endocrine Flashcards
(28 cards)
precipitating factors for hyperglycemia and DKA triggers
- Infection
- Omission or inadequate insulin therapy
- Acute illness or stress (e.g., myocardial infarction, pancreatitis)
- Drugs (e.g., corticosteroids = hyperglycemia)
DKA: 6 I’s
* infection
* infarction
* indiscretion - dont take their meds
* IUP
* Illicit drugs
* iatrogenic
* idiopathic (new onset DM or stress)
uncomplicated hyperglycemia vs DKA vs HHS labs,
uncomplicated:
- hyperglycemia alone = not dangerous
- r/o acute complications of hyperglycemia: NO ACIDOSIS, NO KETOSIS
- management: IV fluids, +/- insulin, metformin on discharge
- ensure close f/u and diabetes education
DKA:
- BG > 250
- acidotic pH <7.3
- bicarb < 15
- elevated anion gap > 10-12
- + KETONES (serum and urine)
- beta-hydroxybutyrate > 3 mmol/L
- CMP: VARIABLE POTASSIUM (but there is a TOTAL BODY POTASSIUM DEFICIT), high BUN, pseudohyponatremia due to polyuria
- EKG: check for precipitating MI
- chest xray: check for precipitating PNA or CHF
- tx: IV fluids, K+ correction, insulin
HHS:
- longer prodrome than DKA
- severe dehydration
- BG: > 600
- pH > 7.3; NO anion gap -> no kusmal breathing
- trace serum ketones
- PROFOUND DEHYDRATION: HYPEROSMOLALITY WITHOUT KETOACIDOSIS
- AMS
- tx: resuscitation with IV fluids, replete K, Mg, phos, insuln, restore renal perfusion, manage the underlying cause
- underlying cause: renal insufficiency, sepsis, PNA, GI bleed
Uncomplicated hyperglycemia lacks acidosis, ketones, and significant dehydration.
DKA involves metabolic acidosis and ketone production due to absolute insulin deficiency. Type 1 DM
HHS features severe hyperglycemia and hyperosmolality without ketoacidosis, usually in older patients with type 2 diabetes.
uncomplicated hyperglycemia vs DKA vs HHS management
uncomplicated:
- IV fluids, +/- insulin, metformin on discharge
- ensure close f/u and diabetes education
DKA:
- tx: IV fluids, K+ correction, insulin
- IV Fluids (5-10L volume deficit): LR/plasmalyte > NS; start with 2L BOLUS RAPIDLY OVER 0-2HRS then do continuous drip
- correct potassium:
- if K < 3.3: hold insulin and until over 3.5 and GIVE K;
- if K is 3.3-5.3: give potassium and start insulin same time
- if K >5.3: start insulin and recheck K in 2 krs
- life threatening effects of hypok: arrhythmias, respiratory paralysis, paralytic ileus, rhabdomyolysis
- GIVE INSULIN IN CONTINUOUS BOLUS: 0.1 UNITS/kg/hr IV*
- if glucose drops < 250-300 mg/dl -> switch fluids to D5NS or D5 1/2 NS and slow insulin rate to 0.05
- continuous insulin infusion till resolution of DKA (D - glucose < 200, K - anion gap 12 or less, beta-hydroxybutyrate < 1; A - pH > 7.3)
HHS: dont know tiny details
- tx: resuscitation with IV fluids slowly, replete K, Mg, phos, insuln, restore renal perfusion, manage the underlying cause
- evaluate for underlying cause: renal insufficiency, sepsis, PNA, GI bleed
- IV Fluids (8-12 L deficit): note HHS develops slowly and deficit should be corrected slowly -> correct 1st 1/2 fluid within 12-24 hrs; give 15-20 mg/kg/hr in first hour (~1-1.5L)
- replete K, mag, phos
- Insulin: SQ to start and switch to IV if persistently hyperglycemic; stop when glucose approaches 300 to prevent cerebral edema from rapid correction
signs and sx of hyperglycemia
Polyuria and polydipsia
Recent weight loss
Nausea, vomiting*
abdominal pain*
Dehydration (especially severe in HHS)
Neurologic symptoms: altered mental status, lethargy, coma, visual disturbances, weakness
DKA-specific: Fruity breath odor (acetone), Kussmaul respirations (rapid deep breathing), DEHYDRATION
HHS-specific: Insidious onset, more profound dehydration, potential focal neurologic deficits and seizures
DKA
-D- diabetes- BS >250
-K- Ketosis- blood beta-hydroxybutyrate -> ketonuria
-A- Acidosis (metabolic anion gap)- pH <7.35, low bicarb <15
-Insulin deficiency → hyperglycemia → hyperosmolality → osmotic diuresis & loss of electrolytes → hypovolemia -> lipolysis & ketogenesis (burning for energy) -> acidosis -> increase gluconeogenesis -> worsens
Triggers:
-Infection!, infarction!, indiscretion! (dont take meds)
-IUP, Illicit drugs, Iatrogenic, Idiopathic
-within 24 hrs and are directly related to:
-HYPERGLYCEMIA
-VOLUME DEPLETION
-ACIDOSIS
-Weakness, confused, AMS
-Blurry vision
-!N/V
-!Abdominal pain
-!Dehydration: Poor skin turgor, dry mucous membranes, tachycardic, orthostatic HoTN, sand paper tongue
-!Rapid/deep breathing (kusmals): compensatory respiratory alkalosis -> this is what kills
-Acetone odor
DKA vs HHS labs
-DKA:
-glucose > 250 (hourly)
-pH < 7.3
-Bicarbonate < 15 (VBG q 2hr)
-Anion gap >10-12
-+ Ketones (serum & urine)
-Beta-hydroxybutyrate >3 (ketones)
-pseudohyponatremia -> high glucose pushes Na into cells but overall Na is normal
-K is low, normal, high but TOTAL K is low!!!!
-high BUN (dehydration)
- mild AMS
-ECG- precipitating MI, hypo/hyperkalemia
-CXR- precipitating PNA/CHF
HHS:
-marked hyperglycemia (600-1000s)
-high serum osmolarity (>320)
-mild/NO ketoacidosis (bc still some insulin)
-severe AMS!
-very mild acidosis pH >7.25
-older pts with T2DM
DKA treatment
-1. FLUIDS
-1st line
-tx dehydration and dilutes hyperglycemia/acidosis
-perfuses kidneys to pee out sugar
-LR/plasmalyte -> 2L bolus rapid over 0-2hrs
-continuous drip 200mL/hr
-too much fluid -> cerebral edema (in kids -> give mannitol or hypertonic saline)
-2. POTASSIUM
-PO or IV K
-!if Mg is low -> 2g IV
-K < 3.3 -> hold insulin until K > 3.5 and GIVE K (20-40/hr)
-K 3.3-3.5 -> GIVE K (20-30/hr) WHILE STARTING INSULIN -> goal K is 4-5
-K > 5.3 -> NO K REPLACEMENT, recheck in 2hrs, start insulin (will close anion gap)
-3. INSULIN
-stops lipolysis/ketosis -> corrects acidemia
-!dont NOT start until you know K
-0.1 U/Kg/hr IV! (no bolus)
-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:
-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
If glucose drops < 200–250 mg/dL:
- Add dextrose (e.g., D5NS)
- Reduce insulin to 0.05 units/kg/hour
K:
- < 3.3 mEq/L HOLD insulin. Give IV KCl. Recheck K⁺.
- 3.3–5.2 mEq/L Give IV KCl while starting insulin. Target K⁺: 4–5 mEq/L
- > 5.2 mEq/L Do not replete. Start insulin. Recheck K⁺ every 2 hrs
insulin:
- 0.1 units/kg/hour IV insulin infusion (no bolus)
- continue until:
- D: Glucose < 200 mg/dL
- K: Anion gap ≤ 12 OR β-hydroxybutyrate < 1 mmol/L
- A: pH ≥ 7.3 or serum HCO₃⁻ ≥ 15
- Patient tolerating PO intake
hyperglycemia hyperosmolar syndrome
-T2DM, elderly, infection, MI, stroke
-!Longer prodrome than DKA (days-weeks)
-!Severe dehydration (> DKA)
-!AMS
-!Abnormal neurologic function
-Often assoc:
-Renal insufficiency
-Gram neg sepsis or PNA
-GI bleed
-Typically NO:
-Abdominal pain
-Kussmauls respirations
-Acetone odor
-BC NO ACIDOSIS
-Tx:
-rehydration
-give K, Mg, phosphate as needed
-SubQ insulin
Recognize Signs and Symptoms of Hypoglycemia
-brain works on sugar -> stroke like sx
-sx start at sugar <60
autonomic/adrenergic sx:
-Sweaty, anxious, tremors, palpitations, dizzy
neuro sx:
-HA, irritable, drowsiness, AMS, difficulty speaking, confusion, inability to concentrate
severe sx: AMS, seizure, death
be aware of: alcohol dependence, malnutrition, and unawareness of hypoglycemia
-factitious hypoglycemia: dont need to know
- normal/low peptide C -> too much insulin
-sulfonylureas, meglitinides, & insulin can cause hypoglycemia
🟦 Hypoglycemia – Rapid Recall Strategy
🔑 Symptoms Start at Glucose < 60 mg/dL
🔷 Think 3 Stages:
Autonomic (“Fight-or-Flight”)
Neuroglycopenic (Brain Starved)
Severe (Life-threatening)
🔹 1. Autonomic/Adrenergic
🧠 Your body’s “alarm system” — early warning signs
Mnemonic: SWAP-DT
Sweating
Weakness
Anxiety
Palpitations
Dizziness
Tremors
🔹 2. Neuroglycopenic
Glucose is the brain’s fuel — now it’s running on empty
Headache
Irritability
Drowsiness
AMS
Confusion
Slurred speech
Poor concentration
Mnemonic: HIDE ASC
🔹 3. Severe
🚨 Medical emergency
Seizures
Coma
Death
🟨 Be Aware of These High-Risk Groups:
Alcoholics (impaired gluconeogenesis)
Malnourished (low glycogen stores)
Elderly / Diabetics with hypoglycemia unawareness
🧪 Lab Pearl for Factitious Hypoglycemia:
Don’t need to memorize deeply for now, but know this clue:
↓ C-peptide → Exogenous insulin overdose
↑ C-peptide → Endogenous (sulfonylureas, insulinoma)
🔄 Common Drug Causes
Insulin
Sulfonylureas
Meglitinides
common causes of hypoglycemia and tx
causes:
- medications: sulfonylureas, meglitinides, & insulin
- illness: sepsis, hepatic failure, adrenal insufficiency
- alcohol, malnutrition
- hypopituitarism
- drugs: salicylates, BBs
tx:
- oral glucose = preferred
- IV dextrose - D50 (adult), D25 kids, d10 infancts
- IM glucagon 1 mg for glycogenolyisis
- sulfonylurea OD recurrent episodes = OCTREOTIDE* (inhibits insulin secretion from pancreas)
hyperthyroidism / thyroid storm
-high CO & and low SV -> activates RAAS -> reabsorb Na to increase preload -> LVH and CHF
-hyperthyroid + end organ damage -> CLINICAL DX
-!Hyperthermia- 104-105F
-!*CNS symptoms: AMS- Agitation, confusion, delirium, seizures, stupor, coma
-!CDV- Tachyarrhythmias, chest pain, CHF (crackles)
-GI/Hepatic- N/V, diarrhea
-Dx:
-CXR- pulmonary edema
-US- nodules, increased flow
-ECG- arrythmias
-thyroid peroxidase antibodies- graves ds
-hyperglycemia, hyperkalemia, LFTs, leukocytosis, leukopenia
signs and symptoms of hyperthyroidism vs thyroid storm
-hyperphagia w/ wt loss
-palpitations, afib, dyspnea
-proximal muscle weakness
-diplopia
-dysphagia, dysphonia, neck full
-pretibial swelling
-decrease menses, libido, gynecomastia
- evidence of HF
-cachexia
- graves: proptosis, pretibial myxedema, lid lag
- -elderly -> SUBTLE sx, depression, wt loss, fatigue
thyroid storm: extreme hyperthyroidism + END ORGAN DAMAGE (CNS!!!!, hyperthermia, cardiovascular) from a TRIGGER
- HYPERTHERMIA: 104F
- CNS SX: AMS - confusion, seizure, delirium**
- CV: tachycardia, chest pain, CHF
- GI: n/v/d
precipitating factors for thyroid storm
thyroid storm = hyperthyroidism + TRIGGER
trigger:
- Infection
- MI
- DKA
- Trauma
- Surgery (especially thyroid surgery)
- Acute illness (e.g. MI, DKA, sepsis)
- Discontinuation of antithyroid drugs
- Iodine exposure (CT contrast, amiodarone)
- pregnancy: Labor and anesthesia induction
hyperthyroid / thyroid storm tx
- ABCs & Supportive care (bc prob suspect sepsis first):
-Fluids (even high output HF will probably need fluids)
-Consider glucose due to low glycogen reserves
-Manage agitation/seizures if present:
-Benzodiazepine: Midazolam 5-10mg IV q5min as needed
-!!Cooling:
-Cooled IV fluids, external cooling!, APAP
-Do NOT! treat fever with NSAIDs or salicylates (ASA) -> use acetaminophen
order of meds:
- 1. cooling meausres
-1. beta blockers - propranolol or esmolol (blocks T4 -> T3)
-1. thioamides: methimazole or propylthiouracil (PTU) -> pref in pregnancy
-PTU blocks thyroid synthesis but ALSO blocks T4 -> T3 -> preferred over methimazole
-2. corticosteroids- hydrocortisone -> give in cooccurring adrenal insufficiency repletes cortisone too!
-3. iodine- 1 hr after thioamide therapy (lugols)
-cooling measures, beta-blocker, thioamide, glucocorticoid!, followed by iodine 1 hour later
-Do NOT delay tx for U/S
-Search and tx for underlying cause including sepsis
-no improvement in 24-48hrs -> thyroidectomy
🔥 What is Thyroid Storm?
An extreme, life-threatening form of hyperthyroidism—usually triggered by:
Infection
Surgery
Trauma
Pregnancy/labor
Stopping antithyroid meds
Iodine contrast
🚨 First Step: Stabilize the Patient (ABCs)
You’re in EM setting, so treat it like sepsis until proven otherwise:
Airway, Breathing, Circulation
Give IV fluids — they may be dehydrated despite heart failure due to high output state.
Check glucose – liver has low glycogen, so hypoglycemia is possible.
Control agitation/seizures – use benzodiazepines like midazolam IV.
Cooling measures – external cooling, cooled IV fluids, acetaminophen ONLY.
❌ Do not give NSAIDs or aspirin – they displace thyroid hormones from binding proteins, worsening the storm.
💊 Specific Medications – IN ORDER
1. Beta-blocker: Propranolol or Esmolol
Blocks symptoms (tachycardia, tremor, anxiety).
Also blocks T4 → T3 conversion (which makes it uniquely useful!).
Esmolol IV is fast, short-acting (good in ICU); propranolol is oral or IV.
- Thioamide: Methimazole or PTU
Block thyroid hormone synthesis.
PTU preferred in thyroid storm because:
It blocks both hormone production and T4 → T3 conversion.
Safer in pregnancy.
Give before iodine to prevent iodine from fueling more hormone production.
- Corticosteroid: Hydrocortisone
Reduces T4 to T3 conversion.
Treats possible adrenal insufficiency (many are depleted due to stress).
Helps with systemic inflammation.
- Iodine solution (e.g., Lugol’s solution, potassium iodide)
Blocks release of preformed T3/T4.
MUST be given 1 hour after thioamide to avoid iodine stimulating more hormone release (“Jod-Basedow effect”).
⚠️ Other Important Points
Don’t delay treatment waiting for imaging or labs (e.g., thyroid ultrasound).
Search for the trigger – infection is common → get cultures, treat with antibiotics if needed.
If the patient does not improve in 24–48 hrs, consider thyroidectomy.
🧠 Mnemonic for Order: “Beta Blocker, Block the Thyroid, Block the Conversion, Block the Release”
Beta blocker
Thioamide (block synthesis)
Steroid (block conversion)
Iodine (block release)
Why is PTU preferred over MMA for thyroid storm management?
thioamides: methimazole or propylthiouracil
PTU:
- pref in pregnancy
-PTU blocks thyroid synthesis but ALSO blocks T4 -> T3 = preferred over methimazole***
- less side effects: but black box liver injury
both can cause agranulocytosis
Is aspirin indicated in thyroid storm for fever?
NO AVOID:
- It displaces T₄/T₃ from binding proteins → worsens thyrotoxicosis
- USE ACETAMINOPHEN
What is needed for concomitant adrenal insufficiency in thyroid storm?
Thyroid storm may cause relative adrenal insufficiency due to high cortisol turnover
- Steroids to jumpstart the HPA and its more responsive to other tx
Treat with IV glucocorticoids:
- Hydrocortisone (preferred)
hypothyroid / myxedema coma: precipitating factors, how is it different than hypothyroidism
MYXEDEMA COMA:
-multiorgan failure
-triggers: hypothermia, infection (blood cx), stroke, MI, trauma, CHF, GIB, missed meds, surgery
-older women in winter
Key findings:
-Hypothermia (<96)
-AMS!
-Hypotension!
-!hypoglycemia
-!hyponatremia
-precipitating factor
-ABG- shallow respiration -> hypercapnia and hypoxia (risk of respiratory failure)
-!ECG- Bradycardia!, heart block!, long QT!, torsades de pointes!, ventricular arrythmias!
-torsades -> mag sulfate
- fluid retention: myxedema facies - puffy eyelids and lips, large tongue (macroglossia)
-low voltage from pericardial effusion
-cardiogenic shcok
- neuro sx: confusion, obtunded, lethargy, depression, psychosis
myexdema coma EKG and cardiac sx
-!ECG- Bradycardia!, heart block!, long QT!, torsades de pointes!, ventricular arrythmias!
-torsades -> mag sulfate
- fluid retention: myxedema facies - puffy eyelids and lips, large tongue (macroglossia)
-low voltage from pericardial effusion: often needs chest tube
- cardiogenic shock
hypothyroidism sx
- Fatigue, lethargy
- Cold intolerance
- GI: Constipation, low motility
- Weight gain
- Bradycardia
- Dry skin, hair thinning
- macroglossia
- Menstrual irregularities
- Depression, cognitive slowing
- puffy hands, ascities
- Myxedema (non-pitting edema, esp. face, hands, pretibial)
hypothyroid / myxedema coma tx
STEROIDS:
-Hydrocortisone FIRST -> jump start adrenals
-Send off cortisol before dosing
REPLACEDMENT OF THYROXINE:
-IV levothyroxine (T4): Gold standard
-Not PO! (Bc AMS and GI is not moving)
SUPPORTIVE CARE:
-Fluids
-Warming
-Correct hypoglycemia and hyponatremia
-ICU
myxedema coma dx
Calculate corrected sodium level (not on test)
why is it useful in DKA?
-1.6 mEq should be added to the reported Na for every 100 mg of glucose >100 mg/dL
Example:
-Na 130, glucose 350
- 350 - 100 = 250
- 250/ 100 = 2.5
-1.6 x 2.5 = 4
-4 + Na 130 = 134 mEq/L corrected sodium
DKA: PSEUDOHYPONATREMIA
- should actually be higher
- If blood sugar is high, sodium looks falsely low on labs. So we “correct” it to see what the sodium would be if sugar were normal.
Find the glucose over 100
(just subtract 100 from the glucose)
Divide that number by 100
Multiply that by 1.6
Add that to the sodium level on labs
hyperkalemia: normal range, causes, sx
-3.5-5.0 normal
- mild: 5.5
- mod: 6
- severe > 7
causes:
-MCC- renal failure
-Acidosis, drugs (spironolactone, BB, ACE, ARBs, K supplements), rhabdo, hemolysis (fictitious)
sx: nonspecific
-muscle weakness
-lethargy
-GI sx
-paresthesias
-SOB
-anxiety/irritable
-arrythmia: long QRS, VFib
