Endocrine and Electrolytes Flashcards
Hyperglycemia is defined as (on this website):
Fasting Blood Glucose (for 8 hrs) > ________ mg/dL
Postprandial Blood Glucose > _______ mg/dL
90 – 130
180
What are the most common precipitating factors to cause DKA?
infections, disruption of insulin therapy, or as the presentation of new onset diabetes
- DKA more common in younger pts
Which has higher mortality, DKA or hyperglycemic hyperosmolar state (HHS)?
HHS
- More common in older pts
Review these causes of hyperglycemia 2/2 increase in insulin counter-regulatory hormones.
Cocaine use Infection / sepsis Myocardial ischemia / infarction Surgery Trauma
Patients with mild hyperglycemia may in fact be asymptomatic. Once the blood glucose level rises above ~ ____ mg/dL (renal threshold), patients will start to develop an osmotic diuresis.
180 mg/dL
List the early sx of hyperglycemia
Polyuria Polydipsia Polyphagia Weight loss Tachycardia Dizziness Lightheadedness Weakness
As the degree of hyperglycemia progresses leading to marked volume depletion, electrolyte disturbance, acidosis, ketosis, etc. additional sx may be seen including:
Abdominal pain Kaussmaul respirations Hypotension Fruity breath (if DKA, from ketones) Marked tachycardia Neurologic sx (seizures, focal weakness, lethargy, coma, death)
Are neurologic sx of severe hyperglycemia (seizures, focal weakness, lethargy, coma) more common in DKA or HHS?
HHS
What labs/tests should be ordered in hyperglycemia?
- Why would you get an EKG?
- bedside glucose
- UA (look for ketones)
- BMP (lytes and AG)
- CBC (infxn)
- ABG
- Phos/Mg2+ (may be off if dehydrated)
- *EKG (extracellular K+ shifts)
- Other (based on presentation)
List how the following values differ b/w DKA and HHS:
Plasma glucose (> what value?) Arterial pH (< or > 7.30) Serum bicarbonate (< or > 18?) Urine ketones (yes or sometimes?) Serum ketones (yes or sometimes?) Serum osmolality (elevated or severely elevated?) Anion gap (yes or no) Mental Status?
DKA HHS
- Plasma glucose (mg/dL) >250 >600
- Arterial pH <7.30 >7.30
- Serum bicarbonate(mEq/L) <18 >18
- Urine ketones +++ – or faintly +
- Serum ketones +++ – or faintly +
- Serum osmolality (mOsm/kg) ↑ ↑↑↑
- Anion gap >>>12 Normal (12-16)
- Mental Status Variable -- from alert to coma (DKA)
Stupor/coma (HHS)Treatment for DKA and HHS is centered around correcting these 4 measures:
- intravascular volume depletion
- management of electrolyte abnormalities
- insulin replacement therapy
- identification of and treatment of any underlying precipitants.
*Discuss the fluid replacement strategy in DKA/HHS (3 steps)
- Start with isotonic saline (0.9%) at 15-20 mL/kg/hour for the first FEW HOURS (in the average adult this will be approximately 1 liter/hr)
- Switch to one-half isotonic saline (0.45%) when the serum SODIUM normalizes
- Add dextrose to the intravenous fluids when serum GLUCOSE reaches 250 mg/dL
In hyperglycemia, what do you need to do before giving insulin?
Correct electrolyte abnormalities
Once electrolytes are corrected, how do you start correcting insulin/glucose?
What should you do if the blood glucose does not fall by 50-70 mg/dL in the first hour?
Start with an infusion of regular insulin at 0.1 U/kg/hour (can give loading dose if you want)
Double the dose of insulin
In correcting hypoglycemia, if the initial potassium is < 3.3 mEq/L, should you correct the potassium or insulin first?
Potassium (delay insulin)
Why is bicarbonate replacement in hyperglycemia tx controversial?
Correction may cause a paradoxical fall in cerebral pH and neurologic deterioration
Certain situations may warrant the use of bicarbonate, such as:
- Severe acidosis with pH < 6.90
- Severe life-threatening hyperkalemia
- Seizures
- Cardiac or persistently hypotensive patient
What requires frequent monitoring in the DKA/HHS pt?
- Blood glucose every hour until stable, then every 2–4 hours
- BMP and blood pH every 2–4 hours during therapy until patient stabilizes
- One very serious complication of DKA/HHS is cerebral edema, with a high degree of morbidity and mortality.
- What types of pts is it seen in?
- When does it occur?
- What sx is it preceded by ?
- It is mainly seen in children and young adults
- Occurring 4-12 hours into tx
- Often preceded by headache, lethargy, then neurologic deterioration (seizures, coma) with bradycardia and respiratory arrest.
Although not completely understood development of cerebral edema is correlated with ___________________ and ___________________.
bicarbonate administration and massive fluid resuscitation
Another name for glucophage?
Metformin
Which hyperglycemia pts always require hospital admission?
DKA
HHS
- Less severe can often be d/c’d w/close f/u
*What range should potassium be kept within during severe hyperglycemia tx?
*4-5
*When treating hyperglycemia, why do you need to make sure to start dextrose containing fluids once the glucose level is lowered to 250 mg/dL
Avoid hypoglycemia
What is the most common condition leading to hyperkalemia?
Missed dialysis in a patient with ESRD
Think of some conditions a/w hyperkalemia.
- Acute renal failure
- Extensive burns
- Trauma
- Severe rhabdomyolysis
- Severe acidosis.
- Acute digoxin toxicity
- Adrenal insufficiency
Patients suspected of having hyperkalemia (chronic renal failure, severe diabetic ketoacidosis, etc.) should have these two things done to monitor their heart:
cardiac monitor and EKG
- Concurrently, IV access should be obtained and a blood sample should be sent to the lab for a BMP
What is a good ddx for someone w/suspected hyperkalemia?
Hyperkalemia Pseudohyperkalemia Thrombocytosis Erythrocytosis Leukocytosis Laboratory error Hemolysis
What s/sx are pathognomonic for hyperkalemia?
Typically underwhelming presentation. No signs or symptoms are pathognomonic for this condition.
While it is not uncommon for a pt with mild to moderate hyperkalemia to be identified by an unexpected lab abnormality, what sx should clue you off to severe hyperkalemia?
- Weakness
- Muscle cramps
- Paresthesias
- Tetany
- Focal or global paralysis
- Dysrhythmia
- N/V/D
(weakness and neuromuscular effects are common)
What types of cardiac dysrhythmias may be seen in hyperkalemia?
- 2nd or 3rd degree heart block
- Wide complex tachycardias
- Progression to v-fib and asystole
What PE signs might be noticed with hyperkalemia? (read)
look for extrasystoles, pauses or bradycardia on cardiac exam, decreased DTRs or decreased strength, or signs of chronic renal failure such as fluid overload
*The most common cause of hyperkalemia is _________________________.
laboratory error resulting from a hemolyzed specimen
*What does pseudohyperkalemia result from?
Thrombocytosis, leukocytosis or erythrocytosis
- What changes occur first on the EKG of pts with hyperkalemia?
- What changes occur later on an EKG of the hyperkalemic pt, once [K+] is > 6.5?
What if it’s > 7?
What if >9?
- T wave changes (peaked)
- QRS widening (bradycardia)
P wave amplitude decreases
See sine wave, v-fib, asystole
*What is the tx for stablizing the cardiac membrane in hyperkalemic pts?
Calcium-gluconate
(10mL (1 ampule) IV over 2-5 minutes)
- Can substitude calcium-chloride, but may see tissue necrosis if it extravasates
*What medications can be used to redistribute
and reduce total body potassium in hyperkalemia? (6)
- Insulin (give w/dextrose if glc < 250)
- Albuterol (always use w/insulin)
- Sodium bicarbonate (+/-, good if acidotic)
- Kayexelate
- Lasix
- Hemodialysis (if DHUS)
How does Kayexelate work to decrease potassium?
Exchanges Na+ for K+ in the colon.
*With a pt w/severe hyperkalemia or HDUS, who should you consult and why?
Nephrology consultation for immediate dialysis
- Consult early in the process
What is the dispo for hyperkalemia pts who are HDS, measured normal or near normal serum K+ conc. after tx, with no ECG manifestations?
Home
In hyperkalemia due to this condition, use caution if administering calcium salts for cardiac membrane stablization.
2/2 dig toxicity
Review a ddx of hypoglycemia.
Coma
Stroke
Seizures
Syncope
Adrenal insufficiency Alcohol abuse (chronic) Diabetics (use of long acting insulin, oral hypoglycemic agents predispose) Insulinoma Liver disease Sepsis
What are the 2 broad categories of hypoglycemia?
- Neuroglycopenic (mental status)
2. Hyperepinephrinemic (sympathomimetic)
What are some neurological manifestations of hypoglycemia?
ALOC
Agitation/combativeness
Confusion/lethargy
Seizures or focal neurologic deficits
In general, how does the body respond to falling glucose levels in the hypoglycemic state?
Counter-regulatory catecholamine response (epinephrine; flight-or-flight stress-response) See: - anxiety/irritability - diaphoresis - nausea/vomiting - nervousness - palpitations/tachycardia - tremor
What’s a method of glucose administration only if the hypoglycemic pt is awake and alert?
PO
- 300g: soda, juice, sandwich, snacks
How is IV glucose given to the adult hypoglycemic pt?
Start with 50 ml of 50% Dextrose in Water (D50)
How is IV glucose given to the pediatric hypoglycemic pt?
Use 1 mL/kg of 25% Dextrose in water or 2-4 ml/kg of 10% Dextrose in water
In correcting hypoglycemia in the alcoholic pt, what should you remember to do?
Remember to consider giving thiamine to alcoholic patients to prevent Wernicke’s Encephalopathy.
If there’s no IV access in a symptomatic hypoglycemic pt who cannot eat, what’s another method of raising the blood sugar?
Glucagon
When might glucagon be ineffective in treating hypoglycemia?
Those w/depleted glycogen stores
- Elderly
- Alcoholics
What medication may be effective for sulfonylurea-induced hypoglycemia?
Octreotide
Review some reasons that a hypoglycemic pt should be admitted.
- *Cause of hypoglycemia due to long acting insulin or oral agents
- No obvious cause
- Persistent neurologic deficits
- Persistent or recurrent hypoglycemic episodes in the ED
Is the mortality rate of thyroid storm (seen in 1% of pop) high or low?
High (10% to 75%)
- 3rd/4th decade of life most common
What are some ocular sx suggestive of Graves disease:?
Proptosis
Periorbital edema
Chemosis
Diplopia
(stare and lig-lag common in most thyroid dz)
How might the BP change in thyroid storm?
Widened pulse pressure
May also see
- Sinus Tachycardia or A-fib
- Hyperdynamic precordium
- Rub
Review some medications/procedures a/w thyrotoxicosis.
Amiodarone Lithium Interferon α Interleukin-2 Iodinated contrast Radioactive iodine Increased iodine intake
Review some common triggers of thyroid storm.
Infection Discontinuing medications for hyperthyroidism MI Stroke Thyroid surgery Self-administration of thyroxine or thyroid supplements Treatment with radioactive iodine Pregnancy DKA Non-thyroid surgery Trauma Iodinated contrast exposure
Specific treatment for thyroid storm utilizes 3 sequential steps:
- Block the peripheral effect of the thyroid hormones,
- Stop the production of hormone in the thyroid, and
- Stop the release of T3 and T4 from the thyroid.
What medications can be used to stop the peripheral effects of thyroid hormones?
Propranolol Esmolol (short T1/2)
What medications can be used to stop the production of hormone in the thyroid?
PTU
Methamizole
What medications can be used to stop the release of T3 and T4 from the thyroid?
*Do Not Start Until at Least __ hour After PTU or Methimazole
Potassium Iodide (SSKI)
Lugol’s Solution
Sodium ipodate
Iopanoic acid
*1 hour
What glucocorticoids may be useful in thyroid storm, and which of the 2 is preferred?
How do they work?
- Dexamethasone (preferred due to its lack of interference on an ACTH stimulation test)
- Hydrocortisone
Inhibit the peripheral conversion of T4 to T3. Promote vascular stability. Treat relative possible relative adrenal insufficiency.
Which BB may be better for CHF pts w/thyroid storm, and why?
Esmolol (short T1/2)
Is PTU or methimazole preferred in thyroid storm?
PTU is preferred as it has the additional benefit of blocking peripheral conversion of T4 to T3
- Can use in pregnancy (some risks)
*In thyroid storm, iodine therapy should not be started any sooner than one hour after the initiation of a thiourea. Why?
In the absence of a thiourea, iodine may actually stimulate release of preformed thyroid hormone
