Endocrinology Test 1
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130 terms
Terms | Definitions |
|---|---|
 Diagnosis of Diabetes Mellitus | Persistent, fasting hyperglycemia WITH glucosuria |
| Significance of fructosamine | Increased levels give evidence for prolonged hyperglycemia. May assist diagnosis in dogs with mild hyperglycemia and subtle clinical signs |
| Most common type of canine diabetes | Type I or insulin-dependent Complete destruction or loss of Beta cells in the pancreas |
| Treatment of canine diabetes | High fiber diet fed with exogenous insulin SQ every 12 hours NEVER give oral hypoglycemic drugs |
| How often should adjustments be made to a dog's insulin therapy? | Should not exceed 10-25% or be made more often than every 7-10 days unless clinical hypoglycemia is noted. If duration of action is longer than 12 hours, then decrease the dose |
| How a blood glucose curve is performed | Owner gives meal and insulin prior to arrival First blood glucose taken within 1-2 hours Subsequent blood glucose values taken every 2 hours until values are less than 200 mg/dl, then hourly until an obvious upward trend is seen |
| Goal of insulin therapy | A nadir of 80-150 mg/dl ocurring 8 hours after insulin injection |
| Most common type of feline diabetes | Type 2 or Non insulin dependent Beta cells still present, but they have been exhausted; 30% of these cases can go into remission with appropriate treatment |
| Treatment of feline diabetes | Low carb, high protein diet; allow cat to graze throughout the day Insulin therapy every 12 hours; no single type of insulin is consistently effective so figure out which one works for each cat Oral hypoglycemic drugs can be used, but not recommended for long-term use |
| How often should adjustments be made to a cat's insulin therapy? | Should not exceed 1 U or be made more often than 2-4 weeks unless clinical hypoglycemia is noted. Insulin requirements may decrease as glucose toxicity, obesity and other contributing factors are treated. |
| Most commonly used types of insulin in feline diabetes | Glargine Detemir Protamine zinc NPH has shorter duration in the cat, so given q 8 hours |
| Somogyi effect | Too much insulin is given, causing hypoglycemia. Counter-regulatory hormones will stimulate glucose release from the liver, causing a serum glucose overswing that can last up to 72 hours. |
| Pathophysiology of diabetic ketoacidosis | When effects of insulin are absent, there is an increase of free fatty acids in circulation. FFA are metabolized into ketone bodies. Ketonemia results in metabolic acidosis, which leads to osmotic diuresis. Diuresis results in loss of ketones and electrolytes. |
| Signs of diabetic ketoacidosis | Total body depletion of sodium - low Na levels on chem panel Total body depletion of potassium - K levels on chem panel normal due to extracellular shift Severe acidemia Vomiting, diarrhea, and anorexia Central nervous system depression in severe cases |
| Therapy of "nonsick" DKA | Look for underlying disease process Blood glucose curve Begin/adjust maintenance dose of insulin Send home and recheck frequently |
| Therapy of "sick" DKA | 1. SLOW fluid restoration over 24 hours; fluid chosen based on Na levels. NEVER use lactate containing fluids. Watch for signs of cerebral edema 2. Insulin (IV or IM) with concurrent dextrose when blood glucose < 250 3. Correct electrolyte imbalances 4. Bicarbonate generally contraindicated |
| Why is bicarbonate contraindicated in treatment of DKA? | Insulin injection facilitates ketone metabolism. Ketone metabolism results in bicarbonate production, which increases blood pH, thereby correcting the metabolic acidosis. |
| Why do you not administer insulin SQ in an animal with DKA? | Severe dehydration compromises the animal's ability to quickly absorb the insulin. |
| Signs of Hyperglycemic Hyperosmolar Syndrome | Blood glucose levels are often elevated above 800 mg/dL Absence of ketoacids Extreme dehydration Renal dysfunction - prerenal/renal azotemia or both Decreased consciousness |
| 3 factors that lead to HHS | Decreased insulin utilization and glucose transport Increased hepatic gluconeogenesis and glycogenolysis Impaired renal excretion of glucose |
| Treatment of HHS | SLOW fluid restoration with isotonic fluids Correct electrolyte imbalances Insulin therapy May need to transfuse blood in small animals in order to correct for constant chem panel tests |
| Clinical signs of hypoglycemia | Blood glucose less than 60 mg/dL Cerebral cortex is the first area to be affected Lethargy, weakness, collapse, ataxia, seizures and coma Muscle tremors, nervousness, restlessness, hunger |
| Insulinoma | Malignant functional beta cell tumors that secrete insulin despite hypoglycemia Signs typically episodic and can be triggered by fasting, exercise, excitement and eating Diagnosed by paired serum insulin and glucose levels |
| Medical management of insulinoma | Frequent feedings high in fat, complex carbs and fiber; limit exercise Prednisone when feedings not effective; gradually increase dose Diazoxide when pred alone not effective Streptozocin directly toxic to beta cells |
| Hypoglycemia associated with hepatic dysfunction | Most commonly associated with portosystemic shunts Toy breeds <3 years old and thin/cachetic Chem panel reveals hypoalbuminemia, hypocholesterolemia, decreased BUN, and elevated liver enzymes |
| Hypoglycemia associated with hepatic disease | Severe destruction of liver by neoplasia, infection, inflammation, or other hepatotoxins 75% of liver function must be lost before signs seen Lab work consistent with severe liver dysfunction |
| Hypoglycemia associated with hypoadrenocorticism | Insufficient secretion of glucocorticoids which are needed to stimulate hepatic mobilization and production of glucose CBC may have eosinophilia, lymphocytosis, and mild nonregenerative anemia Chem panel may reveal prerenal azotemia, hyperkalemia, hyponatremia and hypercalcemia |
| Neonatal and juvenile hypoglycemia | Young animals have limited hepatic glycogen stores, small muscle mass, lack of adipose tissue, and decreased use of FFA as alternative energy sources Manage with frequent small feedings, possibly test for any underlying disorders Disorder should disappear with attainment of adult size |
| Hypoglycemia associated with septic/endotoxic shock | Can be seen with septicemia, a variety of severe bacterial infections, or parvovirus infection Consider if CBC shows severe leukocytosis, leukopenia, left shift, or toxic changes |
| Hunting dog hypoglycemia | Active, lean hunting dogs after extreme exercise; cause not understood Manage with feeding prior to and during hunting; also with proper preseason conditioning (or don't hunt the dog) |
| Medical management of hypoglycemia | Karo syrup applied to the gums (home) 50% Dextrose solution diluted 1:4 IV slowly over 10 minutes (hospital) Feed a small, high protein meal |
| Hypothalamic pituitary adrenal axis | Hypothalamus - secretes corticotropin-releasing hormone (CRH) Anterior pituitary - Stimulated by CRH to produce adrenocorticotropic hormone (ACTH) Adrenal glands - stimulated by ACTH to produce cortisol |
| Pituitary dependent Hyperadrenocoriticism (PDH) | AKA Cushings disease Responsible for 80-85% of HAC cases; due to a functional adenoma of the pars distalis, so secretes excess ACTH |
| Adrenal Tumor | One cause of Cushings syndrome Responsible for 15-20% of HAC cases Functional tumor of adrenal gland that secrete cortisol independent of pituitary control May see atrophy of contralateral adrenal gland cortex |
| Iatrogenic hyperadrenocorticism | One cause of Cushings syndrome Due to excessive administration of exogenous glucocorticoids. Causes suppression of CRH and ACTH, which results in bilateral atrophy of the adrenal cortices. |
| Clinical signs of hyperadrenocorticism | PU/PD; Polyphagia Abdominal enlargement Hepatomegaly Nonpruritic Alopecia; Hyperpigmentation; calcinosis cutis Muscle weakness |
| Differentials for alopecia | Hyperadrenocorticism; Atypical HAC Alopecia X Growth Hormone deficiency Hypothyroidism |
| Differentials for abdominal enlargement | Hyperadrenocorticism Abdominal masses Hepatomegaly/ hepatic insufficiency Right-sided congestive heart failure Psychogenic polydipsia Renal disease Diabetes mellitus/insipidus Hypercalcemia |
| Complications of PDH | Compression of adjacent structures leads to CNS signs Diabetes mellitus occurs in 10% of dogs; more common in cats UTI/pyelonephritis due to dilute urine and suppressed immune system Hypertension which could lead to glomerulopathy |
| CBC, Chem panel, and UA indicators of hyperadrenocorticism | Stress leukogram Mild erythrocytosis Thrombocytosis Elevated ALP isosthenuria or hyposthenuria Cholesterol, triglycerides, and ALT may be elevated |
| Other diagnostic tests for Hyperadrenocorticism | Abdominal rads may show calcified adrenal glands with an adrenal tumor Abdominal U/S can be used to distinguish PDH from an adrenal tumor Thoracic radiographs may show mets of adrenal tumors CT/MRI can be used to diagnose PDH and adrenal tumors |
| How an abdominal U/S distinguishes between PDH and Adrenal tumors | If HAC is suspected and the adrenal glands are both normal-sized, then PDH is most likely Adrenal tumors generally identified as an adrenal mass with the contralateral adrenal gland small or undetectable |
| Screening tests for HAC | ACTH stimulation test Low dose dexamethasone suppression test |
| ACTH stimulation test | Does not distinguish PDH from an adrenal tumor; only test that identifies iatrogenic HAC Hyperplastic/neoplastic adrenal glands should hyper-respond to administration of ACTH. Serum cortisol levels are measured before and after stimulation. Cortisol levels should be above the reference range after ACTH stimulation |
| Low Dose Dexamethasone Suppression Test | Can be used as a screening or differentiating test Sensitivity of 85-90%; Specificity of 50% In normal dogs, small doses of dexamethasone should inhibit pituitary secretion of ACTH In dogs with PDH, cortisol production is variable/suppressed after 4 hours but above the reference range after 8 hours. In dogs with adrenal tumors, cortisol production is not suppressed at all |
| Tests that differentiate PDH from adrenal tumor | Low dose dexamethasone suppression test High dose dexamethasone suppression test Plasma endogenous ACTH concentration |
| High dose dexamethasone suppression test | High doses of dexamethasone will more effectively suppress cortisol production in a dog with PDH Cortisol production will not be suppressed at all, no matter how high the dose of glucocorticoids If cortisol suppressed, dog has PDH If cortisol not supressed, dog could have PDH or adrenal tumor |
| Plasma endogenous ACTH concentration | Can only be used after HAC is diagnosed If dog has PDH, negative feedback is lost so ACTH is in the high to high normal range If dog has adrenal tumor or iatrogenic HAC, ACTH will be in the low range due to negative feedback supression |
| Treatment options for Hyperadrenocorticism | Trilostane Mitotane L-deprenyl Ketoconazole Adrenalectomy |
| Trilostane | Most common treatment for PDH and nonsurgical adrenal tumor Competitive inhibitor of 3-B-hydroxysteroid dehydrogenase Check ACTH stimulation in 10-14 days 4 hours after administration. If ok, recheck in 1 month, then every 3-4 mo. |
| If Post-stimulation test WNL but no clinical improvements seen, how do you adjust trilostane? | Increase dosing to every 12 hours |
| If post-stim cortisol <2 ug/dL, how do you adjust trilostane? | Discontinue trilostane for 5-6 days, reduce the dose by 25-50% and recheck 10-14 days after treatment resumed |
| If dog develops hypoadrenocorticism on trilostane treatment, what do you do? | Discontinue trilostane and perform ACTH stim test Treat clinical signs with glucocorticoids If Na/K ratio is low, treat with mineralocorticoids If clinical signs of HAC recur, restart trilostane on reduced dose |
| Mitotane | Causes progressive necrosis of the zona fasciculata and reticularis of the adrenal cortex. May be used to treat PDH or adrenal tumors (higher dose) Therapy given in two phases Most common side effects are gastric irritation and post-pill vomiting |
| Adjustments for excessive mitotane administration | Discontinue mitotane use Prednisone - should see response within hours. Continue administration for 3-5 days, then tapered off. Reduce mitotane dose and do ACTH stim test 3-4 weeks after resuming treatment |
| L-deprenyl | MAO type B inhibitor, which increases dopamine concentrations Dopamine inhibits secretion of CRH and ACTH Effective for 20-30% of dogs with PDH Alternative therapy should be considered if no improvement after 3 months |
| Ketoconazole | Inhibitor of cytochrome P450, which impairs steroid synthesis Effective in 50-66% of dogs Low incidence of side effects |
| Adrenalectomy | Treatment of choice for adrenal tumors unless metastasized or patient is a poor candidate for anesthesia Hypoadrenocorticism develops post-operatively due to atrophy of the contralateral adrenal cortex Manage with corticosteroids, gradually tapered and discontinued Average survival is 36 months |
| Feline Hyperadrenocorticism | 75-80% due to PDH; iatrogenic is rare Generally associated with diabetes mellitus Difference from dogs is extremely fragile skin and biochemical changes not typically seen. Treatment of choice is adrenalectomy Cats react poorly to mitotane and ketoconazole |
| Primary hypoadrenocorticism | Most common form, but overall the disease is uncommon in dogs Immune-mediated destruction of adrenal cortex; clinical signs occur when >90% of cells are gone Typical form - glucocorticoid and mineralocorticoid deficiency Atypical form - glucocorticoid deficiency only |
| Secondary hypoadrenocorticism | Rare, and results in the loss of ACTH production, causing atrophy of the adrenal cortices. Only affects the zona fasciculata, so mineralocorticoids are still produced |
| Iatrogenic hypoadrenocorticism | Occurs following the rapid withdrawal of chronic glucocorticoid therapy. Exogenous glucocorticoids suppress ACTH secretion, leading to adrenal atrophy |
| Effects of mineralocorticoid deficiency | Hyponatremia, which leads to dehydration, hypovolemia, hypotension and poor perfusion Hypochloridemia Hyperkalemia, which could decrease cardiac responsiveness and slow conduction |
| Effects of glucocorticoid deficiency | Anorexia vomiting Abdominal pain Weight loss Lethargy Possible hypoglycemia |
| Diagnosis of hypoadrenocorticism | Difficult, because signs are vague and may wax and wane |
| CBC, chem panel, and UA changes indicative of hypoadrenocorticism | Lack of stress leukogram with lymphocytosis and eosinophilia Mild normocytic, normochromic, nonregenerative anemia Hyponatremia, Hypochloridemia, Hyperkalemia (typical form) USG below 1.030 despite dehydration |
| Diagnostic tests for hypoadrenocorticism | ACTH stimulation test - basal and post-stim cortisol levels will be below 2 ug/dL Endogenous ACTH test will differentiate between primary (elevated levels) and secondary hypoadrenocorticism (low levels) |
| Management of Addisonian crisis | IV 0.9% NaCl to correct hypovolemia and decrease hyperkalemia Dextrose if hypoglycemic One dose of dexamethasone - rapid onset and will not interfere with ACTH stim test Other therapies as needed |
| Important thing to remember about dexamethasone | 7-10 times more potent than prednisone |
| Values to monitor 48-72 hours after Addisonian crisis | Hydration - maintain IV fluids for at least 48 hours then taper off ECG Electrolytes Renal values, urine output Acid-base status |
| Management after Addisonian crisis | Re-introduce food if patient has gone 24 hours without vomiting Injectable dexamethasone until patient eats, then oral prednisone at 2x physiologic dose for 2 weeks Long term - physiologic dose of prednisone supplemented on days of anticipated stress Replace mineralocorticoid with DOCP or fludrocortisone |
| Causes of hyperparathyroidism | Primary Renal secondary Nutritional secondary |
| Overall effects of Parathyroid hormone | Increases calcium Decreases phosphorous |
| Overall effect of Calcitriol (Vitamin D) | Increases calcium Increases phosphorous |
| 1 alpha hydroxylase | Enzyme responsible for converting calcidiol into calcitriol Activated by high levels of PTH or low levels of phosphorous |
| Calcitonin | Produced by C cells of the thyroid gland Decreases calcium and phosphorous Activated by increased calcium concentrations |
| Diagnosis of primary hyperparathyroidism | Elevated PTH Elevated calcium Low phosphorous Elevated calcitriol |
| Treatment of primary hyperparathyroidism | Surgical removal of parathyroid gland Post-operative hypocalcemia could persist from hours to weeks |
| Renal secondary hyperparathyroidism | Decreased GFR leads to Increased P concentration, which inhibits 1-alpha hydroxylase. This causes decreased calcitriol and iCa. PTH increases in response to low iCa. |
| Nutritional secondary hyperparathyroidism | Caused by meat only diets, which are deficient in calcium and/or vitamin D and contain excessive P. PTH levels increase to compensate |
| Clinical signs of Nutritional secondary hyperparathroidism | Osteopenia Pathologic fractures Muscle twitching Seizures |
| Treatment of renal secondary hyperparathyroidism | Diet modification (Hills k/d or Purina NF) Intestinal phosphate binders Calcitriol Monitor Ca, BUN, and creatinine during treatment |
| Causes of hypercalcemia Remember GOSHDARNIT | Granulomatous - fungal or pyogranulomatous Osteolysis Spurious - lab/sampling error Hyperparathyroidism - primary D toxicosis - rodenticide or over supplementation Addison's disease Renal failure Neoplasia - Lymphosarcoma Idiopathic - cats Temperature - hypothermia |
| Types of malignancy-associated hypercalcemia | Local osteolytic hypercalcemia Humoral hypercalcemia of malignancy |
| Local osteolytic hypercalcemia | Local invasion and dissolution of bone Caused by osteosarcomas, leukemia, and multiple myelomas |
| Humoral hypercalcemia of malignancy | PTH-related protein resembles PTH in genetic sequence and structure Caused by lymphosarcomas and anal gland apocrine adenocarcinoma |
| Diagnosis of humoral hypercalcemia of malignancy | Elevated iCa, Low PTH, elevated PTH-rP PE, bloodwork, imaging, and cytology should reveal the neoplasia responsible |
| Idiopathic hypercalcemia | Young-middle aged cats with vomiting, weight loss, and Ca containing uroliths or nephrocalcinosis Bloodwork shows elevated iCa/total Ca PTH and calcitriol are WNL; PTH-rP undetectable |
| Clinical signs of hypercalcemia | Anorexia, vomiting, constipation PU/PD, hematuria, stranguria, pollakiuria If Ca-P product > 60-70, metastatic calcification will result. Ca precipitates in stomach and kidney, but may also see in arteries, joints and soft tissue |
| Initial treatment of hypercalcemia | Find and treat underlying cause +/- surgery Diuresis with 0.9% NaCl Diuretics AFTER rehydration - Furosemide blocks Ca resorption. Avoid hypophosphatemia. Glucocorticoids - ONLY after definitive diagnosis IV bisphosphonates - blocks osteoclastic bone resorption |
| Primary hypoPTH | Rare in dogs and cats Caused by Immune-mediated destruction Commonly have severe hypocalcemia with low PTH |
| Clinical signs of hypoPTH | Stiff gait, muscle fasciculations/cramping, tetany Pain, tense splinted abdomen Seizures, nervousness, aggression, intense facial rubbing Fever Cataracts |
| Initial treatment options of hypoPTH | Calcium gluconate IV over 10-30 min (monitor HR), then CRI, then switch to intermittent SQ diluted 1:1 w/saline. Calcium chloride (caustic to tissue) |
| Long-term maintenance of hypoPTH | Oral Ca supplementation, started while still on injectable forms of of Ca to prevent relapse Taper off over 2-4 months as vitamin D supplementation reaches steady state Monitor frequently until maintenance is reached, then every 3-6 months |
| Oral vitamin D supplementation options | Vitamin D2 - long time to reach maximal effect, long time to offload; least expensive Dihydrotachysterol - reaches maximal effect and offloads more quickly Calcitriol - Quickest onset and offload; most expensive |
| Clinical signs of hyperthyroidism | Polyphagia with concurrent weight loss Hyperactivity, tachycardia, PU/PD Palpable goiter that may extend into the mediastinum Diarrhea/vomiting |
| Apathetic hyperthyroidism | 10% of cases Lethargy, anorexia Can be extremely ill |
| CBC and chem panel abnormalities of hyperthyroidism | Erythrocytosis Neutrophilia with either lymphocytosis or lymphopenia Increased BUN possible, but normal creatinine ALT and ALP may be elevated |
| Diagnosis of hyperthyroidism | Elevated total T4; may fluctuate so recheck after 1-2 weeks if in the normal range. Concurrent illness may also suppress T4 levels. T3 elevated in 66% of cases T3 suppression test - for thyroid function Thyroid scan if results equivocal |
| Thyroid scan | Tests thyroid function Used to detect ectopic/metastatic thyroid tissue Also used for surgical mapping before thyroidectomy |
| Treatment of hyperthyroidism | Anti-thyroid drugs Surgical management Radioactive iodine Dietary |
| Methimazole | Inhibits thyroid peroxidase, which blocks two steps of T3/T4 production Not curative, requires monitoring of bloodwork Side effects not common, but must monitor CBC, chem panel, and TT4 levels every 2 weeks for 3 months |
| Side effects of methimazole | Blood dyscriasis Liver toxicity Unmasking of renal disease Self-induced excoriations of head and neck Anorexia, vomiting, lethargy |
| Serious complications of methimazole | Occurs in 5% of cases Granulocytosis Thrombocytopenia Immune-mediated hemolytic anemia |
| Anti-thyroid drugs | Methimazole - most popular Carbimazole - not available in U.S. Propylthiouracil - increased side effects Ipodate - does not lower T4, prevents conversion of T4 to T3 in peripheral tissue. Monitor serum T3 |
| Thyroidectomy | 70% of cases bilateral, but 15% will have one lobe that appears grossly normal, so those cases will have a recurrence after 12 months. May cause iatrogenic hypoparathyroidism May not get all tissue if ectopic or metastatic |
| Radioactive iodine | Safest, simplest and most effective treatment of hyperthyroidism Only destroys hypertrophied tissue because the normal tissue is dormant/atrophied. Also does not damage parathyroid glands 95% curative; treats ectopic and metastatic tissue |
| Disadvantages of radioactive iodine | Hypothyroidism (rare) Recurrent hyperthyroidism (rare) Requires specialized facilities/licensing Animal must be hospitalized for 5-7 days |
| Radioactive iodine treatment protocol | Discontinue methimazole about a week prior SQ dose of radioactive iodine Isolate patient for 5-7 days; only allow contact with personnel trained in radiation safety Feed, medicate 2x a day |
| Dietary treatment of hyperthyroidism | Science diet y/d Restricted iodine content May take weeks to months to reach euthyroidism Long term consequences not known |
| Renal connection to thyroid | Hyperthyroidism leads to increased GFR, which may mask renal disease A return to euthyroid will unmask renal disease Test for renal disease by treating thyroid with methimazole; monitor BUN, creatinine and USG. If renal disease present, tailor dose of methimazole to balance between the two dz |
| Thyrotoxic cardiomyopathy | Direct action of excess thyroid hormone on sympathetic nervous system Patient will have tachycardia, gallop rhythm, and/or murmur Often reversible with treatment |
| Canine thyroid tumors | Rare Most are non-functional carcinomas; 30% hypothyroid Locally aggressive, can metastasize Highly vascular |
| Clinical signs of canine thyroid tumor | Visible mass Vomiting or regurgitation Dysphonia or dysphagia |
| Diagnosis of canine thyroid tumor | FNA? Systemic search for metastasis Surgical biopsies Thyroid scan - tissue retains ability to trap iodine |
| Treatment of canine thyroid tumors | Surgery - remember that it is highly vascular Radiation therapy Chemothrapy not usually effective If functional, radioactive iodine |
| Canine hypothyroidism | Most commonly diagnosed endocrinopathy in dogs Easy to treat Clinical signs can be non-specific Diagnosis may not be straight forward |
| Normal functions of thyroid hormone | Increase metabolic rate/oxygen consumption Positive inotropic and chronotropic effects Catabolic effects on muscle and adipose Stimulates erythropoiesis Regulate choleesterol synthesis/degradation Normal growth and development of neurologic and skeletal systems |
| Types of hypothyroidism | Primary Secondary Congenital Iodine deficiency |
| Primary hypothyroidism | >95% of all cases Lymphocytic thyroiditis - auto-immune destruction of thyroid follicles Idiopathic follicular atrophy - replaces thyroid parenchyma with adipose tissue |
| Secondary hypothyroidism | Rare A result of impaired TSH secretion |
| Congenital hypothyroidism | Rare Causes cretinism (retardation of growth and mental development) May result in early death of affected puppies |
| Hypothyroidism due to iodine deficiency | Rare because iodine is added to commercial pet foods |
| Common clinical signs of hypothyroidism | Obesity without increased caloric intake Heat-seeking behavior Lethargy Alopecia, poor hair coat, dry scaly skin Hyperpigmentation Otitis externa/pyoderma |
| Uncommon clinical signs of hypothyroidism | Myxedema or myxedema coma Infertility in females Neuromuscular abnormalities (central and peripheral) Corneal lipid deposits, uveitis Bradycardia, negative inotropy Aggression |
| CBC and chem panel abnormalities of hypothyroidism | Mild normocytic normochromic nonregenerative anemia Fasting hypercholesterolemia +/- Fasting hypertriglyceridemia |
| Diagnosis of hypothyroidism | Low fT4 in conjunction with low TT4 and high TSH TT4 may be low due to euthyroid-sick syndrome, which is why you also test fT4 and TSH |
| Euthyroid sick syndrome | Suppression of thyroid in response to an illness Suppression related to the severity of the illness Causes decrease in T4 and fT4 to a lesser extent; TSH generally normal |
| Drugs that may lower thyroid hormone levels | Glucocorticoids Potentiated sulfa drugs Anticonvulsants Clomipramine |
| Treatment of hypothyroidism | Levothyroxine or Synthroid (synthetic thyroid hormone) Lifelong treatment Takes 6-8 weeks to see clinical improvement Monitor T4 4-8 weeks after supplementation then every 6-8 weeks for first 6 months, then every 6-12 months |
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