Endocrine Flashcards
1
Q
Preop assessment components?
A
- Dx of proposed procedure
- Medical Hx –Review of systems
- Current medications- herbs, minerals, PRn meds
- Allergies
- Physical exam
- Airway Exam
- Lab findings
- Surgical Hx – previous complications
- ASA status
- Consent
2
Q
What is the thyroid gland? Role?
A
Gland:
- Two lobes connected by an isthmus
- 4 parathyroid glands located posteriorly
- Superior larngeal nerve – external branch and RLN (recurrent laryngeal nerve) transverses the boarder
- Produces – T4 (thyroxine - prohormone) and T3 (triiodothyronine - active)
Role:
- Cell differentiation
- Organogenesis
- Thermogenesis
- Metabolic homeostasis
3
Q
What is the HPA axis for thyroid hormone release?
A
- Homeostasis disturbed, low T3/T4 detected at hypothalamus or low body temperature
- hypothalamus releases TRH
- Goes to anterior pituitary to release TSH
- TSH goes to thyroid gland to release T3/T4
- Normal homeostasis maintained with normal T3/T4 and normal body temp
4
Q
Difference between T3/T4?
A
T3
- Active
- 30 mcg/day
- 10% by gland (80% kidney/liver)- peripheral conversion in kidney and liver
- 3-4x’s as potent
- 1 day
T4
- Inactive
- 80 mcg/day- 2-3 x the amount of T3
- Solely by gland
- Potent
- 7 days- keep in mind people can still have s/s hyperthyroidism up to one week after surgery
5
Q
Causes of hyperthyroidism?
A
- Primary
- Graves disease (autoimmune disorder)- tricks receptor to thinking it’s TSH
- Toxic adenoma (gland overgrowth from lack of iodine)
- Multinodular goiter (genetics/lack of iodine)- Similar to toxic adenoms but can have genetic component too
- Secondary- something besides the thyroid causing excess T3/T4 to be made
- TSH secreting pituitary adenoma
- Tertiary
- Amiodarone toxicity
6
Q
S/S Hyperthyroidism?
A
- Neuro
- Anxiety & fatigue
- Ophthalmology
- Exophthalmos
- CV
- HTN, tachycardia, atrial fibrillation, & increased CO
- GI
- Diarrhea and weight loss
- Renal
- Hypercalciuria
- MS
- Muscle weakness
- Goiter
- Weight loss
7
Q
What with Free T4, free T3 and TSH be on labs for graves disease, multinodular goiter, and toxic nodules?
A
- Graves Free T4/T3 elevated, TSH down; TSH antibody present; RAIU diffuse uptake
- Mulinodular T4/T3 elevated, TSH down; RAIU areas of increased and decreased uptake
- Toxic nodule T4/T3 elevated; TSH down; RAIU focal uptake
8
Q
Potential treatment hyperthyroidism?
A
- Anti-thyroid drugs (Inhibits thyroid hormone synthesis)
- Methimazole or Propylthiouracil (PTU) – takes 6 -8 weeks
- Iodine inhibiting drugs (prevent hormone release)
- Potassium iodine
- Steroids (prevents conversion of T4 to T3/decrease secretion)
- Decadron 6 mg
- Hydrocortisone 100 mg
- Beta blockers (block adrenergic stimulation)
- Propranolol (prevents conversion of T4 to T3)
- Esmolol- blocks sympathetic, rapid on/off
9
Q
Anesthesia implications for hyperthyroidism
A
- most important goal is to make the patient euthyroid before surgery-can take 6-8 weeks
- Adequate depth of anesthesia to limit SNS activation
- Avoid medications that stimulate SNS
- Ketamine, pancuronium, ephedrine, or anticholinergics
- HR goal: < 85 bpm
-
Excellent airway exam
- X-ray or CT to evaluate airway compression
- Regional is excellent alternative (avoid adding epinephrine to solution)- avoid epi more theoretical risk with systemic absorption
- Eye protection
- Temperature monitoring – may need to cool
10
Q
S/S and differntial for thyroid storm?
A
Thyroid Storm
- Life-threatening emergency
- Response to stress
- Hyperpyrexia
- Tachycardia
- Myocardia ischemia
- Alterations in consciousness- difficult to see periop
Differential
- Light anesthesia
- Pheochromocytoma
- Neuroleptic malignant syndrome
- Malignant hyperthermia
11
Q
Treatment thyroid storm
A
- IV fluids
- Propylthiouracil via NGT
- Sodium iodide
- Hydrocortisone
- Propranolol/esmolol
- Cooling blanket
- Acetaminophen
- Meperidine
- Digoxin
12
Q
Primary and secondary causes for hypothyroidism?
A
Primary
- Hashimoto thyroiditis (autoimmune)
- Surgical removal of thyroid
- Severe iodine depletion
- Neck radiation
Secondary
- Pituitary disfunction
- Hypothalamic dysfunction
13
Q
s/s hypothyroidism?
A
- Neuro
- Fatigue, memory impairment, depression, or emotional liability
- CV
- Bradycardia, HTN w/ narrowed pulse pressure, or pericardial effusion
- Low voltage EKG
- Prolonged PR, QRS & QT interval
- Resp
- Need thyroid hormone for surfactant production
- Decreased response to hypoxia and hypercarbia
- Optho
- Blurred vision
- Renal
- SIADH – water retention
- Musculoskeletal
- Hyporeflexia
- Large tongue
- Cold intolerance
- Goiter
14
Q
Lab diagnosis of hypothyroidism?
A
- Primary hypothyroidism- TSH elevated, T4 low
- Subclinical TSH elevated; T4 normal
- Secondary TSH normal or low; T4 low
15
Q
Treatment for hypothyroidism?
A
- Hormone replacement with Synthroid
- Be careful with replacement – patient with CAD may not tolerate sudden increase in heart rate
16
Q
Anesthesia considerations with hypothyroidism?
A
- Little reason to postpone elective surgery with mild/moderate hypothyroidism
- Surgery should be postponed with severe hypothryoridism
- Maintain medications up to morning of surgery
- Cardiovascular changes are often the earliest changes
- Get EKG
- Cortisol deficiency is possible – atrophy of gland
- May need replacement therapy- need cortisol for stress response
- Maybe sensitive to sedatives
- Large tongue may lead to difficult airway
- Goiter may compress airway
17
Q
What is a myxedema coma? s/s?
A
- Extreme hypothyroidism
- Medical emergency
- 25 -50% mortality
- Coma
- Hypoventilation
- Hyponatremia (SIADH)
- CHF- incrase fluid retention can cause CHF
- Bradycardia
- Maybe precipitated by surgery, trauma, or infection
18
Q
Treatment myxedma coma?
A
- Tracheal intubation and controlled ventilation
- Levothyroxine 200 -300 mg IV- monitor HR, if CAD, don’t want to increase their HR too high
- Hydrocortisone 100 mg
- Keep warm
- Replace electrolytes as needed
19
Q
What is the parathyroid? Functions?
A
- 4 small endocrine glands located on the back of the thyroid gland
- Chief cells
- Produces parathyroid hormone
- Principal regulator of calcium and phosphate homeostasis
Functions:
- Increases osteoblast activity – increase calcium and phosphorous levels in circulation
- Increases renal tubular reabsorption of calcium
- Stimulates the synthesis of 1,25-dihydroxycholecalciferol (active Vit D)- causes intestine to absorb more Ca
- Increased phosphate excretion- if phophate lowered then Ca can increase because Ca binds to phosphate
20
Q
Role of calcium in body?
A
Regulating heart rate, muscle contraction, nerve impulse, strong bones & teeth, blood clotting, & regulating heart rate
- Total body calcium
- 99% in skeleton
- 1% in blood
- 45% bound to proteins like albumin and globulins- as albumin go down, calcium goes down. need to use albumin corrected Ca level
- 55% unbound ionized
- 45% ionized –ACTIVE form
- 10% complexed with bicarbonate, phosphate, or citrate
21
Q
What is the homeostasis of blood calcium level?
A
- Elevated calcium levels detected
- thyroid releases calcitonin
- calcitonin allows blood calcium levels to fall
- if calcium falls too low, parathyroid detects
- parathyroid releases PTH
- PTH allows blood calcium levels to rise
22
Q
Primary and secondary causes of hyperparathyroidism?
A
- Primary
- Parathyroid adenoma or hyperplasia
- Multiple endocrine neoplasm
- Secondary
- Vitamin D deficiency
- Kidney disease (decreased Vit D conversion)
- Intestinal malabsorption syndrome
35
Q
Diagnosis of diabetes?
A
- Hgb A1C > 6.5%
- Fasting glucose >126 mg/dL
- 2-hour glucose > 200 mg/dL
45
Q
What is stiff joint syndrome in diabetics?
A
- 30 -40% of patients with IDDM have stiff joint
- Up to 30% can have difficult laryngoscopy
- (Reissell)
- Limited atlanto-occipital joint mobility
- Limited temporomandibular joint mobility
- Limited cervical spine mobility
- Positive prayers sign
- Palm print sign
