Exam 4 Flashcards

Question

Pituitary Dwarfism who is the breed most overly represented?

Answer 1

-German shepherd -Autosomal recessive -Pituitary cysts C/S -Lack of growth, endocrine alopecia -Skin hyperpigmentation -Body vs. legs disproportions Tx -Administration of growth hormone Px -Variable

Answer 2

1. Renal disease 2. Hepatic disease 3. Endocrine disease 4. Miscellaneous: elites (low K, low Na, high Ca), drugs, endotoxins 5. Psychogenic polydipsia "Crazy lab syndrome"

Answer 3

-Loss of solutes (Na, Urea) in medulla results in loss of hypertonicity and impaired ability of the kidney to concentrate urine -Due to conditions causing PU/PD -Resolves once the underlying condition is treated -Can interfere with water depravation test. It may take months for animal to re-establish normal osmolality

Answer 4

-Defective synthesis or secretion of Arginine Vasopressin (AVP) AKA ADH by hypothalamus/post pituitary Causes -Insufficient secretion of ADH by hypothalamus/Pituitary (anterior pituitary) can be complete or partial -Idiopathic: young -Head trauma -Neoplasia -Malformations/cysts -Misc: inflammation, parasitic migration Signalment -No breed, sex or age predilection -Primary puppies, kittens, young adults -Secondary - varies depending on underlying cause C/S -PU/PD -Occasionally incontinence -Hypothalamus/pituitary tumor -Head trauma -Hydration WNL as long as animal has access to water and is drinking Dx -Rulo out of acquired secondary -PE -Minimum database: CBC, chemistry panel, urinalysis with culture -T4 (cats) -Adrenal function test (ACTH stim, LDDST)

Answer 5

-Defective Responsiveness of kidney to AVP/ADH in distal tubules Causes -Impaired responsiveness of the kidney to ADH -Primary idiopathic -Primary familial: HUSKIES -Secondary acquired

Answer 6

-Acts on distal convoluted tubules and collecting ducts -ADH (vasopressin) is released when plasma osmolality is increased or when extracellular fluid volume is decreased -Results in decreased urine volume -Promotes FREE water resorption -It also constricts arterioles which increases peripheral vascular resistance and hence blood pressure

Answer 7

1. Response to Desmopressin: preferred test -Evaluate patient's response to trial therapy with desmopressin acetate (DDAVP) -Oral tablets, nasal drops in conjunctiva -Every 12 hours for 7 days Central DI -Owners will notice a definite decrease in PU/PD and increase in USG >1.030 Nephrogenic DI -Minimal to no response will be noted in PU/PD and USG Psychogenic DI -Exhibits mild decrease in PU/PD Hyperadrenocorticism: mimics partial DI - moderate response to DDAVP: must rule out prior to resting to avoid misdiagnosing 2. Modified Water Deprivation Test: labor intense 3. Random plasma osmolality: not very specific, overlaps

Answer 8

First Phase A) Gradual water depravation by owner 3-5 days prior (10% decrease <30ml/lb/d) B) In hospital: initially empty bladder, weigh, measure USG, BUN, etc. Repeat every 2-4 hours Ends when USG >1.030 or loses 5% of body weight Nephrogenic DI -Primary: Can not concentrate urine in the face of 3-5% dehydration -Secondary: rule these out prior to water deprivation test Second Phase Response to DDAVP (desmopressin) -If you hold water and they concentrate urine, then it is psychogenic/behavioral. Central wouldn't be able to concentrate -Differentiates between central vs. Nephrogenic -Central DI: will respond to ADH/AVP by concentration of urine -Nephrogenic: will not respond to ADH/AVP

Answer 9

-No treatment: outdoor cat/dog if access to water -Complete: DDAVP oral or nasal drops in conjunctiva -Partial: DDAVP -Thiazide diuretics: mildly effective -Low Na diet

Answer 10

-Thiazine diuretics -Low Na diet -No treatment

Answer 11

Central on underlying cause: excellent Central due to trauma: good Central due to secondary tumors: usually guarded to poor Nephrogenic: guarded to poor Psychogenic: good

Answer 12

1. Cushing's: chronic disease, lifelong, frustrating disease 2. Pheochromocytoma

Answer 13

-Hypothalamus secretes Corticoid Releasing Hormone, -Pituitary Stimulated by it releases Adrenocortotropic Hormone -ACTH stimulates adrenal glands CORTEX to produce Cortisol and other hormones GFR Zona glomerulosa: Mineralcorticoids Zona Fasciculata: Glucocorticoids = Cortisol Zona Reticularis: Androgen precursors -Dehydroepiandrosterone (DHEA) -DHEA Sulfate -Androstendione Medulla -Catecholamines

Answer 14

Secretion -Stress: hypoglycemia -Infections/fever -Low cortisol levels Inhibition -High cortisol levels -Exogenous steroids -Dopamine: inhibits The Effects/Actions -Increase glucose concentrations in blood -Increase gluconeogenesis -Build up of glycogen for epinephrine and glucagon to act on -Enhances glucagon release **Causes insulin resistance** -Enhances lipolysis and ketogenesis -Increases appetite and caloric intake **Cortisol mobilizes fats and glucose in the body so that we can do all the functions** **Insulin antagonist** Effect on Kidney -Increase GFR -Decrease ADH and its action -Increase free water clearance Effect on CV system -Maintains cardiac output -Maintains Blood pressure -Maintains blood volume **Patients with low cortisol levels are hypovolemic with low BP** Hemopoetic System -Increase RBC formation -WBCs = Neutrophilia, Lymphopenia, Eosinopenia, Monocytosis **Stress leukogram** -Decrease lymphocytes

Answer 15

Disease syndrome resulting from abnormally high levels of cortisol circulating in the body 1. Pituitary dependent = Central -Accounts for 85% of HAC -Functional ACTH producing adenoma. Hyperplastic or reacting too much -Endogenous ACTH levels elevated C/S -Bilateral adrenal hyperplasia -Increased cortisol Excessive CRH from Hypothalamus -Rare -Hypothalamic or CNS disease C/S -Bilateral adrenal hyperplasia -Increased ACTH -Elevated cortisol 2. Adrenocortical dependent or iatrogenic -15-20% of spontaneous HAC -50% adenomas, 50% adenocarcinomas -Excess cortisol secretion = suppression of CRH and ACTH C/S -Decreased ACTH -Unilateral adrenal tumor -One adrenal atrophic -Elevated cortisol Iatrogenic -Excessive administration of glucocorticoids -Exogenous suppress CRH and ACTH -Bilateral adrenal gland atrophy C/S -Decreased cortisol -Everything is suppressed including hypothalamus

Answer 16

-PU/PD -Polyphagia -Panting -Abdominal enlargement "pendulous abdomen" -Muscle weakness -Lethargy **No muscle tone in the abdomen, glycogen in liver production excessive = hepatomegaly likely** -Dermatitis -Pyoderma -Adult onset demodecosis -Endocrine alopecia -Hyperpigmentation -Hyperkeratosis -Calcinosis cutis: dystrophic calcification, Ca normal in the blood but accumulation in the skin. -Prone to calcium oxalate stones in bladder Pituitary tumor C/S -Inappetence -Wandering, pacing, ataxia, head pressing, circling -If the hypothalamus is compressed then ANS dysfunction can occur Potential Complications -Systemic hypertension -Urinary tract infection -Pyelonephritis **Need urine culture** -Proteinuria -Calcium calculi -Dystrophic calcification -Pulmonary thromboembolic disease (PTE) -CHF -Pancreatitis -Diabetes mellitus

Answer 17

-Uncommon but similar signs as dogs Causes -PDH 80% -AT 20% (adrenal tumor, adenoma or carcinoma) -Iatrogenic: rare C/S **Thin, fragile skin, and diabetes** -Hepatomegaly -Skin infections -Pot belly, muscle wasting

Answer 18

Dogs -Elevated ALP (aka SAP) but not specific -Hypercholesterolemia (75% of cases) -Hyperglycemia Cats & Dogs -Stress leukogram -Mildly elevated PCV **Hyposthenuria** -Proteinuria -UTI -Glucosuria if concurrent diabetes mellitus Cats -Consistent with insulin resistant diabetes mellitus -Mildly elevates ALT -Elevated cholesterol -Hyperglycemia Radiographs -Hepatomegaly likely -Adrenal mass maybe identified due to calcification, but not indicative of malignancy for sure -PTE evidence and metastases possible **Bilateral normal or enlarged adrenal glands in dogs with clinical signs is supportive of PDH -Single adrenal mass is consistent with Adrenal tumor Ultrasound -Normal US does not rule out Cushing's -Adrenal tumor maybe visible MRI and CT -If neurologic impairment present -Used for planning and assessment of radiation therapy (stereotactic radio ablation surgery) -Can be used to assess the symmetry of the adrenal glands

Answer 19

1. Diagnostic tests a. Urine cortisol-creatinine ratio (UCC) b. Low-dose dexamethasone suppression (LDDS) c. ACTH stimulation test: adrenal cortex = GFR zones, everything but catecholamines 2. Differentiation PDH vs. AT a. Abdominal ultrasound b. High-dose dexamethasone suppression (HDDS) c. Endogenous ACTH level

Answer 20

SpIN= Rule the condition IN = If the test if positive SnOUT = Rule the condition OUT = If the test is negative

Answer 21

-Sensitive -Not specific -So, if the test is negative = rule out Cushing's **Best used for a dog in which you do NOT suspect cortisol dependent**

Answer 22

-High sensitivity -Moderate specificity -So, if test is negative, the patient does NOT have the disease. Dexamethasone -Suppresses hypothalamus and pituitary -If they are not suppressed, then they have Cushing's -If suppressed at 4 hours, but rebound at 8 hours Pituitary dependent Results -Non-adrenal illness will decrease specificity -Long time: takes 8 hours -Moderate cost -Only assesses CORTISOL

Answer 23

Pros -Quick, 1 hour test -Higher specificity (if positive then rule in the disease) than LDDS test -Gives the baseline values pre-treatment Cons -Lower sensitivity than LDDS (can't rule it out) -Concurrent illness will decrease specificity -Stress can cause a false positive/high result -Cost of the rest: not much **The majority of dogs with classic Cushing's disease screened with an ACTH response or LDDST will have at least one positive test**

Answer 24

-Bilateral adrenomegaly = Pituitary dependent hyperadrenocorticism -Adrenal mass with small contralateral adrenal gland = Adrenal tumor

Answer 25

-Higher dose of dexamethasone will cause PDH cases to suppress at 4 hours and rebound by 8 hours -Adrenal tumor never responds, it would stay high and not suppressed

Answer 26

-PDH = high endogenous ACTH -AT = low endogenous ACTH Technically difficult -Spin and separate plasma immediately -Add proteinase inhibitor aprotinin -Challenging to ship: freeze, dry ice, overnight.

Answer 27

-Routine screening tests LDDS and ACTH stimulation normal -ONe or more sex steroids are elevated in an ACTH stimulation -HS, PE, CBC, Biochemical, chemistry and UA results, and imaging consistent with hyperadrenocorticism

Answer 28

-3Beta hydroxysteroid dehydrogenase enzyme -Trilostane = inhibitor -Trilostane and mitotane are preferred treatment and efficacious

Answer 29

-Signs affecting quality of life of dog and/or owner -Signs concerning to veterinarian (complications) -NOT just because ALP is elevated

Answer 30

-Approved and most widely used -Blocks production of aldosterone and cortisol -Competitive inhibitor of 3Beta hydroxysteroid dehydrogenase enzyme system Side Effects -Excessive ACTH production continues -Adrenal can increase in size during treatment -Transient hypocorticism Dose **Twice daily, lower dosing is safer and effective** **0.5-1.0 mg/kg q12hr** -ACTH stim in 10-14 days following initiation and again in 2 weeks -Then ACTH stim every 3-6 mts **Post cortisol 4 hours after Trilostane dose. Cortisol should be 2-5ug/dL** -If cortisol too low, discontinue or lower dose and re-test in 1-2 weeks

Answer 31

-Potent adrenocorticolytic drug -Induces necrosis of the zona fasciculata and reticular

Answer 32

Adrenalectomy -Treatment of choice for adrenal tumor unless metastases present or patient unstable -MRI, contrast radiographs, prior to surgery -Invasion of caudal vena cava evaluation -Increased risk for PTE during anesthesia, heparin Radiation -Stereotactic radiation treatment of choice for pituitary macro tumor disease -about 33% complete response and several years survival

Answer 33

-Infections -Immune system suppression -Muscle weakness -Peripheral neuropathy -Systemic hypertension -Proteinuria: >0.5 treat -Calcium Oxalate: increased calciuresis from excessive glucocorticoid production. Urinary bladder, renal, biliary/GB -Dystrophic Calcification: Calcinosis cutis -Diabetes mellitus: elevated ALP and diabetic patient NOT enough to test for Cushing's -Pancreatitis: no conclusive data -Pro-coagulant: thromboembolism 10x more at risk -Biliary Mucocele: 29 x more prevalent. Cholestasus, GB dysmotility -CNS signs from pituitary tumor: uncommon

Answer 34

-Melatonin -HMR ligans -SDG ligans (flaxseed) **Supraglan**

Answer 35

Monitor -Blood pressure: q 3-6 mts -Urine culture: q 6mts -Urine protein creatinine ratio: q 6mts. Culture -Minimum database -Q3-6 mts doctor exams

Answer 36

Tumor in medulla of adrenal gland = synthesis of catecholamines -Usually seen in older animals -Insulin antagonist also C/S **Intermittent weakness and collapse, panting or tachypnea, anxious behavior, PU/PD, hypertension, weight loss, lethargy, INAPPETENCE, vomiting, diarrhea, abdominal distention** -Autonomic and CNS -PSNS: cholinergic receptors -SNS: adrenergic receptors = Alpha and Beta -Increased HR, CO, BP -Redistribution of Blood from skin, kidneys and GI towards skeletal muscle -Increased ventilation with dilation of airways -Decreased GI motility and secretions -Increased blood glucose Dx -Often post-mortem -Ante-mortem = signs, abdominal ultrasound, adrenal ultrasound. -Urinary catecholamines concentrations Tx -Surgical resection may be possible -Management of hypertension and arrhythmias during and before surgery Px -Varies -Survival 2 mts to 3 years

Answer 37

Addison's disease RAAS Stimulation of Renin Release -Decreased extracellular fluid volume -Decreased renal perfusion -Hemorrhage -Na depletion -Increase in Serum K+ depolarizes adrenal cells to open up Ca++ channels -Intracellular Ca++ increases to stimulate aldosterone secretions

Answer 38

-Deficiency of both mineralocorticoid and glucocorticoid -Immune mediated or -Infiltrative disease or vascular thrombosis/hemorrhage -Drugs (Mitotane, Trilostane) **ACTH is ELEVATED** **Electrolytes may be normal**

Answer 39

-Only Glucocorticoid deficiency -Destructive pituitary lesion or -Chronic exogenous glucocorticoid administration -Both result in **Decreased ACTH** -Adrenocortical atrophy reversible if exogenous steroid discontinued

Answer 40

Signalment -Young to middle age Breeds with Inherited autosomal recessive suspected -Standard poodle, Portugese, Water dog, Nova Scotia, Duck trolling Retereiver. Others (unknown mode of inheritance) -Great dane, Rottweiler, Berded Collie, West, Soft coated Wheaten, Leonberger Cats -No sex predisposition -Young to middle aged ~6 yo average

Answer 41

History **Slow mimic GI and renal disease** -Can be waxing and waning -Slowly progressive -Can vary from mild to severe -Severe signs - Addisonian Crisis **High K+ cardiac arrhythmias, low Na, Impostor when electrolytes are normal** **Electrolytes normal but lack cortisol, or maybe potassium is low. GI signs, diarrhea in times of stress. Do an ACTH test on them** PE -Lethargy - collapse in severe cases -Weakness -Dehydration -Hypovolemia -Bradycardia -Weak pulses -Abdominal pain

Answer 42

Lab -CBC -Mild Anemia - non-regenerative, combined with lack of stress leukogram -Neutrophilia -Leukocytosis -Eosinophilia - most common finding **Lack of stress leukogram** -Azotemia -Increased BUN/Creatinine ration -Pre-renal = expect high USG maybe Isothenuria -Low Na in serum -Elevated K+ in serum -Low Serum Chloride -Low Na:K ratio (<27:1) Chemistry -Hypoglycemia -Hypercalcemia -Mild low serum Albumin -Mild low serum cholesterol **Metabolic acidosis** Chest Radiographs -Microcardia due to hypovolemia -Megaesophagus: focal Abdominal Ultrasound -Small adrenal glands ECG - Hyperkalemia changes -T wave gets taller -R wave decreases in amplitude -QRS widens -P wave flattens then disappears

Answer 43

-Baseline Cortisol (<2 ug/dl) supportive and diagnostic when ACTH is high = primary -Baseline Cortisol (<2 ug/dl) supportive and diagnostic when ACTH is low = secondary

Answer 44

Acute Crisis -0.9% Saline (NaCl): 40-80 ml/kg/24 hr -Dexamethasone or -Dexamethasone Na Phosphate: IV initially q 12 hr until Prednisone -Bicarbonate: if acidic -50% Dextrose IV if hypoglycemia -Insulin/Glucose IV to lower extremely elevated K+ Maintenance -Desoxycorticosterone Pivalate (DOCP) -Injection every 25-29 days -Monitor electrolytes to determine ideal interval -Mineralcorticoid: FLUDROCORTISONE ACETATE, adjust dose based on electrolytes -Glucocorticoid: -Prednisone or Prednisolone -"Physiological dose" -Amount needs to increase during times of stress/illness or prior to surgery Px -Excellent -Good with owner compliance -Life-long therapy -Follow-ups -Can have normal life expectancy

Answer 45

AKA "Conn Syndrome" -Decreased Renin -Autonomous secretion of aldosterone -Neoplasia of Zona glomerulosa (adenoma or adenocarcinoma) -Idiopathic hyperplasia pf zona glomerulosa

Answer 46

-Increased renin due to decreased effective blood volume -Due to heart failure, kidney disease, liver disease, severe hypoproteinemia

Answer 47

C/S **Hypokalemia, Hypernatremia** -Profound muscle weakness -"Ventral cervical flexion" -Difficulty walking -Muscle damage -Myoglobinuria (renal toxin) -Elevated CK -Cardiac arrhythmias -Systemic hypertension -Retinal detachment/bleeding -Cardiac dysfunction -Renal dysfunction Dx -C/S -Adrenal Ultrasound, adrenal mass (unilateral) or hyperplasia (bilateral) -Elevated Na, Low K+, +/- Azotemia -Urine aldosterone:Creatinine Ratio -Serum Aldosterone Concentrations -Baseline ACTH not always diagnostic Treatment -Neoplasia: surgery -Medical management of low K+, high Na -Slow IV of KCL in 0.45% Saline -Spironolactone: K+ sparing diuretic -K gluconate orally -Hypertension: Amlodipine -Hypernatremia: usually mild Px -Good for hyperplasia with life-long management -Variable for neoplasia

Answer 48

-Multisystemic disease -Excessive circulating levels of T4 and T3 **The most common endocrine disorder in cats** -10% of cats equal or >10 yo get it **T4 is the active form** Causes -Functional thyroid adenomatous hyperplasia (adenoma) is most common -Can affect one or both thyroid glands -1-2% thyroid adenocarcinomas -Hyperactive thyroid tissue exclusively in the mediastinum is 3-5% of cases Etiology -Don't really know Risks -Siamese/Himalayans reduced risk -Cats eating canned diet more at risk -Genetic factors -Cats using cat litter Signalment -Cats middle age to older median 13 yo -Only 5% of cats are <8-10 yo -Most cats have slow progression of disease, may not notice until advanced unless early screening checks C/S -Hypermetabolic signs -Weight loss -Increased appetite, polyphasic -Mild to severe weight loss -Vomiting, diarrhea, large fecal volume -Increased fecal fat associated with malabsorption -Unkept, ragged haircoat, shedding, matting -Restlessness, frantic or aggressive behavior -Stress intolerant -Bad cases hypertrophic cardiomyopathy Renal -Mild Azotemia in 30% cases -Elevated levels of T4 -PU/PD -Renal damage secondary to hypertension and resultant glomerular sclerosis **Chronic renal failure may be masked by hyperthyroidism** -Recommended reversible anti-thyroid treatment trial if CRF suspected, wait 2-4 weeks and check -Early effective treatment can prevent progressive renal disease CV -Thyrotoxic cardiomyopathy HCM or DCM -Hyperthyroidism alters hemodynamics leading to volume overload and high CO -Compensatory mechanism result in dilation and hyperthrophy -Tachycardia, gallop rhythm, systolic murmur -Increased R wave Echocardiography -LV septal hypertrophy -LV or LA dilation -Increased fractional shortening PE -Palpate the thyroid glands -One or both enlarged in 80% of cases -Enlargement may not always be related to clinical signs, but most cases do become hyperthyroid

Answer 49

-Affects <5% of cases -Characterized by depression and weakness -Weight loss -Anorexia instead os polyphasic (incessant hunger) -Ventroflexion of neck -Most cases have concurrent disease

Answer 50

-Diabetes mellitus -Gastrointestinal malabsorption or maldigestion -Neoplasia (GI lymphosarcoma) -Chronic kidney disease -Parasitism

Answer 51

1. Clinical disease -Clinical FHT -Elevated T4 =Consider and recommend Tx 2. Possible FHT with probable NTD -Normal T4 =T4 and fT4 assays 2-4 weeks after initial exam -Evaluate for non-thyroidal disease -Consider suppression of thyroid scintigraphy 3. Enlarged thyroid without clinical FTH -No clinical FHT -Normal T4 =Monitor and repeat assay in 6 mts 4. Subclinical FHT -No over clinical FHT but some PE findings suggest FHT -Elevated T4 =Repeat T4 in 2 weeks -If elevated, Tx -If T4 normal, re-evaluate in 6mts 5. Clinical FHHT with confirmed NTD -Elevated T4 -One or more concurrent diseases =Treat for FHT -Institute management of NTD 6. Clinically normal -No palpable nodule -Elevated T4 =Confirm T4 -If normal, monitor and repeat T4 in 6 mts -If elevated, Tx for FHT

Answer 52

-Nothing specific in CBC and Chemistry Clinical pathology -Elevated ALT, SAP, AST -BUN and Creatinine elevated in 20-40% of cases -SDMA (symmetric dimethylarginine acid) sensitive early marker for decreasing GFR -Elevated PCV -Lymphopenia -Eosinopenia -USG <1.035 in 52% of cases Baseline thyroid hormone testing -T4 and T3 elevated -Free T4 elevated (96% of cases) Radionuclide thyroid scanning -Technetium m99 -Identify ectopic tissue

Answer 53

1. Medication/diet 2. Surgery: falling out of favor 3. Radioactive iodine treatment Choice depends on health, age, renal function, concurrent disease type, etc. Goal of treatment -Normal range 1-4 ug/dl -Thyroid level T4 1-2.5 ug/dl if no renal insufficiency -Creatinine may raise too much, so may need to adjust Tx CV -HCM: beta-blockers (propanolol, atenolol) +/- diuretics -DCM: diuretic, vasodilator (ACE inhibitors), +/- digoxin **Treatment for hyperthyroid state usually reverses signs of HCM but not DCM** Renal -CFR diet management (omega fatty acids, renal diets food) -Control hypertension to decrease GFR (amlodipine, ACE-Inb) -Titrate treatment for hyperthyroidism to evaluate Diet -Ultra low iodine diet -Lower tT4 but may not resolve clinical disease in more advanced cases Anthithyroid medications -Methimazole (Felimazole) FDA approved -Inhibits synthesis of thyroid hormone -Drug of choice -T4 usually returns to normal within 1-2 weeks Adverse Effects -Lethargy -Vomiting -Diarrhea -Mild hematologic changes: cytopenias -Facial pruritic and pinnae scabbing **Discontinue if facial scloration and substitute with iodine** -Hepatic toxicity in small number of cases Radioactive Iodine ->95% resolves -2-4% need second treatment -2% of cases have recurrence in 1-6 years -Side effect: hypothyroidism in only 2% of cases -Cost, limited availability, 8-14 days isolation Surgery -Perform m99 scan prior if possible -Hypocalcemia due to hypoparathyroidism is most serious complication OVerall prognosis -Good -Chronic kidney disease survival up to 5.3 years

Answer 54

XRT chemotherapy

Answer 55

-Functional or structural abnormality of the thyroid gland resulting in deficient production of thyroid hormone THs. T4 - protein bound in plasma fT4 - not bound, goes into cell = active form T3 - does all things inside the cell

Answer 56

-Most common form: direct destruction of the thyroid gland -Lymphocytic thyroiditis: immune mediated cellular infiltration of the thyroid gland -Idiopathic atrophy: loss of normal thyroid tissue with replacement by adipose tissue

Answer 57

-Dysfunction within the pituitary thyrotropic cells -Impaired secretion of thyroid stimulating hormone TSH -Deficiency of thyroid hormone secondary to follicular atrophy of thyroid glands

Answer 58

-Deficiency in thyrotropin releasing hormone from the hypothalamus TRH -Deficiency of thyroid hormone associated with a decrease in TSH and follicular atrophy of thyroid glands -Rare in dogs

Answer 59

-Deficiency dietary iodine intake -Dyshormonogenesis (iodine organification defect) -Thyroid gland dysgenesis -Genetic deficiency of TSH **Giatn Schnauzers and Boxers**

Answer 60

-Primary determinants of basal metabolism -Affect all aspects of lipid metabolism, lipolysis -Interaction with growth hormone is essential for normal growth and development -Nervous and cardia systems important -CNS development in the fetus and neonate -THs increase HR and force of contraction

Answer 61

-Middle age 2-6 yo -Can develop earlier in predisposed breeds -No sex predilection -Apparent breed predilection

Answer 62

Metabolic -Lethargy -Inactivity -Weight gain Dermatologic -Endocrine alopecia "RAT TAIL" -Hyperpigmentation -Dry, brittle haircoat -Seborrhea, dermatitis -Pyoderma, otitis externa

Answer 63

Reproductive -Anestrus -Weak/silent estrus -Prolonged estrual bleeding -Infertility Neuromuscular -Muscular weakness, knuckling -Facial nerve paralysis -Seizures, ataxia -Megaesophagus, laryngeal paralysis CV -Bradicardia -Arrhythmias -GI: diarrhea, constipation Ocular -Corneal lipid deposits, ulceration -Uveitis

Answer 64

-Cretinism -Stunted growth and mental development -Disproportionate body size

Answer 65

-Hyperlipedemia/cholesterolemia -Elevated AST, ALT, SAP, mild-moderate increase in LDH -Mild normocytic, normochromic, non-regenerative anemia (33% of cases) -Coagulopathies, decrease in vonWillebran Factor (unusual) T4 -All serum T4 comes from the thyroid gland -T4, fT4, and cTSH (canine TSH) assess thyroid gland function -Combination of T4, fT4, cTSH has a sensitivity of >99% for hypothyroidism T3 -Serum T3 and rT3 are primarily formed by deiodination outside the thyroid gland -Poor indicators of Thyroid function Factors that can decrease baseline Thyroid hormone -Concurrent illness, non-thyroidal illness NTI -Drug therapy: steroids -Random fluctuations NTI -Physiologic adaptation by body during periods of illness to decrease metabolic rate -T4 suppressed; tT4 fraction more sensitive to alterations than fT4 -In general, the more severe the disease, the more profound effect the thyroid suppression

Answer 66

**The gold standard is measurement by equilibrium dialysis (ED)** Baseline tT4 -Sum of free and protein bound fractions -Easy and less expensive -Check during regular yearly visits for older dogs -Disadvantage: considerable overlap in serum tT4 in hypothyroid and normal dogs, especially with NTI -90% sensitivity -The higher the T4 value the more likely the dog is euthyroid - good negative predictor Baseline fT4 -Gold standard is measurement by equilibrium dialysis (ED) -Low fT4 diagnosed 94% of hypothyroid, sensitivity Baseline cTSH -High cTSH adds specificity to fT4 and tT4 -assay must be validated for canine -Poor screening test values overlap NTI TSH and TRH -Labs -Differentiate between true hypothyroidism and NTI

Answer 67

-3 forms: T3, T4, and thyroglobulin autoantibodies -Antibodies can interfere with RIA tests and produce unusual baseline thyroid hormone values

Answer 68

-MDB -History, PE, CBC, chemistries and urinalysis Screening of pet dogs -Add tT4 -No Tx indicated if inconsistent MDB and tT4 is normal -cTSH and fT4 if tT4 normal but index of suspicion is still high Screening breeding dogs with C/S -MDB, tT4, fT4, cTSH, autobody test -Tx if MDB supportive and thyroid tests abnormal, otherwise no treatment **Repeat in 2-4 weeks if inconclusive** Screening healthy breeding dogs -Annual evaluation of thyroid function recommended -If any test abnormal, do not use for breeding, and re-evaluate in 6 months

Answer 69

-T4 supplementation of choice is -LEVOTHYROXINE -Namebrand: Soloxine -Initial dose every 12 hours -Monitor tT4 levels for 6-8 weeks post induction or -4 weeks following dose adjustment Monitoring -Supplementation ideally should result in normal serum tT4, T3, and cTSH -Measure tT4 levels pre and 4-6 hrs post pill if dosed once daily. It will tell you how long it last and if need to do q 12 hours instead Failure to respond -If no improvement within 8 weeks -Re-evaluate! **Decrease dosage if tT4 >7.5 ug/dl to avoid thyrotoxicosis**

Answer 70

GOSHDARNIT Granulomatous Osteolytic Spurious Hyperparathyroidism (primary) D Hypervitaminosis Addison's disease Renal secondary Hyperparathyroidism Neoplasia Idiopathic (most common in cats) Temperature induced (hyperthermia)

Answer 71

Humeral hypercalcemia of malignancy -Cancer is causing the high ionized calcium

Answer 72

-Total calcium in chemistry panel does not tell you about active calcium -Ionized calcium is what is important because hypercalcemia is high ionized calcium Ionized calcium -45-50% of total calcium -Active form Protein bound calcium -Typically bound to albumin -50-55% of total Complexed calcium -Bound to phosphorous, citrate -Important in kidney disease -Decreases GFR -1-2% of total -Can cause an increase in total calcium without affecting ionized calcium **Bone, gut, and kidney** PTH -The major defense against fluctuations in ionized calcium -PTH = pee out phosphorous, Ca goes up in blood, out of bone into blood. -Calcium always does the opposite of phosphorus -Increases Ca resorption in the kidney -Increases Phosphorous excretion by the kidney -Increases calcium and phosphorous mobilization from the bone -Stimulates increased production of vitamin D -Increases calcium and phosphorous absorption from the intestine

Answer 73

-Histoplasmosis: fungal -Blastomycosis -Coccidiomycosis -Tuberculosis -Schistosomiasis **Increased iCa, decreased PTH** **Macrophages can activate vitD**

Answer 74

-Primary and metastatic bone tumors -Bacterial and mycotic osteomyelitis -Mechanical destruction by infiltrating cells (as in metastatic tumors, osteosarcoma) -Local production of oesteclast-activating factor and other bone resorbing factors (ex: multiple myeloma)

Answer 75

Lipemia -Hemoconcentration -Hemolysis

Answer 76

-Excessive secretion of PTH -Adenomas >> Carcinomas

Answer 77

-Increased iCa, increased PTH -Cholecalciferol rodenticide -Calcipotriene, people cream for psoriasis, dog licks it

Answer 78

-Normal iCa -Total Ca high because they are hemoconcentrated, volume depleted -~30% of dogs -Increased calcium citrate (calcium complexed) -Increased renal resorption of calcium -GFR is down -Increased affinity of serum proteins for calcium

Answer 79

-Chronic renal failure -Hyperphosphotemia -Supression of iCa, compensatory high PTH -Total Ca is elevated NOT iCa (low to normal) -Not physiologically important

Answer 80

-Lymphoma -Multiple myeloma -Anal Sac Adenocarcinoma -Squamous cell Carcinoma -Thyroid carcinoma -Any malignancy (especially those that invade/metastasize to bone) Hypercalcemia of Malignancy = humeral hypercalcemia of Malignancy -Increased osteoclastic bone resorption -Increased renal tubular resorption -Increased intestinal absorption -PTH -PTH-related protein -Transforming growth factor -1,25-dihydroxyvitamin D -Prostaglandin E2 -Osteoclast activating factor -Other cytokines

Answer 81

-Cats -Magnesium restricted, acidifying diets -Lyphoma in cats -Excessive dietary vitD -PTH low to normal, PTHrP negative -PTH independent -Vitamin D and calcitriol levels normal **Long haired cats overrepresented**

Answer 82

Did not discuss

Answer 83

10mg/dl Calcitonin: calcium tone down -Keep it in the bone -Pee it out -Not absorbed from the gut Released by Thyroid glands Parathyroid glands release PTH

Answer 84

-Ionized calcium -PU/PD pee it out

Answer 85

Primary Hypoparathyroidism LOW iCa -Serum iCa = Low to normal -Plasma PTH (parathyroid hormone) LOW PTH independent Hypercalcemia HIGH iCa -Usually due to osteolysis -PTH low -Malignancy, vitaminD toxicity Secondary Hyperparathyroidism LOW iCa -Renal or nutritional -Serum PTH high -Ionized calcium is not high -iCa normal or low Primary Hyperparathyroidism HIGH iCa -High PTH

Answer 86

-Occurs most commonly as a malfunction of one of the glands, usually as a result of benign tumor (adenoma) -Usually bilateral adenoma Dogs -4-16 yo -No sex predilection **Keeshounds common** Cats -8-20 yo -No sex predilection -Mixed and siamese C/S Dogs -PU/PD because ionized hypercalcemia antagonizes ADH receptors -Muscle weakness -Decreased activity -Lower urinary tract signs -Decreased appetite -Weight loss -Muscle wasting -Vomiting -Shivering/trembling Cats -Lethargy -Anorexia -Vomiting -Constipation -PU/PD -Weight loss PE -Most often normal -Generalized muscle atrophy -May have palpable mass cervical region -Cystic calculi in 1/3 of dogs Calcium oxalate or mixed stones Diagnosis -Persistent hypercalcemia -Normal to decreased serum phosphorous Ddx cats and dogs hypercalcemia -Hypercalcemia of malignancy -Primary hyperparathyroidism -Renal failure -Hypervitaminosis vit D -Hypoadrenocorticism -Idiopathic (cats) Diagnosis -Minimum database (CBC, chemistry, UA) -iCa is elevated with Primary hyperparathyroidism -iCa typically normal in chronic kidney disease induced (total) hypercalcemia -Thoracic radiographs looking for cancer -Cervical exam ultrasound structural abnormalities, cancer Specific tests -PTH -PTHrP can be secreted by malignant cells -Specific tests for malignancy **Primary = high PTH, high iCa, low phosphorous and zero PTHrP** Treatment -Surgical excision of affected parathyroid gland -Chemical (ethanol) or heat ablation of mass -Monitor for hypocalcemia -May need to Tx hypocalcemia: Calcium carbonate (Tums) and calcitriol

Answer 87

-Occurs as a result of a metabolic abnormality -Outside of parathyroid glands, which causes a resistance to the function of the parathyroid hormones Chronic Kidney disease -Phosphate retention -Decreased iCa or normal -Increased PTH because phosphorous asking to be excreted -Increased Ionized phosphate excretion

Answer 88

-Feeding a diet with excess phosphorous or low calcium -Ideal calcium:phosphorous is 1.2:1 -Animal fed pure meat diets -Not retaining phosphorous, diet trigger, PTH goes up **Watch for it in reptiles** Prolonged Elevation of PTH leads to -Growth abnormalities -Replacement of normal bone by fibrous tissue -Malformed and pathologic fractures due to osteopenia

Answer 89

-Increased PTH in dogs with hypoadrenocorticism -Compensatory response to calcium loss and or increased phosphorous -Resolves with successful treatment of HAC

Answer 90

-Relative or absolute deficiency of PTH -Leads to hypocalcemia -Hyperphosphatemia -Uncommon in dogs and cats -Lymphocytic infiltration and fibrous tissue scarring of parathyroid gland -Suggest an immune mediated process -Most classified as idiopathic Signalment -Age 6 weeks - 13 yo -Average 5yo -Sex predilection FEMALES Breeds -Toy poodles, miniature schnauzers, labrador retrievers, GSD, Terriers Cats -Any range 6 mts - 7 yo -Mean 5 yo -Sex predilection: MALE -Several breeds -Very few reports of naturally occurring C/S Dogs and Cats -Seizures (when iCa is low, nerves depolarize) -Stiff gait -Muscle tetany, cramping, pain -Focal muscle fasciculations, twitching , tremors -Facial rubbing (intense) -Nervousness, anxiety, vocalizing -Panting, hyperventilation -Aggressive behavior PE -See above -Bradycardia -Paroxysmal tachyarrhythmias -Weak femoral pulses Diagnosis -Persistent hypocalcemia -Hyperphosphatemia -Normal kidney function -Rule out other causes of hypocalcemia (ex: renal, nutritional hyperparathyroidism) -PTH levels undetectable in face of hypocalcemia. Body can't make PTH -Postpartum risks for eclampsia

Answer 91

-Occurs secondary to hypomagnesemia -Suppressed PTH secretion -Increases end organ resistance to PTH -Impairs synthesis of calcitriol -Results in mind hypocalcemia and hyperphosphatemia -Reverses with magnesium supplementation

Answer 92

-Primary hypoparathyroidism -Puerperal tetany (eclampsia) -Renal failure -Secondary nutritional hyperparathyroidism -Hypomagnesemia -Hypovitaminosis D Treatment -Correct underlying cause -Administration of calcium and vitamin D Phase 1: Slow IV calcium gluconate, then CRI Phase 2: Oral supplementation of calcium and vitamin D (calcitriol has fastest onset) Goal calcium maintenance between 8-10 mg/dl Prognosis -Excellent -Requires frequent checks

Answer 93

-Hypercalcemia of malignancy -Tumor producing PTHrP -Vitamin D toxicosis, high dietary levels or accidental ingestion

Answer 94

Endocrine Pancreas

Answer 95

Insulin = Beta cells Alpha cells = Glucagon When blood sugar levels are low, Glucagon is released so that liver breaks down glycogen and releases glucose = blood glucose raises When blood sugar is high, insulin is released into the blood and liver takes up glucose and stores it as glycogen, blood glucose levels declines. Enemies of insulin epi and norepinephrine used in an emergency situation to get Glucagon going and raising blood glucose levels

Answer 96

Type 1 -Destruction or loss of pancreatic beta cells with progressive and eventual insulin insufficiency. Immune mediated, common in people Type 2 -Characterized by insulin resistance and dysfunctional Beta cells -Chronic longterm obesity association Insulin Dependent DM -Permanent hypoinsulinemia and requirement for exogenous insulin therapy -Type 1 commonly Insulin Independent DM -Includes obesity induced down-regulation of insulin receptors, impaired receptor binding affinity and post-receptor defects in insulin action.

Answer 97

-Essentially all dogs have IDDM at time of presentation -NIDDM uncommon -Multifactorial causes: genetic, infection, insulin antagonism with drugs or disease, obesity, pancreatitis and immune mediated insulinitis -Rapidly leads to IDDM -Loss of beta cell function resulting in hypoinsulinemia -Impaired intracellular glucose transport, accelerated hepatic gluconeogenesis -Loss of beta cell function is permanent and results in lifelong requirement for insulin therapy

Answer 98

4 Types Type 1: immune mediated Type 2: common, insulin resistance due to beta cell exhaustion Other -Endocrine pancreatic disease, other endocrinopathies that antagonize insulin -Drug induced **Obesity and free choice feeding may predispose** **Steroid therapy potentially leads to insulin resistance, clients will be angry if they are not aware of side effects**

Answer 99

**Insulin resistance** **Beta cell dysfunction** -Leads to chronic, persistent hyperglycemia which itself is toxic to beta cells -GLUCOSE TOXICITY: leads to abnormal protein folding and beta cell apoptosis -Reversal of glucose toxicity increases chances for diabetic remission -Feline patients may be reversible with rapid glycemic control -Commonly "Brittle diabetic" = dose of insulin needed to control disease is close to dose causing hypoglycemia -C/S may be transient -Insulin often required in advanced cases Risk Factors Amylin -aka Islet Amyloid polypeptide -Co secreted with insulin (antagonizes insulin) -Overproduction causes irreversible amyloid deposits -Leads to progressive islets loss where beta cells are in the pancreas Obesity -Fat is the enemy of glucose regulation -4 times more likely to develop disease -Causes internalization of insulin receptors by fat cells -Reduces insulin receptor affinity -Reversible with weight loss Physical activity -Inactivity regardless of presence or absence of obesity Gender - Cats -Males Age -8-12 yo Genetic -Burmese -Main coon -Russian blue -Siamese Medications -Glucocorticoids -Megestrol acetate **High carbohydrate diet** ?

Answer 100

-Insulin requirements fluctuate in approx 20% of cats -Brittle diabetics (dose of insulin needed to control disease is close to dose causing hypoglycemia) **Neutered males more frequently affected** Age ->6yo, average 10yo Genetic predisposition -Burmese, Maine Coon, Russian Blue, Siamese Medications -Glucocorticoids -Megestrol acetate C/S -PU/PD -Weight loss -Polyphagia -Sudden blindness cataracts -Weight loss when prolonged and untreated -Hepatic lipidosis - hepatomegaly Diabetic Neuropathy -Pelvic limb ataxia: more in dogs -Plantigrade stance: cats more common -hyporeflexia -No specific Tx

Answer 101

-Females twice as likely as males to be affected -Age of onset 4-14 yo, 7-9 yo prevalence Breeds -Keeshound -Cairn -Miniature Schnauzer -Poodle -Daschund -Beagle -Miniature Pinscher C/S -PU/PD -Weight loss -Polyphagia -Sudden blindness cataracts -Weight loss when prolonged and untreated -Hepatic lipidosis - hepatomegaly Diabetic Neuropathy -Pelvic limba ataxia -Plantigrade stance: cats more common -hyporeflexia -No specific Tx

Answer 102

-Suspicion based on clinical signs -Demonstration of persistent, fasting hyperglycemia in conjunction with glucosuria -Difficult to determine NIDDM vs. IDDM **Cats can get stress hyperglycemia, glycosuria, 300-400 mg/dl** -Ketonuria, diabetic ketoacidosis -CBC, Chem, UA with culture. -PLI/TLI -Baseline fructosamine: shorter term 2-3 weeks +/- Glycosylated hemoglobin: longer term 2-3 months -Look closely for concurrent disease Fructosamine -Index of average blood glucose over 2-3 weeks -Can help distinguish stress hyperglycemia -Non-enzymatic, independent of glycosylation insulin serum proteins Glycolated hemoglobin -Index of average blood glucose over previous 4-8 weeks -Insulin independent binding of glucose to hemoglobin in RBCs Fructosamine and Glycosylated Hemoglobin -Separates stress hyperglycemia -Can not identify cause -Clarify discrepancies in history, PE, and BG curves -Every 3-6 months

Answer 103

Goals -Prevent complications: cataracts, bacterial infections, pancreatitis, ketoacidosis, hepatic lipidosis, peripheral neuropathy -Eliminate owner observed c/s Methods -Proper insulin administration, dose, control -Diet -Exercise -Prevention or control of concurrent disease -Avoid potential fatal hypoglycemia due to overzealous insulin administration

Answer 104

Dogs -Provide increased amounts of fiber soluble to slow intestinal absorption of glucose Cats -Important to eliminate obesity -High protein -Low carbs -Moderate fat -Obligate carnivores -Naturally insulin resistant -Don't store glycogen as well as dogs -Maintain euglycemia naturally **Feed 66 kcal/kg/day** for ideal BC Both -Maintain timing and calorie content in order to minimize post prandial glucose fluctuations.

Answer 105

-Promotes weight loss -Helps to increase absorption of insulin from injection site -Daily, moderate is the goal -Overzealous or sporadic can lead to hypoglycemia

Answer 106

1. Inhibit intestinal glucose absorption -Acarbose 2. Improve peripheral insulin sensitivity -Troglitazone -Vanadium -Chromium picolinate -Metformin 3. Promote insulin release from pancreas -Sulfonylureas: type 2 diabetes in humans 4. NEW decrease kidney reabsorption of glucose, pee out more glucose -They don't substitute for insulin -Can not reverse beta cells glucose toxicity -Limited veterinary data **Nutrition and optimal weight control are cornerstone** **SGLT2 receptor inhibitors NEW** -Bexacat: Bexagliflozin tablets -Senvelgo: Velagliflozin oral solution -They block receptor in kidney and increase renal excretion of glucose

Answer 107

Types 1. Onset of duration -Short acting: Regular Crystalline -Intermediate acting: NPH -Long acting: PZY 2. Protein source -Human: Pro-Zinc, NPH, Glargine -Biosynthetic human analogues -Bovine: bovine-porcine protamine zinc, PZI-Vet -Porcine: Veterinary porcine zinc lente insulin, Vetsulin **Cats and cows similar structure** **Pigs, puppies, people** **Never switch needles and bottles, they are calibrated for IU**

Answer 108

Regular -IV CRI -0.5 hrs onset -Peak 1-5 hrs -Duration 8hrs Intermediate acting -NPH -Lente Longer acting -Glargine -Determir -PZI All species origins are effective in cats and dogs, but every patient is individual Immunogenicity and insulin antibodies can alter the effect and duration of the insulin

Answer 109

Dogs -Intermediate acting NHP -BID -0.5-1.0 IU/kg Cats -Glargine: first choice -ProZinc or PZI Hospitalize -Initially for 24-48 hours to ensure that hypoglycemia is managed if occurs BG curve -During hospitalization -Initial goal is to reverse metabolic abnormalities **Re-evaluate in 7-10 days** Glycemic control -Takes 1 about month to establish -Achieved based on 1. Resolution of clinical signs -Pet is healthy and interactive at home -Body weight is stable -Owner satisfied -Blood glucose 100-250 mg/dl dogs -BG 100-300 mg/dl cats

Answer 110

-Owner should keep a log -Never change insulin dose without consulting with veterinarian **At home glucose curves are most useful, no stress hyperglycemia** -Sample taken every 2-4 hours **Urine testing should not be used for adjusting insulin dose** Monitoring -Get a pre-feeding reading -Serum BG after feeding and give insulin -Serum every 2-4 hrs at home ideal -Serum BG every 1-2hrs at hospital if no other option -Jugular catheter to avoid multiple needle sticks

Answer 111

-Pre-feeding reading -Feed same amount and type of food before insulin injection -Take initial blood sample -Have owner give insulin -Assess owner's injection technique -Take blood samples every 1-2 hrs intervals for 12-24 hrs -Help determine insulin dose and frequency of administration required for control of hyperglycemia Monitors for Glucose -Alpha TRAK - feline calibrated

Answer 112

Inappropriate duration of Insulin action

Answer 113

Somogyi effect

Answer 114

-Rapid insulin metabolism -Anti-insulin antibodies -Poor subcutaneous absorption of insulin -Severe obesity -Infection/inflammation: dental disease, UTI, pancreatitis -Drugs: glucocorticoids, pro gestational agents -Endocrine disorders: hyperthyroidism, hyperadrenocorticism, acromegaly, diestrus and progesterone excess

Answer 115

Blood Glucose Curve -Assess the effectiveness -Does it lower BG? -Consider range, BG differential and nadir together For example -A differential of 50mg/dl is acceptable if range is 120-170mg/dl but not if 350-400 mg/dl -Or a differential of 100 mg/dl is acceptable if dose is 0.4 IU/kg but not if dose is 2.2 IU/kg Assess the duration -time from injection to nadir to rise to 200-250 mg/dl -May need extended BG 18-24 hrs -Evaluation of duration is inaccurate if Somogyi effects is occurring -Accurate measurement of duration can help dictate type of insulin and dosing schedule **Always Check for Owner management errors**

Answer 116

1. Initial regulation -Urine glucose monitoring -Blood glucose monitoring 2. Intermediate regulation -Serum fructosamine -Fasting or mean blood glucose 3. Long term regulation -Glycosylated hemoglobin Routine management -Once controlled re-examine every 2-4 months -PE, BW, Glycosylated hemoglobin and fructosamine -Re-evaluate BG curve in hospital if clinical signs change

Answer 117

Hypoglycemia -Common and potentially life threatening -Can occur for several reasons -Excessive overlap of duration in BID dosing -Prolonged inappetence -Unusually strenuous exercise -Insulin-treated cats reverting to NIDDM C/S -Lethargy -Weakness -Head tilt -Ataxia -Seizures Tx -PO Food -Karo syrup on gums -IV dextrose -IM glucagon -Decrease insulin dose 25-50% and re-evaluate BG curve in 2-3 days

Answer 118

**Recurrence of C/S most common** -Usually problems with insulin type, dose, frequency or concurrent disease -Technique factors: outdated, overheated, shaken, syringe type mismatch, faulty injection Somogyi Effect -Insulin overdose -Induces hepatic glycofenolysis and secretion of diabetogenic hormones (epinephrine and glucagon) -Results in rebound hyperglycemia and C/S Recurrence of C/S -Short duration on insulin effect -Inadequate absorption -Circulating insulin antibodies -Concurrent disease interfering with insulin action (HAC, UTI, steroids, hypo or hyperthyroidism, acromegaly chronic inflammation, obesity, hyperlipidemia)

Answer 119

Algorithm for diabetic control

Answer 120

Prognosis -Good to excellent with treatment being effective and owner compliance

Exam 4 Flashcards

(156 cards)