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45 Cards in this Set
- Front
- Back
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What is the pathophysiology of diabetes mellitus?
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type 1: insulin dependent (IDDM)
-pancreatic β-cell destruction --> absolute insulin deficiency type 2: non-insulin dependent (NIDDM) dysfunctional β-cells --> insulin resistance |
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What are some etiologies of DM in:
a. dogs b. cats |
a. most have type 1 (IDDM)
-genetic -immune mediated -chronic pancreatitis --> destruction of endocrine pancreas over time -insulin antagonistic drugs (ex. steroids) -obesity: less common than in cat b. 70% have type 2, 30% have type 1 -pancreatic amyloidosis -chronic pancreatitis: may be relatively silent -obesity -drugs -infection |
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What are common hx & PE findings in dogs w/ DM?
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hx: PU/PD, polyphagia, wt. loss, sudden blindness, cataracts
PE: may be normal -DKA, wt. loss, poor hair coat, obesity, lenticular changes, hepatomegaly |
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How is DM diagnosed?
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criteria for dx of DM: fasting hyperglycemia, glucosuria, & ↑ fructosamine or glycosylated Hb
identify concurrent diseases that may be causing or contributing to carb intolerance (ex. Cushing’s), that may result from carb intolerance (ex. bacterial cystitis), or that may mandate a modification in therapy (ex. pancreatitis) |
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What clin path abnormalities are common in dogs w/ DM?
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U/A: glucosuria, bacteriuria, ketonuria
Chem: hyperglycemia, ↑ ALT, ↑ AP, hypercholesterolemia CBC: usually normal, +/- neutrophilic leukocytosis (d/t stress or inflammatory dz) |
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What are the components of tx for non-complicated DM in dogs?
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insulin therapy: start insulin @ ¼ - ½ unit/kg BID
high fiber diet exercise +/- acarbose: inhibits carb digestion & glucose absorption from gut goal: have insulin protocol set in 1 month post dx |
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What are the various types of insulin used to tx DM in cats & dogs?
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all are recombinant
regular: short acting -used for emergency cases: IV or IM -could use for blocked cat to ↓ K+ NPH, lente: intermediate acting -initial insulin of choice for establishing control of glycemia -most commonly used (BID) -Vetsulin: form of lente insulin -Humulin-N: NPH ultralente: long acting (SID) -not good results PZI: long acting (SID) |
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What are common hx & PE findings in cats w/ DM?
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hx: PU/PD, polyphagia, wt. loss, changing litter box more frequently, lethargy, not grooming, rear limb weakness
PE: may be normal -DKA, obesity, wt. loss, unkempt hair coat, hepatomegaly (d/t diabetes induced hepatic lipidosis), neuropathy -plantigrade stance (ddx: hypokalemia) |
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What are the components of tx for non-complicated DM in cats?
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tx w/ insulin under proven otherwise
+/- glargine: new -insulin analog: prolonged duration of action after administration in humans -designed to provide a sustained mild ↑ in serum insulin conc. to control hepatic glucose production -commonly used in cats: ~40% go into remission -hypoglycemic events may be ↓ diet: prevent obesity -high fiber + low fat, high protein + low carb, or high fat + low carb -all these diets are based on carbohydrate restriction, either by ↓ intake or slowing absorption using fiber +/- oral hypoglycemic drugs -sulfonylureas (glipizide, glyburide): directly stimulate insulin secretion: requires functional β-cells in pancreas -transitional metals (vanadium, chromium): may have insulin-like effects |
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How is DM in cats & dogs monitored?
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clinical signs as noted by owner: monitor PU/PD
spot BG checks, urine glucose at home fructosamine: 2-3 wks. after change in therapy, else every 4-6 mo. glucose curves: vary a lot from day to day |
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What is the Somogyi phenomenon?
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high dose of insulin --> rapid ↓ in BG --> stimulation of hepatic glycogenolysis & secretion of diabetogenic hormones (catecholamines, glucagon: inhibits insulin) --> ↑ BG --> marked hyperglycemia --> signs of hyperglycemia dominate
may be misleading if doing spot BG checks at home -animal is hyperglycemic, yet correct tx is to give dextrose & glucagon |
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insulin resistance
a. suspect when... b. what to do about it |
a. if giving > 2 U/kg BID to a dog or > 6-8 U BID to a cat to control hyperglycemia, animal is considered insulin resistant
b. check dosage, administration technique, storage, & insulin type; consider effects of other drugs (ex. glucocorticoids), other diseases, reproductive cycles |
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What is the pathogenesis of diabetic ketoacidosis?
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stressful disorder (ex. pancreatitis, infection, renal insufficiency) or situation --> ↑ in diabetogenic hormone secretion --> enhanced mobilization of FFA from triglycerides stored in adipose tissue --> hepatic metabolism shifts to fat oxidation --> production of ketones
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What are some etiologies of DKA?
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insulin deficiency
diabetogenic hormones: catecholamines, GH, glucagon, cortisol dehydration anorexia concurrent dz: CRF, hyperthyroidism, Cushing’s, pancreatitis -majority of dogs w/ DKA probably have some degree of pancreatitis |
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What are some PE findings assoc. w/ DKA?
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systemic signs (ex. lethargy, anorexia, vomiting) ensue as ketonemia & metabolic acidosis develop & worsen
common findings: dehydration, depression, weakness, tachypnea, vomiting, sometimes a strong odor of acetone on breath, slow deep breathing if severe metabolic acidosis, vomiting, abdominal pain & distention |
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What clin path findings are assoc. w/ DKA?
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hyperglycemia, glucosuria, ketonuria
electrolyte abnormalities: ↓ Na, K, P, Mg metabolic acidosis |
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What is involved in the tx of DKA?
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replacement fluids: 0.9% saline + KCl +/- KPO4 + Mg
-rehydrate over 24-48 hrs evere hypophosphatemia in cat --> hemolytic anemia -P therapy is indicated if clinical signs of hemolysis are identified or if serum P < 1.5 mg/dl Mg -cofactor for Na/K ATPase -if hypokalemic & refractory to K+ supplementation, Mg supplementation may help ↑ K+ K -if acidemic, most of K+ will be outside cell & K+ in serum may be low normal or low -during tx for DKA, serum K+ ↓ d/t rehydration (dilution), correction of academia (shift of H+ ions out of cells in exchange for K+), insulin mediated uptake of K+ (w/ glucose), & continued urinary losses bicarb?: try not to use if possible -LRS, plasmalyte, & normosol all contain lactate, which is a bicarb precursor manage concurrent disorders insulin: IM or CRI protocol |
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What is the pathophysiology of feline hyperthyroidism?
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thyroid adenoma: most common
adenomatous hyperplasia of thyroid gland >70% are bilateral 1-2% d/t thyroid carcinoma |
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What are common historical & PE findings assoc. w/ feline hyperthyroidism?
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hx: wt. loss, hyperactivity, polyphagia, vomiting, PU/PD, diarrhea, ↓ appetite, large fecal volume, anorexia
PE: goiter: 1 or more small, discrete thyroid masses are palpable in ventral region of neck (thoracic inlet) in ~90% of cats w/ hyperthyroidism -thin, heart murmur, tachycardia, gallop rhythm, aggression, unkempt haircoat, thick claws |
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What clin path abnormalities are commonly assoc. w/ feline hyperthyroidism?
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CBC: usually normal, +/- mild polycythemia (T4 may stimulate BM), neutrophilia, eosinopenia
Chem -↑ AP &/or ALT: present in ~90% of hyperthyroid cats +/- azotemia, hyperphosphatemia U/A: presence of concurrent renal dz? fructosamine: may be falsely lowered d/t ↑ metabolism of fructosamine in hyperthyroid state; may be an issue in cats w/ concurrent DM |
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What are the 2 insulin protocols used in treating dogs & cats w/ DKA?
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regular crystalline insulin recommended: rapid onset of action, brief duration of effect
IM protocol -0.2 U/kg IM followed by 0.1 U/kg q 1 hr. -maintain BG b’twn 150-200 -if BG goes too low, give dextrose -can then switch to longer acting insulin CRI protocol: not used as commonly -very low dosage --> gradual ↓ in BG |
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How is feline hyperthyroidism diagnosed?
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T4
-↑ total T4: diagnostic for hyperthyroidism -cats w/ mild or occult hyperthyroidism & hyperthyroid cats w/ significant non-thyroid illness (ex. neoplasia, systemic infection, organ system failure) can have “normal” T4 •measure T4 & fT4 using MED in 1-2 wks & R/O non-thyroid illness other: fT4 (not for use as a screening test), T3 suppression test, TRH stim, radionuclide thyroid scanning |
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What are the 3 main treatment modalities for feline hyperthyroidism?
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hyperthyroid cats should be treated medically 1st w/ oral anti-thyroid drugs to reverse hyperthyroid induced metabolic & cardiac derangements, ↓ anesthetic risk assoc. w/ thyroidectomy, & assess impact of tx on renal function
anti-thyroid drugs: inhibit thyroid hormone synthesis w/o damaging gland methimazole: oral or transdermal -after initial 3 mos. of therapy, monitor CBC (platelets), T4, renal values q 3-6 mo. -may be necessary to maintain a mild hyperthyroid state to improve renal perfusion & GFR & avoid uremia radioactive iodine -selectively destroys thyroid gland: kills those cells that are functioning (+): 95% effective, no problem w/ parathyroid glands, quick, no pills or sx (-): patient must be hospitalized, lack of facilities doing procedure in some areas -may become hypothyroid post tx surgical thyroidectomy -U/S of ventral neck or radionuclide scan should be performed before sx to ID location of abnormal thyroid tissue, differentiate unilateral from bilateral lobe involvement, & provide some insight into possibility of hypocalcemia post-op -hypocalcemia is a possibility post-op d/t removal of parathyroid glands -other complications: lar par other: chemical ablation w/ ethanol |
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What is the pathophysiology of canine hypothyroidism?
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1º dz of thyroid: 95% of cases
-lymphocytic thyroiditis: immune mediated: genetic factors play a role -idiopathic atrophy: may be a 1º degenerative disorder &/or may represent an end stage of autoimmune lymphocytic thyroiditis 2º: pituitary dz --> ↓ TSH -may occur d/t suppression of thyrotroph function by glucocorticoids |
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What clinical signs are assoc. w/ canine hypothyroidism?
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insidious onset
signs result from ↓ cellular metabolism & its effects on dog’s mental status & activity lethargy, anorexia, wt. gain, dry coat/shedding, anestrus, hyperpigmentation, cold intolerance, bradycardia |
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What PE findings related to the following body systems are common w/ canine hypothyroidism
a. metabolic b. derm c. repro d. ocular e. CV f. neuromuscular |
a. wt. gain, mental dullness, lethargy, inactivity
b. alopecia: classic finding is bilaterally symmetric nonpruritic truncal alopecia that tends to spare head & extremities; may be local or generalized & symmetric or asymmetric, may involve only the tail (“rat tail”), often initially starts over sites of wear -dry & brittle haircoat, hyperpigmentation, seborrhea, otitis, pyoderma, myxedema c. anestrus, silent estrus, enlarged mammary glands (gynecomastia), inappropriate milk production (galactorrhea) d. lipid deposits in cornea (d/t hypercholesterolemia), corneal ulceration, uveitis e. mild, asymptomatic ↓ contractility, bradycardia, arrhythmias f. weakness, ataxia, knuckling, seizures (uncommon), facial paralysis, laryngeal paralysis, esophageal hypomotility (megaesophagus) |
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What are common clin path abnormalities assoc. w/ canine hypothyroidism?
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CBC: +/- mild normocytic normochromic nonregenerative anemia
Chem: hypercholesterolemia (80%) |
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How is canine hypothyroidism diagnosed?
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standard of dx: ↓ T4, ↓ fT4, ↑ TSH
normal T4 R/O hypothyroidism fT4: less affected by concurrent dz, no effect d/t circulating antithyroid Abs endogenous TSH: 80% sensitivity & specificity other: TSH, TRH stim tests, T4, T3, thyroglobulin auto-Abs |
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What is the tx for canine hypothyroidism?
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L-thyroxine: synthetic T4
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What is the pathophysiology of canine hyperadrenocorticism?
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pituitary dependent: 85% of dogs
-functional ACTH secreting micro- (most common) or macro- adenoma of pars distalis -excessive secretion of ACTH --> bilateral adrenocortical hyperplasia & excessive cortisol secretion -normal feedback inhibition of ACTH secretion by physiologic levels of glucocorticoids is missing adrenal dependent -adrenocortical tumor: 50% adenomas, 50% carcinomas -carcinomas tend to appear larger than adenomas on abdominal U/S -tumors are autonomous & functional & randomly secrete excessive amounts of cortisol independently of pituitary control -cortisol suppresses hypothalamic CRH & circulating plasma ACTH conc. --> cortical atrophy of uninvolved adrenal & atrophy of all normal cells in involved adrenal -most, if not all, tumors appear to retain ACTH receptors in that they respond to administration of exogenous hormone iatrogenic -typically results from excessive administration of glucocorticoids --> suppression of hypothalamic CRH & circulating plasma ACTH conc. --> bilateral adrenocortical atrophy |
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What clinical signs are common in dogs w/ hyperadrenocorticism?
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PU/PD: ADH antagonism, possible concurrent DM
bilaterally symmetric alopecia: usually non-prurtic -thin skin, hyperpigmentation, comedones pot bellied appearance d/t muscle atrophy panting, dyspnea (d/t PTE), insulin resistance (hyperglycemic or concurrently treating for DM) if macroadenoma expanding into hypothalamus/thalamus: dull, listless attitude, seizures, blindness, circling UTI: assoc. w/ ↑ cortisol PTE: contributing factors: inhibition on fibrinolysis, systemic hypertension, protein losing glomerulopathy, ↓ serum antithrombin III conc., ↑ coag factor conc., ↑ PCV |
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What clin path abnormalities are common in dogs w/ hyperadrenocorticism?
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CBC: stress leukogram (d/t ↑ cortisol)
Chem: ↑ ALP (95%), hyperglycemia (cortisol inhibits insulin), hypercholesterolemia (75%), ↑ ALT U/A: isosthenuria (steroids interfere w/ ADH), proteinuria (may be hypertensive or have other glomerulonephropathy) |
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What miscellaneous findings are assoc. w/ canine hyperadrenocorticism?
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hypertension (80%)
hepatomegaly: lipid accumulation & glycogen storage in liver imaging: mineralization of adrenal tumors (~50%), pulmonary mets, adrenal hyperplasia (may be d/t general illness) |
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How is canine hyperadrenocorticism diagnosed?
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low dose dex suppression (LDDS)
- in normal dog, relatively small doses of dexamethasone given IV can inhibit pituitary secretion of ACTH --> prolonged (up to 24 hrs) ↓ in circulating cortisol conc. -give low dose of IV dex: measure cortisol at 0, 4, & 8 hrs post injection -better sensitivity & specificity than ACTH stim: ~85% accuracy -may be able to differentiate PDH vs. ADH *suppresses at 4 & 8 hrs: normal animal *suppresses at 4 hrs only: consistent w/ PDH *no suppression: consistent w/ Cushing’s (PDH or ADH) ACTH stim baseline cortisol level, give ACTH, measure cortisol 2 hrs. later very sensitive, specificity based on clinical signs -~20% of dogs w/ Cushing’s have normal test results only test that readily IDs iatrogenic Cushing’s cortisol can increase w/ any dz urine cortisol:creatinine ratio -get 1st urine sample of the morning -cortisol > 35 is suggestive of Cushing’s -cortisol will be elevated in any sick patient: not diagnostic for Cushing’s -high negative predictive value: normal ratio rules out Cushing’s & can be used as a screening test for normalcy |
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How are pituitary dependent vs. adrenal dependent canine hyperadrenocorticism differentiated?
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sometimes LDDS
high dose dexamethasone suppression -not commonly used anymore: can look at adrenal w/ US -give high dose of IV dex: measure cortisol at 0, 4, & 8 hrs post injection -patients w/ ADH & perhaps pituitary macroadenomas will not suppress endogenous ACTH -should be ↑ in PDH -should be ↓ in ADH: somewhat unpredictable (may be normal) abdominal U/S: finding of bilaterally normal sized or large adrenals in an animal diagnosed w/ Cushing’s is considered evidence of adrenal hyperplasia caused by PDH |
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What is the most commonly used tx for canine hyperadrenocorticism?
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mitotane (Lysodren)
-adrenocorticolytic drug: selectively destroys adrenal cortex induction phase: 50 mg/kg/day for 7-10 d. -if not PU/PD or polyphagic & does not have DM: ↓ induction dose (harder to monitor response to tx) -if PU/PD or polyphagia resolves after x days of induction, stop -ACTH stim at end of induction phase -goal: ACTH stim test result that is suggestive of hypoadrenocorticism maintenance phase: 50 mg/kg/wk divided into several doses -relapses may be common -may be used for adrenal tumors: adrenal tumors are usually refractory (need huge dose); esp. in aged dogs or dogs w/ worrisome concurrent dz monitor response to tx w/ ACTH stim |
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What are other possible treatments for canine hyperadrenocorticism?
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ketoconazole: inhibits production of cortisol by inhibiting synthetase enzyme (doesn’t destroy adrenals)
-use if refractory to mitotane or adverse effects occur on mitotane (ex. anorexia, GI signs) -monitor w/ ACTH stim q 3-6 mo. medical adrenalectomy: give high dose mitotane to completely destroy adrenal cortex --> hypoadrenocorticism L-deprenyl: approved for tx of PDH -monamine oxidase B inhibitor --> ↑ dopamine conc. --> negative feedback of dopamine inhibits ACTH secretion -no evidence of benefit in most Cushing’s patients, but probably does no harm adrenalectomy -tx of choice for ADH -larger tumors are harder to remove & are more likely to metastasize |
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What are the characteristics of feline hyperadrenocorticism?
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uncommon
strong assoc. w/ DM signs: wt. loss, fragile skin syndrome difficult to dx & tx |
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What is the pathophysiology of canine hypoadrenocorticism?
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1º: destruction of adrenal cortex --> lack of glucocorticoids & mineralocorticoids
-most common etiology -causes: immune mediated, thromboembolism, neoplasia (usually considered idiopathic) 2º: ↓ ACTH secretion --> deficiency in glucocorticoids only -causes: destructive lesions (ex. neoplasia or inflammation) in pituitary gland or hypothalamus, long term administration of exogenous steroids -adrenal function usually returns w/in 2-4 wks of discontinuation of exogenous steroids unless long acting depot forms are used |
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What are common clinical signs in dogs w/ hypoadrenocorticism?
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anorexia, vomiting, depression, lethargy, waxing & waning course, wt. loss, weakness/shaking, dehydration, diarrhea w/ melena or hematochezia, PU/PD, bradycardia, regurgitation
Addisonian crisis: severe weakness & collapse, dehydration, weak pulses, poor CRT, bradycardia |
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What clin path abnormalities are commonly found in dogs w/ hypoadrenocorticism?
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CBC: non-regenerative anemia, lymphocytosis, eosinophilia, lack of stress leukogram
Chem: hyponatremia, hyperkalemia (Na:K < 27; ddx: renal failure, uroabdomen, severe SI dz), hypochloremia, azotemia, hyperphosphatemia, hypoglycemia, hypercalcemia (usually mild), metabolic acidosis U/A: USG < 1.030 (medullary washout: loss of Na) |
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What are some common misc. findings in dogs w/ hypoadrenocorticism?
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ECG changes, megaesophagus, microcardia, small caudal vena cava
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How is canine hypoadrenocorticism diagnosed?
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ACTH stim
-Addison’s confirmed by abnormally ↓ post-ACTH plasma cortisol conc. -normal post-ACTH cortisol conc. rules out Addison’s basal cortisol: good to R/O ≥ 2: 98% chance animal is not Addisonian |
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What is the tx for a dog in an Addisonian crisis?
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restore volume: replacement fluid
-physiologic saline is fluid of choice b/c it aids in correcting hypovolemia, hyponatremia, & hypochloremia correct electrolyte disorders -hyperkalemia is ↓ by simple dilution & by improved renal perfusion -can use calcium gluconate, insulin + glucose, glucose, sodium bicarb if needed control arrhythmias correct hypoglycemia: supplement glucose if necessary (dextrose) replace glucocorticoids -use Dex: pred will interfere w/ ACTH stim results -do ACTH stim ASAP b/c repeated Dex will cause negative feedback replace mineralocorticoids -usually do not need to supplement: fluids have Na -injectable DOCP preferred for tx of sick animal |
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What is the long term therapy for canine hypoadrenocorticism?
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physiologic glucocorticoids
-↑ glucocorticoid requirements of hypoadrenal animals during sx or illness w/ non-adrenal dz: double dose on days when ↑ stress is anticipated mineralocorticoids: fludrocortisone PO SID or DOCP (Percorten) q 21-30 d. -not needed in animals w/ 2º Addison’s monitor q 3-6 months |
