Term
| What is the most common cause of abnormal PLRs in a geriatric pet? |
|
Definition
iris atrophy
*** although the PLR is incomplete, these patients will have a normal menace response |
|
|
Term
| Why is using skin elasticity a less accurate method of determining hydration status of geriatric pets? |
|
Definition
| skin elasticity decreases with age, don't over interpret skin tent measures of hydration in older patients |
|
|
Term
| How common is senile cognitive dysfunction in dogs? In cats? |
|
Definition
20-25% of dogs >9rs (females overrepresented)
30-35% of cats >11yrs |
|
|
Term
| What five historical findings are consistent with senile cognitive dysfunction in dogs or cats? |
|
Definition
Disorientation
Altered interactions with humans or other anmials Sleep-wake cycle alterations
Deterioration of house training and other learned behaviors
change in activity (increased or decreased) |
|
|
Term
| What is the main drug used to treat cognitive dysfunction in geriatric pets? |
|
Definition
selegiline (MAO-B inhibitor)
**** the drug takes a couple of weeks to begin having an effect, having owners keep a behavior log is a good way to assess response to therapy |
|
|
Term
| T/F patients with old dog vestibular disease may present with vertical nystagmus |
|
Definition
FALSE
*** old dog vestibular disease is peripheral (ie. affects the inner ear) so nystagmus will be rotary or horizontal ONLY, if you see vertical nystagmus be worried about cranial dz (ex. brain tumor) |
|
|
Term
| What treatment is warranted to old dog vestibular disease? |
|
Definition
neurologic signs are self limiting
Nursing case and control of nausea +/- fluids if not drinking are generally sufficient until patient improves |
|
|
Term
| What are the two presentations of urinary incontinence that develops in geriatric patients? |
|
Definition
urethral sphincter incontinence (usually spayed female dogs)
neurologic- lumbosacral myelopathy (IVDD, tumors, degenerative and vascular diseases that affect this region of the spinal cord) |
|
|
Term
| What is the treatment of choice for urethral sphincter incontinence in dogs (esp. geriatric spayed females)? |
|
Definition
phenylpropanoamine
*** alpha adrenergic agonist --> increases sympathetic tone at the uretheral sphincter |
|
|
Term
| What is the most common etioloy of constipation in cats? |
|
Definition
idiopathic (62%)
*** R/O dehydration, neurologic dysfunction, obstructive dz/FB, behavioral |
|
|
Term
| What are two non-invasive treatment options for feline constipation? |
|
Definition
warm water/lube enemas
Go-lytely (oral electrolyte solution --> retained in intestinal lumen --> induces osmotic diarrhea)
*** if conservative medical management fails sedation with manual evacuation, or surgery (sub-total colectomy) are options |
|
|
Term
| What are the two most important elements to consider when developing a palliative care treatment plan? |
|
Definition
pain management (NSAIDs for musculoskeletal pain, cannot be given with steroids and even selective COX-2 inhibitors can cause ARF)
nutritional support (mitrazapine is a TCA and can be used to stimulate appetite in dogs(SID) and cats(q 3days)) |
|
|
Term
| What is the most common pathologic basis of hypoadrenocorticism? |
|
Definition
| destruction of glucocorticoid AND mineralocorticoid secreting cells of the adrenal cortex **** hypoA secondary to inadequate central secretion of ACTH or CRF from the pituitary/hypothalamus --> just glucocorticoid deficiency is RARE |
|
|
Term
| What are two potential etiologies of primary hypoA (destruction of zona granulosa and fasiculata of the adrenal cortex)? |
|
Definition
irreversible idiopathic atrophy or autoimmune injury
reversible secondary to inflammation, infarcts, neoplasia, amyloid deposition and drugs (esp. mitotane and trilostaine <- used to tx cushings) |
|
|
Term
| What are two potential etiologies of secondary hypoA (central- failure of pituitary/hypothalamus to secrete sufficient ACTH or CRF)? |
|
Definition
spontaneous (lack of ACTH or CRF --> just corticosteroid deficiency)
iatrogenic (exogenous glucocorticoid administration --> adrenal cortical atrophy) |
|
|
Term
| What pathology is associated with mineralocorticoid deficiency? |
|
Definition
inability to conserve sodium -> HYPONATREMIA/CHLOREMIA --> impaired renal concentrating capacity --> severe dehydration, hypovolemia and hypotension --> decreased CO, decreased GFR --> prerenal azotemia and metabolic acidosis
inability to excrete potassium --> HYPERKALEMIA --> bradyarrythmias and can also cause myasthenia gravis |
|
|
Term
| Where in the kidneys does aldosterone (mineralocorticoid) exert an effect? |
|
Definition
| acts at the distal convoluted tubules and collecting ducts *** normal function is to reabsorb sodium and water from the lumen in exchange for potassium which is excreted with the urine |
|
|
Term
| What physical and laboratory findings are consistent with cortisol deficiency? |
|
Definition
| depressed mentation; non-regenerative anemia (ie. anemia of inflammation/chronic disease) with eosinophilia and lymphocytosis; hypercalcemia (glucocorticoids promote renal calcium excretion); hypolglycemia/cholesterolemia/albuminemia; anorexia, vomiting, and abdominal pain |
|
|
Term
| What hemogram pattern is consistent with hypoadrenocorticism? |
|
Definition
| mild non-regenerative anemia (animals may initially present with marked hemoconcentration secondary to dehydration) lymphocytosis +/- eosinophilia (ie. this is a really sick animal with NO neutrophilia) |
|
|
Term
| What are 4 potential causes of hyperkalemia other than hypoA? |
|
Definition
metabolic acidosis
drugs (NSAIDs, ace inhibitors, TMS etc.)
muscle injury
heat stroke |
|
|
Term
| T/F hypoglycemia is uncommonly associated with hypoadrenocorticism |
|
Definition
TRUE
*** if present generally appears as CNS abnormalities (seizures, nystagmus, paresis) |
|
|
Term
| What is the mechanism driving the development of metabolic acidosis in hypoA patients? |
|
Definition
| impaired renal excretion of hydrogen ions (b/c aldosterone is normally responsible for retaining sodium, chloride and water in exchange for pottasium and hydrogen, hypoA-> hyperkalemia and increased H+) , impaired renal absorption of bicarbonate, and decreased GFR |
|
|
Term
| What findings on rads and ultrasound are consistent with hypoA? |
|
Definition
microcardia and microhepatica (secondary to hypovolemia) and rarely megaesophagus (secondary myasthenia) on survey rads
atrophied adrenals and microhepatica on abdominal ultrasound |
|
|
Term
| What is an excellent first line screening test to r/o hypoA in suspected patients? |
|
Definition
resting cortisol
**** normal is 1-4 ug/dl
resting cortisol of <1 is highly sensitive and specific for hypoA
resting cortisol >2 rules out hypoA |
|
|
Term
| If you suspect hypoA and wish to initiate treatment in a sick patient prior to diagnostic testing which drug will NOT cross react with plasma cortisol assays? |
|
Definition
dexamethazone
*** do NOT use pred |
|
|
Term
| How can you distinguish primary hypoA (destruction of zona granulosa and fasiculata of the adrenal cortex) for secondary hypoA (inadequate pitutitary or hypothalamic release of ACTH, CRF respectively) on endogenous plasma ACTH assay? |
|
Definition
ACTH will be markedly elevated in primary hpyoA (no negative feedback from adrenal cortex)
ACTH will be low or non-detectable in secondary hypoA (ACTH is not released from the pituitary) |
|
|
Term
| What are the five treatment goals to be followed when managing a patient in an acute addisonian crisis? |
|
Definition
correct hypovolemia and hypotension (isotonic fluid therapy)
improve vascular integrity
provide exogenous glucocorticoids
reverse electrolyte imbalances
manage acidosis and hypoglycemia |
|
|
Term
| Is it possible to distinuish primary from secondary hypoA using the ACTH stimulation test? |
|
Definition
| NO both primary (destruction of adrenal cortex) and secondary (inadequate central secretion of ACTH or CRF) will have minimal to no increase on plasma cortisol levels following administration of exogenous ACTH **** need to measure endogenous ACTH to differentiate primary (high) from secondary (low) |
|
|
Term
| What fluid should be chosen for volume resecitation of patients in acute addisonian crisis? |
|
Definition
0.9% NaCl, these patients are HYPERKALEMIC and need copious isotonic fluid therapy to restore circulating volume and correct dehydration
** can also add dextrose (intracellular translocation of potassium) to help manage hyperkalemia, in severe cases can also give insulin |
|
|
Term
| What is considered a physiologic dose of prednisone? |
|
Definition
0.2mg/kg/day
**** tx for life in patients with hypoA |
|
|
Term
| T/F judicious fluid therapy for patients in acute addisonian crisis is generally sufficient to resolve acidosis |
|
Definition
|
|
Term
| What drug is used to replace mineralocorticoids in patients with primary hypoA? |
|
Definition
DOCP (aka percortin-V) SQ injections q 25 days
***for large dogs Fludrocortisone acetate (florinef) is a glucocorticoid AND mineralocorticoid <-- may need to supplement occasionally with pred
MONITOR ELECTROLYTES |
|
|
Term
| Hyperthyroidism is characterized by excessive production and secretion of which two hormones? |
|
Definition
| thyroxine (T4) and triiodothyronine (T3 |
|
|
Term
| What is the most important predisposing risk factor for the development of hyperthryroidism in cats? |
|
Definition
AGE
95% of cases occur in patients >8yrs old
*** indoor cats are also predisposed (anecdotal) |
|
|
Term
| What is the most common etiology of hyperthryroidism in older cats? |
|
Definition
functional thyroid adenoma or hyperplasia
*** 3-5% due to functional thyroid carcinoma |
|
|
Term
| What two clinical signs are most commonly reported in hyperthyroid cats? |
|
Definition
polyphagia with weight loss
hyperactivity
***also patchy alopecia, PU/PD, and regurgitation/vomiting |
|
|
Term
| What three PE findings are most commonly identified in hyperthyroid patients? |
|
Definition
palpable thyroid
low BCS
hyperactivity
***also tachycardia, alopecia, small kidneys (concurrent CKD), and heart murmur/arrythmias |
|
|
Term
| T/F you can R/O hyperthyroidism in a cat with palpable thyroid nodules but a normal T4 |
|
Definition
FALSE
***continue monitoring thryoid values, palpable abnormalities can develop prior to detectable hormone derangement |
|
|
Term
| What is the minimum database needed to work up a case of suspected hyperthyroidism? |
|
Definition
CBC (stress leukogram +/- mild polycythemia)
Chem (elevated ALT/ALP, +/- elevated BUN/Cr/phosphorus if underlying CKD)
UA (R/O other causes of PU/PD ex. CKD, DM, pyelonephritis)
T4 (elevated)
+/- thoracic rads and EKG if cardiac abnormalities are noted on PE
*** unlike HYPOthyroidism, elevated T4 is adequate to diagnose hyperthyroidism in cats |
|
|
Term
| Why can occult CKD become symptomatic in older cats starting treatment for hyperthyroidism? |
|
Definition
| hyperthyroid cats have increased GFR (secondary to increased renal blood flow) which ameliorates chemistry abnormalities usually present with CKD. Before initiating treatment for hyperthyroidism assess renal function with urine SG. |
|
|
Term
| What test is used to diagnose hyperthyroidism? |
|
Definition
Basal T4 concentration
**** 2-10% of hyperthyroid cats will have baseline T4 within normal ranges <-- if hyperthyroidism is highly suspected repeat T4 in a couple of weeks, r/o concurrent illness (euthyroid sick syndrome) |
|
|
Term
| T/F T4 is the active form of thyroid hormone |
|
Definition
FALSE
T4 his protein bound and represents 99% of the thyroid hormone in circulation. "Free" T4 is less than 1% of total thyroid hormone but is the active form than enters cells to modify metabolism |
|
|
Term
| Why is it important to not overinterpret elevated "Free" T4 values in cats? |
|
Definition
| 5% of cats with normal thyroid function but serious non-thyroid illness have elevated "Free" T4 |
|
|
Term
| When might you consider doing a radionuclide scan in a hyperthyroid patient? |
|
Definition
to plan for surgical excision
*** used to identify unilateral vs. bilateral (probs. thyroid carcinoma) vs. ectopic thyroid tissue (mediastinal) |
|
|
Term
| What are the three major treatment options for feline hyperthyroidism? |
|
Definition
surgical excision (curative)
oral antithyroid drugs (lifetime tx)
radioactive iodine (curative) |
|
|
Term
| What is the most common drug used to treat hyperthyroid cats medically? |
|
Definition
methimazole --> blocks thyroid hormone synthesis
*** remember, this drug is NOT cytotoxic, patients treated with methimazole will become hyperythroid again if drugs are discontinued |
|
|
Term
| What are some advantages of using methimazole to treat hyperthyroidism (vs. radioactive iodine or surgery)? |
|
Definition
| inexpensive; no special facilities or hospitalization required - owners administer at home; no risk of permanent HYPOthyroidism; relatively safe and adverse effects reverse upon cessation of drug administration |
|
|
Term
| Once starting medical therapy for hyperthyroidism (methimazole PO) what parameters should you monitor and how frequently? |
|
Definition
CBC(blood dyscrasias- esp. thrombocytopenia have been reported in 15% of cats)/Chem (assess renal function) every 2-4 weeks for the first 8-12 weeks of treatment
*** don't bother rechecking T4 until patient has been on methimazole >2wks |
|
|
Term
| When can clients expect to start seeing a clinical response to oral methimazole in their hyperthyroid cat? |
|
Definition
| 2-6 weeks after T4 normalizes <-- remember, T4 normalizes 1-2 weeks after initiating treatment, so no clinical response should be expected until 3-8 weeks of therapy have elapsed |
|
|
Term
| Because methimazole is a lifelong therapy for hyperthyroid cats, following calibration of the initial dose, how frequently should you monitor the patient? |
|
Definition
after the initial 3 month period monitor (CBC/CHEM/T4/PE) every 3-6 months for LIFE
*** development of side effects (blood dyscrasia, GI, facial pruritis, reversible hepatopathy) following the initial 3 month period is rare but not unheard of |
|
|
Term
| What is the best initial treatment option for a cat with concurrent hyperthyroidism and CKD? |
|
Definition
| methimazole trial, if renal values remain stable over a 6 week trial period it is reasonable to consider continuing methimazole, or surgery/radioactive iodine therapy as alternatives |
|
|
Term
| T/F even if you intent to treat a hyperthyroid cat with surgery, the patient should be normalized by treating with methimazole for 6-12 weeks preoperatively |
|
Definition
TRUE
*** failure to pre-treat patients is associated with increased post-surgical complications (CHF, decompensated CRF, cachexia etc.) |
|
|
Term
| When are beta blockers (propranolo/atenolol) indicated in the treatment of a hyperthyroid cat? |
|
Definition
used to address marked tachycardia or supraventricular arrythmias
*** contraindicated in CHF patients b/c they increase stroke volume and cardiac output --> volume overload and pulmonary edema |
|
|
Term
| What are some complications associated with surgical treatment of hyperthyroidism? |
|
Definition
hypoparathyroidism
laryngeal paralysis
horner's syndrome
inadequate excision of thyroid tissue with recurrent or persistent hyperthyroidism
hypothyroidism |
|
|
Term
| How often should you check T4 levels in patients that receive surgical treatment for hyperthyroidism? |
|
Definition
recheck 1-2x yearly
*** recurrent or persistent hyperthyroidism following surgery is possible in the event that not all of the diseased tissue was removed, or development of disease in tissue that was normal at the time of the procedure |
|
|
Term
| What are some benefits associated with radioactive iodine therapy in the treatment of hyperthyroidism? |
|
Definition
only functioning thyroid tissue takes up the radioactive iodine so that atrophied normal thyroid tissue is not irradiated
minimal risks to the cat with high curative success rate |
|
|
Term
| What are some disadvantages associated with radioactive iodine therapy in the treatment of hyperthyroidism? |
|
Definition
cost and availability
radiation exposure requires 10-14 days of isolation |
|
|
Term
| What are the two primary endocrinopathies that produce alterations in serum calcium metabolism |
|
Definition
hyper and hypoparathyroidism
*** the paraythyroid glands normally act to maintain serum calcium within a narrow physiologic range by secreting PTH |
|
|
Term
| What is the function of parathyroid hormone? |
|
Definition
| effects bone, kidney, and GI to increase serum ionized calcium concentration |
|
|
Term
| What form of calcium is metabolically active? |
|
Definition
ionized
*** the majority of calcium is protein bound (with albumin) or complexed (with anions) |
|
|
Term
| What chemistry abnormalities are associated with hypocalcemia? |
|
Definition
hypoalbuminemia (b/c majority of serum calcium is protein bound)
alkelemia (less anions (H+), a large component of serum calcium exists complexed with anions) |
|
|
Term
| What six biologic functions/organ systems require calcium? |
|
Definition
skeletal integrity
muscle contraction (striated and cardiac)
blood vessles
nerve conduction
blood clotting cascade
enzyme function |
|
|
Term
| What effect does Parathyroid hormone (PTH) have on the kidneys? |
|
Definition
| promotes renal excretion of phosphorus and retention of calcium |
|
|
Term
| What affect does PTH have on the bone? |
|
Definition
| stimulates osteoclasts to remodel bone and increase serum calcium and phosphorus |
|
|
Term
| What is the trigger for the feedback loop causing the parathyroid glands to release PTH? |
|
Definition
low serum ionized calcium
*** remember PTH acts at the kidney, GI, and bone, all to increase serum calcium levels (also promotes renal excretion of phosphorus) |
|
|
Term
| What gland is responsible for producing calcitonin and what function does calcitonin have in the body? |
|
Definition
The thyroid gland produces calcitonin which counteracts PTH to prevent hypercalcemia
*** specifically calcitonin
inhibits Ca2+ absorption by the intestines, inhibits osteoclast activity in bones, inhibits renal tubular cell resorption of Ca2+ allowing it to be excreted in the urine |
|
|
Term
| Which hormone, other than PTH, acts to increase serum calcium levels? |
|
Definition
Calcitriol (1,25-dihydroxycholeciferol aka active vitamin D3)
*** synergystic with PTH in increasing GI absorption of calcium, also increases osteoclast activity and renal resorption of calcium |
|
|
Term
| How would you characterize the relationship between serum ionized calcium levels and serum levels of PTH? |
|
Definition
inverse
as serum ionized calcium drops PTH levels rise, and vice versa |
|
|
Term
| What two organs are involved in the bioactivation of calcitriol (1,25-dihydroxycholecalcierol, Vit D3)? |
|
Definition
liver and kidney
*** both hydroxylation reactions |
|
|
Term
| What are four common causes of hypercalcemia (not including primary hyperparathyroidism)? |
|
Definition
lymphoma
CKD (uremic anions bind to calcium increasing amount of complexed calcium and therefore total serum calcium)
hypoadrenocoricism
artifact (lipemia, hyperalbuminemia)/lab error |
|
|
Term
| What should always be done when significant hypercalcemia is noted in the absence of lipemia, hemolysis, and/or dehydration (which can artifactualy elevate serum calcium) on a chemistry panel? |
|
Definition
| repeat the test to R/O lab error (one of the most common "causes" of hypercalcemia) |
|
|
Term
| What is the MOST common cause of hypercalcemia in small animals? |
|
Definition
hypercalcemia of malignancy -> increased local osteolytic activity and humoral factors (ex. PTHrP -parathyroid related protein) that promote hypercalcemia
***** generally secondary to lymphoma, but less frequently associated with anal sac adenocarcinoma, multiple myeloma, other carcinomas (including mammary, squamous cell, and thyroid) |
|
|
Term
| What is the most common signalment and clinical presentation associated with primary hyperparathyroidism? |
|
Definition
aged (mean=11yrs) large breed dogs, rarely cats
Present with GI (anorexia, vomiting, constipation, rare pancreatitis); renal (PU, PD, signs of LUTD-dysuria, hematuria, pollakiuria, and urolithiasis (calcium oxylate, calcium phosphate), also depressed mentation |
|
|
Term
| How does hypercalcemia affect the body? |
|
Definition
| nephrotoxic, impairs renal concentrating ability (interferes with ADH) and can progress to ARF if severe or prolonged |
|
|
Term
| What serum chemistry abnormalities are associated with primary hyperparathyroidism or hypercalcemia of malignancy? |
|
Definition
| elevated serum total calcium with normal to low serum phosphorus (remember PTH increases renal reabsorption of calcium and EXCRETION of phosphorus) |
|
|
Term
| Hypercalcemia with concurrent hyperphosphatemia is most consistent with what disorder in calcium metabolism |
|
Definition
hypervitaminosis D (ex. cholecalciferol rodenticide, calciptrene lotions)
*** Vit D3 increases GI absorption of Calcium and phosphorous, as well as bone resorption with release of additional calcium and phosphorus into the blood stream |
|
|
Term
| In a patient presenting with hypercalcemia AND azotemia, how can you differentiate primary hyperparathyroidism (persistent hypercalcemia is nephrotoxic) from hypercalcemia secondary to primary renal disease? |
|
Definition
run an ionized calcium test
Patients with primary hyperparathyroidism have increased total serum calcium and increased ionized calcium, while patients with primary renal disease rarely have increased ionized calcium (<10% of cases) |
|
|
Term
| Why do most dogs with primary hyperparathyroidism have dilute urine despite normal renal function? |
|
Definition
| hypercalcemia interferes with ADH function (also does cause renal tubular damage and eventually direct injury to the kidney <-- will be azotemic at this point) |
|
|
Term
| Can you use serum PTH levels to distinguish between hypercalcemia secondary to hyperparathyroidism or CKD? |
|
Definition
NO
**** PTH levels will be elevated in both circumstances, low PTH with concurrent hypercalcemia is more commonly associated with hypercalcemia of malinancy
Remember: In normal animals PTH levels should drop as serum calcium increases |
|
|
Term
| If minimum database doesn't allow for a diagnosis of hypercalcemia what three tests should be considered next in the course of the work up? |
|
Definition
ionized calcium (differentiate hyperparathyroidism or hypercalcemia of malignancy (high) from renal disease(low to normal)
serum PTH and PTHrP (differentiate hyperparathyroidism from hypercalcemia of malignancy) |
|
|
Term
| When would a therapeutic drug trial (pred) not be appropriate for the treatment of hypercalcemia? |
|
Definition
if suspecting CKD (low ionized calcium) or hypercalcemia of malignancy (low PTH, high PTHrP)
*** may make the patient more azotemic or hide the tumor further complicating diagnosis |
|
|
Term
| What medical strategies can be employed to manage severe or symptomatic (cardiac arrythmias, neurologic signs, azotemia) hypercalcemia? |
|
Definition
saline diuresis + loop diuretics (furosemide), calcium follows sodium
*** also mild alkalinization and bisphosphonate ($$$$$) are options |
|
|
Term
| What is the treatment of choice for primary hyperparathyroidism? |
|
Definition
surgical excision
*** usually a single well circumscribed mass is present but explore both thyroid glands for enlarged or abnormal parathyroid tissue |
|
|
Term
| How should patients be monitored post-op when surgically managing primary hyperparathyroidism? |
|
Definition
| monitor for hypocalcemia (can develop if hypercalcemia (esp >14g/dl) causes atrophy of non-affected parathyroid glands over the course of the disease) for 5 days post-op and if present supplement with vitamin D and calcium gluconate |
|
|
Term
| Do patients with post-op hypocalcemia secondary to surgical treatment of hyperparathyroidism require life-long calcium and vitamin D supplementation? |
|
Definition
NO
supplement calcium to levels slightly below normal to stimulate atrophied parathyroid tissue. Recheck calcium values periodically and taper dose until normal stable serum calcium concentrations have been achieved |
|
|
Term
| What is the prognosis for primary hyperparathyroidism? |
|
Definition
GOOD if no concurrent severe renal disease is present at diagnosis
**** surgical excision is generally curative |
|
|
Term
| What is the most common etioloy of hypercalcemia in cats? |
|
Definition
idiopathic, often in cats receiving an acidifying diet
*** primary hyperparathyroidism is very rare in cats |
|
|
Term
| What are the six most important R/O for hypocalcemia? |
|
Definition
parathyroid disorders (primary hypoparathyroidism is rare, females predisposed)
CDK
hypoalbuminemia
acute pancreatitis (secondary to hypoalbuminmia and fat saponification)
impaired GI absorption
eclampsia (post-parturient, lactating dogs) |
|
|
Term
| what clinical sings are associated with primary hypoparathyroidism? |
|
Definition
| Nervousness, generalized seizures, rear leg cramping or pain, focal muscle fasciculations, ataxia, facial rubbing (intense), aggression |
|
|
Term
| What laboratory findings are consistent with a diagnosis of primary hypoparathyroidism? |
|
Definition
| hypocalcemia, hyperphosphatemia, very low PTH |
|
|
Term
| How long must patients receive calcium and vitamin D supplementation for the treatment of hypoparathyroidism? |
|
Definition
require lifelong treatment with vit D and initial calcium supplementation (once serum calcium levels have stabilized can be phased out)
** recheck weekly for first 6 months, and then q 2-3 months for the lifetime of these patients; need to have calcium levels monitored as iatrogenic hypercalcemia can induce irreversible renal disease |
|
|
Term
| T/F canine diabetes mellitus is associated with an absolute or relative insulin deficiency and almost ALWAYS requires insulin treatment |
|
Definition
|
|
Term
| What five endogenous hormones antagonize the effects of insulin? |
|
Definition
Cortisol
Epinephrine
Glucagon
Growth hormone
Progesterone |
|
|
Term
| What is the pathophysiology of type 1 DM (most common in dogs)? |
|
Definition
immune destruction and lymphocytic infiltration of beta pancreatic islet cells --> insulin deficiency
*** may be incited by genetic, toxic, infectious or other inflammatory damage to beta islet cells |
|
|
Term
| What two medications can induce DM in dogs? |
|
Definition
| glucocorticoids and megesterol acetate |
|
|
Term
| What two disease processes can result in the development of DM in dogs? |
|
Definition
chronic pancreatitis
pancreatic neoplasia |
|
|
Term
| What signalment, history, and PE findings are most consistent with DM in dogs? |
|
Definition
| middle aged, female dogs, PU/PD, polyphagia, cataracts, weight loss and hepatomegally |
|
|
Term
| Why do diabetic cats rarely develop cataracts? |
|
Definition
| older cats (DM is rare in young cats) have low aldose reductase activity in their lens -> less sorbitol is produced. Sorbitol is one of the molecules implicated in the development of diabetic cataracts (draws water into the lens resulting in disruption of the lens fibers and opacity ie. cataracts) |
|
|
Term
| What two laboratory findings are sufficient for diagnosing DM in a dog? |
|
Definition
elevated fasting glucose (>200mg/dl)
glucosuria +/- ketonuria
*** ALT and ALP are almost always elevated |
|
|
Term
| What physiologic states can result in falsely elevated or falsely depressed serum fructosamine values in diabetic patients? |
|
Definition
hyperprotinemia --> false elevation
hypoprotinemia --> false depression
*** remember this assay quantifies protein glycosylation secondary to sustained hyperglycemia |
|
|
Term
| What are the two types of intermediate acting insulin? |
|
Definition
|
|
Term
| What are the three types of long acting insulin? |
|
Definition
Insulin glargine
ProZinc (PZI)
Insulin detemir |
|
|
Term
| what type of insulin is indicated for the treatment of DKA in dogs? |
|
Definition
regular insulin <-- rapid acting, short duration
****yup, that's what it's really called |
|
|
Term
| What category of insulin is the treatment of choice for dogs with DM? |
|
Definition
Intermediate acting: Humulin N, Novolin
*** administer SQ only, BID |
|
|
Term
| What is the only type of insulin that is dosed with U-40 syringes? |
|
Definition
|
|
Term
| What glucose monitoring plan is indicated for a patient that is just starting insulin therapy? |
|
Definition
measure BG 2-3x q 3 hours following initial dose (0.25-0.5 units/kg), if BG is <150mg/dl reduce the dose of insulin by 25%
BG curve 5-7 days post initiation of insulin therapy |
|
|
Term
| T/F urine glucose is a non-invasive way to assess patient response to therapy and adjust insulin dosage |
|
Definition
FALSE
need to assess blood glucose! |
|
|
Term
| How should you use BG curve to adjust insulin dosage? |
|
Definition
| adjust based off lowest BG value NOT duration of action |
|
|
Term
| What three criteria can be assess to determine if a diabetic patient is well regulated? |
|
Definition
| clinical signs have resolved, weight is stable, BG between 90 and 270 mg/dL |
|
|
Term
| What are some ideal diet characteristics for maintenance of a diabetic dog? |
|
Definition
high fiber low in simple sugar
*** in general most commercial maintenance diets are sufficient |
|
|
Term
| What category of insulin is suitable for use in a diabetic cat? |
|
Definition
long acting: glargine and ProZinc
glargine is associated with highest rate of diabetic remission and lowest risk of hypoglycemia
*** initial dose is 0.25units/kg/ BID |
|
|
Term
| T/F if you do not see a decrease in BG while monitoring for the first week following initiation of insulin treatment in a cat, you should increase the dose by 25% |
|
Definition
| FALSE *** rarely see change in BG for the first week of therapy |
|
|
Term
| What two values can be determined from a BG curve? |
|
Definition
nadir (lowest BG value)
average BG over 10-12hrs |
|
|
Term
| What is the main element in dietary management of feline diabetes? |
|
Definition
low carbohydrate diet
*** and portion control for overweight cats |
|
|
Term
| What are some medical options for diabetic cats that are extremely sensitive to even the smallest insulin doses, or for patients with owners that are unwilling to administer insulin injections? |
|
Definition
| oral hypoglycemic agents like darglitazone |
|
|
Term
| What is the pathologic mechanism of diabetes mellitus in cats? |
|
Definition
hyperinsulinemia coupled with insulin resistance (ie. lower tissue sensitivity to insulin)
*** some degree of decreased insulin secretory capacity may also play a role in some patients (vs. almost all k9 DM patients are insulin deficient) |
|
|
Term
| What are five ways that feline DM is similar to human type 2 diabetes? |
|
Definition
onset in middle age
associated with obesity and inactivity
low but measurable levels of insulin
presence of islet amyloidosis
relatively resistant to ketosis |
|
|
Term
| What is the physiologic role of islet amyloid polypetide? |
|
Definition
soluble molecule: co secreted by beta islet cells with insulin, acts to regulate glucose homeostasis
insoluble form: isomer forms secondary to chronic hyperglycemia --> precipitates into amyloid fibrils which are cytotoxic --> impairs insulin secretion |
|
|
Term
| What are six consequences of prolonged hyperglycemia in cats? |
|
Definition
PU/PD (osmotic diuresis)
neuropathy (plantigrade stance, hindlimbs most commonly affected)
pulmonary changes (congestion, edema, mineralization, fibrosis etc.)
increased deposition of amyloid in beta islet cells (reduced insulin secretion)
acromegally (facial deformities secondary to
hypersecretion of growth hormone by a functional pituitary tumor <-- complicates regulation)
worsens heart disease (serum hyperosmolarity -> volume overload and cardiac pump failure) |
|
|
Term
| What diagnostic tests are recommended when working up a cat for diabetes mellitus? |
|
Definition
confirm no exposure to drugs that antagonize insulin (glucocorticoids and progestagens)
CBC (r/o or characterize inflammatory diseases)
Chem (assess organ function)
UA (monitor for glucosuria,ketonuria, assess renal function, and culture (r/o UTI))
T4 (r/o hyperthyroidism) |
|
|
Term
| What are the three diabetic emergencies? |
|
Definition
ketoacidosis
hyperglycemic hyperosmolar syndrome
insulin induced hypoglycemia (iatrogenic) |
|
|
Term
| What laboratory findings are consistent with diabetic ketoacidosis? |
|
Definition
hyperglycemia, glucosuria, ketonuria, metabolic acidosis
+/- ketonemia |
|
|
Term
| What laboratory findings are consistent with hyperglycemic hyperosmolar syndrome? |
|
Definition
profound hyperglycemia, hyperosmolarity (>320 mOsm/kg)
NO ketonuria/emia or metabolic acidosis |
|
|
Term
| What is the pathophysiology of DKA? |
|
Definition
| *** characterized by increased glucagon:insulin ratio diabetes mellitus AND concurrent disease results in increased the secretion of glucagon and cortisol --> antagonizes insulin (in addition to inhibited insulin secretion (beta cell amyloidosis) and insulin resistance) --> perceived hypoglycemia by tissues results in hyperglycemia, ketone production and accumulation, and lactic acidosis; concurrent osmotic diuresis and medullary wash out result in massive urinary losses of water and electrolytes --> profound dehydration, hypovolemia and metabolic acidosis + CRTZ stimulation with vomiting and further fluid and electrolyte losses |
|
|
Term
| How does glucagon contribute to the development of DKA? |
|
Definition
| glucagon is secreted by islet alpha cells in response to hypoglycemia and induces production of large amounts of glucose and FFAs by the liver. Diabetic cats are hyperglycemic but insulin resistance results in percieved hypoglycemia by the tissues. Large amounts of glucagon are secreted resulting in massive accumulation of ketones and lactic acid --> metabolic acidosis |
|
|
Term
| If your previously regulated feline diabetic patient develops DKA what concurrent diseases should you R/O? |
|
Definition
bacterial and viral infections (esp. UTI, stomatitis, and dental disease)
inflammatory diseases (ex. pancreatitis, IBD)
CKD
neoplasia |
|
|
Term
| What are the five basic goals in treatment of DKA? |
|
Definition
fluid therapy (volume resuscitation and dilution of hyperglycemia)
slow administration of "regular" insulin (ie. rapid onset, admin at low dose continuous IM/IV) to gradually reverse hyperglycemia and ketoacidosis
monitor potassium, phosphorus and magnesium
reverse metabolic acidosis
identify and treat underlying diseases |
|
|
Term
| Why is low dose insulin therapy preferable to high dose therapy in the treatment of DKA? |
|
Definition
| low dose is as effective at reducing hyperglycemia and more effective at minimizing ketone formation than high dose therapy. Additionally there is a decreased risk of developing complications (hypoglycemia, cerebral edema, hypokalemia/phosphatemia, hemolytic anemia) |
|
|
Term
| When can you switch from regular rapid onset insulin to long acting insulin (glargine) as maintenance for recovering DKA patients? |
|
Definition
| once BG is stable (monitor BG every hour) and patient is alert and eating can convert to long acting insulin (glargine) |
|
|
Term
| What is the mechanism and clinical consequence of hypokalemia in DKA patients? |
|
Definition
potassium is lost in vomit, diarrhea, and urine, serum potasium is further depleted by intracellular translocation secondary to insulin therapy and correction of metabolic acidosis, which is further augmented by the dilutional effect of fluid therapy
can result in profound muscle weakness |
|
|
Term
| What is the maximum amount of potassium that can safely be supplemented in the fluids? |
|
Definition
0.5meq/kg/hr
feeding can additionally supplement potassium and magnesium
*** monitor daily (minimum) with EKG for bradyarhythmias |
|
|
Term
| T/F supplemental HCO3 is generally not necessary to ameliorate ketoacidosis in DKA patients? |
|
Definition
TRUE
ketone production ceases once insulin is administered allowing the body to metabolize and excrete accumulated ketones and normalize serum pH
***additionally HCO3 administration has been associated with serious paradoxical cerebral acidosis |
|
|
Term
| What are three adverse reactions associated with treatment of DKA? |
|
Definition
cerebral edema (overhydration via fluid therapy)
hypophosphatemic hemolytic anemia (insulin induces intracellular translocation of phosphorus in patients with depleted tissue phosphorus stores due to increased renal excretion)
paradoxical cerebral acidosis (HCO3 induced) |
|
|
Term
| What two clinical syndromes are associated with hypophosphatemia in cats? |
|
Definition
DKA (renal losses and intracellular translocation following insulin therapy)
starvation re-feeding in cats with lipidosis (rapid intracellular translocation of glucose, phosphorus follows) |
|
|
Term
| What are some complications associated with phosphorus supplementation? |
|
Definition
Hyperphosphatemia --> soft tissue mineralization and hypocalcemia (precipitates out of serum)
Hypotension
Renal failure |
|
|
Term
| What organ is always affected secondarily to DM in both dogs and cats? |
|
Definition
the liver (all patients with DM have some degree of triglyceride deposition in the liver) --> elevated ALP/ALT
*** partially reversible upon treatment of DM |
|
|
Term
| What is the most common reason that a diabetic patient would need to be anesthetized? |
|
Definition
removal of diabetic cataracts
*** minimize stress at induction and recovery, schedule as first surgery and check BG prior to induction (because animals need to be NPO and BG may be high (give some insulin) or low (give some dextrose)) |
|
|
Term
| How frequently should you monitor BG in diabetic patients under anesthesia? |
|
Definition
every 30-45 minutes under general anesthesia and post op until animal is eating normally
*** adjust dextrose or insulin depending on trends in BG |
|
|
Term
| Although DKA patients rarely need to be anesthetized what are some important treatments to stabilize these patients in the event that they need general anesthesia? |
|
Definition
Fluid therapy (correct dehydration, hypovolemia and hypotension)
correct electrolyte imbalances (hyperkalemia (secondary to acidosis) or hypokalemia (secondary to hyperglycemia and hyperinsulinemia)) |
|
|
Term
| What is the most important consideration when managing anesthesia for a patient with diabetes insipidus? |
|
Definition
always give patient access to water and provide generous IV fluids (D5W) <-- otherwise patients get extremely dehydrated and hypovolemic/hypotensive
monitor sodium, if hypernatremic (~160meq/L) adjust SLOWLY prior to induction, otherwise hypertonic encephalopathy |
|
|
Term
| What four complications are patients with hyperadrenocorticism at risk for when undergoing general anesthesia? |
|
Definition
impaired ventilation (muscle weakness, organomegally, pulmonary and bronchial mineralization) <-- may need intermittent positive pressure ventilation
prone to thromboembolism, esp. pulmonary thromboembolism (elevated PCV and blood viscosity, hypercoagulable <- increased clotting factors and decreased antithrombin, increased susceptibility to endothelial damage and blood flow stasis in recumbent animals during the surgical procedure)
hypertension (increased responsiveness to pressors <- endogenous or exogenous, and elevated renin-angiotensin)
fragile veins and skin <-- bruising with venipuncture and challenging IV catheterization |
|
|
Term
| Which drug, used to treat hyperadrenocorticism, interacts with full mu-agonists to cause serotonin syndrome in humans (and possibly dogs)? |
|
Definition
Selegiline
*** massive release of serotonin --> vasodilation and CV arrest |
|
|
Term
| What three treatments are indicated for patients with hypoadrenocorticism that need to be anesthetized? |
|
Definition
fluid therapy for volume resuscitation
correct hyperkalemia
supplement with glucocorticoids (if untreated or have missed a dose) |
|
|
Term
| T/F polyuria and polydipsia usually occur concurrently |
|
Definition
|
|
Term
| What are three options for confirming PU/PD? |
|
Definition
measure water intake
measure urine excretion
measure urine SG on one or more morning urine samples (caveat:glucosuria can falsely elevate SG) |
|
|
Term
| What is the upper limit of urine production in a day in dogs? in cats? |
|
Definition
k9: 45ml/kg/day
feline: 40ml/kg/day |
|
|
Term
| What is the upper limit of water intake per day in dogs? In cats? |
|
Definition
k9: 90ml/kg/day
feline: 45ml/kg/day |
|
|
Term
| Where are volume receptors involved in water homeostasis located? |
|
Definition
aortic arch
cardiac atria
glomerular afferent arterioles
*** primarily moderate sodium excretion (water follows sodium) |
|
|
Term
| Where does ADH act, and how does it affect water homeostasis? |
|
Definition
| ADH acts at the collecting ducts and distal tubules to increase permeability to water (by inserting aquaporin channels) --> water moves out of the collecting duct and into the hypertonic medulary interstitum resulting in concentration of urine |
|
|
Term
| What two mechanisms are responsible for the development of primary polyuria? |
|
Definition
inadequate quantity of functional ADH is release from posterior pituitary (dramatic response to exogenous ADH administration)
Kidneys fail to respond appropriately to ADH (primary nephrogenic diabetes insipidus is congenital and very rare) |
|
|
Term
| What two mechanisms are responsible for the development of primary polydipsia? |
|
Definition
Stimulation to the central thirst center
behavioral |
|
|
Term
| What are four etiologies associated with central diabetes insipidus in small animals? |
|
Definition
pituitary neoplasia
trauma or inflammation of the brain (esp. cats)
post-op hypophsectomy (tx. for hyperadrenocorticism)
idiopathic (no lesions on necropsy) |
|
|
Term
| What historical features and clinical signs are associated with central diabetes insipidus? |
|
Definition
insatiable PU/PD
nocturia and incontinence
+/- behavioral changes if pituitary neoplasia is the inciting cause |
|
|
Term
| What two tests can employed to diagnose central diabetes insipidus? |
|
Definition
ADH response test (PU/PD is minimized, urine is concentrated)
water deprivation test (no effect on PU/PD, urine remains dilute (<1.030), monitor SG and body weight hourly until animal has lost 5% of BW) |
|
|
Term
| What is the therapy for central DI? |
|
Definition
exogenous administration of synthetic ADH (aka. DDAVP)
DDAVP is extremely expensive, owners may elect not to treat, animals must be managed with free access to unlimited water and location for frequent urination |
|
|
Term
| What are six causes of PU/PD that are associated with osmotic diuresis (SG >1.013)? |
|
Definition
DM
CKD
post-obstructive diuresis
diuretic drugs
ingestion of large amount of solutes
primary renal glucosuria (uncommon heritable disorder in certain dog breeds) |
|
|
Term
| What are three causes of PU/PD secondary to water diuresis (SG <1.006)? |
|
Definition
central diabetes insipidus
congenital nephrogenic diabetes insipidus
behavioral (ie. primary polydipsia) |
|
|
Term
| How can you distinguish primary polyuria from primary polydipsia based off serum sodium levels? |
|
Definition
primary polyuria is associated with normal to high levels of serum sodium
primary polydipsia is associated with normal to low levels of serum sodium |
|
|
Term
| What are the top four differentials for young patients that have been PU/PD since birth? |
|
Definition
congenital nephrogenic or cental diabetes insipidus
portovascular anomalies
congenital renal disease |
|
|
Term
| What are the top six differentials for a patient that develops PU/PD in middle age or older? |
|
Definition
hyperadrenocorticism
diabetes mellitus
CKD
hyperthyroidism
pyometra
pituitary or hypothalamic neoplasia |
|
|
Term
| What are the three most common causes of PU/PD in dogs? in cats? |
|
Definition
K9: DM, CKD, hyperadrenocorticism
feline: DM, CKD, hyperthyroidism |
|
|
Term
| When is iohexol clearance test indicated? |
|
Definition
R/O early CKD, impaired clearance is associated with deceased GFR
*** make sure patient is well hydrated |
|
|
Term
| What are two contraindications for a water deprivation test? |
|
Definition
|
|
Term
| How does the body maintain glucose levels between meals? |
|
Definition
| hepatic gluconeogenesis and glycogenolysis |
|
|
Term
| What is the most important hormone affecting recovery from acute hypoglycemia? |
|
Definition
glucagon --> increased hepatic gluconeogensis within minutes
*** glucagon, norepinephrin, and epinephrine respond early; cortisol and growth hormone respond to persistent hypoglycemia |
|
|
Term
| What clinical signs are associated with hypoglycemia? |
|
Definition
neurologic (glucose is the primary energy substrate for the brain --> depression, ataxia, blindness and coma)
muscle tremors, tachycardia, nervousness (secondary to release of norepinephrine and epinephrine in response to hypoglycemia) |
|
|
Term
| What are six rule outs for hypoglycemia secondary to increased utilization? |
|
Definition
insulinoma
sepsis
late pregnancy
large extra-pancreatic tumors (often hepatic)
exertional (usually hunting dogs)
severe polycythemia |
|
|
Term
| What are three rule outs for hypoglycemia secondary to decreased production or availability? |
|
Definition
hepatic failure
hypoadrenocorticism
puppy hypoglycemia (esp. small breeds, limited glucose stores and inadequate gluconeogenic capacity) |
|
|
Term
| What is the first thing you should rule out before investigating hypoglycemia? |
|
Definition
rule out lab error! Most common cause of hypoglycemia is a sample that has not been spun down to separate RBC from serum
****RBC continue to utilize glucose in the serum sample resulting in artifactual hypoglycemia) |
|
|
Term
| T/F fasting DOES NOT generally induce hypoglycemia in dogs |
|
Definition
TRUE
*** caveat: small breed puppies have limited glucose stores and inadequate hepatic gluconeogenesis and may develop hypoglycemia if not fed frequently |
|
|
Term
| What species has the highest incidence of insulinoma? In what species is this neoplasia extremely rare? |
|
Definition
very common in ferrets, very rare in cats
*** does occur in older large breed dogs |
|
|
Term
| What clinical signs are associated with insulinoma? |
|
Definition
| symptoms are intermittent and present as convulsions or collapse in most patients (often misdiagnosed as epilepsy) |
|
|
Term
| What laboratory findings are consistent with insulinoma? |
|
Definition
hypoglycemia, no other abnormalities on CBC/CHEM/UA
further Dx with serum insulin assay (75% are hyperinsulinemic) |
|
|
Term
| What imaging modality is most useful for identifying insulinoma and looking for mets (generally to the liver or regional LN)? |
|
Definition
| ultrasound, masses are usually small and survey rads are not sensitive enough to detect primary tumors or mets very well |
|
|
Term
| What is the therapy of choice for treatment of insulinoma? |
|
Definition
surgical excision
***manage pre-op with multiple small meals a day, high in protein and complex CHO +/- IV dextrose |
|
|
Term
| What are the two most common complications following surgical excision of insulinoma? |
|
Definition
paradoxical DM (usually transient, due to down regulation of normal islets secondary to prolonged hypoglycemia, rarely requires chronic insulin therapy)
persistent hypoglycemia (if not all of the tumor or mets can be excised) |
|
|
Term
| Other than frequent feedings, what medical therapy is available for the treatment of insulinoma if surgery is not an option or if hypoglycemia is persistent post op? |
|
Definition
prednisone --> promotes hepatic gluconeogenesis
+/- oral hyperglycemic agents (diazoxide), somatostatin analogs, and islet toxic drugs |
|
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