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42 Cards in this Set

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