Endocrine Flashcards
Preop assessment components?
- 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
What is the thyroid gland? Role?
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

What is the HPA axis for thyroid hormone release?
- 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

Difference between T3/T4?
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
Causes of hyperthyroidism?
- 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
S/S Hyperthyroidism?
- 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
What with Free T4, free T3 and TSH be on labs for graves disease, multinodular goiter, and toxic nodules?
- 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

Potential treatment hyperthyroidism?
- 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
Anesthesia implications for hyperthyroidism
- 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
S/S and differntial for thyroid storm?
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
Treatment thyroid storm
- IV fluids
- Propylthiouracil via NGT
- Sodium iodide
- Hydrocortisone
- Propranolol/esmolol
- Cooling blanket
- Acetaminophen
- Meperidine
- Digoxin
Primary and secondary causes for hypothyroidism?
Primary
- Hashimoto thyroiditis (autoimmune)
- Surgical removal of thyroid
- Severe iodine depletion
- Neck radiation
Secondary
- Pituitary disfunction
- Hypothalamic dysfunction
s/s hypothyroidism?
- 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
Lab diagnosis of hypothyroidism?
- Primary hypothyroidism- TSH elevated, T4 low
- Subclinical TSH elevated; T4 normal
- Secondary TSH normal or low; T4 low

Treatment for hypothyroidism?
- Hormone replacement with Synthroid
- Be careful with replacement – patient with CAD may not tolerate sudden increase in heart rate
Anesthesia considerations with hypothyroidism?
- 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
What is a myxedema coma? s/s?
- 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
Treatment myxedma coma?
- 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
What is the parathyroid? Functions?
- 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
Role of calcium in body?
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
What is the homeostasis of blood calcium level?
- 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

Primary and secondary causes of hyperparathyroidism?
- Primary
- Parathyroid adenoma or hyperplasia
- Multiple endocrine neoplasm
- Secondary
- Vitamin D deficiency
- Kidney disease (decreased Vit D conversion)
- Intestinal malabsorption syndrome
S/S Hyperparathyroidism?
- Neuro
- Mental status changes – delirium, psychosis, or coma
- CV
- Hypertension, ECG changes (prolonged PR, short QT & wide T waves), & arrhythmias
- GI
- N/V, constipation, & pancreatitis
- Renal
- Stones (r/t excess calcium), polyuria, polydipsia, impaired renal concentrating ability, & dehydration
- Musculoskeletal
- Muscle weakness and osteoporosis
Diagnosis hyperparathyroidism?
- Total calcium: > 10.4 mg/dl
- Ionized calcium: > 1.5 mmol./L; >6 mg/dL
- Elevated PTH
- Increased 1,25 Vit D
- Decreased Phosphate
Hyperparathyroidism treatment?
- Mild (10.4 – 11.5 mg/dl)
- IV normal saline (dilution) & loop diuretics (reduce reabsorption)
- Moderate (> 11.5 mg/dl)
- Continue normal saline & loop diuretics
- Bisphosphonates (inhibit osteoclasts)
- Calcitonin ( inhibits osteoclasts)
- Chloroquine (inhibits Vit D conversion)
- Mithramycin (Inhibits osteoclasts)
- Toxic side effects – thrombocytopenia, hepatic & renal toxicity, azotemia
- Severe
- Dialysis
Anesthesia management for hyperparathyroidism?
- Low threshold to get EKG
- No evidence that a specific anesthetic drug or technique has advantages over another
- Scheduled
- No special monitors usually required
- Emergency
- A-line (frequent lab draws), central line, & Foley
- Unpredictable response to neuromuscular blockade
- May require decreased dosing & frequent monitoring
- Careful positioning- osteoporosis
Primary and secondary causes hypoparathyroidism?
- Primary
- Parathyroid surgery (removal for hyperparathyroidism)
- Accidental removal during thyroid surgery
- Secondary
- Suppression (severe hypomagnesemia, burns, or sepsis)
- Vitamin D deficiency
- Renal failure (hyperphosphatemia)
- Idiopathic hypoparathyroidism (congenital)
- Acquired hypoparathyroidism (autoimmune disease)
- Genetic (DiGeorge Syndrome)
- Heavy metal damage (copper)
S/S hypoparathyroidism?
- Neuro
- Anxiety, depression, or psychosis
- CV
- Hypotension, ECG changes (prolonged QT interval), CHF
- Resp
- Apnea or laryngeal spasms
- Neuromuscular
- Tetany
- Chvostek’s
- Trousseau’s
- Paresthesia
- Tetany
Diagnosis hypoparathyroidism?
- Total calcium: < 8.5 mg/dl
- Ionized calcium : < 4.0
- Increased phosphate
- Decreased PTH
- Decreased 1,25 Vitamin D
What is trousseau’s sign?
- Induction of carpopedal spasm by inflation of sphygomomanometer above SBP for 3 min
- Response- carpopedal spasm characterized by:
- adduction of thumb
- flexion of metacarpopharlangeal joints
- extension of the interphalangeal joints
- flexion of wrist
What is chvostek’s sign?
- Contraction of ipsilateral facial muscles elecited by tapping the facial nerve just anterior to the ear
- Reponse: twitching of the lip to spasm of all the facial muscles
Treatment of hypoparathyroidism? symptomatic v asymptomatic?
Symptomatic
- Intravenous Calcium
- Calcium gluconate 10 -20 mls of 10% solution (90 mg elemental calcium)- preferred method of admin
- Calcium chloride 10 ml’s of 10% solution (273 mg elemental calcium)- caustic to veins if given peripherally
- Intravenous magnesium
- Magnesium 2 -4 mg IV
Asymptomatic
- Oral calcium supplements
- Oral vitamin D supplements
Anesthesia management of hypoparathyroidism?
- Low threshold to get EKG
- No evidence that a specific anesthetic drug or technique has advantages over another
- Correct calcium and magnesium – have symptoms under control prior to anesthesia
- Judicious use of albumin or large amounts of blood products- will bind Ca and decrease ionized calcium present
- Avoid respiratory alkalosis – (decreases ionized calcium)
S/S hyperglycemia?
- Polydipsia
- Polyphagia
- Polyuria
- Weight loss
- Irritability
- Recurrent infections
- Visual changes
- Paresthesia
- Lethargy/fatigue
Diagnosis of diabetes?
- Hgb A1C > 6.5%
- Fasting glucose >126 mg/dL
- 2-hour glucose > 200 mg/dL

Classifications of diabetes?
- Type I (5 -10%)
- T-cell mediated destruction of the beta cells
- Type II (80 – 90%)
- Deficiency in production or insensitivity in peripheral tissue or both
- Gestational (3-5% of pregnancies)
- Body becomes less sensitive to insulin
- Diabetes due to other causes (surgery, drug, or diseases)
- Stress response, steroids, or Cushing’s/acromegaly
- pre-diabetic in 3:1 ratio with normal diabetes. tons of prediabetics
Type 1 vs type 2 diabetics?
Type I
- Requires exogenous insulin
- Usually normal/thin
- Autoimmune mediated
- Symptomatic
- FBS: 300 – 500 mg/dl
- Suppressible by insulin
- Unresponsive to oral medications
- Prone to ketoacidosis and hypoglycemia
Type II
- Non-insulin dependent
- Usually obese/sedentary
- Gland/receptor problem
- Maybe asymptomatic
- FBS: 150 -300 mg/dl
- High levels of glucagon
- Can be both responsive and resistant to insulin
- Responsive to oral hypoglycemics
- Prone to hyperglycemia hyperosmolar nonketotic acidosis
Onset, peak duration of rapid, short, intermediate and long acting insulins? SQ admin
- Rapid Acting (Lispro/Aspart)
- O: 15-30 M; P: 30 – 90 M; DOA 3-5 H
- Short (regular)
- O: 30 -60 M; P: 2 -5 H; DOA: 4 – 6 H
- Intermediate (NPH)
- O: 1 – 4 M; P: 4 -14 H; DOA: 10 -20 HR
- Long Acting (Glargine/Detemir)
- O: 1 -2 H; P: None; DOA: 24 hours
Drugs used to treat Type 2 DM?
- Acarbose (Precose)
- Alpha-glucosidase inhibitor
- Diarrhea
- Meglitinide (Repaglinide)
- Increase insulin release (ATP dependent K+ ATPase pump)
- Hypoglycemia
- Biguanide (Metformin)
- Decrease gluconeogenesis
- N/V/D; Lactic acidosis (high doses – Hold 24 hours?)- Some hospitals may not hold. lactic acidosis is theoretical risk and not seen commonly?
- Sulfonylureas (Glyburide)
- Increase insulin release (ATP dependent K+ ATPase pump)
- Hypoglycemia and weight gain
- Thiazolidinediones (Rosiglitazone)
- PPAR receptor agonist (Increase fatty acid storage – decrease insulin resistance)
- Heart failure/Death
- Dipeptidyl Peptidase-4 inhibitors (Sitagliptin)
- Headache, leg swelling, ANGIOEDEMA
Goals of periop diabetes managmeent?
- Optimal perioperative glucose target is unclear
- Most information comes from ICU patients
- Most bodies recommend glycemic targets between 110-180 mg/dL
- American Diabetes Association – 80-180 mg/dL
- Treatment threshold 180 mg/dl
- Determining end organ complications
- Understand the patients medication regime
- Avoidance of hypoglycemia and hyperglycemia
- Especially severe <40 mg/dL
- Try to make first case of day
End organ complications of diabetes?
- Atherosclerosis
- CAD, PVD, CVD, HTN, cardiomyopathy & silent MI
- Diabetic nephropathy (20 – 40%)
- Microalbuminuria, proteinuria, & elevated serum creatinine
- Chronic renal failure
- Neuropathies
- Stroke
- Polyneuropathy
- Autonomic neuropathy
- GI (gastroparesis)
- Musculoskeletal
- Stiff-joint syndrome
- Other
- Infections
What is autonomic dysfunction prevalence in diabetics? complications?
- Autonomic Dysfunction
- 20-40% of diabetics affected
- Affects CV and GI system most
Complications
- Intraoperative hypotension
- Increased vasopressor support
- Perioperative arrest
- Exaggerated response to intubation
- Intraoperative hypothermia
S/S Autonomic dysfunction?
- Ophthalmology
- Impaired adaption to light
- Sudomotor
- Dry skin
- Anhidrosis
-
CV (green on ppt)
- Tachycardia @ rest
- Exercise intolerance
- Orthostatic hypotension
- Silent MI
- Loss of beat to beat variability
- GI
- Esophageal dysmotility
- Gastroparesis
- Constipation/diarrhea/incontinence
- GU
- Neurogenic bladder
- Erectile dysfunction
Preop tests for diabetics?
- CV
- EKG – others as need
- May display old infracts – Q waves, prolonged QT interval, or LV hypertrophy
- Resp
- Chest x-ray not usually required
- Labs
- A1C
- > 9% is indicative of poor control
- Electrolytes
- US
- CBC
- A1C
What is stiff joint syndrome in diabetics?
- 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

Preop and introp managment of diabetics?
- Preop and intraoperative management
- Several methods of control
- Questions to ask yourself?
- How tight of control does the patient need
- Will the patient take oral hypoglycemics on the DOS
- Will the patient take insulin on the DOS
- How often will the blood glucose need to be monitored
- Will the patient require an insulin drip
- Will the patient require glucose IV solution
- How will the patient be managed in the postop period
Managmenet of type 1 DM insulin preop? PM night before and AM dose?
- Quick
- PM - Normal
- AM - Hold
- Regular
- PM – Normal
- AM - Hold
- Intermediate
- PM – 80%
- AM – 50 -80%
- Long
- PM – 80%
- AM – 50 -80%
- Pump
- AM – Basal rate
Managemet of type 2 meds around sx?
- Oral
- PM – Take
- AM – Hold – Restart as soon as possible
- Quick
- PM – Usual
- AM - Hold
- Regular
- PM – Usual
- AM – 1/2 to 2/3 normal dose
- Intermediate
- PM – 80%
- AM – 50 – 80%
- Long
- PM – 80%
- AM – 50 – 80%
S/S DKA? DX?
- Signs & Symptoms
- FSBS 300 -500 mg/dl
- Acute abdominal pain
- Lethargy
- Hypovolemia
- Diagnosis
- Ketone > 7 mmol/L
- Bircarb < 18 mEq/L
- pH < 7.25
Treatment DKA?
- Restore intravascular volume
- Normal saline vs. 0.45% NS
- Start D5W @ FBS 250 - 300
- Insulin
- 10 – 20 IV unit bolus
- 1 -2 units/HR
- Electrolytes
- Potassium
Who is most likely to experience HHNC (hyperosmolar, hyperosmotic, non-ketotic coma)? S/S?
- Elderly with minimal DM
- Signs/symptoms
- FSBG > 600 mg/dl
- Thirst
- Dry mouth
- Fever
- Increased urination
- Confusion
- Seizures
- Coma
Treatment HHNC?
- Restore intravascular volume
- Normal saline vs. 0.45% NS
- Start D5W @ FBS 250 - 300
- Insulin
- 10 – 20 IV unit bolus
- 1 -2 units/HR
- Electrolytes
- Potassium
- Goal
- Decrease 50 mg/dl /hour
- Rapid correction may lead to cerebral edema
What is hypoglycemia dx?
- Low blood glucose
- Blood glucose < 50 -70 mg/dl
- Or signs and symptoms of hypoglycemia
- Difficult under anesthesia – need to have high index of suspicion
S/S hypoglycemia?
- Neuro
- Fatigue
- Anxiety
- Confusion
- Seizures
- LOC
- CV
- Tachycardia then to bradycardia
- Irregular rhythms
- Hypotension
- Resp
- Embarrassment- rapid shallow breathing with inspiratory dyspnea……
- Optho
- Blurred vision
Risk factors for hypoglycemia? What are situations where you could be unaware pt is hypoglycemic?
Risk factors
- Decreased oral intake
- Renal insufficiency
- Liver disease
- Infection
- Pregnancy
- Adrenal insufficiency
Unawareness
- Beta blockers
- Sedation
- Advanced age
- Long history of diabetes
- Diabetic neuropathy
Treatment hypoglycemia?
- Hospital:
- 25 – 50 ml’s D50
- 1 mg IM/IV glucagon
- D5 or 10 W
- Take quickly absorbed carbs such as
- half glass juice
- 5-7 jellybeans
- 3 tsp honey or sugar
- glucose that contains 15 g carb
- THEN follow up with slowly absorbed carb such as:
- sandwich
- biscuits
- glass of milk
- piece of fruit
- Retest after 15 min
- Goal: BG > 100 mg/dl