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198 Cards in this Set
- Front
- Back
what provides verification of canine diabetes?
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persistent, fasting hyperglycemia combined with glucosuria
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why do most dogs quickly progress to clinical diabetes?
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as a result of an absolute insulin deficiency
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type 1 diabetes
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insulin dependent, destruction or loss of beta cells in the pancreas
|
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glucocorticoids and females in disestrus can contribute to
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insulin resistance
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when do clinical signs occur
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when the BG surpasses renal threshold and glucosuria ensues resulting in an osmotic diuresis
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what occurs to offset polyuria
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compensatory polydipsia
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renal threshold in the dog
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180-200mg/dl
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renal threshold in the cat
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250-300 mg/dl
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primary goal in the tx of diabetes
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minimize clinical signs and prevent potential sequala/complications such as ketoacidosis, UTIs, and cataracts
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what kind of diet is recommended?
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increased insoluble and soluble fiber - to decrease post prandial hyperglycemia
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how should insulin be qdjusted
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adjustments should not exceed 10-25% or be made more than every 7-10 days unless clinical hypoglycemia is noted
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most commonly used insulin
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human recombinant neutral protamine hagedorn (NPH) or humulin-N
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typical canine starting dose
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.25u/kg
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standard of care for monitoring a diabetic
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blood glucose curve
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why should insulin not be increased during the first week of treatment
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to allow for the reversal of hyperglucagonemia, reduction in hepatic gluconeogenesis and insulin senesitivity to improve
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goal of insulin therapy
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a nadi of 80-150 mg/dl occuring 8 hours after the insulin injection. Goal is also to minimze client observed clinical signs
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why does diabetes usually occur in dogs
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destruction or loss of insulin producing islet cells in the pancreas
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when can misdiagnosis of diabetes in cats occur?
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cats can have marked increaes in serum glucose secondary to stress with glucose values, occasionally into the 400mg/dl range
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will stress hyperglycemia cause glucosuria?
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rarely, but if present, it is transient
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the majority of cats are type __ diabetics
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type 2, non insulin depdenent
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what are the major pathophysiologic abnormalities resulting in the development of diabetes?
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peripheral insulin resistance and impaired insulin secretion
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what does pancreatic amyloidosis cause? What does this result in?
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loss of b cells decreasing the capacity to secrete insulin
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what is amyloid composed on?
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pancreatic amylin, a substance secreted from the pancreas concurrently with insulin
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chroni hyperglycemia leads to
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b cell exhaustion and decreased insulin secretion
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effect of obesity on insulin sensitivity
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obesity decreases insulin sensitivity by post-rc mechanisms
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the endocrine pancreas of cats in remission is:
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able to produce just enough insulin to maintain glucose valuse beneath renal threshold, minimizing PU/PD
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how should cats in remission be treated?
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with a low carb/high protein diet and the avoidance of insulin antagonistic medications (such as steroids)
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because most cats are non insulin dependent diabetics, their insulin requirements will usually ______ as glucose toxicity, obesity and other factors are addressed with treatment
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decrease
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standard of care for monitoring a diabetic
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blood glucose curve
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what information does the curve provide?
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info regarding the duration of insuln (type of insulin) and the dose of insulin (nadir or lowest glucose value).
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nadir
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lowest glucose value or peak effect of insulin. Should occur at the halfway point
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what happens in response to hypoglycemia
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the body will release counter regulatory hormones in order to stimulate glucose release from the liver
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when does the somogyi effect occur?
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when too much insulin is given tand the BG drops below 60mg/dl
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what is the most important thing to remember about a somogyi overswing?
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that the resulting hyperglycemia usually lasts up to 72 hours. The animal will not be responsive to subsequent doses of insulin administration
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what test can give evidence for prolonged hyperglycemia and may assist in dx of cats with mild hyperglycemia and subtle clinical signs?
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fructosamine
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40% of newly diagnosed diabetics are ___
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ketotic
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presenting complaints of DKA
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inappropriate urination, vision changes in dogs, peripheral neuropathy in cats, polyphagia, weight loss, lethary
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Physical exam of a DKA pt often shows
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dehydration, acetone smell to breath, cataracts in dogs, hepatomegaly, planti or palmigrade (in cats), dermatitis.
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lab tests on a DKA pt might show:
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serum liver enzyme elevations, hyperlipidemia, hyperlipasemia, hyperamylasemia, metabolic acidosis, serum hyperosmolality, prerenal azotemia, hematuria, pyuria, bacteriuria, ketonuria
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basic pathophysiology of DKA
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imbalance between insluin and counter reg hormones -> increase lipolysis and FA availability -> hepatic metabolism of FFA to ketone bodies -> ketonemia results in metabolic acidosis -> ketones exceed renal tubular threshold resulting in osmotic diuresis
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idioosmoles
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created in the brain to prevent a fluid shift from the CNS into the vascular space
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how to treat a healthy dog/cat with mild ketoacidosis and persistent ketonuria
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regular insulin q8hrs along with 1/3 caloric requirements. Continue until ketonuria resolves, then use longer acting insulin regimen. Reasses/BG in 7-10days
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how to treat a healthy dog/cat with no metabolic acidosis, persistent ketonuria and who is eating normally with no vomiting
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maintainence insulin q12hrs after feeding and reassess with BG in 7-10days
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sick DKA: goals of therapy
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restore fluid loss, provide regular insunl in decrease hyperglycemia and metabolize ketones, correct electrolyte imabalances, correct acidosis, monitor closely for CNS signs, address any underlying dz process causing insulin resistance, institute maintainace insulin therapy
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what two electrolyte imbalances occur with insulin therapy and correction of dehydration and acidosis?
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hypokalemia and hypophosphatemia
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metabolism of ketons and lactate results in ____ production
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bicarbonate
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decreasing serum osmolality quickly can result in
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cerebral edema, due to the idioosmoles in the brain
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criteria for diagnosing hyperglycemic hyperosmolar syndrome (HHS)
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BG levels often elevated above 800mg/dl; serum osmolality >330osm/L, absence of ketoacids
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HHS signalment/clinical signs
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middle aged to older, variable duration of clinical signs, PUPD, weight loss, extreme dehydration, renal dysfunction, decreased consciousness (hyperosmolarity-induced dehydration on the brain parenchyma)
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three main factors in development of HHS
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1) decreased insulin utilization and glucose transport 2) increased hepatic GNG and glycogenolysis and 3) impaired renal excretion of glucose
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treating HHS
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slowly restablish normal hydration and adequate urine output. Use isotonic fluids. Decrease BG levels with insulin therapy. Supplement potassium.
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exogenous/dietary energy provides enough fuel for ____ hours of cell metabolism
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4-8 hours
|
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the liver provides glucose via
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glycogenolysis
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as glycogen stores decrease, hepatic glucose production augmented by
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gluconeogenesis
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what other tissue can contribute to GNG?
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renal cortex
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the kidney also contributes to glucose ___ in the event of hypoglycemia
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counter regulation
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what can suppress endogenous glucose production and increase glucose utilization?
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insulin
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functions of insulin
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bind to membrane rc, muscle cells, adipocytes and other cells causing them to become highly permeable to glucose. Ehnances fornation of glycogen by the liver and increases uptake of glucose by hepatocytes. When quantity of glucose entering hepatocytes exceeds the amount that can be stored as glycogen, insulin converts excess glucose to fatty acids. inhibits GNG.
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glucose raising hormon
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function to increase hepatic glucose production and ihibit glucose utilization
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glucagon
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key counter regulatory hormone in acute hypoglycema and opposes the actions of insulin. Secreted by a cells in the pancreas. Actas exclusively on the liver to activate glycogenolysis and gluconeogenesis. Less influcence in recovery from chronic hypoglycemia
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epinephrine
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stimulates hepatic glycogenolysis and hepatic and renal gluconeogenesis. Provides muscle tissue with alternative source of fuel by mobilizaing muscle glycogen and stimulating lipolysis. Mobilizes gluconeogenic precurosors. Inhibhts glucose utilization by insulin-sensitive tissues (ie, skeletal muscle)
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growth hormone
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promotes lipolysis and antagonizes the action of insulin on glucose utilization in muscle cells
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cortisol
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faciliates lipolysis, promotes protein catabolism and the conversaion of amino acids to glucose by the liver and kidney. Limits glucose utilization by insulin dependent tissues
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hypoglycemia
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BG <60mg/dl
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animals with chronic/recurring hypoglycemia tend to tolerate lower BG leves for prolonged periods of time without ______. Why?
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exhibiting clinical signs; thought to be due to the upregulation of high affinity glucose transporters on the vascular cells of the BBB
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first area to be affected by hypoglycemia
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cerebral cortex
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will a normal dog or cat become hypoglycemic from fasting?
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no
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clinical signs of hypoglycemia
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neuroglycopenia signs (lethargy, weakness, collapse, syncope, ataxia, bizarre behavior, blindness, seizures, coma), and smypathoadrenal signs (muscle tremors, nervousness, restlessness and hunger)
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differentials for hypoglycemia
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insulinoma, congenital hepatic dysfunction, acquired hepatic dz, addisons, non beta cell tumors, endotoxic or sepsis induced hypoglycemia, artifact, iatrogenic, hunting dog hypoglycemia (exertional hypglycermia)
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insulinoma
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malignant functional tumors arising from the beta cells of the pancreas that secrete insulin despite hypoglycemia. They are not completely autonomous because they will respond to increases in glucose by secreting insulin, often in excessive amounts
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insulinoma signalment
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middle aged to older, large breed dogs, very rare in cats
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insulinoma signs
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seizures, weakness, collapse, ataxia, fasciculations, bizarre behavior. Signs typically episodic and can be triggered by fasting, exercise, excitement and eating.
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insulinoma PE
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often WNL. Weakness and lethargy most common findings. Weight gain seen in some due to anabolic effects of insulin. Can also see peripheral neuropathies
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insulinoma labwork
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hypoglycemia is only consistent finding
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diagnosing insulinoma
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paired serum insulin and glucose values (hypoglycemia with high insulin levels). But SX exploration is best dx, therapeutic and prognostic tool
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insulinoma medical management
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goal is to control clin signs, not to establish euglycemia. Feed small meals high in fat, complex carbs and fiber. Limit exercise. Prednisone (initiate when frequent feedings ineffective and gradually increase dose as needed to control signs). Diazoxide (use when prod alone not effected. inhibits insulin secretion, stimulates hepatic gluconeogenesis and glycogenolysis and inhibits tissue use of glucose), streptozocin (directly toxic to beta cells),
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congenital hepatic dysfunction
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assoc with PSS. Hypoglyc due to insufficient hepatic glycogen stores and inadequate hepatocellular fxn to support GNG. Cbc may show microcytosis. Chem - hypoalbuminemia, hypocholesterolemia, decreased BUN, elevaed liver enzymes. Ammonium biurate crytals in urine. bile acids elevated.
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glycogen storage dz
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rare congenital hepatic disorders in dogs in which hypoglycemia results from an inability to convert glycogen to glucose
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acquired hepatic dz
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severe destriction of liver. Hypoglycemia due to inaduate amounts of functional hepatic tissue for storage of glycogen or for sufficient gluconeogenesis. >75% liver function lost. Hypoglc usually mild
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hypoadrenocorticism (addisons)
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mild hypoglyc due to insufficient secretion of glucocorticoids needed to stimulate hepatic mobilization and production of glucose.
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addisons signalment
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young to middle aged female dogs.
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non beta cell tumor
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hepatocellular carcinoma, hepatoma, leiomyoma, leiomyosarcoma and tumors with extensive hepatic mets of many different neoplasia types, hemangiosarc, gastrinoma, mammary carcinoma. Pathogenesis: excessive glucose utilization by tumor, tumor induced hepatic destruction, inhibition of counter regulatory hormones, secretion of an insulin like growth factor
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neonatal and juvenile hypoglycemia
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limited hepatic glycogen stores, small muscle mass, lack of adipose tissue and decreased use of free fatty acids as an alternative energy source place neonates at risk for hypoglycemia. Often occurs in conjunction with hypothermia (in neonates, leades to decreased digestive function and sepsis). in toy/mini dogs <6mo. alanine deficiency implicated. manage with small frequent feedings, test for underlying disorders. disorder dissapears when reach adult size.
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endotoxic or sepsis induced hypoglycemia
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pathogenesis believed to result from increased tissue utilization of glucose in conjunction with decreased hepatic glucose production. Consider if significian leukocytosos or leukopenia, left shift, toxic changes found, fever or hypothermia seen.
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spurious hypoglycemia
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artifactual, sample handling artifact
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iatrogenic hypoglycemia
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overdose of insulin or oral sulfonylurea drugs in patients with DM
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hunting dog hypoglyc / exertional hypoglycemia
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active lean dogs after extreme exercise. Manage with feeding prior to and during hunting, proper pre season conditioning
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diagnostic approach to the hypoglycemia pt
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PE may be normal or may have evidence of neuro dysfunction or other dz proecess. CBC/chem/UA. Emergency tx okay, but withhold others until after diagnosis made. Always confirm low BG value.
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medical management of hypoglycemia
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goal is to provide glucose substrate for CNS. For hypoglycemia seizures use sugar solution on gums or IV dextrose solution (diluted). Feed small meal once pet is sternal. CRI dextrose to prevent reoccurance. Pursue underlying etiology
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anterior pituiary consists of
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pars distalis and pars intermedia
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where is corticotrophin releasing hormone produced?
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hypothalamus
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CRH stimulates the _______ to produce adrenocorticotropic hormone
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anterior pituitary
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ACTH stimulates ___ production from the adrenal glands
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cortisol
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effects of cortisol
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stim of hepatic GNG, promotoion of glycogen storage by the liver, reductions of cellular utilization of glucose, reduction of protein synth and promotion of protein catabolism, increased mobilization of fat and altered immune function
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pathophys of hyperadrenocorticism
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results from overproduction of cortisol.
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cushing syndrome refers to
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any dz process that causes the clinical signs brought about by excessive circulating cortisol and can include pituitary dependent hyperadrenocorticism, functional adrenal tumors, bilateral nodular adrenal hypertrophy and iatrogenic cushings.
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the most common cause of spontaneous hyperadrenocorticism
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pituitary dependent hyperadrenocorticism
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pituitary dependent hyperadrenocorticism
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due to functional tumor of the pituiary gland (adenoma of the pars distalis) that inappropriately secretes excessive levels of ACTH. Excessive production of ACTH causes bilateral adrenocortical hyperplasia.
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adrenal tumor
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adrenocortical dependent hyperadrenocorticism = 15-20% HAC in dogs
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iatrogenic hyperadrenocorticism
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due to excessive admin of exogenous glucocorticoids often seen with admin of glucocorticoids for allergies or immune mediated dz.
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clinical signs of cushings
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PUPD, polyphagia, panting, abdominal enlargement, hepatomegaly, muscle weakness and atrophy. Bilateral symmetric nonpruritic alopecia --> truncal alopecia. Hyperpigmentation, calcinosis cutis, poor wound healing, bruising, secondary pyometra
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DDx for alopecia
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adrenal associated (atypical HAC, alopecia X, non adrenal, growth hormone deficiency, hypothyroidism)
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DDx for abdominal enlargement
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abdominal masses, hepatomegaly, CHF, psychogenic polydypsia, renal dz, hepatic insufficiency failure, DM, DI, hypercalcemia
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potential complications of large pituitary tumors
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compression of adjacent structures and CNS signs - lethargy, dullness, inappetance, wandering, circling, behavioral changes. Pulmonary thromboembolism post-tx
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what disease occurs in ~10% dogs with HAC?
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diabetes mellitus
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HAC diagnostic testing
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CBC (stress leukogram, mild erythrocytosis and thrombocytosis.) CHEM (elevated aLP, ALT, cholesteral, triglycerides). UA (isosthenuric or hyposthenuric, UTI, proteinurea)
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____% of adrenal tumors are calcified
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50%
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discriminitory test to help distinguish PDH from AT
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abdominal US
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ACTH stim
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a screening test that cant differentiate between PDH and AT. Results can be used as a baseline for comparision during tx of HAC with mitotae or trilostane
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what is the only test that will ID iatrogenic hyperadrenocorticsm
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ATCH stim
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LDDST
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low dose dex suppressiontest - screening test that may also serve as a differentiating test. More sensitive but less specific
|
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HDDST
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differentiating test that Should NOT be used to dx HAC. Discriminates PDH from AT
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plasma endogenous ACTH concentration
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not used to dx. Good for determining that HAC is due to PDH, but is not reliable with AT
|
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urine cortisol:creatinine raton
|
very sensitive, help rule out HAC but positive should not be used to dx
|
|
trilostane
|
for PDH or nonsx AT. FDA approved for dogs. Works by competitive inhibition
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mitotane
|
causes progressive necrosis of zona fasciculata and zona reitcularis of the adrenal cortex. Tx AT at higher dose. Given in two phases
|
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l-deprenyl
|
MAO type b inhibitor, increases dopamine concentrations --> inhibit CRH and ACTH
|
|
ketoconazole
|
impairs steroid synth (p450 inhib)
|
|
adrenalectomy
|
tx of choice for AT unless mets or local invasion detected. Hypoadrenocort develops on post-op.
|
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role of sex hormones in hyperadrenocorticism
|
excessive production reported in some dogs with HAC,
|
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feline hyperadrenocorticsm % PDH cases
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75-80%
|
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feline hyperadrenocorticsm
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half are adenomas, half carcinomas.
|
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feline hyperadrenocorticism, % AT
|
20-25
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feline HAC signalment
|
older, female cats.
|
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what dz is feline HAC assoc with?
|
diabetes mellitus
|
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feline HAC clinical signs
|
PUPD, weight loss, cachexia, fragile skin, patchy alopecia, muscle wasting, hepatomegaly
|
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how to dx feline HAC
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atch stim, dex suppression test, ab US
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feline hac tx of choice
|
adrenalectomy
|
|
zone glomerulosa
|
synthesizes and secretes aldosterone
|
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zona fasciculata
|
synth and secrete glucocorticoids
|
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zona reticularis
|
synth and secrete sex hormones
|
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mineralcorticoids main effect
|
at the renale tubule where it promotes renal tubular resorption of sodium and chloride and excretion of potassium
|
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what controls the secretion of aldosterone
|
renin angiotensin system
|
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what is the major glucocorticoid
|
cortisol
|
|
some actions of cortisol
|
maintain vascular tone and endothelial integrity, stim GNG and glycogenesis, suppress glucose uptake by peripheral tissues, stim erythryocytosis, maintain GI integrity, counteract effects of stress
|
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what regulats glucocorticoid secretion
|
hypothalamic pituitary axis
|
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Corticotropin releasing hormone secreted by
|
hypothalamus
|
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CRH stimulates ____ secretion by the pituitary gland
|
ACTH
|
|
ACTH stimulates secretion of
|
adrenal corticosteroids
|
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_____have a neg feedback effect on CRH And ACTH secretion
|
glucocorticoids
|
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pathophys of primary hypoaderenocorticism
|
most common form but overall not common in dogs. Clinical signs when >90% cells of adrenal cortex nonfunctional. Idiopathic. (immune mediated??)
|
|
pathophys of secondary hypoadrenocorticism
|
rare, results in loss of production of ACTH causing atrophy of adrenal cortices. Result is impared secretion of glucocorticoids
|
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pathophys of iatrogenic hypoadrenocort
|
occurs after rapid withdrawal of chronic glucocorticoid therapy. Exogenous glucocorticoids suppress the acth secretion by the pituitary gland leading to adrenal atrophy.
|
|
effects of mineralocorticoid deficiency
|
lack of aldosterone -> hyponatremia, hypchloridemia, hyperkalemia. The loss of sodium results in concurrent loss of body water (Dehydration, hypovolemia, hypotension, poor perfusion). Sodium loss can cause PUPD, hyperkalemia can have life threatening heart effects.
|
|
effects of glucocorticoid defic
|
lack of cortisol -> GI signs (anorexia, vomiting, abdominal pain, and weight loss). Hypoglyc due to altered energy metabolism. Lethargy
|
|
hypoadrenocorticism signalment
|
young to middle aged female dogs. Increased risk in poodles, great danes, westies
|
|
how can hypoadrenocort pts present
|
for an acute adrenal crisis or for chronic signs. Signs are non specific (lethargy, weight loss, shaking, shivering, pupd)
|
|
PE exam abnormalities
|
lethargy, weakness, hypovolemic, CV shock. Inappropriate bradycardia that is expected in a shocky pt may NOT be present
|
|
DX testing
|
LACK of a stress leukogram. Lymphocytosis, eosinophilia. Norm/norm nonregen anemia common (may be masked by hemoconc/dehydration). NA/K <27. hypnatremia, hypochloridemia, hyperkalemia.
|
|
only definitive test for hypoadrenocorticism
|
ACTH stim
|
|
what is needed to differentiate between primary and secondary hypoadrenocorticism
|
endogenous ACTH concentration
|
|
ACTH stim for a hypoadrenocorticism dog
|
basal and post acth cortisol conc <1.oug/dl. Pre and post <2.0ug/dl
|
|
treatment of the addisonian crisis
|
actm stim performed when patient is stable. IV saline. May need dextrose. Dex SP once. Monitor hyperkalemia. Sodium bicarb if acidotic.
|
|
management after the addisonian crisis
|
pred, long term physiologic dose. Extra dose on days of stress. Replace mineralocorticoid with DOCP or fludocortisone.
|
|
atypical addisons
|
glucocorticoid defic with normal mineralocorticoid production. Serum electrolytes are normal. Dx based on aCTH stim. May progress to typical case.
|
|
DDX for hyperkalemia and hyponatremia
|
mineralocorticoid defic (typical, primary), renal and urinary tract dz, severe GI dz, severe metabolic or resp acidosis, artifact.
|
|
diseases causing ca metabolism disorders are either caused by ________ or ________
|
a dysfunction of the parathyroid gland or due to other dzs that alter calcium kinetics in the body
|
|
primary hyperparathyroidism is usually the result of
|
an autonomous adenoma of a single parathyroid gland
|
|
primary hypoparathyroidism usually results from
|
mmune mediated destruction of the parathyroid glands
|
|
most common cause of hypercalcemia in dogs. Other common causes?
|
hypercalcemia of malignancy. Hypoadrenocorticism, renal failure
|
|
cats develop an idiopathic hypercalcemia that often leads to the development of
|
calcium containing uroliths
|
|
hypercalcemia clin signs
|
anorexia, vomiting, constipation, pupd, hematuria, stranguria, pollakiuria, ataxia, muscle weaknesss, obtundation, listlessness, muscle twitching, seizures, coma
|
|
DDx for hypercalcemia
|
neoplasia, hypoadrenocorticism, renal failure, granulomatous diseases, vit d toxicosis, primary hyperparathyroidism. Less common: osteolytic dz
|
|
DX testing
|
cbc chem ua. - renal dz, hypadrenocort, evidenice of granulomatous dz. Thoracic rads, ab rads/US, cytology, histopath, ionized calcium, serum PTH
|
|
increases in ionized calcium typically equivalent to increases in
|
total calcium
|
|
the combo of elevated iCa, elevated PTH-rP and low PTH levels in an animal is strongly suggestive of
|
nonparathyroidal malignancy
|
|
hypocalcemia clinical signs
|
often episodic, stiff gait, fasciculations, cramping, pain, tense, splinted abdomen, tetany, seizures, intesnse facial rubbing, nervousness, fever, cataracts
|
|
what can cause hypocalcemia
|
primary parathyroid dz, dz causing redistribution of calcium in the body, nutritional defic of ca or vit D.
|
|
hypoalbumnemia alters the __________ even though the ionized calcium concentration is normal
|
total calcium concentration
|
|
corrected total calcium -
|
patients measured total calcium - patients albumin + 3.5
|
|
why is the use of corrected formulas out of favor?
|
there is equipment to measure ionized calcium concentration
|
|
____ levels are often elevated in patients with hypoparathyroidism
|
phosphorus
|
|
ECG of hypocalcemia
|
bradycardia with deep wide T waves and prolonged Q-T intervals. Supravent tachycard.
|
|
pathophys
|
pth release is closely regulated by serum concentrations of ionized calcium. Because of the very tight range of alterations in calcium that regulate the negative feedback mechanism, alterations in serum calcium by an dz rocess affects the pth gland and release of pth
|
|
hypercalcemia etiologies
|
(GOSHDARNIT) - granulomatous dz, osteolytic dz, spurious, hyperparathryoidism, d toxicosis, addisons, renal failure, neoplasia, idiopathic, temperature (hypotherm)
|
|
most common cause of hypercalcemia?
|
neoplasia
|
|
primary hyperparathyroidism signalment
|
rare in dogs, rare in cats. Average age in dogs is 10.5 years.
|
|
90% of priamry hyperparathyroidism cases are due to
|
adenoma
|
|
secondary hyperparathyroidism
|
excessive parathyroid hormone secretion due to calcium and phosphorus imbalances. Most commonly caused by CRF and diet imbalances.
|
|
whey is there secondary hyperparathyroidism with CRF?
|
decreased glomerular filtration rate -> icreased phosphate in the body
|
|
hyperphosphatemia leads to the bodys perceptiom of
|
decreased serum ionized calcium levels
|
|
nutritional hyperparathyroidism
|
due to inappropriate diet. Skeletal abnormalities seen with CaP rations greater to or equial to 1:2. clinical signs - reluctance to move, lameness, incoordination. Pathologic fractures.
|
|
hypocalcemia can occur due to
|
primary parathryoid dysfunction, lack of dietary Ca/vit D, lack of absorption of Vit D/Ca or a problem causing systemic redistribution of calcium
|
|
primary hypoparathyroidism signalment
|
rare, average age of dogs 4-8 years
|
|
most common cause of primary hypoparathyroidism
|
immune mediated dz
|
|
therapy for hypercalcemia
|
find and treat underlying cause. (primary hyperparathyroidism - remove affected glands). Diurses, diuretics after rehydration, glucocorticoids after diagnosis, bisphosphaonates, calcitonin
|
|
therapy for hypocalcemia
|
find and treat underlying cause. (primar hypoparathyroidism - intitial tx of tetany (IV ca containing fluids). Begin oral vit D and Ca supplementation.
|
|
goal of vit D therapy
|
maintian serum total calcium in the 8-9.5mg/dl range
|
|
Furosemide (Class, route, indications)
|
loop diuretic, IV, hypercalcemia (after rehydrated)
|
|
prednisole (Class, route, indications)
|
glucocorticoid, PO, hypercalcemia (after dx of etiology)
|
|
pamidronate disodium (Class, route, indications)
|
bisphosphanate, IM, hypercalcemia
|
|
calcium gluconate 10% (Class, route, indications)
|
calcium containing IV fluid, IV, hypocalcemia (initial therapy or transitional therapy.) Can dilute and give SQ,
|
|
calcium chlorid 10% (Class, route, indications)
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calcium containing IV fluid, IV, hypcalcium- perivascular irritation
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oral calcium supplements / calcium carbonate (Class, route, indications)
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antacids, PO, hypocalcemia
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ergocalciferol (Class, route, indications)
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vitamin D2, PO, hypoparathyroidism
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dihydrotachysterol (Class, route, indications)
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synthetic vitD, PO, hypoparathyroidism
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calcitriol (Class, route, indications)
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vit D3, PO, hypoparathyroidism
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DOES NOT INCLUDE CA SUPPLEMENTAL READING
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GO READ!
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