Unit 2 Endocrine & Metabolic

Question 1

Types of diabetes

Answer 1

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

Question 2

Metabolic syndrome

Answer 2

HTN
Insulin resistance
Dyslipidemia
Truncal obesity

Question 3

Latent autoimmune DM of adulthood

Answer 3

Initially appear to have DM II, but develop antibodies to pancreatic islet cells and become insulin dependent

Question 4

Complications of DM

Answer 4

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

Question 5

Effects of Chronic hyperglycemia

Answer 5

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

Question 6

Vascular disease complications from DM

Answer 6

Microvascular - nephrophathy, retinopathy, neuropathy

Macrovascular - arterial atherosclerorosis

Increased risk of MACE

Question 7

Diabetic autonomic neuropathy

Answer 7

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

Question 8

DKA

Answer 8

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

Question 9

DKA treatment

Answer 9

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

Question 10

HHS

Answer 10

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

Question 11

Preoperative exam for DM patient

Answer 11

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

Question 12

Preoperative testing for DM

Answer 12

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

Question 13

HbA1c

Answer 13

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

Question 14

DM Need to know

Answer 14

Medication regime
Normal BG level
How compliant?
How often do they check BG?
Presence of end organ damage?

Question 15

Metformin

Answer 15

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

Question 16

DM patient considerations

Answer 16

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

Question 17

Most common cause of perioperative hyperglycemia?

Answer 17

Stress
So avoid stressful situation: pain, PONV

Question 18

BG target?

Answer 18

Typically 140-180
Usually don’t treat unless >180

Question 19

How long for decadron to increase BG?

Answer 19

About 120min

Question 20

what to look for with delayed emergence?

Answer 20

Always rule out hypoglycemia

Question 21

POST OP risk to DM patients

Answer 21

MACE: prothombotic state, increased platelet aggregation and adhesiveness
Pulmonary complications (PPCs)
Renal injury
Altered immune function
Poor wound healing
Infection

Question 22

Whipple triad

Answer 22

Defines hypoglycemia
symptoms of neuroglycopenia: weakness, dizziness, confusion, coma
Blood glucose < 40
relief of symptoms with glucose administration

Question 23

Hypoglycemia treatment

Answer 23

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

Question 24

Biologically active thyroid hormones

Answer 24

Thyroxine T4 90%
Triiodonthyroninine T3 10%
T4 prohormone converted to deiodinases to T3

Question 25

Circulating thyroid hormone

Answer 25

Majority of thyroid hormone is protein bound, primarily to thyroid binding globulin Remaining unbound (free) hormone is metabolically active

Question 26

Thyroid function

Answer 26

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

Question 27

Thyroide hormones regulated by?

Answer 27

Hypothalamic pituitary thyroid axis

Question 28

Mild or moderate thyroid dysfunction

Answer 28

Generally does not put the patient at any higher risk for perioperative complications

Question 29

Severe thyroid dysfunction

Answer 29

Can precipitate myxedema coma or thyroid storm

Question 30

Hyper thyroidism

Answer 30

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.

Question 31

Hyperthyroidism S/S

Answer 31

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

Question 32

Hyperthyroidism Diagnostic testing

Answer 32

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,

Question 33

Hyperthyroidism management

Answer 33

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

Question 34

Perioperative anesthesia considerations in hyperthyroidism

Answer 34

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

Question 35

Hypothyroidism

Answer 35

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

Question 36

Hypothyroidism S/S

Answer 36

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

Question 37

Hypthyroidism diagnostic testing

Answer 37

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

Question 38

Hypothyroidism management

Answer 38

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

Question 39

Anesthesia considerations in hypothyroidism

Answer 39

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

Question 40

Thyroid storm

Answer 40

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

Question 41

Myxedema coma

Answer 41

Rare in longstanding hypothyroidism Triggered by stressful event (surgery) Clinical manifestations: cardiac: labile BP, bradycardia, pulm: hypoventilation/OSA hypothermia Management: levothyroxine, corticosteroids, supportive measures

Question 42

Plasma calcium

Answer 42

Protein bound: 50% Ionized: 45% (physiologically active and regulated) Diffusable non ionized: 5%

Question 43

Parathyroid hormone

Answer 43

Maintain extracellular serum calcium through bone reabsorption, renal calcium reabsorption, and indirectly through Vit D synthesis

Question 44

Renal effects of parathyroid hormone

Answer 44

phosphaturia bicarbonaturia, in addition to enhanced Ca2+ and magnesium resorption.

Question 45

PTH secretion regulated by?

Answer 45

serum ionized Ca phosphate metabolism magnesium Increases Ca+2, decreases PO4-3 ↓ Mg+2 → ↓ Ca+2 → ↓ PTH secretion

Question 46

PTH Effects on bone, kidney, and intestine

Answer 46

↓ 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

Question 47

Types of Hyperparathyroidism

Answer 47

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

Question 48

Hyperparathyroidism S/S

Answer 48

Often asymptomatic Altered LOC Hypertension Peptic ulcer disease Renal calculi and polyuria Pathologic fractures secondary to bone destruction and muscle weakness (Positioning)

Question 49

DX hyperparathyroidism/hypercalcemia

Answer 49

Ecg and electrolyte/metabolic panel

Question 50

Hyperparathyroidism Goal of management:

Answer 50

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.

Question 51

Hypoparathyroidism

Answer 51

An underproduction of PTH or resistance end-organ tissue to PTH Hypocalcemia < 8mg/dL

Question 52

Hypoparathyroidism etiology

Answer 52

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

Question 53

S&S: manifestations of Hypocalcemia!!!

Answer 53

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)

Question 54

Chvostek sign

Answer 54

contracture of facial muscle

Question 55

Trousseau sign:

Answer 55

contraction of fingers/wrist after BP cuff inflated on forearm

Question 56

The treatment of hypoparathyroidism

Answer 56

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.

Question 57

Adrenal Hormones

Answer 57

Adrenal Medulla: Epinephrine and Norepinephrine Adrenal Cortex: Glucocorticoids (Cortisol), Mineralocorticoids (Aldosterone), Androgens

Question 58

Cortisol (hydrocortisone

Answer 58

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.