Endocrine Flashcards
A 7-year-old girl presents with her mother for lethargy and weight loss. Her mother reports she has lost seven pounds over the past several weeks, has excessive thirst, and has been wetting the bed. This morning, she appeared to have difficulties breathing and was difficult to arouse from sleep. She has minimal verbal response and only states her “tummy aches.”
HR 130, BP 70/50, RR 34, Temp 37°C (98.6°F).
potential warning signs of diabetes
Thrush, candida, balanitis
glucose regulatory hormones
-INSULIN:
-Post-prandial release from pancreas
-Stores glucose in the form of glycogen
-GLUCAGON:
-Counterrgulatory hormone
-Releases glucose from glycogen stores
Type one DM occurs by autoimmune destruction of pancreatic beta-cells
Occurs at any age but mostly in CHILDREN
Typically, lean body type with NORMAL lipid profiles
Absolute insulin deficiency, parenteral insulin is required for survival
Prone to ketosis and decompensates into DKA
TYPE 2 DM occurs due to insulin resistance
Insulin levels can be low, normal, or high
May be asymptomatic for a long period of time
Typically, OVERWEIGHT/OBESE body type (80%), with underlying hypertriglyceridemia
Ketosis is rare and decompensates into HHS
Long term (~15 yrs) : Fat deposition into pancreas can destroy insulin production
morbidity and mortality of DM
-cardiovascular
-cerebrovascular
-renal failure
-eyesight
underlying triggers
-new onset DM
-uncomplicated hyperglycemia
-DKA
-HHS
uncomplicated hyperglycemia
-!Hyperglycemia by itself is NOT usually dangerous
-!Acute complications of hyperglycemia need to be ruled out
-If no acidosis/ketosis can manage uncomplicated hyperglycemia with:
-!IV fluids
-Consider insulin
-Consider metformin on discharge from ER
-There is no “magic number” for discharge
-Diabetic teaching (diet, resources, nutritionist)
-Ensure close follow up: long term problem = long term care
DKA
-life threatening complication of DM (usually type 1)
-D: Diabetes- BS>250
-K: Ketosis- blood beta-hydroxybutyrate -> ketonuria
-A: Acidosis (metabolic anion gap)- pH < 7.35, anion gap, low bicarb <15
pathophysiology of DKA
-!!No insulin = no glucose uptake
-Hyperglycemia
-Glycosuria & osmotic diuresis
-Volume depletion and electrolyte loss
-Impaired renal function and worsening acidosis
-Increased lipolysis
-Increased free-fatty acids and ketogenesis causing acidosis
-Protein breakdown
-More release of amino acids that increase gluconeogenesis
-Worsens the hyperglycemia and osmotic diuresis
DKA triggers: 6 I’s
!-Infection*
!-Infarction
!-Indiscretion*- dont take meds
-IUP- intrauterine pregnancy
-Illicit drugs
-Iatrogenic
-Idiopathic (New onset diabetes [25%], or even stress)
-Also consider hyperthyroidism, Cushing’s syndrome, hemorrhage, stroke, pancreatitis, renal failure
DKA S&S
-Usually due to type 1 diabetes mellitus (new or known)
-Manifestations develop within 24 hrs and are directly related to:
-HYPERGLYCEMIA
-VOLUME DEPLETION
-ACIDOSIS
-Weakness
-Blurry vision
-!Nausea, vomiting
-!Abdominal pain
-Confusion, drowsiness
-!Dehydration: Poor skin turgor, dry mucous membranes, tachycardic, orthostatic HoTN, sand paper tongue
-!Rapid / deep breathing (kusmals): Due to burning of fats for energy -> ketones/ketoacids -> compensatory respiratory alkalosis
-abn breathing is what kills -> try not to intubate, try to match respirations to when they came in (not when they started to get tired)
-Acetone odor
-Altered mental status
-Coma
-Severe DKA can eventually lead to coma
DKA dx!!!!
-Blood glucose > 250mg/dL
-Acidosis pH < 7.3
-Bicarbonate level < 15mEq/L
-Elevated anion gap >10-12
-AG = Na - [Cl + HCO3]
-+ Ketones (serum and urine)
-Beta-hydroxybutyrate >3 mmol/L (ketones)
DKA labs
-Rapid bedside glucose check
-CBC - Evaluate for leukocytosis
-CMP + magnesium + phosphorus + calcium:
-↓ Sodium due to pseudohyponatremia! (high glucose pushes Na into cells)
-Potassium may be low, normal, or high on labs* -> never tx with kayexalate
-TOTAL K is low, but can appear high -> give insulin to push it back in cells
-↑ BUN in dehydration
-↑ glucose
-↑ Amylase, lipase can be non-specific finding
-VBG:
-Assess acidosis and bicarbonate levels
-Lactic acid
-Beta-hydroxybutyrate (ketones)
-Calculate anion gap
-Urine:
-Glucosuria
-Ketones
-ECG:
-Evaluate for precipitating MI
-Look for changes associated with hypo-hyperkalemia
-CXR- Evaluate for precipitating PNA or CHF
electrolyte disturbances
-SODIUM (NORMAL 135-145):
-Pseudohyponatremia
-1.6 mEq should be added to the reported sodium value for every 100 milligrams of glucose >100 milligrams/dL
-Example:
-Na 130, glucose 350
-1.6 x 2.5 = 4
-4 + Na 130 = 134 mEq/L corrected sodium
-!!!!POTASSIUM (NORMAL 3.5-5.0):
-Blood potassium can be low, normal, high
-Low due to diuresis, vomiting, diarrhea
-High due to acidosis causing extracellular shift or renal failure
-Do not be fooled! There is a
-TOTAL BODY POTASSIUM DEFICIT
What electrolyte may be falsely decreased in patients with hyperglycemia or DKA?
Phosphorus
Potassium
Magnesium
Sodium!!!!!!
Calcium
goals of DKA management
-volume repletion
-reverse metabolic derangements
-electrolyte correction
-recognize and treat precipitating causes
-avoid complications
-3 PILLARS OF TX:
-FLUIDS
-POTASSIUM
-INSULIN
DKA: IV fluids
-!!IVF fluids is the first line therapy
-Treats dehydration! and dilutes hyperglycemia/acidosis!
-Also increases response to insulin therapy
-Perfuses the kidneys to urinate out ketones/sugar
-Generally, 5-10 L volume deficit by the time you diagnose DKA
-LR / Plasmalyte might be a better fluid than NS.
-Start with !2L bolus rapidly over 0-2 hours!
-Once fluid boluses are given, consider providing continuous drip of 200 mL/hr of IV fluid
-Fluid replacement in children with DKA can be tricky (mortality 1%) bc too much can cause cerebral edema, consult pediatric intensivist
DKA: correct potassium
-Total body potassium deficit! (up to 3-5mEq/L true deficit)
-The measured blood K can be unpredictable
-Aggressive replacement is usually necessary, and must occur prior to insulin
-Replete with PO or IV potassium!
-Replete low magnesium 2g! IV if needed
-The rapid development of severe hypokalemia is potentially the most life-threatening electrolyte derangement during the treatment of DKA
-Cardiac arrythmias, respiratory paralysis, paralytic ileus, rhabdomyolysis
-If K <3.3 -> hold insulin until K>3.5 and GIVE POTASSIUM (20-40 per hour)
-If K 3.3-3.5 -> GIVE POTASSIUM (20-30 per hour) WHILE STARTING INSULIN -> goal K is 4-5
-If K>5.3 -> NO K REPLACEMENT, recheck in 2hrs, start insulin (will close anion gap)
DKA: START INSULIN
-!Insulin stops lipolysis/ketosis and corrects acidemia
-!Do NOT START until you know the potassium
-!STOP if there is hypokalemia
-Insulin concontinuous infusion at * 0.1 U/kg/hr IV *
-Bolus no longer recommended
-If glucose !drops to < 250-300 mg/dL
-!Switch fluids to D5NS or D5 ½ NS @ 50-200 mL/hr and ↓ insulin rate to 0.05U/kg/h
-!!Continue infusion until resolution of DKA:
-D: glucose <200
-K: Anion gap ≤12 ± 2 or beta-hydroxybutyrate <1mmol
-A: pH≥7.3 or serum bicarbonate ≥15
-Tolerating PO
-INSULINS PURPOSE IS TO STOP ACIDEMIA NOT TO LOWER SUGAR
-KEEP GIVING INSULIN UNTIL ANION GAP IS GONE -> IF SUGAR STARTS TO GET LOWER BEFORE ANION GAP IS CLOSED GIVE SUGAR
Iatrogenic DKA complications
-Hypokalemia
-Hypoglycemia
-Pulmonary edema
-!Cerebral edema; rare (0.3-0.9%) but fatal (mortality 21-24%)
-Occurs 6-10 hours after treatment
-Rare, more common in young children <5yo, most feared complication in children
-Warning sign: Headache! after treatment initiation, incontinence, change in behavior such as irritability or lethargy, bradycardia, papillary edema, seizures, AMS
-Management: Mannitol IV! or hypertonic saline! by specialist
-No specific cause, but best way to prevent is slow correction of osmolality and glucose, and avoid dangerously low electrolyte levels (sodium, potassium magnesium, phos, hypoxia)
be sure to monitor DKA pts
-General guidelines, will vary by hospital
-Serial ECGs – don’t miss an evolving STEMI
-Hourly glucose finger sticks
-Repeat VBG every 2 hours
-Repeat BMP every 4 hours
-To the ICU!
-RECHECK- dont memorize bc every hospital is diff but this is general^^
What is the electrolyte complication that could arise when you administer insulin?
Hyponatremia
Hypomagnesemia
Hypocalcemia
Hypokalemia!!!!!!!!
hypophosphatemia
An 86-year-old woman with a history of cerebral vascular accident, hypertension, type 2 diabetes and chronic kidney disease presents to the emergency department with confusion, low grade fever, and tachycardia per the ECG. She is unable to add to the history.
Vital signs are as follows: HR 130, BP 88/56, RR 28, Temp 38.5°C (101.3°F).
Her mucous membranes are dry, neck veins are flat, and she has poor skin turgor. Paramedics reported a bedside glucose as “high” (greater than 500).
-blood cultures (for HHS not DKA)
-WBC
-lactate
-VBG
-CXR- pna
-U/A- UTI
hyperglycemia hyperosmolar syndrome (HHS)
-Mortality 15-30%
-Syndrome of:
-!Marked hyperglycemia (600-1000s)
-!↑ Serum osmolarity (>320 mOsm/kg)
-!Mild to no ketoacidosis (bc still some insulin)
-!!!!!Altered mental status * - HHS can also cause seizures, hemiparesis, coma
Usually very mild acidosis pH >7.25
-Epidemiology:
-!T2DM > T1DM
-!Elderly > young
-!Nursing home
-!Recent change in DM medications
-!The 6 “I”s (see slide 18)- Esp infection, MI, stroke
