Unit 2 Endocrine & Metabolic Flashcards
Types of diabetes
Type 1 - Autoimmune, no production of endogenous insulin. Absolute insulin deficiency.
Type 2 - polygenic and influenced by environment. Cellular resistance and or impaired insulin release
Gestational - relative insufficiency of insulin production and insulin resistance with pregnancy. aggressive clinical progress, may persist after pregnancy
Secondary - side effect of medications or pancreas dysfunction
Genetic - genetic defects in insulin secretion or action
Metabolic syndrome
HTN
Insulin resistance
Dyslipidemia
Truncal obesity
Latent autoimmune DM of adulthood
Initially appear to have DM II, but develop antibodies to pancreatic islet cells and become insulin dependent
Complications of DM
Multi-organ dysfunction and increased risk of perioperative complications
^ CV morbidity & mortality
associated with chronic kidney disease
increased risk of peripheral nerve injury
wound infections
Effects of Chronic hyperglycemia
Tissue glycosylation
Oxidative stress
PKC activation (inflammation)
Soft tissue changes and cellular swelling of airway anatomy
stiff tissue/joints cervical region
potential for difficult airway
Vascular disease complications from DM
Microvascular - nephrophathy, retinopathy, neuropathy
Macrovascular - arterial atherosclerorosis
Increased risk of MACE
Diabetic autonomic neuropathy
BP/HR lability/variabliity
S/S: postural hypotension, resting tachycardia, peripheral sensory neuropathy, lack of respiratory pulse variation. ^ risk of MI and cardiopulmonary arrest
Delayed gastric emptying
increased aspiration risk
DKA
Mortality about 5%
1% of diabets related emergencies, more common than HHS (10% mortality)
Diagnosis:
ketonemia/ketonuria
blood glucose > 250
serum HCO3 < 18mmol/L
arterial pH < 7.3
Treatment:
insulin administration
fluid and electrolyte replacement
DKA treatment
Regular insulin 10-unit IV bolus
Insulin infusion at (BG/150) units/h
Isotonic fluids (4-10L deficit)
When UOP > 0.5/hr, check lytes for possible K replacement, give k 10-40mEq/h with continuous ECG
When serum glucose is decreased to 250 add dextrose 5% at 10ml/h
Consider sodium bicarb if pH <6.9
HHS
10-20% mortality
BG > 600mg/dL
Dehydration 9-12L
Combination of imparied thirst response and mild renal insufficiency
makred hyperosmolarity may lead to coma and seizures
increased plasma viscosity may produc intravascular thrombosis
Responds quickly to rehydration and small doses of insulin
Preoperative exam for DM patient
Silent myocardial ischemia, weak pulses, orthostatic hypotension
Hx of stroke, neuropathy
GERD
Renal function
Glucose control and hx of DKA/HHS
Complete airway evaluation including neck mobility assessment
Preoperative testing for DM
All patients get fasting BG, >126 should be repeated and get AIC to confirm diagnosis
Intermediate to high risk surgery
get AIC, k level,
cardiac testing based on ACC/AHA guidlines
HbA1c
Shows average blood glucose level over past 2-3 months
ADA reccomends <7%
American college of endocrinology <6.5%
Pre-op hyperglycemia with long term glycemic control may proceed to surgery
Poor glycemic control, joint decision with surgeon considering co-morbidities and surgical risk
Postpone surgery for complications of DKA, HHS, dehydration
DM Need to know
Medication regime
Normal BG level
How compliant?
How often do they check BG?
Presence of end organ damage?
Metformin
Weight loss, decrease lipds etc
Overall reduction of mortality
Worry about risk of lactic acidosis (uncommon)
Usually hold day of surgery.
If quick surgery or short fasting period it’s okay if they still take it
DM patient considerations
Try to schedule as first case of the day
Day of surgery
Type 1: 1/3-1/2 of normal long acting insulin
type 2: none - 1/2 of normal long acting insulin
pt with insulin pump: continue basal rate (unless BG drops then you can turn it off)
Short acting oral agents: DC day of surgery
talk with patient about how to handle DOS hypoglycemia symptoms
Most common cause of perioperative hyperglycemia?
Stress
So avoid stressful situation: pain, PONV
BG target?
Typically 140-180
Usually don’t treat unless >180
How long for decadron to increase BG?
About 120min
what to look for with delayed emergence?
Always rule out hypoglycemia
POST OP risk to DM patients
MACE: prothombotic state, increased platelet aggregation and adhesiveness
Pulmonary complications (PPCs)
Renal injury
Altered immune function
Poor wound healing
Infection
Whipple triad
Defines hypoglycemia
symptoms of neuroglycopenia: weakness, dizziness, confusion, coma
Blood glucose < 40
relief of symptoms with glucose administration
Hypoglycemia treatment
25g IV dextrose, glucagon, juice
Goal: BG > 100mg/dL
If diabetic pt gets insulin or sulfonylureas without supplemental glucose their actions will be prolonged in renal insufficiency
Biologically active thyroid hormones
Thyroxine T4 90%
Triiodonthyroninine T3 10%
T4 prohormone converted to deiodinases to T3
Circulating thyroid hormone
Majority of thyroid hormone is protein bound, primarily to thyroid binding globulin
Remaining unbound (free) hormone is metabolically active
Thyroid function
General increase in most of the bodies metabolic processes (gene transcription, growth, glucose use and pathways, etc)
Synergistic actions with SNS stimulation
increase number and sensitivity B-adrenergic receptors
Thyroide hormones regulated by?
Hypothalamic pituitary thyroid axis
Mild or moderate thyroid dysfunction
Generally does not put the patient at any higher risk for perioperative complications
Severe thyroid dysfunction
Can precipitate myxedema coma or thyroid storm
Hyper thyroidism
Prevalence about 1.2%
Half of them are subclinical
Increase with age
More common in women than men, happens in places of iodine deficiency
True hyper thyroidism: thyroid gland has increased metabolic activity.
Graves disease: autoantibodies stimulate TSH receptor.
toxic multinodular goiter
toxic adenoma
Thryrotoxicosis without hyperthyroidism
metabolic activity of the thyroid gland is decreased.
subacute lymphocytic thyroiditis: inflammation damages follicular cells and release stored T3 / T4
drug induced (contain iodine): amiodarone, contrast dye, lithium, interferon-a, interlukin-2
short period of hyperthyroidism, followed by hypothyroid stage, and eventual return to euthyroid state.
Hyperthyroidism S/S
Mimic sympathetic stimulation
Caridac: tachycardia, HTN, afib
Neuro: fatigue, weakness, nervouseness, tremor,
GI: changes in appetite, bowel movement frequency, weight lost despite increased appetite
Endocrine: increased perspiration, irregular menses
HEENT: tracheal deviation, goiter, dysphagia, orthopnea, hoarseness
Hyperthyroidism Diagnostic testing
Don’t screen asymptomatic patients
Symptomatic patients:
TSH level is most specific/sensitive
Free T4 and T3 improves diagnostic accuracy
Subclincial hyperthyroidism
low TSH with normal T3 and T4
Endocrinology guides testing for new Dx
radioactive iodine uptake
ultrasonography
thyroid receptor antibodies
Meds that can effect thyroid labs: glucocorticoids, dopamine, TSH secretion, iodine, amiodorone,
Hyperthyroidism management
All non emergent procedures are delayed until a euthyroid state
Definitive therapy:
antithyroid drugs (monitor LFTs)
Radioactive iodine
surgery (thyroidectomy)
Sympathetic outflow managed with B-adrenergic blockade
Pain controlled with NSAIDs and or corticosteroids
Perioperative anesthesia considerations in hyperthyroidism
Check for S/S see how they are feeling
Evaluate fluid and electrolyte status
Continue antithyroid and b-blockade on DOS
Airway, airway, airway
Plan to avoid SNS stimulation (up-regulated)
intubation, surgical stimulation, extubation
Positioning
Hypothyroidism
0.3% prevelance
4-8.5% prevelance of subclinical hypothyroidism
Primary: deficiency in endogenous production of thyroid hormone
Hasimoto thyroiditis: autoimmune lymphocytic disease (most common)
desruction of gland from radiation (cancer)
surgery (head&neck)
medications: amiodorone, lithium, interferon-a, interleukin-2
Secondary: dysfunction of HPT axis
damage to pituitary gland from radiation and or surgery
hypertension
Hypothyroidism S/S
General: slow movements, slow speech, cold intolerance, anemia and left shift oxy-hgb curve
CV: bradycardia, low voltage EKG,
Pulm: hypoventilation, decreased response to hypoxia and hypercarbia, OSA
Neuro: fatigue, sleepiness, depression, paresthesias delayed DTRs, autonomic dysfunction
GI: weight gain, constipation
HEENT: periorbital edema, tracheal deviation, goiter, dyspnea, etc
Hypthyroidism diagnostic testing
No screening for asymptomatic patients
Normal TSH rules out primary hypothyroidism
Primary hypothyroidism
high TSH and low T3 & T4
Subclinical hypothyroidism
high TSH with normal T3 & T4
absence of systemic illness
Hypothyroidism management
Levothyroxine: prohormone converted to active T3
continue perioperatively, half life 7-10 days
Elective surgery postponed with moderate-severe disease until euthyroid state
Urgent surgery with moderate disease should not be delayed
No delay with mild hypothyroidism
GA and surgery (stress) can precipitate myxedema coma
Anesthesia considerations in hypothyroidism
If possible, delay surgery until euthyroid state
mild-mod symptoms probably OK
sever symptoms consult endocrinology
Airway Airway Airway
Hemodynamic monitoring
Temp management (avoid hypo/hyperthermia)
Pharmacology
preoperative anxiolysis/pain management (thyroid emergencies usually precipitated by stress)
consider stress dose corticosteroids
myocardial-depressant activity of anesthetic agents so they are prone to hemodynamic swings
Thyroid storm
Life threatening
S/S mimic malignant hyperthermia
Acute stress in untreated hyperthyroid state
S/S: HTN, tachycardia, CHF, A-fib, MI, hyperthermia
Management:
anti-thyroid medications
supportive measures
Myxedema coma
Rare in longstanding hypothyroidism
Triggered by stressful event (surgery)
Clinical manifestations:
cardiac: labile BP, bradycardia,
pulm: hypoventilation/OSA
hypothermia
Management:
levothyroxine, corticosteroids, supportive measures
Plasma calcium
Protein bound: 50%
Ionized: 45% (physiologically active and regulated)
Diffusable non ionized: 5%
Parathyroid hormone
Maintain extracellular serum calcium through bone reabsorption, renal calcium reabsorption, and indirectly through Vit D synthesis
Renal effects of parathyroid hormone
phosphaturia bicarbonaturia, in addition to enhanced Ca2+ and magnesium resorption.
PTH secretion regulated by?
serum ionized Ca
phosphate metabolism
magnesium
Increases Ca+2, decreases PO4-3
↓ Mg+2 → ↓ Ca+2 → ↓ PTH secretion
PTH Effects on bone, kidney, and intestine
↓ Ca+2 → PTH stimulates osteoclasts to release Ca+2
↓ Ca+2 → PTH augments reabsorption of Ca+2 in the renal tubules
↓ Ca+2 → PTH promotes Vitamin D formation in the kidneys and Ca+2 absorption from intestine
Types of Hyperparathyroidism
Primary: autonomous secretion of PTH from
Responsible for > 90% of hypercalcemia in ambulatory
population
Secondary: associated with renal failure
Tertiary: occurs after successful renal transplantation
Planned parathyroidectomy most common reason to encounter a hypercalcemic patient preoperatively
Hyperparathyroidism S/S
Often asymptomatic
Altered LOC
Hypertension
Peptic ulcer disease
Renal calculi and polyuria
Pathologic fractures secondary to bone destruction and muscle weakness (Positioning)
DX hyperparathyroidism/hypercalcemia
Ecg and electrolyte/metabolic panel
Hyperparathyroidism Goal of management:
normal CA2+ levels and correct hypovolemia (CA2+ < 12mg/dL)
Serum calcium >14 mg/dL requires hospitalization and urgent fluid resuscitation, loop diuretics, and possible bisphosphonate therapy.
Hypoparathyroidism
An underproduction of PTH or resistance end-organ tissue to PTH
Hypocalcemia < 8mg/dL
Hypoparathyroidism etiology
Most common cause is unintentional removal parathyroid glands during thyroid/parathyroid surgery
Therapy for thyroid disease (radiation/medicine)
Neck trauma
Malignancy
Severe hypomagnesemia
Renal insufficiency and Vit D deficiency
Pancreatitis and burns
S&S: manifestations of Hypocalcemia!!!
Neuronal irritability, parasthesias, fatigue, skeletal muscle spasm, tetany, seizures
Chvostek & Trousseau signs
CV: CHF, hypotension, insensitivity to B-agonists secondary catecholamine release
Acute onset after thyroid/parathyroid surgery manifest as stridor and apnea (know this)
Chvostek sign
contracture of facial muscle
Trousseau sign:
contraction of fingers/wrist after BP cuff inflated on forearm
The treatment of hypoparathyroidism
electrolyte replacement. The objective is to have the patient’s clinical symptoms under control before anesthesia and surgery.
Hypocalcemia caused by magnesium depletion is treated by correcting the magnesium deficit. Serum phosphate excess is corrected by the removal of phosphate from the diet and the oral administration of phosphate-binding resins (aluminum hydroxide). The urinary excretion of phosphate can be increased with a saline volume infusion.
Ca2+ deficiencies are corrected with Ca2+ supplements or vitamin D analogs. Patients with severe symptomatic hypocalcemia are treated with IV calcium gluconate (10 to 20 mL of 10% solution) given over several minutes and followed by a continuous infusion (1 to 2 mg/kg/hr) of elemental Ca2+.
The correction of serum Ca2+ levels should be monitored by measuring serum Ca2+ concentrations and following clinical symptoms. When oral or IV calcium is inadequate to maintain a normal serum–ionized calcium level, vitamin D is added to the regimen.
Adrenal Hormones
Adrenal Medulla: Epinephrine and Norepinephrine
Adrenal Cortex: Glucocorticoids (Cortisol), Mineralocorticoids (Aldosterone), Androgens
Cortisol (hydrocortisone
Cortisol is produced under the control of adrenocorticotropic hormone (ACTH) and released by the anterior pituitary gland. ACTH, which in turn is regulated by the corticotropin-releasing factor from the hypothalamus. ACTH release follows a diurnal pattern, with maximal activity occurring soon after awakening. Psychological or physical stress (trauma, surgery, intense exercise) also promotes ACTH release
Cortisol has multiple effects on intermediate carbohydrate, protein, and fatty acid metabolism, as well as maintenance and regulation of immune and circulatory function. The anti-inflammatory actions of cortisol relate to its effect in stabilizing lysosomes and promoting capillary integrity.
