Endocrine Exam 1

Front 1

What are the basic hormonal mechanisms responsible for maintain water balance?

Back 1

ADH!!! Aldosterone from the RAAS system antagonizes ADH.

Front 2

List the renal functions or factors that contribute to urine concentration and dilution.

Back 2

Properly functioning transport mechanisms in the pct and dct, medullary gradient, and functioning adh receptors in the collecting ducts.

Front 3

What is considered normal water intake for cats and dogs?

Back 3

Less than 100 ml/kg/day

Front 4

What does it mean to say that normal does not equal appropriate?

Back 4

If water loss is higher than normal, eg. a hot dry day, increased water intake above normal would still be appropriate.

Front 5

Pu/pd mechanism-Primary polydipsia

Back 5

1. Primary polydipsia
2. Splenomegaly

Front 6

Pu/pd mechanism-reduced or absent ADH

Back 6

1. Polycythemia
2. Central diabetes insipidus

Front 7

Pu/pd mechanism-loss of medullary gradient

Back 7

1. Hyponatremia
2. Liver failure
3. Portosystemic shunt
4. Medullary washout
5. Chronic kidney disease
6. Leptospirosis
7. Hyperthyroidism (cats only)
8. Hypoadrenocorticism (Addisons)

Front 8

Pu/pd mechanism-osmotic diuresis

Back 8

1. Post obstructive diuresis
2. Polyuric acute renal failure
3. Diabetes mellitus
4. Fanconi's syndrome
5. Primary renal glucosuria
6. Acromegaly(cats only)-growth hormone interferes with insulin, leads to diabetes

Front 9

Pu/pd mechanism-impaired response to ADH

Back 9

1. Pyelonephritis(LPS antagonizes ADH)
2. Pyometra/prosthetitis
3. Primary hyperaldosteronism (Blunts ADH response)
4. Primary Nephrogenic DI
5. Hypercalcemia
6. Pheochromocytoma
7. Leiomyosarcoma
8. Hyperadrenocortisism (Cushings)

Front 10

Pu/pd mechanism-Aquaporin 2 down-regulation

Back 10

1. Chronic partial ureteral obstruction
2. Hypokalemia

Front 11

Pu/pd mechanism-other things that don't fit

Back 11

Diet, drugs, and toxins

Front 12

What three pu/pd differentials cause extreme (hyposthenuric) urine dilution?

Back 12

Central DI
Primary polydipsia
Cushings

Front 13

What are the most common causes of Pu/pd in dogs?

Back 13

Cushings, diabetes mellitus, chronic kidney disease

Front 14

What are the most common causes of Pu/pd in cats?

Back 14

Hyperthyroidism, diabetes mellitus, chronic kidney disease

Front 15

Which causes of pu/pd only occur in cats?

Back 15

Acromegaly, hyperthyroidism

Front 16

Which causes of pu/pd only occur in dogs?

Back 16

primary/psycogenic polydypsia

Front 17

What are hormones, what is their basic function?

Back 17

A hormone is a biochemical molecule that alters the function of cells to keep body systems in balance.

Front 18

Understand and describe the different types of regulation/feedback loops used to control hormones.

Back 18

Negative feedback-hormone suppresses its own production
Hormone levels are maintained by release of the hormone, not by clearance from the body.
Control of hormone effect by binding to a carrier molecule or by transport of a precursor state.
Receptor concentration in different tissues control uptake in each tissue.
Antagonistic hormone production-different hormone has the opposite effect of original hormone (eg. Insulin and glucogon).

Front 19

Differentiate between a hypo- and hyperfunctional endocrine gland. Be able to describe the different mechanisms of each.

Back 19

Hypo-decrease in function of a gland. Occurs due to destruction of tissue, replacement of tissue with non-functional neoplastic tissue, destruction of a precursor gland, or outside suppression of the gland.
Hyper-increase in gland function. Due to benign or malignant neoplastic hyperplasia, overstimulation from an upstream gland or exogenous source, or deficiency of a suppressive hormone.

Front 20

What are the basic types of endocrine testing and what are the advantages or limitations of each? What is each test best used for?

Back 20

Single assay-measures a single hormone at a single point in time. Ruling in or out a differential.
Paired assay-measures multiple hormones in a loop, or a trigger and response pair. Assessing the entire hormone loop, or the appropriateness of an abnormal result.
Stimulation test-stimulates hormone production. Diagnosing a hypofunctional gland.
Suppression test-suppresses hormone production. Diagnosing a hyperfunctional gland.

Front 21

What is the difference between normal/abnormal and appropriate/inappropriate?

Back 21

Normal/abnormal refers to a test results relationship to the reference interval. Appropriate/inappropriate refers to the presence or absence of a normal physiologic cause for a test result.

Front 22

Describe the hypothalamic-pituitary-thyroid axis in the healthy animal. How does this axis differ in the hypothyroid animal?

Back 22

Normal: The hypothalamus produces TRH, which stimulates the pituitary to produce TSH, which stimulates the thyroid gland to produce T3 and T4. T3 and T4 have inhibitory effects on the hypothalamus and pituitary.
Hypothyroid: T3 and T4 are not produced either due to a lack of response from the thyroid tissue, lack of TRH production, or lack of TSH production.

Front 23

Distinguish between the different types of hypothyroidism.

Back 23

Primary: Lack of functional thyroid tissue. Aquired-lymphocytic thyroiditis, idiopathic follicular atrophy, secondary to neoplasia. Iatrogenic-surgery, 131-I therapy, anti-thyroid medications. Congenital-cretinism, disproportionate dwarfism.
Secondary: decreased pituitary secretion of TSH. Aquired-neoplasia (most common), pituitary suppression, illness, malnutrition. Congenital (rare).
Tertiary: Lack of TRH production in the hypothalamus. This has never been reported in a dog.

Front 24

Basic functions of unbound (physiologically active) T3 and T4.

Back 24

T4-provides negative feedback to the hypothalamus and pituitary.
T3-increases basal metabolic rate and tissue O2 consumption, promotes calorigenesis, promotes protein and enzyme synthesis, promotes muscle and adipose catabolism, regulates cholesterol metabolism, maintains the strength and rate that the heart contracts (inotropic and chronotropic effect), promotes erythropoiesis, allows for normal hypoxic and hypercapnic drives, essential for normal neurologic and skeletal development.

Front 25

What is reverse T3?

Back 25

reverse T3 is an inactive form of T3 that is produced in illness, starvation, or catabolic states.

Front 26

What is euthyroid sick syndrome?

Back 26

Non-thyroidal illnesses cause a decrease in serum T3 and T4, even though the patient is not truly hypothyroid. This occurs due to decreased protein binding of T3 and T4, decreased conversion of T4 to T3, and decreased TSH release. This can be difficult to distinguish from true hypothyroidism, and euthyroid sick patients will respond to soloxine treatment.

Front 27

Describe the pathophysiologic mechanism of clinical signs of hypothyroidsims: Dullness, lethargy, exercise intolerance, cold intolerance, and obesity without polyphagia.

Back 27

Dullness,lethargy, and cold intolerance-decrease in metabolic rate, inhibited calorigenesis
Exercise intolerance-same as above, plus decrease in the heart's ability to pump blood through the body.
Obesity-decreased BMR, decreased muscle and fat catabolism, disregulation of cholesterol.

Front 28

Describe the pathophysiologic mechanism of clinical signs of hypothyroidsims: dermatologic abnormalities

Back 28

Thyroid hormone is necessary for the anagen phase of hair growth. This lack leads to hair loss, failure of hair to grow back, and retention of brittle hair (telogen phase). Manifestations include: dry skin/coat, bilaterally symmetrical alopecia, non-puritic hair loss, "puppy coat", dull coat. Hair loss further results in hyperpigmentation, seborrhea, lichenification, and comedones.

Front 29

Describe the pathophysiologic mechanism of clinical signs of hypothyroidsims: Recurrent infection

Back 29

Decreased thyroid hormone lowers immune function, and the changes in dermatologic function also decrease the skin's barrier function.

Front 30

Describe the pathophysiologic mechanism of clinical signs of hypothyroidsims: Myxedema

Back 30

Mechanism of mucopolysaccharide and hyaluronic acid accumulation is undetermined.
Obtundation, stupor, coma, hypothermia-decreased BMR, inhibited calorigenesis, decreased cellular O2 consumption.
Hypoventilation-T3 effect on hypoxic and hypercapnic drive.
Hypotension, bradycardia-decreased inotropic and chronotropic effects.

Front 31

Describe the pathophysiologic mechanism of clinical signs of hypothyroidsims: Cardiovascular effects

Back 31

Decreased inotropic and chronotropic effects lead to sinus bradycardia, weak apex beat, low voltage complexes on ECG, and decreased fractional shortening on Echo.

Front 32

Describe the pathophysiologic mechanism of clinical signs of hypothyroidsims: ocular abnormalities

Back 32

Anterior uveitis and corneal lipid deposits occur due to hyperlipidemia caused by disregulation of cholesterol.
Horner's syndrome and Keratoconjunctivitis sicca can also occur (mechanism undefined).

Front 33

Describe the pathophysiologic mechanism of clinical signs of hypothyroidsims: Gastrointestinal abnormalities

Back 33

Constipation, diarrhea, and vomiting may occur secondary to decreased myoelectric and mechanical responses of the GI tract, but the true mechanism is unknown.
Pancreatitis occurs secondary to hypertriglyceridemia.

Front 34

Describe the pathophysiologic mechanism of clinical signs of hypothyroidsims: Neurological impairment

Back 34

Occurs secondary to demyelination of the nerves. Includes: periperal neuropathies, myopathies, cranial nerve dysfunction.
Central neurologic signs occur secondary to neoplasia of the pituitary in secondary hypothyroidism.

Front 35

Describe the pathophysiologic mechanism of clinical signs of hypothyroidsims: Reproductive dysfunctions

Back 35

Infertility, shortened estrus, prolonged estrual bleeding, prolonged anestrus, glalctorrhea, and testicular atrophy all occur. Mechanism unknown, but suspected due to disregulation of the pituitary gland.

Front 36

Describe the pathophysiologic mechanism of clinical signs of hypothyroidsims: Concurrent endocrine disorders

Back 36

Diabetes mellitus, hypoadrenocorticism, hypoparathyroidism, gonadal failure. Where one endocrine disorder goes, others often follow.

Front 37

List the clinical pathologic abnormalities associated with hypothyroidism.

Back 37

CBC: normocytic, normochromic, nonregenerative, mild anemia; leukocytosis secondary to infections.
Chemistry: increased cholesterol, triglycerides, and lipemia; increased ALP, AST, and ALT; decreased sodium.
Urinalysis: usually normal; cases of lymphocytic thyroiditis may also have glomerulonephritis and proteinuria.

Front 38

Contrast the advantages and disadvantages of diagnostic tests for hypothyroidism: Total T4

Back 38

Test of thyroid gland function.
Advantages: Screening test. Normal tT4 in the upper half of reference interval excludes hypothyroidism. 75-80% accuracy.
Disadvantages: Affected by daily fluctuations, breed differences (Greyhounds always lower), anti-T4 antibodies will cause falsely increased levels.

Front 39

Contrast the advantages and disadvantages of diagnostic tests for hypothyroidism: Free T4

Back 39

Test of thyroid function
Advantages: Indicates thyroid status at the tissue level. Less affected by external factors. 90% accuracy.
Disadvantage: still affected by anti-T4 antibodies if done by RIA.

Front 40

Contrast the advantages and disadvantages of diagnostic tests for hypothyroidism: Total T3

Back 40

Advantages: None. T3 is conserved in the hypothyroid state.
Disadvantages: T3 is not a good diagnostic indicator of thyroid dysfunction. Anti-T3 antibodies will affect T3 done by RIA

Front 41

Contrast the advantages and disadvantages of diagnostic tests for hypothyroidism: Baseline TSH

Back 41

Advantages: TSH will increase with primary hypothyroidism, but not secondary. 90% specific when paired with tT4 or fT4. RIA is most precise.
Disadvantages: 20-40% of hypothyroid dogs will have normal TSH (pituitary anergy)

Front 42

Contrast the advantages and disadvantages of diagnostic tests for hypothyroidism: TRH or TSH stimulation test

Back 42

Measures thyroid response
Advantages: Can differentiate between hypothyroid dogs (no response) and euthyroid sick dogs (normal response).
Disadvantages: $$$ typically cost prohibitive, and can be difficult to obtain.

Front 43

Contrast the advantages and disadvantages of diagnostic tests for hypothyroidism: Autoantibodies

Back 43

Advantages: Sensitive and specific for thyroiditis.
Disadvantages: Not diagnostic for other causes of hypothyroids; only useful in 35-60% of cases.

Front 44

Contrast the advantages and disadvantages of diagnostic tests for hypothyroidism: Ultrasound

Back 44

Advantages: Useful for cases of thyroid carcinoma. May be able to differentiate hypothyroid from euthyroid sick.
Disadvantages: Limited diagnostic value in most cases. Breed specific references ranges.

Front 45

Contrast the advantages and disadvantages of diagnostic tests for hypothyroidism: Thyroid scintigraphy

Back 45

Advantages: may be useful for canine thyroid carcinoma. Mainly used for diagnosis of hyperthyroidism.
Disadvantages: Limited diagnostic value.

Front 46

How do certain drugs affect thyroid hormone levels: Glucocorticoids, phenobarbital, TMP-sulfa antibiotics, NSAIDs?

Back 46

Glucocorticoids and phenobarbitol: decreased tT4, fT4, and tT3; normal to decreased TSH. Glucocorticoids will also cause decreased T4 to T3 conversion.
TMP-sulfa antibiotics: decreased tT4 and fT4, increased TSH
NSAIDs: decreased tT4, +/- decreased fT4 and TSH

Front 47

Develop an appropriate therapeutic monitoring plan for hypothyroidism.

Back 47

Therapy: Levothyoxine supplementation @ 0.02 mg/kg PO q 12 hours. Always start with synthetic name brand (works best). Decrease to 50% dose if concurrent heart disease.
Monitoring: 1st recheck at 4 weeks, peak level 4-6 hours post pill, aim for high end of reference interval. Recheck every 6-8 weeks for 6 months, then every 6 months.

Front 48

What are the most common reasons for therapeutic failure?

Back 48

Poor compliance
Inadequate dose or frequency
Misdiagnosis
Poor absorption from GI tract
Generic or animal origin supplement (name brand really does work best *shrug*).

Front 49

What are the signs of thyrotoxicosis? What causes it, and how is it treated?

Back 49

Panting, PU/PD, polyphagia, weight loss.
Caused by excess supplementation, individual sensitivity, or renal/hepatic insufficiency.
Treatment: decrease frequency of dosing, may need to stop supplementation for 1-3 days.

Front 50

What are the primary causes of feline hypothyroidism? What tests are used to diagnose it, and what is the appropriate therapy?

Back 50

Causes: Iatrogenic hypothyroidism secondary to treatment for hyperthyroidism. Can be euthyroid sick.
Diagnosed by tT4, and canine TSH assay can be used. TSH stim is not recommended.
Therapy: 0.05-0.1 levothyroxine/cat q 24 hours. Recheck in 4-6 weeks. Goal is tT4 of 1-3 ug/dL

Front 51

Compare the hypothalamic-pituitary thyroid axis in normal and hyperthyroid animals.

Back 51

In the hyper thyroid animal, abnormal thyroid tissue continues to overproduce thyroid hormone, even when TSH release has stopped due to negative feedback.

Front 52

What are the two causes of hyperthyroid? Which is more common?

Back 52

Benign hyperplasia or adenoma (97-99% of cases).
Malignant carcinoma.

Front 53

List possible risk factors for the development of hyperthyroid.

Back 53

Diet-canned foods, esp fish, liver and giblets
Diets high in iodine or other goitrogens.
BPA in pop top can lids
Single cats
Cats that use litter (more likely indoor cats that live long enough to get the disease)
Exposure to PBDEs (a fire retardant)-carpet, furniture. This compound is also found in cat foods (dry and canned). Statistical significance is questionable.

Front 54

Describe the pathophysiologic mechanisms of clinical signs: weight loss and polyphagia

Back 54

Increased metabolic rate

Front 55

Describe the pathophysiologic mechanisms of clinical signs: Polyuria/Polydipsia

Back 55

Increased cardiac output causes increased renal blood flow and GFR. May have concurrent renal disease with azotemia masked by the high GFR.
Psycogenic component has also been suggested.

Front 56

Describe the pathophysiologic mechanisms of clinical signs: Vomiting and diarrhea

Back 56

Vomiting-thyrotoxic effect on emetic center
Diarrhea-Hypermotility and maldigestion

Front 57

Describe the pathophysiologic mechanisms of clinical signs: Systemic hypertension

Back 57

Due to increased cardiac output.
4 effects: Retinal lesions (detachment, blindness), Glomerular damage (proteinuria), and Myocardial damage (cardiac dysfunction). Brain effects are not as noticable in cats as they are in humans.

Front 58

Describe the pathophysiologic mechanisms of clinical signs: Cardiac disease

Back 58

Thyrotoxic effect on myocardium causes hypertrophy. Will reverse when euthyroid state is restored.
May also have concurrent HCM. This will not reverse with treatment.

Front 59

Describe the pathophysiologic mechanisms of clinical signs: Behavioral changes

Back 59

Mechanism unexplained.
Increased friendliness or agression. Hyperactivity.

Front 60

Describe the pathophysiologic mechanisms of clinical signs: Other

Back 60

Dyspnea-from heart disease or thromboembolism
Weakness-increased muscle breakdown
Tremors, heat and stress intolerance-hyperthyroid cats are "tightly wound" individuals.

Front 61

Describe the pathophysiologic mechanisms of clinical signs: Apathetic hyperthyroid

Back 61

<10% of cases.
Inappetance and lethargy.
Probably either very advanced hyperthyroidism, or concurrent illness.

Front 62

List clinical pathologic abnormalities associated with hyperthyroidism

Back 62

CBC: polycythemia, macrocytosis; stress leukogram; may have mild anemia if concurrent disease.
Chem: increased ALT, or ALP; azotemia, increased phosphorus, increased glucose (stress)
Urinalysis: decreased USPG (not necessarily isosthenuric), occult urinary tract infection.

Front 63

List radiographic findings associated with hyperthyroidism.

Back 63

Radiographs: cardiomegaly, pulmonary edema or pleural effusion secondary to congestive heart failure, metastatic nodules if malignant carcinoma.

Front 64

Contrast advantages, disadvantages and uses of diagnostic tests for hyperthyroidism: Total T4

Back 64

Use: primary method of diagnosing hyperthyroidism
Advantages: Relatively accurate, does not typically require further confirmatory testing.
Disadvantages: Daily fluctuations, early or mild hyperthyroidism, and depression by non-thyroidal illness can cause borderline values.

Front 65

Contrast advantages, disadvantages and uses of diagnostic tests for hyperthyroidism: Free T4

Back 65

Use: diagnosing "occult" hyperthyroidism
Advantages: can confirm hyperthyroidism in high normal cases.
Disadvantages: does not really tell you anything you did not know from the tT4.

Front 66

Contrast advantages, disadvantages and uses of diagnostic tests for hyperthyroidism: T3 suppression test

Back 66

Use: Tests negative feed back mechanism on thyroid
Advantages: None
Disadvantages: Not much reason to run it.

Front 67

Contrast advantages, disadvantages and uses of diagnostic tests for hyperthyroidism: TRH stimulation test

Back 67

Use: Tests pituitary response to stimulation
Advantages: None
Disadvantages: Not much reason to use this test.

Front 68

Contrast advantages, disadvantages and uses of diagnostic tests for hyperthyroidism: Serum TSH

Back 68

Use: low TSH diagnostic of hyperthyroidism
Advantage: can support diagnosis.
Disadvantage: no feline specific assay in the US. All feline samples register below detectable limits on the canine assay.

Front 69

Contrast advantages, disadvantages and uses of diagnostic tests for hyperthyroidism: Nuclear scintigraphy

Back 69

Use: Gold standard confirmation for hyperthyroidism.
Advantages: detects ectopic tissue, metastatic tissue (carcinomas), and indicates whether overactive tissue is unilateral or bilateral.
Disadvantages: Pet has to have special handling for a period of time after procedure. If special facility is not already available, the hospitalization can be very expensive.

Front 70

Compare the hypothalamic-pituitary-adrenal axis in normal animals compared to typical addison's, atypical addison's, and the animal receiving exogenous glucocorticoids.

Back 70

Normal: 1. Hypothalamus releases CRF->Pituitary releases ACTH->Cortisol (and androgens) released from zona fasciculata and reticularis of the adrenal cortex->Negative feed back to H&P; fast response to rate of cortisol change, slow response to [cortisol]. Cortisol also released at a basal rate irregardless of ACTH. 2. Aldosterone released from zona glomerulosa in response to change in blood pressure.
Typical Addison's: Entire adrenal cortex is affected, no release of cortisol or aldosterone.
Atypical Addison's: Only zona fasciculata and reticularis are affected. Cortisol release will be affected, but aldosterone will remain the unaffected.
Exogenous glucocorticoid administration: Negative feedback on the pituitary from the meds causes decrease in ACTH release, and atrophy of the adrenal gland. These patients will present with clinical signs of HYPERadrenocortisism, but have Addisonian crisis when meds are stopped.

Front 71

Describe the pathophysiology of clinical signs in hypoadrenocorticism: Depression, lethargy, weight loss, weakness, hypoglycemia

Back 71

Most changes in body condition and mentation are due to a decrease in gluconeogenesis and glycogenesis that is normally stimulated by glucocorticoids. Without the ability to utilize glucose as an energy source, body condition and normal activity levels decline.

Front 72

Describe the pathophysiology of clinical signs in hypoadrenocorticism: Dehydration

Back 72

Dehydration is a result of the PU/PD condition caused by changes in electrolyte balance found in the TYPICAL Addisonian.

Front 73

Describe the pathophysiology of clinical signs in hypoadrenocorticism: GI bleeding, diarrhea and vomiting

Back 73

The mechanism for GI signs seen with hypoadrenocorticism is currently unknown. GI signs are more common in atypical cases.

Front 74

Describe the pathophysiology of clinical pathologic changes in hypoadrenocorticism: Anemia

Back 74

Glucocorticoids are one of the many mechanisms responsible for stimulating erythropoeisis. Because it is not the only mechanism, anemia is not seen in the majority of cases, or may be mild. Anemia is more common in atypical cases.

Front 75

Describe the pathophysiology of clinical pathologic changes in hypoadrenocorticism: Lack of a "stress leukogram"

Back 75

Although the mechanism is not entirely known, glucocorticoids are responsible for triggering the shift in WBC's that result in a stress leukogram.

Front 76

Describe the pathophysiology of clinical pathologic changes in hypoadrenocorticism: Hyperkalemia, hyponatremia, hypochloridemia, azotemia, decreased USPG

Back 76

Aldosterone is responsible for increasing sodium reuptake (with Cl and H2O), and potassium excretion in response to low blood pressure. Without aldosterone, sodium and chloride are lost, and potassium is retained causing electrolyte imbalances; water is also lost with sodium causing inappropriately dilute USPG; and because decreased blood flow to the kidney is never corrected, GFR decreases, leading to azotemia.

Front 77

Describe the pathophysiology of clinical signs in hypoadrenocorticism: Hypotension

Back 77

All types: glucocorticoids are responsible for maintaining vascular tone and mediates the vasoconstrictive response to epinephrine. Lack of glucocorticoids leads to hypovolemia, decreased blood pressure, and decreased cardiac output.

Front 78

Describe the pathophysiology of clinical pathologic changes in hypoadrenocorticism: Hypoalbuminemia

Back 78

Possibly due to protein losing nephropathy or enteropathy. Mechanism not entirely known.

Front 79

Describe the pathophysiology of clinical signs in hypoadrenocorticism: Hypocholesterolemia

Back 79

Mechanism unknown.

Front 80

Describe the pathophysiology of clinical signs in hypoadrenocorticism: Megaesophagus

Back 80

Thought to be due to muscle weakness caused by changes in membrane potential (from decreased sodium and increased potassium), and unexplained weakness associated with decreased cortisol.

Front 81

Describe the pathophysiology of clinical signs in hypoadrenocorticism: Electrocardiogram changes

Back 81

DUE TO HYPERKALEMIA!
Bradycardia, peaked T waves, Widened QRS complex, decreased or absent P wave amplitude, ventricular asystole.

Front 82

Name the test used for diagnosis of Addison's disease.

Back 82

ACTH stimulation test.
Sensitive and specific for both types (typical and atypical) of Addison's as long as no steroids are given prior.
Exogenous ACTH is given and cortisol is measured (aldosterone may also be measured at this time); Addisonian animals will have little or no increase in cortisol.

Front 83

Develop a treatment plan for a dog in Addisonian crisis

Back 83

Treat for shock: Aggressive fluid therapy. Always calculate deficit/losses/maintenance. 4x maintenance will not cut it because patient comes in excessively dehydrated.
Glucocorticoid replacement: larger dose than normal given because animal is in SHOCK (would normally be producing more). Dexamethasone SP is best because it does not interfere with ACTH stim test.
Correct hyperkalemia and ECG abnormalities: in most cases hyperkalemia will correct with aggressive administration of NaCl 0.9%. If ECG abnormalities persist, give Calcium Gluconate. Can give sodium bicarbonate or dextrose (+/- insulin) as a secondary resort.

Front 84

Develop a maintenance and monitoring plan for typical and atypical addisonian patients.

Back 84

Typical: DOCP ~every 25 days, and daily prednisone. DOCP dosing interval is adjusted based on electrolytes. Once stable, prednisone should be tapered to the lowest effective dose. Double doses of prednisone should be given before/during stressful events (eg. grooming and kenneling). Alternatively, fludrocortison can be given alone, dose increased or decreased to affect.
Atypical: Only require supplementation with prednisone. Dose is tapered to lowest effective dose. Therapy frequency is based on the resolution of original presenting clinical signs.

Front 85

Compare the hypothalamic-pituitary-adrenal axis in the normal animal to the cushinoid animal (pituitary or adrenal neoplasia), and an animal receiving exogenous glucocorticoids.

Back 85

Pituitary neoplasia: Pituitary production of ACTH does not respond to negative feedback from cortisol. Constant stimulation causes hypertrophy of all adrenal tissue.
Adrenal neoplasia: Cortisol is produce regardless of stimulation pattern from the pituitary, excess cortisol leads to decreased production of ACTH. All non-neoplastic adrenal tissue will atrophy.
Exogenous glucocorticoids: Drug provides negative feedback to the pituitary, decreased ACTH production, which causes adrenal tissue to atrophy. When drug is discontinued, cortisol is no longer produced leading to a hypoadrenocortical state.

Front 86

What is "atypical" hyperadrenocorticism?

Back 86

Atypical hyperadrenocorticism is the overproduction of cortisol precoursers rather than an overproduction of cortisol.

Front 87

What are the 5 most common signs of Cushings?

Back 87

Polyuria
Polydipsia
Polyphagia
Pot-belly
Panting

Front 88

Describe the pathophysiologic mechanism of common clinical signs in the hyperadrenocortical dog: PU/PD

Back 88

Excess glucocorticoids interfere with the release and action of ADH

Front 89

Describe the pathophysiologic mechanism of common clinical signs in the hyperadrenocortical dog: Polyphagia

Back 89

Polyphagia is a direct effect of glucocorticoids

Front 90

Describe the pathophysiologic mechanism of common clinical signs in the hyperadrenocortical dog: Abdominal enlargement

Back 90

Catabolic effect of glucocorticoids causes abdominal muscles to weaken; fat deposition increases in the intra-abdominal tissues; excess glucocorticoids cause hepatomegaly. Because the animal is PU/PD, the bladder is often distended with excess urine.

Front 91

Describe the pathophysiologic mechanism of common clinical signs in the hyperadrenocortical dog: Panting

Back 91

Fat deposition increases in the intra-thoracic tissues. Catabolic effects weaken the intercostal muscles and diaphragm. Abdominal distention prevents the diaphragm from moving easily. Panting may also be a result of thromboembolic complications.

Front 92

Describe the pathophysiologic mechanism of common clinical signs in the hyperadrenocortical dog: Neuromuscular signs

Back 92

Muscle weakness and ligamentous damage are both due to catabolic changes
Fibrous myopathy, facial nerve paralysis, and behavioral changes do not have well understood mechanisms.

Front 93

Describe the pathophysiologic mechanism of common clinical signs in the hyperadrenocortical dog: Dermatologic changes

Back 93

Excess cortisol directly causes atrophy of hair follicles (alopecia), comedones, hyperpigmentation, and thinning of the skin.
Due to effects on vessel endothelium, excessive bruising and poor wound healing also occur.

Front 94

Describe the pathophysiologic mechanism of common clinical signs in the hyperadrenocortical dog: Calcinosis cutis

Back 94

Excess cortisol causes dysregulation of calcium homeostasis.

Front 95

Describe the common clinical pathologic abnormalities in the hyperadrenocortical dog.

Back 95

CBC: mild polycythemia, stress leukogram, thrombocytosis
Chem: Increased ALP activity, mildly increased ALT activity, hyperlipidemia/hypercholesterolemia, hyperglycemia.
Urinalysis: Decreased USPG (often hyposthenuric), proteinuria, +/-active sediment and calcium oxalate crystals.
Thyroid testing: Decreased total T4.
Bile acids: increased in 30% of dogs.

Front 96

Advantages, disadvantages and uses of tests for hyperadrenocorticism: Urine cortisol:creatinine ratio

Back 96

First morning urine sample should be collected at home, three days in a row.
Advantages: Highly sensitive, cheap and easy to perform.
Disadvantages: Not specific, sensitive to concurrent disease or any stress.
Use: Quick and cheap test to rule out cushing's if it is not high on your differential list.

Front 97

Advantages, disadvantages and uses of tests for hyperadrenocorticism: ACTH stim

Back 97

Baseline sample taken, administration of exogenous ACTH, sample taken at 1 hr; testing cortisol levels. Tests adrenal response to ACTH.
Advantages: High sensitivity and specificity; least affected by concurrent disease or medication. Quick to perform. Diagnoses atypical cases when coupled with a full adrenal panel.
Disadvantages: ACTH is expensive. 40% of adrenal dependent cases do not respond.
Uses: "gold standard" test for Cushing's in specialty situations. Only test that can be used to monitor therapy.

Front 98

Advantages, disadvantages and uses of tests for hyperadrenocorticism: Low-dose Dexamethasone suppression test

Back 98

Cortisol measured at baseline, 4 hour, and 8 hour; low dose dex given IV. Measures negative feed back loop. Baseline and 8 hr reading are diagnosic; all three readings can be used to differentiate some cases of pituitary dependent.
Advantages: Highly sensitive, very cheap, sometimes useful for differentiation.
Disadvantages: less specific, affected by concurrent disease or medications. Long time required to perform (can be confounding if the animal becomes stressed during testing, no other procedures can be done at the same time).
Uses: Back up for ACTH stim; used widely in general practice as a cheaper alternative (time constraint less problematic).

Front 99

Advantages, disadvantages and uses of tests for hyperadrenocorticism: High-dose Dexamethasone suppression test

Back 99

Cortisol measured at baseline, 4 hour, and 8 hour; high dose dex given IV. Measures negative feed back loop.
Advantages: Diagnostic for a higher percentage of pituitary dependant cases than the low dose test.
Disadvantages: Can not diagnose adrenal dependent cases, time consuming
Uses: used as a differentiation test AFTER the diagnosis of cushing's has been made.

Front 100

Advantages, disadvantages and uses of tests for hyperadrenocorticism: Endogenous ACTH levels

Back 100

Single sample is taken and endogenous ACTH levels are tested.
Advantages: Can diagnose adrenal dependent and pituitary dependent cases. Quick.
Disadvantages: Labile-special handling and fast shipping required.

Front 101

Advantages, disadvantages and uses of tests for hyperadrenocorticism: Imaging (x-rays, ultrasound, brain MRI)

Back 101

X-rays: adrenal calcification can be detected in <50% of ADH cases.
Ultrasound: Adrenal shape and symmetry can be used to guide differentiation of ADH vs PDH; however, incidental adrenal nodules, bilateral adrenal masses, can confound interpretation. Best used for staging/planning once diagnosis has been made.
Brain MRI: Used to detect pituitary nodules. Nodules may or may not be visible, does not mean they aren't there.

Front 102

Advantages, disadvantages, and risks of treatments for hyperadrenocorticism: Mitotane

Back 102

Dose dependent destruction of zona fasciculata and reticularis; will destroy the glomerulosa at really high doses.
Uses: PDH, inoperable ADH, and "Utrecht protocol"
Advantages: Stops adrenal hypertrophy/growth; can be used for medical adrenalectomy (Atypicals, patients intolerant of medication).
Disadvantages: Expensive, overtime will require higher doses to maintain hypoadrenal state. ADH requires longer induction and higher maintenance doses. Utrecht protocol only has 80-85% success rate; must be supplemented with glucocorticoids and mineralocorticoids.
Risks: Toxic effect on GI, over dosage can cause iatrogenic Addison's (typically during induction), undesired idiosyncratic adrenal necrosis (permanant).

Front 103

Advantages, disadvantages, and risks of treatments for hyperadrenocorticism: Trilostane

Back 103

Competitively inhibits enzymes in the cortisol production pathway.
Advantages: May work in cases refractory to mitotane.
Disadvantages: Labeled dose is way too high, so best guess dose must be used. May have ongoing signs in spite of good ACTH stims. Does not stop adrenal enlargement.
Risks: Sudden death with labeled dose. Adrenal necrosis, iatrogenic Addison's, makes some atypical cases worse. Does not stop adrenal enlargment.

Front 104

Advantages, disadvantages, and risks of treatments for hyperadrenocorticism: Ketoconazole

Back 104

Competitively inhibits steps in the cortisol production pathway.
Advantages: Inhibits more steps than Trilostane.
Disadvantage: Does not stop adrenal enlargement.
Risks: Hepatocellular damage, iatrogenic Addison's.

Front 105

Advantages, disadvantages, and risks of treatments for hyperadrenocorticism: L-deprenyl (selegiline)

Back 105

Pilot study-83% efficacy.
Peer reviewed studies-NO EFFECT.

Front 106

Advantages, disadvantages, and risks of treatments for hyperadrenocorticism: Adrenalectomy

Back 106

Surgical removal of the adrenal gland.
Advantages: Treatment of choice for ADH. 2 year survival time for carcinomas, much longer survival for adenomas (unknown-study ended with no deaths). If it works, it is a permanent cure.
Disadvantages: 20% perioperative mortality. Not an option if tumor has spread/invaded other tissue.
Risks: Transient post-op Addison's expected, atrophied adrenal tissue must rebound.

Front 107

Advantages, disadvantages, and risks of treatments for hyperadrenocorticism: Hypophysectomy

Back 107

Used for pituitary dependent; typically microadenomas.
Advantages: 75% success with 28 month mean survival. Prevent further complications and neurologic sequelae.
Disadvantages: Can be hard to perform on macroadenomas. Causes permanent hypothyroidism and Addison's. Not many places offer this, and it is very expensive.
Risks: Transient to permanant central diabetes insipidus; 8% perioperative mortality.

Front 108

Advantages, disadvantages, and risks of treatments for hyperadrenocorticism: Pituitary irradiation

Back 108

Primarily used for pituitary macroadenomas
Advantages: Decreases neuro signs, aids in control of HAC.
Disadvantage: Rare for this to be fully curative. Not readily available and expensive. Must be anesthetized daily for treatment.
Risks: Radiation effects-skin lesions, brain edema and necrosis, intracranial neoplasia. Anesthetic risks.

Front 109

Describe how cats with HAC differ from dogs with regards to presentation and clinical signs.

Back 109

Presentation-similar to dogs, 80% PDH. >50% of cats will also be unregulated diabetics.
Clinical signs: Same clinical signs as dogs, plus excessively fragile (will tear off in panels).
Clin path: Rare to have inc ALP; typically inc cholesterol, BUN; and proteinuria will be more marked than that in dogs.
Imaging: Hepatomegaly on rads. Calcification of adrenals may be idiopathic.

Front 110

Describe how cats with HAC differ from dogs with regards to diagnosis.

Back 110

Diagnosis: ACTH stim less sensitive than dogs (60%), requires two post samples. LDDS requires 10x the dose for dogs.
Differentiation: HDDS also requires 10x dose for dogs; less sensitive for PDH (50%). eACTH very useful in cats (correct in most cases).

Front 111

Describe how cats with HAC differ from dogs with regards to treatment.

Back 111

Mitotane and ketoconazole have no effect in cats.
Metyrapone may have some effect.
Treatment of choice is Trilostane, but must be used with extreme caution (not uncommon for cat to die suddenly during treatment).
Surgery-Pituitary irradiation is probably the best choice for cats. Adrenalectomy may be done for both ADH and PDH, but reported cases are rare. Not good perioperative survival with any surgical treatments.

Front 112

Describe the physiology of glucose homeostasis with attention to the hypo- and hyperglycemic hormones.

Back 112

Hyperglycemic state:
1. Insulin-promotes uptake and utilization of glucose, amino acids, and fatty acids in peripheral tissues; increases uptake and storage of fatty acids in adipose tissue; promotes glycogen production, fatty acid synthesis, and protein synthesis in the liver while down regulating gluconeogenesis.
Hypoglycemic state:
1. Glucagon (fast)-promotes glycogenolysis and gluconeogenesis in the liver. Will also increase ketone production during starvation.
2. Epinephrine (fast)-Transiently decreases insulin secretion, increases gluconeogenesis, glycogenolysis, and lipolysis. Also decreases tissue glucose utilization for a longer period.
3. Cortisol (slow)-In peripheral tissues, decreases glucose uptake and cellular process, increases protein breakdown and lipolysis. In the liver, promotes glycogen synthesis and glucose synthesis.
4. Growth hormone (slow)-increases lipolysis, and decreases peripheral tissue uptake and utilization of glucose.

Front 113

Know the numerical definition of hypoglycemia, and the organs most commonly affected.

Back 113

BG <60mg/dL
The brain is the organ most severely affected by hypoglycemia because it can only utilize glucose! However, other major organs in the body are also affected.

Front 114

Identify factors that erroneously affect blood glucose measurement results.

Back 114

Increase in RBCs or WBCs in the sample
Delay in sample handling
Use of portable glucometers

Front 115

Describe the pathophysiology of common clinical signs of hypoglycemia:.

Back 115

1. Compensatory mechanisms: Increased appetite
2. Nervous system effects: Depression, mental dullness, bizarre behavior, tremors, seizures, coma, apnea, death.
3. Muscle effects: muscle twitching, weakness, ataxia.
4. Misc/Whole body effects: Hypothermia.

Front 116

Formulate a treatment plan for a clinical patient with hypoglycemia.

Back 116

1. Treat the underlying cause.
2. Glucose supplementation-feed a meal (+/- high fiber, blunts post-prandial insulin spike), karo syrup on mucous membranes, IV dextrose. Route of treatment should be based on clinical presentation of the animal, not BG values.
3. Prednisone-used in Insulinoma patients.
4. Glucagon-used in insulineoma patients or refractory hypoglycemia.

Front 117

Describe the mechanisms of hypoglycemia for commonly associated diseases: Juvenile Hypoglycemia

Back 117

Toy and miniature breed dogs, less than 6 months of age.
High glucose needs, low body mass and glycogen stores, any concurrent stress, hyporexia, or infection.

Front 118

Describe the mechanisms of hypoglycemia for commonly associated diseases: Neonatal hypoglycemia

Back 118

Occurs in neonates.
Similar causes to juvenile hypoglycemia; most commonly due to inadequate nursing (runt, too many babies, mother won't allow nursing).

Front 119

Describe the mechanisms of hypoglycemia for commonly associated diseases: Insulin overdose

Back 119

Iatrogenic: owner error, overlapping doses (happens when insulin has high duration of affect).
Increased insulin sensitivity/decreased need: Strenuous activity, inappetence, resolution of insulin antagonism, cats.

Front 120

Describe the mechanisms of hypoglycemia for commonly associated diseases: Cortisol deficiency

Back 120

Hypoadrenocorticism-typical and atypical
Relative adrenal insufficiency
Iatrogenic-overcontroled Cushing's patients

Front 121

Describe the mechanisms of hypoglycemia for commonly associated diseases: Sepsis

Back 121

Impaired glycogenolysis and gluconeogenesis, increased peripheral use, consumption of glucose by bacteria and leukocytes.

Front 122

Describe the mechanisms of hypoglycemia for commonly associated diseases: Hepatic failure.

Back 122

Occurs when >70% of hepatocytes are lost.
Glycogen synthesis and gluconeogenesis functions decrease.

Front 123

Describe the mechanisms of hypoglycemia for commonly associated diseases: Insulinoma

Back 123

Functional beta cell tumor: small to microscopic, most commonly carcinomas on the pancreatic limbs, very common in ferrets, sort of common in dogs.
Tumor secretes insulin autonomously.
Diagnosed by paired glucose and insulin levels (inappropriately normal or high insulin, while hypoglycemic. Normo- or hyperglycemic reading voids the test).
Treatment: surgical removal is best if tumor can be found. Can be managed with frequent feeding of high fiber diet and administration of insulin-antagonizing agents (pred, diazoxide, glucagon). Glucose should not be given, may worsen insulin release, exacerbating hypoglycemia!

Front 124

Describe the mechanisms of hypoglycemia for commonly associated diseases: Hunting dog hypoglycemia

Back 124

Occurs in lean bodied hunting dogs after several hours of vigorous/prolonged exercise. Possibly due to increased utilization and depletion of glycogen stores. Can be avoided by feeding a meal before and after long periods of activity.

Front 125

Describe the mechanisms of hypoglycemia for commonly associated diseases: Paraneoplastic Hypoglycemia

Back 125

Non-pancreatic neoplasms secrete insulin-like polypeptides; also possible that the neoplastic tissue overutilizes glucose, and potentially decreases hepatic gluconeogenesis.

Front 126

Describe the mechanisms of hypoglycemia for commonly associated diseases: Xylitol

Back 126

In dogs, causes a mass release of insulin. May also cause hepatic failure and coagulopathies. Not-necessarily dose dependent.

Front 127

Describe the mechanisms of hypoglycemia for commonly associated diseases: Beta-blockers

Back 127

Suppresses counter-regulatory hormones and gluconeogenesis. Requires ingestion of large quantities.

Front 128

Describe the mechanisms of hypoglycemia for commonly associated diseases: Epidurals

Back 128

Hypoglycemia occurs when lumbar anesthesia infiltrates the thoracic region. Mechanism unknown.

Front 129

Describe the mechanisms of hypoglycemia for commonly associated diseases: Pre- and Postpartum

Back 129

Late gestation and during prolonged labor. Post-partum, 1st time mothers will often let pups over-nurse. Occurs concurrent with eclampsia.

Front 130

Describe the mechanisms of hypoglycemia for commonly associated diseases: Hepatozoonosis

Back 130

Increased glucose utilization by infected mononuclear cells and endothelial cells.

Front 131

Distinguish between insulin dependent diabetes mellitus and non-insulin dependent diabetes mellitus.

Back 131

IDDM-absolute deficiency of insulin; more common in dogs; patient will be supplemented with insulin for life.
NIDDM-relative deficiency in insulin; more common in cats, rarely occurs in dogs, may convert to IDDM; patient requires insulin therapy to begin with, then may be weaned off insulin as insulin resistance factors are corrected.

Front 132

Describe physiology for the different components of insulin resistance.

Back 132

1. Changes in counter-regulatory hormones: Increase in hormone production due to concurrent disease process. a. Cortisol (Cushing's, stress, drug therapies). b. Growth hormone (Acromegaly). c. Catecholamines (Pheochromocytoma). d. Progesterone (Diestrus, Gestation). e. Glucagon (Glucagonoma).
2. Glucose toxicity/carb intolerance: constant presence of glucose from over consumption of carbohydrates leads to overstimulation that down regulates insulin secretion, expression of glucose transporters, and causes defects in the post-transport insulin action.
3. Peripheral insulin resistance: Obesity decreases the number of insulin receptors and the ability of insulin to bind to receptors, changes the post-receptor action of insulin, and increases the build up of Amylin (leads to damage of the B-cells).

Front 133

Describe the pathophysiology of common clinical signs of diabetes mellitus: PU/PD

Back 133

Amount of glucose in the blood exceeds the renal threshold->glucosuria->osmotic diuresis.

Front 134

Describe the pathophysiology of common clinical signs of diabetes mellitus: Polyphagia

Back 134

Feeding center of the brain is always on, unless inhibited by signals from the satiety center. The satiety center is always off, unless activated by insulin-facilitated glucose uptake. Without insulin/glucose uptake, the satiety center is not activated, and the feeding center is not suppressed; the animal is always hungry.

Front 135

Describe the pathophysiology of common clinical signs of diabetes mellitus: Weight loss

Back 135

Without insulin or with increase in counter regulatory hormones, the liver decreases production of protein and increases production of glucose. In other tissues, the cells cannot uptake glucose to use it even though it is there, and tissue atrophy occurs.

Front 136

What two clinicopathologic abnormalities are REQUIRED to make a diagnosis of diabetes mellitus?

Back 136

Persistent fasting hyperglycemia WITH glucosuria.

Front 137

Be able to distinguish between diabetes mellitus and stress hyperglycemia.

Back 137

Stress hyperglycemia: Hyperglycemia, +/- glucosuria. BG can be greater than 300.
If glucosuria not present, not diabetes mellitus. If glucosuria present, recheck in a non-stressed enviroment or check fructosamine.

Front 138

List the common clinical pathologic abnormalities identified in diabetic animals.

Back 138

CBC: None
Chem: Hyperglycemia. Secondary hepatopathy-lipemia, hypercholesterolemia, hypertriglyceridemia, increased ALT and ALP. Concurrent pancreatitis-increased PLI.
Urinalysis: USPG >1.025, glucosuria, +/-ketonuria, proteinuria.
Urine culture: 50% have occult UTI.
Fructosamine: Increased (reflects glycemic state from the last 1-3 weeks).

Front 139

Compare and contrast the advantages, disadvantages, and uses of the different types of insulin with attention to their duration and potency: Regular crystalline insulin.

Back 139

Advantages: Rapid onset, very potent, multiple routes.
Disadvantages: Short duration of action.
Uses: Insulin of choice for managing sick or ketotic patients.

Front 140

Compare and contrast the advantages, disadvantages, and uses of the different types of insulin with attention to their duration and potency: Vetsulin

Back 140

Mixed amorphous and crystaline zinc.
Advantages: Veterinary specific. Mix allows for increased initial potency with longer duration of action. Kinetics may allow SID dosing in some.
Disadvantages: Currently off market. Porcine insulin-good for dogs, not as good for cats.
Uses: First choice for use in dogs when available.

Front 141

Compare and contrast the advantages, disadvantages, and uses of the different types of insulin with attention to their duration and potency: NPH

Back 141

Neutral Protamine Hagedorn
Advantages: Intermediate duration of action and potency.
Disadvantages: Duration may be <12 hours in cats, requiring TID dosing. Human formulation.
Uses: Second choice in dogs and third in cats. Currently first choice in dogs because Vetsulin off the market.

Front 142

Compare and contrast the advantages, disadvantages, and uses of the different types of insulin with attention to their duration and potency: Glargine (Lantus)

Back 142

Advantages: Slow release due to microprecipitation when pH changes decreases peaks and troughs. Long duration of action allows for BID dosing.
Disadvantages: Giving SID increases risk of ketosis. Dilution will cause insulin to precipitate.
Use: First choice in cats.

Front 143

Compare and contrast the advantages, disadvantages, and uses of the different types of insulin with attention to their duration and potency: PZI

Back 143

Human recombinant protamine zinc.
Advantages: Veterinary label. Long duration, low potentcy. BID dosing.
Disadvantages: Duration of action is unknown and highly variable in dogs.
Uses: Second choice in cats.

Front 144

Compare and contrast the advantages, disadvantages, and uses of the different types of insulin with attention to their duration and potency: Levemir

Back 144

Super long acting human insulin. Used as a last resort.

Front 145

Developing a diabetes theraputic plan: Management of causes of insulin resistance.

Back 145

Most important is to treat any other concurrent diseases. ANYTHING going on with the animal will change the animal's insulin requirements and response to insulin.

Front 146

Developing a diabetes theraputic plan: Insulin choice.

Back 146

Dogs: Vetsulin>NPH>Glargine
Cats: Glargine>PZI>NPH
Ultimately each individual's response to a given insulin should be assessed to determine dose, frequency, and type of insulin that is best for the patient.

Front 147

Developing a diabetes theraputic plan: Nutritional recommendation.

Back 147

All: Twice daily feeding; SID insulin-1/2 prior to insulin and 1/2 at nadir, BID insulin-1/2 at each dose.
Dogs (obese): High fiber, low carb diet. Slows CHO absorption and aids weight loss. Can cause Constipation or diarrhea.
Dogs (not obese): Moderate fiber, low carb diet (most "senior" diets). Advantages of high fiber, low carb diet, but without the GI side effects, and prevents unnecessary weight loss.
Cats: High protein, low carb, low fiber, CANNED diet. (Kitten food is just as good as specialty diet.) Increased rate of remission. Can use higher fiber diets if morbidly obese or if cat refuses to eat canned food.

Front 148

Developing a diabetes theraputic plan: Oral hypoglycemic agents.

Back 148

Uses: not used often. Can be used as a last resort adjunct for poorly controlled diabetics, or as a start up treatment to give owners time to adjust to the idea of treating with insulin.
Alpha-glucosidase inhibitors: used mostly in dogs, sometimes in cats. Delays glucose absorption, which decreases post-prandial BG conc.
Glipizide: Requires functional beta cells, only useful in NIDDM cats. Increases insulin secretion. Cons-variable efficacy, worsens islet amyloidosis. Must monitor glucose and UA weekly, and hepatic enzymes at 2 weeks.

Front 149

Developing a diabetes theraputic plan: Exercise recommendations

Back 149

DAILY exercise will reduce insulin requirements by increasing insulin mobilization, glut-4 upregulation, and glucose effectiveness.

Front 150

Developing a diabetes theraputic plan: Starting insulin therapy.

Back 150

Patient should be hospitalized and a BG curve performed when giving the first dose of insulin. If hypoglycemic, the dose should be decreased. If hyperglycemic, dose should be left alone, as it takes several weeks to adjust to equilibrate. Recheck BG curves should be done no less than 7 days apart, ideally no less than 2 weeks apart.
It is imperative to watch for hypoglycemia, and change dose if it occurs.

Front 151

Integrate understanding of the pathophysiology of diabetes with knowledge of the 3 major components of glucose curve evaluation to accurately interpret glucose curves.

Back 151

Three portions of a glucose curve: Time of onset, nadir, and duration of effect. Ultimately indicates efficacy.
Samples should be taken at T0 and every two hours while BG is above 150. If below 150, sample every hour, and if below 100, sample every 30 minutes. Decreases risk of missing nadir if patient becomes hypoglycemic and has a physiologic BG spike response (Somogyi effect). This response will negate the curve results, and BG concentrations may remain high for 24-72 hours.

Front 152

Recognize and describe the pathophysiology of common complications of diabetes mellitus and their relative prevalences in dogs vs. cats: Cataracts.

Back 152

Formation of cataracts in diabetes is related to sorbitol dehydrogenase in the lens. Causes changes in lens osmolarity that lead to an influx of water and swelling/rupture of the lens fibers.
Will cause a secondary lens-induced uveitis.
Very common complication in dogs, rarely happens in cats.

Front 153

Recognize and describe the pathophysiology of common complications of diabetes mellitus and their relative prevalences in dogs vs. cats: Diabetic neuropathy

Back 153

Mechanism is not completely understood.
Most common complication in cats.
Signs: inability to jump, plantigrade posture, decreased reflexes/postural reactions.
Treated with aggressive glucose regulation and B12 supplements.
If caught early, may be reversible.

Front 154

Recognize and describe the pathophysiology of common complications of diabetes mellitus and their relative prevalences in dogs vs. cats: Diabetic nephropathy

Back 154

Pathogenesis unknown, secondary to diabetic effect on the kidneys. May be due to concurrent disease.
Signs: Proteinuria, azotemia, uremia. Can lead to oliguric/anuric renal failure.
Not common in either species because it takes too long to develop.

Front 155

Recognize and describe the pathophysiology of common complications of diabetes mellitus and their relative prevalences in dogs vs. cats: Hypertension (+ retinopathy)

Back 155

Mechanism unclear. Suggested due to sub-clinical renal disease, disturbed lipid metabolism, or immune-mediated microangiopathy.
~50% prevalence in dogs, incresed chance with chronic diabetes. Retinopathy occurs in ~20%.

Front 156

Describe in scientific terms the pathophysiology of ketone formation.

Back 156

Ketone bodies are formed from Acetyl CoA and used by tissues as an energy source when glucose is deficient.

Front 157

Describe the pathophysiology underlying diabetic ketoacidosis: Common concurrent illnesses.

Back 157

Acute/chronic pancreatitis
Bacterial infections
Cholangiohepatitis
Renal insufficiency
Cardiac disease
Hormonal disorders

Front 158

Describe the pathophysiology underlying diabetic ketoacidosis: Clinical features

Back 158

PU/PD-diuresis from glucosuria as well as ketonuria
Vomiting/Diarrhea-Unabsorbed glucose in the food can cause osmotic diarrhea. Vomiting from acidosis.
Dehydration-from osmotic diuresis, vomiting, diarrhea, and cellular dehydration due to hyperglycemia. May be severe (>12-14%).

Front 159

Describe the pathophysiology underlying diabetic ketoacidosis: Hematologic/biochemical sequelae.

Back 159

Acidosis-ketoacids as well as lactic acid
Hyperglycemia, glucosuria-duh.
Inc ALP/AST-glycogen hepatopathy
Decreased Na and Cl-osmotic diuresis, GI losses (diarrhea/vomiting), compensation for increased osmolarity due to hyperglycemia (correction: +2.4 mEq/L Na for every 100 mg/dL increase in glucose).
Decreased potassium-extracellular shift from acidosis, osmotic diuresis, GI loss and decreased intake; will worsen with therapy.
Decreased phosphorus-no dietary intake, no insulin triggered cellular uptake, increased urinary loss; will worsen with therapy.
Decreased magnesium-common in cats, but hard to measure. Suspect if refractory hypokalemia, hypocalcemia, or ventricular arrhytmias.

Front 160

Develop an appropriate initial theraputic and monitoring plan based on a strong understanding of DKA pathophysiology.

Back 160

1. Fluid therapy: 0.9% saline is best for correcting low Na and Cl. Add potassium 40mEq/L, half as KPO4, to prevent both K and PO4 deficits from worsening (or appearing) with therapy. If PO4 is <2.0 mg/dl, supplement as CRI and monitor levels every 6-8 hrs. Magnesium supplement only when suspect hypomagnesemia. Fluid therapy and electrolyte correction will often correct acidosis and a large chunk of the hyperglycemia by itself.
1.5 Bicarb may be given only AFTER 1-2 hours of rehydration IF tCO2 <12!
2. Insulin-start after 1-2 hours of rehydration. If still hypokalemic, delay until K is normal. Regular crystalline insulin may be given hourly IM, intermittently(4-6 hours) IM and SQ, or as a CRI. Goal is to gradually decrease BG (~50mg/dl/hr). When glucose reaches <250, add dextrose fluids. Continued insulin therapy is required to correct ketoacidosis; dextrose prevents hypoglycemia without decreasing insulin.
4. Switch to long term insulin when patient is stable, maintaining fluid/electrolyte balance without supplementation and hematologic/UA abnormalities have corrected.
5. Treat any concurrent diseases
**In the healthy DK patient-regular insulin is used until ketonuria resolves, then long term insulin is instituted. Because patient is healthy, no other steps needed.

Front 161

Describe the physiology of normal calcium/phosphorus homeostasis with attention the interrelationship of PTH, PTHrP, calcitriol and calcitonin.

Back 161

PTH-Negative feedback loop directly with iCa. Maintains serum levels between 10.5-11.5. Short half life with minute correction. Causes increased bone resorption (inc Ca and P), stimulates kidney to inc Ca absorption and P excretion (inc Ca, dec P). Also stimulates calcitriol production in the kidney. Overall effect is increased Ca with decreased P.
PTHrP-Identical biological activity to PTH, only secreted in detectable levels by cancers.
Calcitriol-metabolited of Vit D3 produced in response to PTH. Negative feedback on PTH production, as well as on the enzyme pathway for it's own production. Stimulates Ca and P absorption in the intestine. Also stimulates bone deposition to counteract some of PTH effect.
Calcitonin-Secreted by C-cells of the thyroid gland in response to digestive secretions. Decreases bone resorption and increases Ca and P excretion in the kidney. Blunts postprandial hypercalcemia.

Front 162

Describe the pathophysiologic mechanisms of hypocalcemia commonly associated with diseases: hypoalbuminemia

Back 162

Because some of Ca is bound to albumin, hypoalbuminemia will cause a falsely decreased tCa (bound fraction is low even though ionized fraction is normal).

Front 163

Describe the pathophysiologic mechanisms of hypocalcemia commonly associated with diseases: Eclampsia

Back 163

Acute increase in calcium demands associated with lactation.
Can also be caused by parathyroid gland atrophy caused by excessive prepartum calcium supplementation.
Features: often associated with nervous, first time mothers that do not make babies stop nursing. Rapidly progressive signs of hypocalcemia.
Tx: Intravenous calcium supplementation, forced separation of mother and babies to allow recovery time.

Front 164

Describe the pathophysiologic mechanisms of hypocalcemia commonly associated with diseases: Hypoparathyroidism

Back 164

Immune-mediated parathyroid destruction; genetic predisposition in mini schnausers and german shepards. Causes decreased PTH, tCa, and iCa, with increased P.
Treatment: Calcitriol and oral calcium supplementation.

Front 165

Describe the pathophysiologic mechanisms of hypocalcemia commonly associated with diseases: Chronic renal failure

Back 165

Increased P (from dec GFR) and decreased production of calcitriol cause hypocalcemia. This will cause increased PTH production; and Ca levels usually stay normal until end-stage. However, the increased Ca and P pulled from the bone will cause mineralization of other tissues (inc Ca/P product).

Front 166

Describe the pathophysiologic mechanisms of hypocalcemia commonly associated with diseases: Pacreatitis

Back 166

Mild hypocalcemia due to saponification of adipose.

Front 167

Describe the pathophysiologic mechanisms of hypocalcemia commonly associated with diseases: Ethylene glycol toxicity

Back 167

Metabolites chelate calcium to form calcium oxalates. Acidosis will often maintain iCa levels at normal because of shift away from bound fraction. Clinical signs result when acidosis is corrected too quickly.

Front 168

Describe the pathophysiologic mechanisms of hypocalcemia commonly associated with diseases: Phosphate enemas

Back 168

Cause toxicity in cats. Increased Phophate will trigger a decrease in Calcium.

Front 169

Describe the pathophysiologic mechanisms of hypocalcemia commonly associated with diseases: Hypercalcitonism

Back 169

Rare. Due to C-cell neoplasm.

Front 170

Describe the pathophysiologic mechanisms of hypocalcemia commonly associated with diseases: Iatrogenic

Back 170

Bilateral thyroidectomy with removal of the parathyroid glands, or complete parathyroidectomy.

Front 171

Develop and appropriate diagnostic plan for a patient with clinical hypocalcemia.

Back 171

Diagnostic plan is based on clinical signs, suggestive history of disease processes, tCa and P levels, iCa levels, and PTH/PTHrP assay.

Front 172

Develop and appropriate treatment plan for a patient with clinical hypocalcemia.

Back 172

Emergency: Start 10% calcium gluconate IV over 10-15 minutes, monitor ECG while administering. If BG is concurrently decreased, correct BG first (clinical appearance is very similar).
Chronic: Oral calcitriol, oral calcium (adjunct to calcitriol). Monitor ionized calcium.

Front 173

Describe the pathophysiologic mechanisms of hypercalcemia for commonly associated diseases: Hyperparathyroidism

Back 173

Abnormal gland produces PTH with no feedback from Ca.
Typically solitary adenomas.
Primary clinical signs is PU/PD. Clin path: inc tCa and iCa; dec or normal P; no PTH-rP; and inc to normal PTH.
Diagnose by ultrasound of neck. Surgical removal is best.

Front 174

Describe the pathophysiologic mechanisms of hypocalcemia commonly associated with diseases: Osteomyelitis

Back 174

Septic bone disease; secondary hypercalcemia due to osteoclastic activity.

Front 175

Describe the pathophysiologic mechanisms of hypocalcemia commonly associated with diseases: Granulomatous disease

Back 175

Macrophages produce the enzyme which increases calcitriol production. Both Ca and P will be increased.

Front 176

Describe the pathophysiologic mechanisms of hypocalcemia commonly associated with diseases: Idiopathic hypercalcemia

Back 176

Miled to moderate inc in tCa and iCa, with decrease to normal PTH, and normal Phos and Vit D.
Mechanism unknown.

Front 177

Describe the pathophysiologic mechanisms of hypocalcemia commonly associated with diseases: Neoplasia.

Back 177

Top cause of hypercalcemia in dogs!!!!
Mechanisms: PTHrP production by the tumor; induced osteolysis; induced cytokines promoting bone resorption.
Lymphoma and apocrine gland adenocarcinoma (anal sac) most common in dogs; squamous cell and pulmonary carcinomas most common in cats.

Front 178

Describe the pathophysiologic mechanisms of hypocalcemia commonly associated with diseases: Youth

Back 178

Normal increase in Ca due to bone growth.

Front 179

Describe the pathophysiologic mechanisms of hypocalcemia commonly associated with diseases: Addisons/Hypoadrenocorticism

Back 179

Mechanism poorly understood. Possibly due to inc excretion, hemoconcentration, or increased protein binding. Increase is only in total calcium, ionized fraction will be normal. Does not cause clinical signs of hypercalcemia.

Front 180

Describe the pathophysiologic mechanisms of hypocalcemia commonly associated with diseases: Renal Failure

Back 180

Decreased Calcitriol and renal excretion->inc tCa and P (iCa normal to dec)->normal to inc PTH b/c of dec iCa.

Front 181

Describe the pathophysiologic mechanisms of hypocalcemia commonly associated with diseases: D-Hypervitaminosis

Back 181

Increased intestinal calcium and phosphorus absorption. Leads to tissue mineralization.

Front 182

Develop and appropriate diagnostic plan for a patient with hypercalcemia.

Back 182

Confirm hypercalcemia in a fasted, non-lipemic, non-hemolyzed sample to rule out spurious increase.
Assess: iCa, phosphorus, BUN/Cr, electorlytes, PTH/PTHrP, +/-Vitamin D.
Do a thorough neoplasia hunt, then hunt some more.
Parathyroid ultrasound or exploratory of the neck.

Front 183

Formulate an appropriate treatment plan for a clinical patient with hypercalcemia.

Back 183

Short term: collect any necessary diagnostic samples pre-treatment! Fluid therapy, then diuretics (furosemide is best) to increase renal calcium excretion.
Long term: Glucocorticoids (will decrease irregardless of cause, do not start until cause is identified), Bisphosphonates (decreased osteoclast function), Bicabonate (corrects acidosis, shifts iCa to protein bound fraction).
Rescue therapy: Calcitonin, Na-EDTA

Front 184

Interpret an ionized calcium/PTH/PTHrP panel in a clinical patient.

Back 184

Primary hyperparathyroidism: Inc tCa, iCa, PTH; no PTHrP; dec phos.
Malignancy: Inc tCa, iCa; dec PTH; inc/present PTHrP; dec phos.
Renal failure: Inc tCa, PTH, phos; no PTHrP; iCa may be increased or decreased.
Hypervitaminosis-D: Inc tCa, iCa; dec PTH; no PTHrP; inc phos.
Hypoparathyroidism: dec tCa, iCa, PTH; no PTHrP; inc phos.