Endocrine Flashcards
Endocrine system
Includes pituitary gland, hypothalamus, adrenal glands, thyroid gland (and others).
Regulate growth, metabolism, sexual development.
Serum osmolality
275-295 mOsm/kg
(about double normal Na level)
Helps maintain fluid balance.
Measure of solute in relation to available fluid or plasma.
If >295, pt is volume depleted (high = dry)
…body will attempt to retain fluid by releasing ADH.
If <275, pt os volume overloaded and body doesn’t release ADH
SIADH
Too much ADH is released.
Pt retains water.
Oliguria (decreased output)
…will have high specific gravity (>1.030)
Dilutional hyponnatremia
Serum osmolality <270
Edema is NOT present
Neuro sx caused by cerebral edema
Pulmonary edema and dyspnea
Causes:
carcinoma of the lung
…produces a substance like ADH
Head problems
…trauma, tumors, CVA, meningitis
Hypoxemia
Nephrogenic causes
…anesthetics, narcotics, Tylenol, anticonvulsants
SIADH treatment
Fluid restriction
Consider hypertonic saline
…1-2mL/kg/hr until asymptomatic
Raise serum sodium 0.5mEq/L per hour
Can raise Na faster if the drop was faster
Consider lasix 1mg/kg
Avoid hypotonic solutions
Don’t use D5W
Diabetes Insipidus
Opposite of SIADH - not enough ADH
Constant urination (polyuria)
Low urine specific gravity (clear)
Dehydration
Elevated serum Na
Elevated serum osmolality
urine hypo-osmolality
Causes:
head injury, infection, tumors, lithium, dilantin
Results in:
Hypovolemia, shock, electrolyte imbalances
Treatment of Diabetes Insipidus
Aggressive IV fluid replacement.
Raise sodium slowly
Consider vasopressin (synthetic ADH)
Monitor urine specific gravity and cardiac changes.
DKA
Not enough insulin, body breaks down fat
…Buildup of ketones
Leads to acidosis.
Characterized by hyperglycemia, dehydration, and acidosis.
Acidosis with elevated glucose is an indication of DKA rather than HHS
Symptoms:
Acidosis (elevated ketones)
Ketones can cause fruity breath
Kussmaul respirations (rapid, shallow to breath off CO2
Increased serum osmolality
Dilutional hyponatremia.
Potassium loss from inside cell to oudside cell (trying to offset hydrogen
…potassium may be elevated initially
Hypokalemia is most common cause of death
For every 100mg/dL glucose over 100, serum sodium decreases by 1.6 mEq/L
DKA treatment
Aggressive fluid: 100-150mL/kg
…1/2 in first 8-12 hrs and rest in 16-24hr
Switch to D5NS when glucose = 300
Insulin drives glucose, K, and H2O back into cells, so if they haven’t been hydrated they could go into circulatory collapse.
When managing DKA, focus on treating acidosis prior to administration of insulin.
…focus on improving acidosis, not glucose.
Prevent hypokalemia
Add 10-40 mEq/L/hr to fluids
Add insulin after hydrating and managing K
0.1 units/kg bolus. Same dose/hr drip
Don’t reduce glucose > 100mg/dL/hr
…glucose is a large molecule; water follows it easily which can cause fluid to third space back into the tissue, especially the brain…causing cerebral edema.
Bicarb will be low due to metabolic acidosis but not routinely given because when insulin is given, lactate and ketones will be metabolized into bicarb.
Corrected Sodium (DKA)
measured sodium + (serum glucose-100)0.016
Hyperosmolar Hyperglycemic State (HHS)
Similar to DKA but these pts still have some insulin…aren’t breaking down fatty acids
Acidosis NOT present
Blood sugar range 1000-2000
…Takes longer for sx to present themselves
Dehydration
HHS treatment
Aggressive fluid (1-2L in first 2 hrs)
Switch to 1/2NS once blood pressure and urine output stabilize.
Switch to D5NS when glucose = 300
Add insulin 0.1units/kg bolus, same dose/hr drip
Do not reduce glucose >100 mg/dL/hr
Prevent hypokalemia
…start K replacement at 5 or less because giving insulin will cause lower K.
Thyroid Storm
Life threatening exacerbation of HYPERthyroidism
Excess circulating thyroid hormone
Impacts many systems
O2 demand quickly exceeds supply
Anaerobic metabolism…increased lactate
Triad:
Hyperthermia - up to 104
Tachycardia
AMS
Diaphoresis, N/V/D
Decreased TSH, increased T3 and T4
Cardiovascular collapse, hypovolemia
Treatment:
Propranolol, esmolol (B-adrenergic blocker
Block new hormone production
…PTU and methimazole
Treat adrenal insufficiency w/glucocordicoids (dex or hydrocortisone
Supportive care:
Aggressive cooling
Acetaminophen (only) for fever
D5NS for dehydration and hypoglycemia
Benzos for agitation
May have crackles but not from overload
Myxedema Coma
Extreme manifestation of HYPOthyroidism
Compensatory response to hypothyroidism is overwhelmed by precipitating factors, leading to a loss of brain function.
Findings:
hypothermia, puffy face, edema, dry skin
AMS, bradycardia, hypotension
Free T4/T3 low. TSH high
90% cases occur during winter months.
Treatment:
IVF resuscitation, vasopressors if needed.
IV corticosteroids
IV thyroid hormone replacement
Cushing’s syndrome
prolonged exposure to glucocorticoids or pituitary tumor.
Weight gain, buffalo hump, moon face.
Treatment:
Surgical removal of tumor
adrenal steroid inhibitors
Gradual removal of glucocorticoids.
Adrenal Insufficiency
Occurs when the adrenal glands fail to supply the body’s demand for glucocorticoids; cortisol and aldosterone.
Cortisol:
helps regulate blood sugar
holds back immune response
released in response to stress
Aldosterone
Helps maintain BP and water/salt balance
Adrenal insufficiency findings:
Hypotension, not responsive to IVF/pressors
Hypoglycemia
Abdominal pain/tenderness
Fever
confusion/lethargy
Low bicarb, non anion gap metabolic acidosis
Treatment:
IVF = D5 NS (2-3L)
Administer steroids (hydrocortisone, dexamethasone, prednisone)
Vasopressors if not responsive to IVF
Sickle Cell Crisis
Autosomal recessive disorder most common in ppl with African ancestry
Sickle shaped RBCs
Increases risk of infection due to damaged cells clogging the spleen.
Symptoms: most commonly severe pain
Treatment:
pain management
Maybe PRBC transfusion
Sepsis
Systemic inflammatory response to infection
Clotting cascade
- Vasoconstriction
Vessel walls constrict, causing reduced blood flow to injury - Platelet plug formation
Platelets aggregate to the injury site and stick together, forming a ‘plug.’ - Clot formation
Fibrin proteins stick together in a mesh-like structure, forming a clot
Clot is then broken down after bleeding stops
DIC (disseminated intravascular coagulopathy)
Not a specific disease - always secondary
Overstimulation of the clotting cascade, secondary to massive tissue damage.
Causes blood clots to form through body’s small blood vessels.
Clots can reduce or block blood flow leading to organ/tissue damage.
Excessive clotting uses up platelets and other clotting factors which can lead to significant bleeding.
True danger lies not in excessive bleeding but in formation of clots within small blood vessels - leading to tissue ischemia and organ failure.
Contributing factors: sepsis, surgery, trauma, cancer, pregnancy/childbirth
Treatment:
Treat underlying condition.
Heparin (inhibits conversion of prothrombin to thrombin)
Anti-thrombin 3
TXA -tranexamic acid if active bleeding only
SIRS (systemic inflammatory response syndrome)
Sepsis screening criteria:
temp >38C or <36C
HR >90
RR >20 or PaCO2 <32 mmHg
WBC >12k or <4k
Septic Shock
Sepsis with profound circulatory, cellular, and metabolic abnormalities.
Requires vasopressors to maintain MAP of 65 or greater.
Serum lactate >2 in absence of hypovolemia
Sepsis pathophysiology
Immune system over-activated
Inflammatory cascade:
pro inflammatory cytokines and mediators
Capillary leakage –> profound vasodilation and hypotension
Neutrophils release nitric oxide which is a potent vasodilator
Inflammation - coagulation
Clot formation
Production of thrombin leads to fibrin clots –> potential to develop DIC
Cardiovascular insufficiency
multi-organ failure
Sepsis presentation
Initially hyperdynamic (high cardiac output), but become hypodynamic as sepsis progresses
Ventricular dilation
Loss of sympathetic responsiveness
Hyperventilation with respiratory alkalosis
Sepsis treatment
Rapid fluid resuscitation and early abx
30mL/kg IVF based on actual body weight
Fluids started within 1 hour and completed within 3 hrs of initial presentation
Large, rapid fluid boluses w/reassessment
abx should be started within 1 hr
Vasopressors if IVF no longer effective
…norepinephrine first line
Possibly epinephrine or vasopressin
If IVF and vasopressors are not sufficient within the first 6 hrs, consider dobutamine or PRBC transfusion
In hypovolemic shock, anticipate this type of renal failure…
pre-renal failure.
Kidneys are not being perfused enough, so there is a failure ‘before’ the kidneys.
