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55 Cards in this Set
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This is a manifestation of severe insulin deficiency. It is often in association with stress (infection). High blood sugar, acidosis, and high levels of ketone bodies. Potentially fatal.
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Diabetic ketoacidosis
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What are the only things that don't depend on insulin to absorb glucose?
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RBC, neurons, some intestinal tissues and pancreatic B cells.
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This stimulates formation of glycogen from glucose. Stimulates fatty acid uptake and storage. Inhibits protein breakdown. Inhibits gluconeogenesis (amino acids leading to glucose).
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Insulin
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These 2 ketone bodies enter the blood and increase the osmolar load of the blood and decrease the pH.
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B-hydroxybutyrate
Acetoacetate |
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What are the signs and symptoms of diabetic ketoacidosis?
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Sluggishness, extreme tiredness
Extreme thirst, despite large fluid intake Constant urination Fruity smell to breath (acetone) Hyperventilation - first rapid and shallow, then progressively deeper and less rapid (Kussmaul breathing) Muscle wasting and weight loss Nausea, vomiting, abd pain Pain in shoulders, neck and chest Agitation, irratiation, aggression, confusion, lethargy |
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What happens after prolonged DKA?
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Unconsciousness, diabetic coma, medical attention is imperative.
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What are the first considerations in DKA treatment?
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Preferably close monitoring in the ICU
Fluid replacement Adequate insulin administration Potassium repletion |
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What are other considerations to take into account when treating DKA apart from the first considerations?
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Bicarbonate
Phosphate Magnesium |
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When treating DKA, you should use a flow sheet to measure?
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Urine glucose and ketones
Serum pH Plasma glucose Acetone Bicarbonate BUN Electrolytes Osmolality |
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What is involved with fluid replacement in DKA?
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Restore circulating volume:
NS as rapidly as 1 L/h X 2 hours If Na >155, may give 1/2 NS Replenish total body water deficit: 1/2 NS @ 150-500ml/h depending on renal and cardiac function. Maintenance fluid replacement: Until patient is about 6L positive Complete fluid replacement may take up to 12-24 hours. |
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What is involved in insulin therapy for a DKA patient?
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IV bolus 0.15 units/Kg of regular insulin
Then 0.1 units/kg/h continuous infusion (this may be replaced by 5-10 units every 1 hour intramuscular - but may be less reliable). |
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What is the expected blood glucose response after initially treating DKA?
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Decrease in glucose by 50-75mg/dl/h
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What is a risk of rapidly correcting glucose at a rate of over 100mg/dl/h?
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Risk of osmotic ecephalopathy
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When glucose level is less than 250mg/dl what are you meant to do in the DKA patient?
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infuse D5N5
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Once patient takes in orally, IV insulin may be converted to what?
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SC insulin, with about 30 minutes IV and SC insulin overlap
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This should always be assumed in DKA, regardless of plasma levels?
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Hypokalemia
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What are important things to do in monitoring kypokalemia in a DKA patient?
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Insulin therapy results in a rapid shift of K back into the intracellular compartment.
Monitor K serum levels every 2 hours. Check EKG May add 10-20 meq/h K to IVF If pt presents with hypokalemia start 40 meq/h of K |
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What are three other tx considerations for DKA apart from hypokalemia, insulin and fluid management?
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May consider bicarb if pt. is in shock or a coma. Severe acidosis (pH 6.9-7.1)
May need to replete magnesium and phosphate Consider Abx if pt's DKA was triggered by infection. |
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What are three complications associated with diabetic ketoacidosis?
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Arterial thrombosis
Cerebral edema Rebound ketoacidosis |
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This can be a complication of DKA associated with stroke, MI or ischemic limb. Routine anticoagulation is NOT recommended. The mechanism is unknown.
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Arterial thrombosis
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This is a complication of DKA that is more common in children than adults. It occurs 2/2 overhydration with free water and excessively rapid correction of hyperglycemia. Monitor serum Na to recognize early. May be diagnosed on head CT. TX: is IV Mannitol.
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Cerebral edema
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This is a complication that occurs in DKA that is a result of premature cessation of insulin therapy.
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Rebound ketoacidosis
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What are three important points of patient education to avoid DKA?
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1. Take insulin.
2. Body's need for more, rather than less insulin during illness. 3. Testing the urine for ketones 4. Procedures for obtaining timely and preventive medical attention |
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This was previously called hyperglycemic, hyperosmolar nonketotic coma. It is when someone is severely hyperglycemic >600 mg/dl with an absence of ketosis, The serum osmolality is > 310 osm/kg with normal being 280-300. Dehydration is involved and it is mainly involved in middle aged to elderly patients with mild or occult DM. Most patients have underlying renal insufficiency or CHF.
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Hyperglycemic hyperosmolar state.
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What are examples of precipitating events that can cause hyperglycemic hyperosmolar state?
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Infection, MI, stroke or recent surgery.
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What are the drugs that are implicated with hyperglycemic hyperosmolar state.
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Phenytoin, corticosteroids and diuretics.
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What are the signs and symptoms of a hyperglycemic hyperosmolar state?
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Insidious onset over days to weeks
Weakness Polydipsia Polyuria Dehydration Lethargy and confusion There is no Kussmaul breathing because the patient is not trying to blow off CO2 to correct low pH. |
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What are the lab findings with hyperglycemic hyperosmolar state?
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Glucose > 600 mg/dl
Initially serum Na of 120-125 mEq/L (2/2 dilution and urine Na losses) Later Na > 140 mEq/L (2/2 dehydration) leads to increased serum osmolality Increased BUN > 100 mg/dl Ketosis or acidosis are either absent or mild |
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What are the first line considerations for treatment of hyperglycemic hyperosmolar state?
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Fluid replacement
Insulin therapy Correction of electrolyte deficits Detection and treatment of precipitating factors |
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With is involved with the initial fluid replacement in HHS?
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Initial fluid therapy - NS @ 1L/h until intravascular volume is restored.
Free water deficit - 1/2 NS to replace 1/2 of the H20 deficit over the first 12 h and the remainder over the next 24 h, guided by serum Na levels. Consider cardiac and renal status in the elderly. Maintenance fluid replacement - Guided by clinical status especially urinary output and e/o overload Patients may require as much as 10-12 L positive fluid balance over 24-36 hours to restore total deficits. |
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What is involved with insulin therapy in HHS?
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Insulin is indicated in all patients.
If glucose is > 600 mg/ml give 5-10 unites regular insulin IV bolus, then 0.1-0.15 units/kg/h or 0.15 units insulin/kg/h bolus followed by 1-2 units/h Once glucose level is 250-300 change regimen to 1-2 units/h and change IVF to D5 1/2 NS. |
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What is involved with electrolyte management in HHS?
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Hypokalemia should always be assumed regardless of plasma levels.
Insulin therapy results in a rapid shift of K back into the intracellular compartment Monitor K serum levels Check EKG May add 10-20 meq/h K to IVF If patient presents with hypokalemia start 40 meq/h of K |
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What are other considerations, apart from initial tx, for HHS?
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Diabetic education and weight loss
Abx therapy, even empiric broad spectrum Abx in a septic pt pending results of Blood Cx Consider nephrology consult if oliguria persists in spite of correction of volume deficits Risk of coagulopathy exists (either thrombotic or bleeding), may require specialist management |
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What are the two principle types of hypoglycemia?
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Fasting and postprandial.
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When do the symptoms of hypoglycemia start?
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Sx start at plasma glucose level of approximately 60 mg/dl
Impaired brain function at approximately 50 mg/dl |
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What can diagnose hypoglycemia?
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Whipple triad - Hx of hypoglycemic Sx, Fasting blood glucose = 40 mg/dl, Immediate recovery upon administration of glucose.
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What is the etiology of fasting hypoglycemia?
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Hyperinsulinemia 2/2 pancreatic B cell tumors, Islet hyperplasia, Surreptitious administration of insulin - (patient is taking insulin already).
Non insulin producing extra pancreatic tumors. |
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Fasting hypoglycemia can be a secondary feature in some endocrine disorders such as?
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Hypopituitarism, Addison's dz, myxedema, In liver malfunction (acute alcohol or liver failure), Renal failure (especially in patients on dialysis).
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B cell tumors = B cell adenoma = insulinoma
Mechanism - inappropriately high insulin secretion at time of hypoglycemia. What are the symptoms? |
CNS dysfunction e.g. blurred vision, diplopia, HA, slurred speech, weakness, anxiety, psychotic behaviour - leading to convulsions - leading to coma.
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When dose fasting hypoglycemia 2/2 a b cell tumor occur?
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Early in the morning, after missing a meal or after exercise.
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What studies do you do to diagnose a B cell tumor?
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Supervised fast up to 72 hours
Serum insulin level of 6 microunit/ml and blood glucose less than 40 mg/dl Elevated proinsulin level in B cell tumor, but not in factitous administration of insulin (patients sneeking insulin) |
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With this pancreatic B cell tumor, which causes hypoglycemia, you will usually see symptoms of epigastric distress, renal stones, menstrual/erectile dysfunction. This is diagnosed by checking calcium, gastrin and prolactin levels.
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MEN 1 (multiple endocrine neoplasia type 1) = insulinoma + parathyroid tumor + pituitary tumor
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How do you localize pancreatic b cell tumors?
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Using spiral CT or ultra sound
Ca stimulated angiography - injection of Ca gluconate into the gastroduodenal A. - pancreatic head. into the sup. mesenteric artery - uncinate process, into the splenic artery - body and tail. |
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What is the tx of fasting hypoglycemia 2/2 pancreatic b cell tumor?
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Tx: surgical removal of insulinoma
If an insulinoma is metastatic it will go to the liver and bone. |
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What are the diet and medical Tx's of hypoglycemia 2/2 pancreatic b cell tumors.
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Frequent po intake of carbs every 2-3 hours to prevent hypoglycemia - risk of obesity
Diazoxide 300-600mg po in 2-3 doses, mechanism - inhibits insulin release from the insulinoma leading to increased blood glucose within an hour. side effects - GI upset, hirsuitism and edema HCTZ 25-50 mg po qd, purpose - to counteract Na retention and edema from diazoxide. |
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What is the tx for islet hyperplasia?
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Partial pancreatectomy
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These are rare and include mesenchymal tumors such as retroperitoneal, hepatocellular, and adrenocortical carcinomas. Insulin like growth factor-2 (IGF-2) binds to insulin receptors - on muscle cells promoting glucose transport into the cell. On liver cells reducing glucose output. On pancreas B cells reducing insulin output.
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Non insulin producing extra pancreatic tumors.
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How do you diagnose a non insulin producing extra pancreatic tumor?
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Fasting hypoglycemia with undetectable serum insulin levels.
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How do you tx a non insulin producing extra pancreatic tumor?
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Dietary management (diazoxide is ineffective)
Surgical resection |
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Postprandial hypoglycemia occurs early and late when?
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Early is 2-3 hours after a meal
Late is 3-5 hours after a meal |
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Mechanism : Rapid discharge of ingested carbs into the small bowel + rapid glucose absorption + hyperinsulinism
Sometimes seen after gastric bypass for obesity. Pt have also been found to have islet hyperplasia Tx: More frequent PO intake of smaller portions of less rapidly assimilated carbohydrates combined with slowly absorbed fat and protein |
Postgastrectomy Alimentary Hypoglycemia
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Not explained by prior GI surgery
Sx: Chronic fatigue, anxiety, irritability, weakness, poor concentration, decreased libido, HA, hunger after meals and tremulousness Dx: Postprandial hypoglycemia after high carbohydrate breakfast (better than glucose tolerance test) |
Functional Alimentary Hypoglycemia
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Delay in insulin release leads to initial hyperglycemia leads to exaggerated insulin response leads to hypoglycemia (4-5h postprandial)
Sx: Can lead to obesity Tx: Weight loss, reduced carbohydrate intake with multiple small meals |
Late Hypoglycemia (Occult Diabetes)
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Epidemiology: Malnourished alcoholics or anybody w/ ETOH induced gastritis and vomiting
Mechanism: Hepatic glycogen depletion (2/2 no po intake) + ETOH induced inhibition of glucogenesis Tx: Glucose administration until glycogen stores replenished (18-24 h) |
Fasting Hypoglycemia after ETOH
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Mechanism: sugar-containing soft drinks mixed with ETOH leading to greater insulin release than soft drink alone leading to hypoglycemia 3-4 h later
Tx: Avoid mixed drinks and take in food |
Post ETOH reactive Hypoglycemia
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