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
clinical presentation of HHS
-!Longer prodrome than DKA (days-weeks)
-!Severe dehydration (more than DKA)
-!Altered mental status
-!Abnormal neurologic function
-Often associated with…
-Renal insufficiency
-Gram negative sepsis or PNA
-GI bleed
-Vital signs
-Tachycardic
-Low blood pressure
-± fever
-Typically NO
-Abdominal pain
-Kussmauls respirations
-Acetone odor
-BC NO ACIDOSIS
typical labs of DKA and HHS
-dont know diff of mild mod severe
HHS management (dont need to know details)
-!Resuscitation via Rehydration*
-Deficit 8-12L
-HHS develops slowly, it should be corrected slowly
-First half of fluid deficit should be corrected within first 12-24 hours
-First hour should be given 15-20mg/kg/hr (approximately 1-1.5 L in avg adult)
-IVF at 250-500mL/hr
-Replete potassium, magnesium, phosphate as needed
-Insulin
-Subcutaneous is usually fine to start with
-If persistently hyperglycemic, start IV insulin at 0.05 U/kg/hr (except if ↓ K)
-Stop when glucose approaches 300mg/dL to prevent cerebral edema from rapid correction
-Evaluate for underlying cause
-Dispo: ICU
-GOALS:
-Expand volume
-Restore renal perfusion
-Correct sodium & osmolarity
-Manage underlying cause
HHS complications
-Large vessel thromboembolism
-Disseminated intravascular coagulation
-Nontraumatic rhabdomyolysis
-Cerebral edema- Complication of therapy d/t the quick infusion of fluids
hyperglycemia (POC)
-start fluids
-U/A for ketones, serum electrolytes, and glucose, VBG, CXR, ECG
-negative ketones, normal AG, normal pH -> hyperglycemia -> tx with fluids
-(dont need to know) positive ketones, normal AG, normal pH -> diabetic ketosis
-positive ketones, elevated AG, pH <7.3 -> DKA
-trace or neg ketones, normal AG, normal pH, elevated serum Osm -> HHS
A 32-year-old female with a history of diabetes presents with loss of strength in her right hand and arm and an inability to speak. Her family member states that she was fine when she went to bed last night, but on awakening this morning had difficulties walking downstairs and was unable to speak and unable to move her right arm. The patient’s diabetes is managed with an insulin pump, and she has been dieting recently.
why does hypoglycemia happen
-too little food
-burning too many calories
-too much insulin
-oral hypoglycemia agents
hypoglycemia
-Brains work on sugar! (stroke like sx!)
-Develop symptoms when blood sugar <60mg/dL
-Common sxs:
-Adrenergic: !Sweaty, anxious, tremors, palpitations, dizziness
-Neurologic: !Headache, irritability, drowsiness, confusion, inability to concentrate, difficulty speaking
-Severe hypoglycemia can cause AMS, seizures, death
-Beware: hypoglycemic unawareness - dont realize these sx
-Beware: alcohol dependence or malnutrition- dont realize these sx
hypoglycemia dx
-Check their serum blood glucose level
-<50-60 mg/dL is low
-If you are suspicious of factitious hypoglycemia:
-Normal or low levels of peptide C -> means they are giving too much insulin
-High levels of insulin
hypoglycemia management
-GIVE GLUCOSE:
-Oral glucose preferred
-IV dextrose
-D50 in adults
-D25 in children
-D10 in infants
-IM glucagon 1mg
What class of oral hypoglycemic agents can cause prolonged and severe hypoglycemia?
Sulfonylureas!!!
Alpha-glucosidase inhibitors
Dipeptidyl peptidase-4
Thiazolidinediones
Biguanides
possible sulfonylurea overdose
-Long half-life = Prolonged and Recurrent hypoglycemic episodes
-Initial treatment = oral sugar or IV dextrose
-Recurrent episodes may require octreotide!!!*
-Inhibits insulin secretion from pancreas
-Subcutaneous or IV infusion
-Dispo: Often admission
hypoglycemia conclusion
-Glucose metabolism is regulated by insulin and glucagon
-Hyperglycemia can be a result of uncomplicated hyperglycemia, DKA or HHS. Labs, history, physical can help distinguish between these.
-In DKA and HHS, look for an underlying cause
-Do not begin insulin treatment until a potassium level is resulted
-Check a finger stick for all patients who present with altered mental status
-Hypoglycemia is common in diabetics and malnourished patients and requires prompt treatment to prevent seizures and coma
potassium and hyperkalemia
-Regulated by the kidney
-Normal K is 3.5 – 5.0 mEq/L
-Primarily intracellular cation
-Kidney failure, or, dialysis patients are at higher risk of hyperkalemia
-Cardiotoxicity
-Arrythmias (long QRS, Vfib)
-Cardiac arrest
-Increased membrane excitability
-Hyperkalemia = too much outside the cells, > 5.5
-Mild 5.5 – 5.9 mEq/L
-Moderate 6.0-6.9 mEq/L
-Severe >7.0 mEq/L
-MOST DANGEROUS ELECTROLYTE ABNORMALITY
hyperkalemia etiology
-Renal failure- MC
-Acidosis
-Drugs
-Spironolactone
-Beta-blockers
-ACE-I or ARBs
-Potassium supplements
-Cell breakdown in rhabdomyolysis or burns
-Lab hemolysis causes fictitious hyperK (tourniquet, gauge, shake)
hyperkalemia sx
-Nonspecific
-Muscle weakness
-Lethargy
-GI symptoms
-Paresthesias
-SOB
-Anxiety/Irritability
-Cardiac arrythmias
hyperkalemia: EKG stat
-As K+ level rises you get…
-Peaked T waves and prolonged PR intervals
-Widened QRS and flattened P waves -> Ectopic beats, escape rhythms
-Sine wave pattern - Vfib, asystole
-top pic is starting to get widened QRS
hyperkalemia
-the QRS is getting so wide -> sin wave
hyperkalemia tx goals
-place on cardiac monitor, STAT ECG
-#1 stabilize the cardiac membrane: IV calcium
-#2 Shift the potassium intracellularly: Insulin+D50 / Albuterol
-#3 Excrete total body potassium
-other measures
-If all else fails -> def tx is hemodialysis
HYPERKALEMIA: STEP 1: IV CALCIUM
-Use in pts with !ECG changes!
-Stabilizes the cardiac membrane
-protects the heart
-Effect lasts 30-60 minutes
-doesnt actually treat at all
-IV calcium
-1g calcium chloride or
-3g of calcium gluconate
HYPERKALEMIA TX: STEP 2: INTRACELLULAR SHIFT
-Insulin + D50*
-Administer IV insulin (5-10U IVP)
-Caution in end stage renal ds (ESRD), use lower dose of 5U (hard on kidney)
-Peak effect in 30 minutes, lasts 2-4 hours
-1 amp D50 is to prevent hypoglycemia
Give if glucose <250 or glucose unknown
-Beta-2-agonist:
-Nebulized albuterol 10-20mg / 10 min
-Very high dose needed
-Peak effect 30 minutes
-Lasts 2-6 hours
-Sodium bicarb
-Not really given, can consider if extremely acidotic
HYPERKALEMIA: STEP 3: POTASSIUM EXCRETION
-!!1. Dilute the potassium : IV fluids -> dilutes, increases blood flow to kidneys for excretion
-!!2. THROUGH THE URINE:
-Furosemide! (loop diuretic)
20-40 mg IVP , Onset 30-60 minutes
-Esp good in fluid overload with functioning kidneys, tumor lysis or rhabdomyolysis
-!!3. THROUGH THE STOOL: Cation exchange resins
-!Sodium zirconium cyclosilicate (LOKELMA) (PATIROMER [VELTASSA])
-Sodium polystyrene sulfonate [Kayexalate] is generally no longer recommended due to potential risk of intestinal necrosis
-Takes effect >4 hours , is NOT used for emergency treatment for life threatening hyperK
-ex. pt with 5.7 and no ECG changes, stop meds that may be causing it and send home with give lokelma
-!4. THROUGH A MACHINE:
-Hemodialysis; Definitive treatment
-Most effective, usually reserved for those with ESRD or critically ill
HYPERKALEMIA: STEP 4: OTHER MEASURES
-Renal diet
-Avoid potassium-sparing diuretics (spironolactone)
-Use potassium-losing diuretics if needed (furosemide)
hyperkalemia: dispo
-Mild hyperK can be managed on an outpatient basis
-All moderate to severe hyperK should be admitted to a monitored unit
-Unstable to ICU
A 54-year-old woman presents with the sudden onset of palpitations and mild shortness of breath. She denies any chest pain or lower extremity swelling. She has no history of alcohol use. Review of systems is positive for an unintentional 20-lb weight loss over last 2 months, despite an increased appetite.
Vitals: Pulse 180, blood pressure 150/86, respiratory rate 26, temperature 101.3F.
On exam, she is diaphoretic and appears anxious. Heart and lung exams reveal tachycardia with no murmurs and clear lung sounds.
thyroid: overview
-TYPICALLY
-Elevated TSH => hypothyroidism
-Low TSH => hyperthyroidism -> Unless pituitary failure…
-TSH screening
-Pathophysiology of hyperthyroidism
-Excess endogenous T3/T4, or exogenous ingestion
-↑ Cardiac output & ↓ SVR which activates RAAS to reabsorb sodium to increase preload
-Long term untreated causes LV hypertrophy and CHF
etiology of hyperthyroidism (she did go over this)
-GRAVES DS:
-MC
-women 20-50yo
-autoantibodies that bind to TSH receptors
-Toxic multinodular goiter:
-2nd MC
-women >50yo
-multiple, autonomously functioning, nodules
-milder presentation than graves
-Thyroiditis:
-Autoimmune (Hashimoto’s) (Post partum)
-Drug-induced (Amiodarone, lithium, contrast, factitious)
-Infectious (subacute, suppurative)
-Traumatic
-Other causes include a !toxic adenoma, TSH-producing adenoma or pituitary adenoma!, significant physiologic stressors, underdosing or overdosing of any home medications.
S&S of hyperthyroidism
-constitutional- wt loss despite hyperphagia, fatigue
-metabolic- heat intolerance, excessive perspiration
-cardiorespiratory- palpitations, afib, dyspnea, DOE
-GI- N/V, dysphagia
-neuropsychiatric- anxiety, restlessness, insomnia
-neuromuscular- myopathy, proximal muscle weakness
-ophthalmologic- diplopia, FB
-thyroid gland- dysphagia, dysphonia, neck fullness
-dermatologic- flushed, thinning hair, pretibial swelling
-reproductive- decreased menses, decreased libido, gynecomastia
-elderly- more subtle sx!!!, depression, fatigue, wt loss
signs of hyperthyroidism
-Cachectic
-Hyperthermic
-Diaphoretic
-Anxious
-Tachycardia / Atrial fibrillation
-Tremors
-Hyperreflexia
-Evidence of heart failure
-May have a goiter, palpable thrill, nodules
-Grave’s may have proptosis with lid lag and pretibial myxedema
thyroid storm
-Extremely rare
-Extremely dangerous- 100% mortality if untreated
-Due to:
-!Untreated / undertreated thyrotoxicosis
-!Acute stressors: Thyroid surgery, trauma, infection, pulmonary embolus
-Ultimately leads to cardiovascular collapse
-HYPERTHYROIDISM WITH END ORGAN DAMAGE- NO LABS WILL DIFFERENTIATE: DO PE:
-must be clinical dx:
-!Hyperthermia- 104-105F
-!*CNS symptoms: AMS- Agitation, confusion, delirium, seizures, stupor, coma
-!Cardiovascular- Tachyarrhythmias, chest pain, CHF
-GI/Hepatic- Nausea, vomiting, diarrhea
STORM = HYPERTHYROID STATE + TRIGGER
-Infection
-MI
-DKA
-Pregnancy
-Trauma
-Surgery
-Amiodarone (iodine)
-CT contrast
EVAL in hyperthyroidism/thyroid storm
-Hyperthyroidism exists on a continuum of severity
-Suspect storm based on clinical picture (fever, cardiac, CNS sxs)
-Fever
-Cardiac: Tachyarrhythmias, chest pain, SOB, CHF (crackles)
-CNS: Agitated, confused, psychotic, seizures
-Hemodynamic instability is expected
-!!Low TSH: depressed or undetectable
-!!Elevated Free T4 and T3 (bioactive markers)
-CBC, BMP, Cultures -> May also reveal hyperglycemia, hypercalcemia, abnormal liver function tests, leukocytosis, or leukopenia.
-CXR for pulmonary edema
-U/S for nodules or increased vascular flow
-ECG to look of arrythmias or afib
-Thyroid peroxidase antibodies present in 75% of Grave’s disease
-DDX
-Heat stroke
-Sepsis
-Toxins (sympathomimetics, serotonin, NMS)
thyroid storm management
-#1 ABCs & Supportive care (bc you prob suspect sepsis first):
-Fluid resuscitation
-Many will need fluids, and even high output heart failure will probably need fluids
-Consider adding glucose due to low glycogen reserves
-Manage agitation / seizures if present
-Benzodiazepine: Midazolam 5-10mg IV q5min as needed
-!!Cooling measures
-Cooled IV fluids, external cooling!, APAP
-Do NOT! treat fever with NSAIDs or salicylates (ASA)
-Initial treatment: !cooling measures, beta-blocker, thioamide, glucocorticoid!, followed by iodine 1 hour later
-Do NOT delay treatment for an ultrasound study
-Search and treat for underlying cause including sepsis
thyroid storm management
-#1 Beta blockers : BLOCK THYROID EFFECTS
-Propranolol or esmolol
-Inhibits peripheral conversion of T4 -> T3
-Non-selective to help with tremors, agitation
-Target heart rate 100bpm
-#1 Thioamides: BLOCK THYROID SYNTHESIS
-Methimazole - Loading dose: 20-25mg PO ->Longer acting
-!Propylthiouracil (PTU) - Loading dose: 600-1000mg PO -> Preferred in early pregnancy
-Black box liver injury warning
-Also blocks conversion of T4->T3 * preferred
-Both can be PO or PR (no IV version in USA)
-Both can cause agranulocytosis
-#2 CORTICOSTEROIDS: Use because of HPA depression
-Hydrocortisone 300mg IV
-Improved survival with early steroid administration
-Also inhibits T4->T3
-#3 IODINE: BLOCK THYROID RELEASE
-Inhibit release of preformed thyroid hormone
-NOT administered immediately!!
-Given at least 1 hour after thioamide therapy!
-Saturated solution of potassium iodide (SSKI) – 5 drops by mouth q6h
-Lugol’s solution
-Sodium iodide
thyroid storm disposition
-ICU (usually intubated)
-Endocrine consult
-No improvement in 24-48 hours will likely require thyroidectomy
-Takes weeks for TFTs to normalize after management
What beta blocker is used primarily for the management of thyrotoxicosis?
Bisoprolol
Timolol
Carvedilol
Atenolol
Propanolol!!!!!!!!!!
A 67-year-old man presents from an extended care facility with increased lethargy and inability to assist with his activities of daily living. He has been undergoing an aggressive bowel regimen for constipation over the last week, which has largely been unsuccessful. A chart review shows a history of congestive heart failure and longstanding hypertension. His current medications include hydrochlorothiazide and amlodipine. He is unable to participate in the history.
HR 54, BP 100/85, RR 12, and Temp of 95.6F.
He is sleepy but arousable.
Laboratory analysis shows: Na 125, Cl 98, K 3.8, BUN 60, Creatinine 1.77, glucose 78. His TSH is elevated and free T4 is low.
hypothyroidism
-thyroid gland fails to produce adequate amounts of thyroid hormone
-PRIMARY (99%):
-Due to gland failure itself
-Autoimmune: Hashimoto’s
-Infiltrative
-Pregnancy
-Congenital
-SECONDARY:
-Lack of stimulation of the gland (pituitary or hypothalamus issues)
Hypothyroidism S&S
-varied symptoms -> from vague to over organ failure
-fatigue, weakness
-wt gain
-bradycardia
-cold intolerance
-low GI motility
-dry skin, coarse brittle hair
-macroglossia
-puffy hands, ascites
myxedema coma (a misnomer)
-dont always have the myxedema or coma
-clinical dx
-Life-threatening (mortality as high as 30-60%)
-Severe hypothyroidism -> multiorgan failure
-History of hypothyroid, thyroidectomy, pituitary surgery
-Precipitated by:
-Hypothermia
-Infection: sepsis
-Stroke
-MI
-Or any other stress! -Trauma, CHF, GIB, missed/underdosed meds, surgery
myxedema coma key findings
-Classically: Older woman in winter with known hypothyroidism / thyroidectomy
-Key findings:
-Hypothermia (<96.0 F) (<35.5 C)*
-Altered mental status*
-Hypotension* , Bradycardia*
-Precipitating factor
-Hypoglycemia
myxedema coma: resp, cardio, neuro
-Resp:
-Slow, shallow respirations -> hypercapnia and hypoxia
-High risk of respiratory failure
-Cards:
-!ECG: Bradycardia, heart blocks!, long QT!, torsades de pointes!, and ventricular arrythmias!
-mag sulfate for torsades!!!
-May have low voltage from pericardial effusion!
-Cardiogenic shock!
-Fluid retention causing myxedema facies! – puffy eyelids and lips, large tongue
-Neuro:
-Confusion, obtundation, lethargy, coma, seizures, poor cognitive function, depression, psychosis
-Chronic hypothyroidism – skin, hair, ↓ DTR
-pleural effusion
-myxedema coma
-thoracentesis
-also get pericardial effusion
hypothyroid dx
-Thyroid: High TSH, Low T4/T3!
-BMP: Hypoglycemia! and hyponatremia!
-LFTS: Elevated liver function tests
-Blood cultures to rule out sepsis
-Cortisol levels
-Blood gas: Hypoxemia, hypercapnia
-Before treating… rule out MI/Adrenal crisis
-Aggressive T4 replacement can increase risk of MI and adrenal crisis
-Check cortisol levels
-ECG, troponins
hypothyroid tx
-STEROIDS:
-Hydrocortisone 100mg first
Jump start adrenals
Send off cortisol level before dosing
-REPLACEDMENT OF THE THYROXINE:
-IV levothyroxine (T4) 200-400mcg loading dose : Gold standard
-Not PO! (Bc AMS and GI is not moving)
-SUPPORTIVE CARE:
-Fluids
-Warming
-Correct hypoglycemia and hyponatremia
-ICU
