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198 Cards in this Set

  • Front
  • Back
what provides verification of canine diabetes?
persistent, fasting hyperglycemia combined with glucosuria
why do most dogs quickly progress to clinical diabetes?
as a result of an absolute insulin deficiency
type 1 diabetes
insulin dependent, destruction or loss of beta cells in the pancreas
glucocorticoids and females in disestrus can contribute to
insulin resistance
when do clinical signs occur
when the BG surpasses renal threshold and glucosuria ensues resulting in an osmotic diuresis
what occurs to offset polyuria
compensatory polydipsia
renal threshold in the dog
180-200mg/dl
renal threshold in the cat
250-300 mg/dl
primary goal in the tx of diabetes
minimize clinical signs and prevent potential sequala/complications such as ketoacidosis, UTIs, and cataracts
what kind of diet is recommended?
increased insoluble and soluble fiber - to decrease post prandial hyperglycemia
how should insulin be qdjusted
adjustments should not exceed 10-25% or be made more than every 7-10 days unless clinical hypoglycemia is noted
most commonly used insulin
human recombinant neutral protamine hagedorn (NPH) or humulin-N
typical canine starting dose
.25u/kg
standard of care for monitoring a diabetic
blood glucose curve
why should insulin not be increased during the first week of treatment
to allow for the reversal of hyperglucagonemia, reduction in hepatic gluconeogenesis and insulin senesitivity to improve
goal of insulin therapy
a nadi of 80-150 mg/dl occuring 8 hours after the insulin injection. Goal is also to minimze client observed clinical signs
why does diabetes usually occur in dogs
destruction or loss of insulin producing islet cells in the pancreas
when can misdiagnosis of diabetes in cats occur?
cats can have marked increaes in serum glucose secondary to stress with glucose values, occasionally into the 400mg/dl range
will stress hyperglycemia cause glucosuria?
rarely, but if present, it is transient
the majority of cats are type __ diabetics
type 2, non insulin depdenent
what are the major pathophysiologic abnormalities resulting in the development of diabetes?
peripheral insulin resistance and impaired insulin secretion
what does pancreatic amyloidosis cause? What does this result in?
loss of b cells decreasing the capacity to secrete insulin
what is amyloid composed on?
pancreatic amylin, a substance secreted from the pancreas concurrently with insulin
chroni hyperglycemia leads to
b cell exhaustion and decreased insulin secretion
effect of obesity on insulin sensitivity
obesity decreases insulin sensitivity by post-rc mechanisms
the endocrine pancreas of cats in remission is:
able to produce just enough insulin to maintain glucose valuse beneath renal threshold, minimizing PU/PD
how should cats in remission be treated?
with a low carb/high protein diet and the avoidance of insulin antagonistic medications (such as steroids)
because most cats are non insulin dependent diabetics, their insulin requirements will usually ______ as glucose toxicity, obesity and other factors are addressed with treatment
decrease
standard of care for monitoring a diabetic
blood glucose curve
what information does the curve provide?
info regarding the duration of insuln (type of insulin) and the dose of insulin (nadir or lowest glucose value).
nadir
lowest glucose value or peak effect of insulin. Should occur at the halfway point
what happens in response to hypoglycemia
the body will release counter regulatory hormones in order to stimulate glucose release from the liver
when does the somogyi effect occur?
when too much insulin is given tand the BG drops below 60mg/dl
what is the most important thing to remember about a somogyi overswing?
that the resulting hyperglycemia usually lasts up to 72 hours. The animal will not be responsive to subsequent doses of insulin administration
what test can give evidence for prolonged hyperglycemia and may assist in dx of cats with mild hyperglycemia and subtle clinical signs?
fructosamine
40% of newly diagnosed diabetics are ___
ketotic
presenting complaints of DKA
inappropriate urination, vision changes in dogs, peripheral neuropathy in cats, polyphagia, weight loss, lethary
Physical exam of a DKA pt often shows
dehydration, acetone smell to breath, cataracts in dogs, hepatomegaly, planti or palmigrade (in cats), dermatitis.
lab tests on a DKA pt might show:
serum liver enzyme elevations, hyperlipidemia, hyperlipasemia, hyperamylasemia, metabolic acidosis, serum hyperosmolality, prerenal azotemia, hematuria, pyuria, bacteriuria, ketonuria
basic pathophysiology of DKA
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
idioosmoles
created in the brain to prevent a fluid shift from the CNS into the vascular space
how to treat a healthy dog/cat with mild ketoacidosis and persistent ketonuria
regular insulin q8hrs along with 1/3 caloric requirements. Continue until ketonuria resolves, then use longer acting insulin regimen. Reasses/BG in 7-10days
how to treat a healthy dog/cat with no metabolic acidosis, persistent ketonuria and who is eating normally with no vomiting
maintainence insulin q12hrs after feeding and reassess with BG in 7-10days
sick DKA: goals of therapy
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
what two electrolyte imbalances occur with insulin therapy and correction of dehydration and acidosis?
hypokalemia and hypophosphatemia
metabolism of ketons and lactate results in ____ production
bicarbonate
decreasing serum osmolality quickly can result in
cerebral edema, due to the idioosmoles in the brain
criteria for diagnosing hyperglycemic hyperosmolar syndrome (HHS)
BG levels often elevated above 800mg/dl; serum osmolality >330osm/L, absence of ketoacids
HHS signalment/clinical signs
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)
three main factors in development of HHS
1) decreased insulin utilization and glucose transport 2) increased hepatic GNG and glycogenolysis and 3) impaired renal excretion of glucose
treating HHS
slowly restablish normal hydration and adequate urine output. Use isotonic fluids. Decrease BG levels with insulin therapy. Supplement potassium.
exogenous/dietary energy provides enough fuel for ____ hours of cell metabolism
4-8 hours
the liver provides glucose via
glycogenolysis
as glycogen stores decrease, hepatic glucose production augmented by
gluconeogenesis
what other tissue can contribute to GNG?
renal cortex
the kidney also contributes to glucose ___ in the event of hypoglycemia
counter regulation
what can suppress endogenous glucose production and increase glucose utilization?
insulin
functions of insulin
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.
glucose raising hormon
function to increase hepatic glucose production and ihibit glucose utilization
glucagon
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
epinephrine
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)
growth hormone
promotes lipolysis and antagonizes the action of insulin on glucose utilization in muscle cells
cortisol
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
hypoglycemia
BG <60mg/dl
animals with chronic/recurring hypoglycemia tend to tolerate lower BG leves for prolonged periods of time without ______. Why?
exhibiting clinical signs; thought to be due to the upregulation of high affinity glucose transporters on the vascular cells of the BBB
first area to be affected by hypoglycemia
cerebral cortex
will a normal dog or cat become hypoglycemic from fasting?
no
clinical signs of hypoglycemia
neuroglycopenia signs (lethargy, weakness, collapse, syncope, ataxia, bizarre behavior, blindness, seizures, coma), and smypathoadrenal signs (muscle tremors, nervousness, restlessness and hunger)
differentials for hypoglycemia
insulinoma, congenital hepatic dysfunction, acquired hepatic dz, addisons, non beta cell tumors, endotoxic or sepsis induced hypoglycemia, artifact, iatrogenic, hunting dog hypoglycemia (exertional hypglycermia)
insulinoma
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
insulinoma signalment
middle aged to older, large breed dogs, very rare in cats
insulinoma signs
seizures, weakness, collapse, ataxia, fasciculations, bizarre behavior. Signs typically episodic and can be triggered by fasting, exercise, excitement and eating.
insulinoma PE
often WNL. Weakness and lethargy most common findings. Weight gain seen in some due to anabolic effects of insulin. Can also see peripheral neuropathies
insulinoma labwork
hypoglycemia is only consistent finding
diagnosing insulinoma
paired serum insulin and glucose values (hypoglycemia with high insulin levels). But SX exploration is best dx, therapeutic and prognostic tool
insulinoma medical management
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),
congenital hepatic dysfunction
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.
glycogen storage dz
rare congenital hepatic disorders in dogs in which hypoglycemia results from an inability to convert glycogen to glucose
acquired hepatic dz
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
hypoadrenocorticism (addisons)
mild hypoglyc due to insufficient secretion of glucocorticoids needed to stimulate hepatic mobilization and production of glucose.
addisons signalment
young to middle aged female dogs.
non beta cell tumor
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
neonatal and juvenile hypoglycemia
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.
endotoxic or sepsis induced hypoglycemia
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.
spurious hypoglycemia
artifactual, sample handling artifact
iatrogenic hypoglycemia
overdose of insulin or oral sulfonylurea drugs in patients with DM
hunting dog hypoglyc / exertional hypoglycemia
active lean dogs after extreme exercise. Manage with feeding prior to and during hunting, proper pre season conditioning
diagnostic approach to the hypoglycemia pt
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.
medical management of hypoglycemia
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
anterior pituiary consists of
pars distalis and pars intermedia
where is corticotrophin releasing hormone produced?
hypothalamus
CRH stimulates the _______ to produce adrenocorticotropic hormone
anterior pituitary
ACTH stimulates ___ production from the adrenal glands
cortisol
effects of cortisol
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
pathophys of hyperadrenocorticism
results from overproduction of cortisol.
cushing syndrome refers to
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.
the most common cause of spontaneous hyperadrenocorticism
pituitary dependent hyperadrenocorticism
pituitary dependent hyperadrenocorticism
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.
adrenal tumor
adrenocortical dependent hyperadrenocorticism = 15-20% HAC in dogs
iatrogenic hyperadrenocorticism
due to excessive admin of exogenous glucocorticoids often seen with admin of glucocorticoids for allergies or immune mediated dz.
clinical signs of cushings
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
DDx for alopecia
adrenal associated (atypical HAC, alopecia X, non adrenal, growth hormone deficiency, hypothyroidism)
DDx for abdominal enlargement
abdominal masses, hepatomegaly, CHF, psychogenic polydypsia, renal dz, hepatic insufficiency failure, DM, DI, hypercalcemia
potential complications of large pituitary tumors
compression of adjacent structures and CNS signs - lethargy, dullness, inappetance, wandering, circling, behavioral changes. Pulmonary thromboembolism post-tx
what disease occurs in ~10% dogs with HAC?
diabetes mellitus
HAC diagnostic testing
CBC (stress leukogram, mild erythrocytosis and thrombocytosis.) CHEM (elevated aLP, ALT, cholesteral, triglycerides). UA (isosthenuric or hyposthenuric, UTI, proteinurea)
____% of adrenal tumors are calcified
50%
discriminitory test to help distinguish PDH from AT
abdominal US
ACTH stim
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
what is the only test that will ID iatrogenic hyperadrenocorticsm
ATCH stim
LDDST
low dose dex suppressiontest - screening test that may also serve as a differentiating test. More sensitive but less specific
HDDST
differentiating test that Should NOT be used to dx HAC. Discriminates PDH from AT
plasma endogenous ACTH concentration
not used to dx. Good for determining that HAC is due to PDH, but is not reliable with AT
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
mitotane
causes progressive necrosis of zona fasciculata and zona reitcularis of the adrenal cortex. Tx AT at higher dose. Given in two phases
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.
role of sex hormones in hyperadrenocorticism
excessive production reported in some dogs with HAC,
feline hyperadrenocorticsm % PDH cases
75-80%
feline hyperadrenocorticsm
half are adenomas, half carcinomas.
feline hyperadrenocorticism, % AT
20-25
feline HAC signalment
older, female cats.
what dz is feline HAC assoc with?
diabetes mellitus
feline HAC clinical signs
PUPD, weight loss, cachexia, fragile skin, patchy alopecia, muscle wasting, hepatomegaly
how to dx feline HAC
atch stim, dex suppression test, ab US
feline hac tx of choice
adrenalectomy
zone glomerulosa
synthesizes and secretes aldosterone
zona fasciculata
synth and secrete glucocorticoids
zona reticularis
synth and secrete sex hormones
mineralcorticoids main effect
at the renale tubule where it promotes renal tubular resorption of sodium and chloride and excretion of potassium
what controls the secretion of aldosterone
renin angiotensin system
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
what regulats glucocorticoid secretion
hypothalamic pituitary axis
Corticotropin releasing hormone secreted by
hypothalamus
CRH stimulates ____ secretion by the pituitary gland
ACTH
ACTH stimulates secretion of
adrenal corticosteroids
_____have a neg feedback effect on CRH And ACTH secretion
glucocorticoids
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
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)
calcium containing IV fluid, IV, hypcalcium- perivascular irritation
oral calcium supplements / calcium carbonate (Class, route, indications)
antacids, PO, hypocalcemia
ergocalciferol (Class, route, indications)
vitamin D2, PO, hypoparathyroidism
dihydrotachysterol (Class, route, indications)
synthetic vitD, PO, hypoparathyroidism
calcitriol (Class, route, indications)
vit D3, PO, hypoparathyroidism
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