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42 Cards in this Set
- Front
- Back
ENDOCRINE EM
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ENDOCRINE EM
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Define neuroglyopenic
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an autonomic catagory of hypoglycemia. Shortage of glucose in nerve cells of the brain.
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Define hyperepinephrinemic
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A sympathomimetic catagory of hypglycemia.
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Define hypoglycemia
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an abnormally low concentratrion of glucose in the circulating blood
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Define diabetic ketoacidosis
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DKA: buildup of ketones in blood due to breakdown of stored fats for energy: untreated can lead to death
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Define hyperosmolar hyperglycemic nonketotic
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complication seen in DM. marked hyperglycemia occurs causing osmotic shifts in water in brain cells and resulting in coma. Can be fatal or lead to permanent neurologic damage
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Define alcoholic ketoacidosis
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an accumulation of ketones in the blood, caused by excessive alcohol consumption
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When serum glucose levels are <50mg/dl what is it called
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hypoglycemia
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What clinical situations may be associated with hypoglycemia
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DM, sepsis, liver disease, alcohol intoxication, starvation and certain toxic ingestions.
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What are the 2 main catagories of hypoglycemia
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neuroglycopenic (autonomic) and hyperepinephrinemic (sympathomimetic)
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Describe signs and symptoms of hypoglycemia
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potential cause of altered mentation, can mimic sxs of stroke, TIA, seizures, narcolepsy, MS, psychosis, drug OD, hysteria just to name a few
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Explain the primary metabolic derangement and precipitating factors in DKA
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lack of insulin & exces counterregulatory hormones result in hyperglycemia (due to excess production and underutilization of glucose), osmotic diuresis, pre-renal azotemia, ketone formation, & wide-anion gap metabolic acidosis
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Discuss clinical features of DKA
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Abnormal vitals may be only PE finding. Tachycardia, orthorstasis or hyptension. Poor skin turgor, acidemia, Kussmaul resp, fruity odor, hypothermia, abd px
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Discuss typical changes in chem panel and CBC for DKA
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↑anion gap, acidosis, glycosuria, hyperglycemia, ↓pH,(↑amylase but↑lipase more specific to pancreatitis & used to differentiate)
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What ECG changes might you see with DKA
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May be transient due to rapidly changing metabolic status. Underlying rhythm is sinus tachycardia then progresses: Tall peaked T, short QT interval → prolonged PR → wide WRS flat P → V-fib, complete heart block & asystole
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What diagnostic tests help in evaluating and managing DKA
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glucose test strip, urine dip, ECG, blood gas, serum electrolytes evaluating for wide anion gap and metabolic acidosis
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Identify the treatment goals for DKA
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volume repletion, reversal of metabolic consequences of insulin insufficiency, correction of electrolyte & acid base imbalances, recognition & tx of causes and avoid complications
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Discuss the treatment of DKA with respect to fluid administration
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Rapid fluid administration single most important initial step. helps restore volume & normal tonicity, perfuse organs, improve GFR & ↓ serum glucose & ketones
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Discuss the treatment of DKA with respect to insulin
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Avoid IM/subQ insulin. Absorption erratic when volume depleted delaying adequate insulin level. Delayed absorption can cause later hypoglycemia
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Discuss the treatment of DKA with respect to Potassium
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Large amounts of K+ necessary 1st 24-36h. Goal is to maintain normal extracellular K+ during acute phase and replace intracellular deficit over days
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Describe signs nad symptoms of alcoholic ketacidosis AKA-AKA and precipitating factors
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No specific PE soley w/AKA. Most common: tachycardia, tachypnea, mild-moderate abd tenderness. Volume depletion from anorexia, diaphoresis, NV.
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Explain the basis for the diagnosis of AKA and the use of confirmatory laboratory testing
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electrolytes, BUN, creatinine, hepatic/pancreatic enzymes, WBC, hematocrit, UA, anion gap, serum lactic acid, osmolarity, ABG
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Describe the general treatment of AKA
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glucose & volume repletion: D5NS.
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What do DKA and HHNS (hyperosmolar Hyperglycemic Nonketotic Syndrome) have in common
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hyperglycemia, hyperosmolality, severe volume depletion, electrolyte disturbances, sometimes acidosis.
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What do pt's with DKA have that pt's with HHNS don't have
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higher levels of lipolysis and more profound acidosis.
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Describe the presentation and PE findings in HHNS
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poor skin turgor, dry membranes, sunken eyes, hypotension, hyperglycemia, hyperosmolality, hypothermia, 15% seizures resistant to anticonvulsants
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What precipitating causes may be present with the non-diabetic pt with HHNS
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Acute CVA, burns, MI, infection, pancreatitis or other acute illness.
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Discuss the treatment of HHNS including the importance of fluid rescuitation
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tissue perfusion key to effective recovery in HHNS. correct hypovolemia, underlying causes, electrolyte abn, hyperglycemia, osmolarity.
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Discuss thyroid storm as it relates to precipitating events
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infection, truama, DM ketoacidosis, MI, CVA, pulmonary thromboembolic disease, general surgery, withdrawal of thyroid rx, iodine, palpation of thyroid gland, ingestion of thyroid hormone, idopathic 20-25%
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Discuss thyroid storm as it relates to mortality rates
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mortality rates high even with tx: 10-75%
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Discuss thyroid storm as it relates to confirmatory lab findings
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lab analysis not helpful. nonspecific findings might include: leukocytosis, hyperglycemia, increased transaminases and bilirubin. Further tests aimed at underlying causes
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Describe the treatment of thyroid storm
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1.ABC 2.↓ de novo synthesis: propylthioracil / methimazole 3.Prevent relase of hormone: iodine, lithium carbonate 4. Prevent peripheral effect: B-blocker, guanethidine, reserpine 5. Other considerations: corticosteroids, antipyretics
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What consideration must be factored before administering iodine in pt with thyroid storm
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Do not administer iodine until the synthetic pathway has been blocked. Otherwise may promote further hormone production
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describe myxedema coma
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rare clinical state with long standing preexisting hypothyroidism presents with life threatening decompensation. Mostly common in elderly
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Describe precipitating events for myxedema coma
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infection, cold exposure, rx (sedatives, lithium, amiodarone) trauma, stroke, CHF, inadequate thyroid hormone replacement & undx hypthyroidism
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Describe clinical features of myxedema coma
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severe decompensated metabolic state, ↓ mental status, hypothermia, bradycardia, hypoventilation, periorbital edema, nonpitting edema, delayed DTR, hypoglycemia, hyponatremia
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Describe treatment for myxedema coma
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Recognition, supportive including vent, thyroid replacement, glucocorticoid, hyothermia, electrolyte correction, hypoglycemia, Tx cause, admit for monitoring
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Why is glucocorticoids recommended for myxedema coma
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avoids the portential of precipitating adrenal crisis in pts with unrecognized adrenal insufficiency or hypothyroidism secondary to hypopituitarism. Baseline cortisol level should be obtained
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Identify the most common cause of tertiary adrenal insufficiency
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chronic administration of exogenous glucocorticoids, leading to failure of anterior pituitary to secrete ACTH resulting in adrenal atrophy
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Discuss the cause and presentation of adrenal crisis
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life-threatening hypotension resistant to catecholamine and IV fluids. If cortisol not replaced - death.
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Discuss the response to treatment and the main causes of death in adrenal crisis
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tx w/glucocorticoids, several liters of D5NS to correct hypovolemia/glycemia
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Suspected what when unexplained hyponatremia & hyperkalemia in setting of hypotension & unresponsive to catecholamine & fluid administration?
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Adrenal crisis
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