cells)
Insulin (beta cells)
Somatostatin (delta cells)
Pancreatic polypeptide (F cells)
What hormones are primarily involved in the regulation of carbohydrate, fat and protein metabolism
Insulin and glucagon
What does somatostain do
Involved in the regulation of insulin and glugagon (and other hormones) secretion
What does pancreatic polypeptide do
Modulates pancreatic secretory response to food
True or False in a normal animal feeding and strenuous exercise can increase serum glucose appreciably
FALSE
Glucose homeostasis is tightly regulated
What counters glucose influx
Glucose influx is largely countered by insulin
What does insulin do
Increases protein synthesis and lipogenesis
Decreases fat and protein catabolism
Inhibits hepatic gluconeogenisis and ketogenisis
What does glucagon do
Increases gluconeogenisis, glycogenolysis and ketogenisis
What are the hormonal abnormalities with diabetes mellitus
Hypoinsulinemia
Hyperglucagonemia
Why is there polyuria associated with Diabetes mellitus
Increased glucose spills over into the urine cause an osmotic effect -> polyuria and a compensatory polydipsia
Why is there weight loss associated with untreated diabetes mellitus
The caloric loss of glucose in the urine and decreased peripheral utilization of glucose
What are the two causes of diabetes mellitus
Decreased insulin secretion
Decreased insulin action
What is the most common type od diabetes in the dog
Inulin dependent DM with onset in middle to old aged dogs
True or False Males are more affected 2X as much as females with insulin dependent DM
FALSE Females are 2X as likely as males to get this
What are the etiopathogenic factors for diabetes melitus
Genetics
Increased diabetogenic hormones
Infection (viral)
Obesity
Autoimmunity
Pancreatitis
Diabetogenic medications
Stress or other illness
What is the typical presentation of diabetes mellitus in cats
Domestic shorthair cats >5 years of age

neutered males > females

most have absolute insulin deficiencey
Compare and contrast the insulin characteristics of diabetes mellitus in cats and dogs
Dogs juvelile form - normal absolute insulin level - but still needs exogenous insulin
Dogs adult for - absolute insulin level decreased
Cats - absolute insulin deficiency
What are the four classic clinical signs of uncomplicated diabetes mellitus
polyuria
polydipsia
polyphagia
weight loss
Aside from the classic clinical signs of uncomplicated diabetes mellitus what OTHER signs might be present
An obese patient may have hepatic lipidosis and hepatomegaly
Cataracts secondary to prolonged hyperglycemia
Sudden blindness from cataracts (see above)
Plantigrade stance in cats from diabetic neuropathy
What can cause a misdiagnosis of diabetes mellitus
Evaluating only the urine glucose because dogs with FANCONI syndrome will have a persistant glucosuria

Evaluating only the blood glucose in a cat under stress
What does it take to make a diagnosis of diabetes mellitus
Hx of polyuria, polydipsia, polyphagia and weight loss in conjunction with a persistant fasting hyperglycemia and glucosuria
True or False diabetes in the cat should only be diagnosed if a persistant hyperglycemia and glucosuria are present
TRUE
What can be used to diagnose cats where it is difficult to rule out stress hyperglycemia
Fructosamine concentration can be evaluated
What additional diagnostics should every potential diabetic have performed
Serum lipase analasys and a urine culture (prefeably by cystocentesis)
What abnormal lab results can be seen with diabetic patients
Leukocytosis
Normal to increased serum alanine aminotransferase
Normal to increased ALP
Hypercholesteremia
Ketonuria
Proteinuria
Bacteriuria

A lot of dogs will have pancreatitis and/or UTI
Why is fructosamine a good test in diabetic animals
It reflects blood glucose over the previous 1-2 weeks
What are the types of insulin available for the dog and cat
Based on origin -
Beef
Beef-pork
Human (synthetic)

Based on formulation -
Regular (crystalline)
NPH insulin
Lente
Ultralente
True or false porcine and human insulin are fairly similar to canine insulin
TRUE

Feline insulin is more different
Who metabolizes insulin faste cats or dogs
Cats
What type of insulin would be used to treat an unstable ketoacidotic diabetic
Regular (crystalline) insulin until they are stabilized
What are the primary choices of insulin (in Canada) to treat the diabetic patient at home
NPH
Lente
Glargine
What is the protocol for the intitial treatment for diabetes
Insulin is given twice daily
Blood glucose concentrations are measured every 3-4 hours for a 12-24 hour period
Feed 1/2 the daily caloric requirement at time of injection
Adjust the next days insulin dose based on the glucose determinations if required
What should you be aware of when performing an in clinic blood glucose evaluation in cats
Stress hyperglycemia can sometimes make it dificult or impossible
What do you need to tell your client about feeding with a diabetic patient
The diet of a diabetic patient must be consistent as it will be based on the patients weight and activity level
Does exercise increase or decrease insulin requirements
It decreases insulin requirements due to increeased blood flow and insulin delivery to working skeletal muscle
Should diabetic working dogs get increased or decreased insulin under working conditions
Decreased insulin or insulin will drive glucose into the cells --> excessive exercise may lead to hypoglycemic seizures
How does the estrus cycle have an effect on diabetes control
Progesterone stimulates release of growth hormone which is a diabetogenic hormone and diabetic control may be difficult for the next 2 months after an estrus cycle some bitches may die despite all attempt at diabetic control
What should be done with diabetic bitches
They should be spayed as soon as their diabetes is under control
What are the complications of diabetes mellitus
Cataract formation
Hepatic lipidosis
Diabetic retinopathies
Nephropathies
Neuropathies
Atherosclerosis
What are acute complications of diabetes mellitus
Diabetic ketoacidosis
Nonketotic hyperosmolar
Infection
Hyperlipidemia
Hypertension
Possibly pancreatitis
What might cause insulin therapy to not work properly
Improper insulin administration by the owner
Inadequate mixing of insulin prior to withdrawal from the syringe
Outdated insulin
Inactive insulin (from improper storage)
Inaccurate or outdated ketodiastix
True or False the effects of insulin on a patient can be evaluated after two consecutive blood glucose samples
FALSE it will take serial blood glucose levels to determine the effectiveness
What can cause post hypoglycemic hyperglycemia
Excessive insulin administration
What is the pathophysiology of post hypoglycemic hyperglycemia
Excessive insulin administration causes blood glucose to drop below 3.6 mmol/L this causes the release of diabetogenic hormones which cause an increase in blood glucose
What should be done with patients that have a rapid metabolism of insulin
Insulin administration must be changed to
A more frequent administration schedule
A longer acting insulin
What is Somogyi phenomenon
Post-hypoglycemic hyperglycemia
What is the issue of patients with somogyi phenomenon
When you test in the morning the blood glucose is unchecked and too high so the owner increases the insulin dose exacerbating the syndrome
What happens with insulin antagonism/resistance
Something is interfering with the action of insulin --> persistant hyperglycemia and blood glucose does not decline significantly with insulin therapy
What are causes of insulin resistance
Exogenous glucocorticoid administration
Hyperadrenocortism
Acromegaly (mostly cats)
Estrus
Pregnancy
Infections
Prolonged stress
What can happen with hypoglycemic reactions
Patient recieves too much insulin or exercises too much hypoglycemia and associated reactions may occur before diabetogenic hormones are released or have an effect
What types of insulin must be given SQ
NPH
Lente
Ultralente
How can regular/crystalline insulin be administered
IV
IM
SQ
What is the pathogenisis of diabetic ketoacidosis
With diabetes mellitus lipase is not inhibited by insulin properly ->excess free fatty acids delivered to the liver -> ultimately converted to beta-hydroxybutyric acid and acetone (ketoacids) ->ketone accumulation and metabolic acidosis -> resultant osmotic diuresis
What are common presenting complaints for ketoacidosis
Anorexia
Not drinking
Vomiting
Diarrhea
Severe depression
What should you do when preesented with a case of diabetic ketoacidosis
ALWAYS look for another disease process
What disease processes are associated with diabetic ketoacidosis
Pancreatitis
UTI
CHF
Pyometra
What is the prognosis for diabetic ketoacidosis
Guarded
Requires fast and accurate recognition and agressive therapy even then pronosis is guarded
How is a presumptive diagnosis of diabetic ketoacidosis confirmed
Both ketones and glucose is present in the urine or hyperglycemia and hyperketonemia
What are the initial goals of therapy for diabetic ketoacidosis
Provide adequate insulin to reverse hyperglycemia and ketone production
Correct dehydration and electrolyte abnormalities
Correct severe metabolic acidosis
Identify any precipitaing factors
What are the diabetogenic hormones
Glucagon
Epinephrine
Cortisol
Growth Hormone
What are the causes of decreased glucose production
Puppy hypoglycemia
Hepatic insufficiency
Glycogen storage disease
Hypoadrenocorticism
Sepsis
What are causes of increased glucose utilization
Beta cell tumor
Extrapancreatic neoplasia
Sepsis