Endocrine & Metabolic Disorders Part 1 Flashcards

1
Q

Autoimmune, insulin-dependent, potential association with other autoimmune diseases.
-No production of endogenous insulin, obligatory need for exogenous insulin, disease of childhood/adolescence, DKA risk

A

Type 1 Diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Polygenic & influenced by environment, increasing incidence with higher life span and western cultural habits.
-Cellular insulin resistance and/or impaired insulin release, infrequent DKA, prevalence correlates directly with obesity
-Metabolic Syndrome: HTN, insulin resistance, dyslipidemia, truncal obesity

A

Type 2 Diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Patients initially appear to have DM2, but actually developed antibodies to pancreatitis islet cells & become insulin dependent.

A

Latent Autoimmune DM of adulthood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Relative insufficiency of insulin production & insulin resistance with pregnancy
-Aggressive clinical progress and may persist after pregnany

A

Gestational Diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Due to the side effects of meds, pancreas dysfunction, may also influence ocular and lacrimal function → search for underlying cause!
-Pancreatic surgery, pancreatitis, cystic fibrosis, hemochromatosis

A

Secondary Diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Defects in insulin secretion or action, potential ocular associated malformations

A

Genetic Diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Increased risk of perioperative complications:
-Increased CV morbidity & mortality, CKD, increased risk peripheral nerve injury, wound infections

A

Multi-organ dysfunction complications of Diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Causes Tissue glycosylation, oxidative stress, protein kinase C activation (inflammation), soft-tissue changes & cellular swelling of airway anatomy (potential for difficult airway!!!)

A

Chronic Hyperglycemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Microvascular: nephropathy, retinopathy, neuropathy
Macrovascular: arterial atherosclerosis
Increased risk of Major Adverse Cardiac Event (MACE)

A

Vascular complications of Diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

BP/HR lability/variability → S&S: postural hypotension, resting tachycardia, peripheral sensory neuropathy, lack of respiratory pulse variation
-Increased risk of Myocardial ischemia & cardiopulmonary arrest!!!!
-Delayed gastric emptying → increased aspiration risk!!!

A

Diabetic Autonomic Neuropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

-Increased risk of peripheral nerve injury (check pressure points), soft-tissue compromise, increased risk of infection
-Poor wound healing, limited wound tensile strength, vascular disease diminishes perfusion to tissues

A

Diabetes Infection/Immune Complications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Has a risk of lactic acidosis (rare), weight loss, favorable w/ lipids, improve resistance to insulin, decreases mortality. Does not cause significant hypoglycemia. Usually hold day of surgery unless renal impairment or use of contrast is expected.

A

Metformin (Biguanides)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Scheduled first case of day, monitor BG, continue all insulin regime until DOS.

A

Diabetic Periop Management

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Type 1: receive 1/3-1/2 normal long acting dose
Type 2: nothing - 1/2 long acting dose
Pump: continue basal rate
D/c short acting oral agents on DOS
D/c metformin DOS and do not restart if hepatic or renal failure

A

DOS Diabetic Management

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the most common cause of periop hyperglycemia?

A

Stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Target BG 140-180
-Check BG preop and PACU
-Avoid stressful situations (pain, PONV)
-Always r/o hypoglycemia with delayed emergence
-Inc risk of complications: MACE (prothrombotic state, inc plt aggregation/adhesion), pulmonary complications, acute renal injury, altered immune function, poor wound healing, infection.

A

Anesthesia Management of Diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Average glucose level over past 2-3 months, goal <7%, patients w/hyperglycemia but long-term control can proceed to surgery, patients w/ poor control=convo w/ surgeon, postpone surgery if complications (dehydration, DKA, HHS)

A

HgbA1c

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Triad: Ketonemia, Hyperglycemia, and Acidemia.
-Insufficient insulin = ketone bodies
-Unable to block lipolysis, so fatty acids are metabolized
-Inc unmeasured anion gap
TX: insulin, fluid, electrolyte replacement

A

Diabetic Ketoacidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Ketonemia, BG > 250, Serum bicarb <18, and pH < 7.3

A

Diagnostic criteria for DKA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Hyperglycemia (BG > 600) and profound dehydration (9-12 L).
-Impaired thirst response and mild renal insufficiency
-Hyperosmolarity -> coma, seizures
-Inc plasma viscosity -> intravascular thrombosis
Tx: rehydration, small insulin doses

A

Hyperglycemic Hyperosmolar State (HHS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Whipple Triad: symptoms of neuroglycopenia (weakness, dizziness, confusion, coma), BG <40, and relief of symptoms with glucose administration.
Tx: Sugar, IV dextrose, glucagon, juice. Goal BG > 100.

A

Hypoglycemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

T4 is 90%
-T4 is converted to T3
-Majority are protein bound
-Unbound (free) hormones are metabolically active
-Has synergistic actions with SNS stimulation (B adrenergic receptors -> Inc contractility and HR)
-Regulated by the Hypothalamic-pituitary-thyroid axis

A

Thyroid Hormones

23
Q

1) Primary: deficiency in endogenous production thyroid hormones
-Hashimoto thyroiditis (autoimmune destruction), destruction from radiation, surgery, Meds: amio, lithium, interferon a & interleukin2
2) Secondary: dysfunction in hypothalamic-pituitary-thyroid axis
-Damage to pituitary gland from radiation/surgery, HTN

A

Hypothyroidism

24
Q

S/Sx:
-slow movements, slow speech, dry sallow skin, myxedema, cold intolerance, anemia, decreased 2,3-DPG (left shift), bradycardia, labile BP, hypoventilation, OSA, fatigue, sleepy, depression, weight gain, constipation, periorbital edema, tracheal deviation, goiter, tracheal deviation, hoarse → airway difficulty

A

Hypothyroidism

25
No recommended screening of asymptomatic patients. -Normal TSH value rules out primary hypothyroidism -Primary hypo → high TSH & low T3&T4 -Subclinical hypo → high TSH with normal T3&T4, absence of systemic illness
Diagnostic Testing of Hypothyroidism
26
Tx: Levothyroxine: prohormone converted to active T3 (continue perioperatively; half life of 7-10 days). Takes 6+ months to feel better
Hypothyroidism
27
Elective: postponed with moderate/severe until euthyroid state achieved, no delay with mild Urgent: proceed with mild/moderate
Hypothyroidism Surgery Implications
28
Severe → chronic clinical symptoms (myxedema coma), AMS, HF, low T4; consult endo Moderate → overt disease (high TSH, low free T4) Mild → subclinical disease (elevated TSH, normal T4) How are you feeling? Any recent changes in your thyroid medicine?
Hypothyroidism
29
-Mod/Severe - advanced monitoring (Arterial line, TEE, or PAC) -Goiter - issues with airway -Avoid hypo/hyperthermia -GA/surgery (Stress) can precipitate myxedema coma! Pre-op anxiolysis and multi-modal pain management necessary -Consider stress dose steroid -Myocardial depressant activity of anesthetics
Anesthesia Considerations for Hypothyroidism
30
More common in women and in countries with iodine deficiency. -Overactive synthesis/release of T3 and T4 from the thyroid gland
Hyperthyroidism
31
Occurs when the thyroid gland has increased metabolic activity -Graves disease: autoantibodies stimulate TSH receptor -Toxic multinodular goiter & toxic adenoma
True Hyperthyroidism
32
Occurs when metabolic activity of the thyroid gland is decreased. -Subacute & lymphocytic thyroiditis: inflammation damages thyroid follicular cells & release stored T3 & T4 -Drug-induced (iodine): amiodarone, contrast dyes, lithium, interferon-a, interleukin-2 -Short period of hyperthyroidism, followed by hypothyroid stage, and eventual return to euthyroid state
Thyrotoxicosis without Hyperthyroidism
33
Mimic SNS stimulation: hyperkinesis, warm moist skin, carpal tunnel syndrome, tremor, HTN, tachycardia, fatigue, weakness, nervousness, weight loss, inc perspiration, tracheal deviation, exophthalmos, goiter, dysphagia, hoarse (difficult airways!!)
Hyperthyroidism
34
No recommended screening in asymptomatic pts. -Symptomatic: TSH level = most sensitive/specific test; free T4 & total T3 improves diagnostic accuracy -Primary hyperthyroidism: low TSH, high T3/T4 -Subclinical hyperthyroidism: low TSH, normal T3/T4 -Endocrinology guides testing for new diagnosis: radioactive iodine uptake, ultrasonography, thyroid receptor antibodies
Diagnostic Testing for Hyperthyroidism
35
All non emergency procedures are delayed until euthyroid state! -evaluate fluid/electrolyte status, continue antithyroid & beta blockade DOS! (consider esmolol), AIRWAY!, avoid SNS stimulation (intubation, surgery, extubation), positioning (reverse trendelenburg) -Hemodynamic monitoring, temperature monitoring -Consider stress dose steroids, preoperative anxiolysis/pain mgmt -Remember that anesthetic agents are myocardial depressants.
Anesthesia Considerations for Hyperthyroidism
36
Definitive therapy: antithyroid drugs (side effect of hepatotoxicity), radioactive iodine, surgery (thyroidectomy) -Sympathetic outflow managed with beta blockers -Pain controlled with NSAIDS & corticosteroids
Treatment of Hyperthyroidism
37
1) Regular Insulin, 10 unit IV bolus, followed by an insulin infusion nominally at (BG/150) units/hr 2) Isotonic IV fluids guided by VS and UOP (anticipate 4-10 L deficit) 3) When UOP > 0.5mL/kg/hr, give KCl 4) When BG < 250, add D5W at 100 mL/hr 5) Consider Na bicarb when pH <6.9
DKA management
38
Rare in longstanding hypothyroidism, triggered by stressful event -S/Sx: labile BP, bradycardia, hypoventilation, OSA, hypothermia -Mgmt: levothyroxine, corticosteroids, supportive measures
Myxedema Coma
39
1) Tracheal Intubation and ventilation 2) Levothyroxine 200-300 micrograms IV over 5-10 min, then 100 micrograms IV q 24 hrs 3) Hydrocortisone 4) Fluid and electrolyte therapy 5) Cover to conserve body heat; no warming blankets
Management of Myxedema Coma
40
Acute stress in untreated hyperthyroid state, life-threatening! -S/Sx: HTN, tachycardia, CHF, Afib, MI, hyperthermia -Mgmt: anti-thyroid meds, supportive measures
Thyroid Storm
41
1) IVF 2) Sodium Iodide 3) PTU 4) Hydrocortisone 5) Propanolol or esmolol 6) Cooling blankets, acetaminophen, meperidine (shivering) 7) Digoxin for HF
Management of Thyroid Storm
42
Acts to maintain extracellular Ca directly via bone reabsorption and renal reabsorption (phosphaturia and bicarbonaturia; enhanced Ca and Mg reabsorption) and indirectly via effects on Vit. D synthesis -regulated by serum ionized Ca, phosphate metabolism, & Mg (Mg is required for PTH release)
Parathyroid Hormone
43
Works via negative feedback mechanism to maintain normal Ca levels; increases Ca, decreases PO4, decreased Mg = decreased Ca = decreased PTH
Parathyroid Hormone
44
Stimulates osteoclasts to release Ca, augments reabsorption of Ca in renal tubules, promotes Vit D formation in the kidneys & Ca absorption from intestine
Decreased Calcium (PTH effects)
45
An underproduction of PTH or resistance of end-organ tissue to PTH; results in hypoCa (< 8 mg/dl) -Most common cause = unintentional removal of parathyroid glands during thyroid/parathyroid surgery (also radiation, neck trauma, malignancy, severe hypoMg bc suppresses PTH secretion, renal insufficiency, VitD insufficiency, pancreatitis, burns)
Hypoparathyroidism
46
S/Sx: manifestations of hypocalcemia. -Neuronal irritability, paresthesias, fatigue, skeletal muscle spasm, tetany, seizures, CHF, hypotension, insensitivity to B agonists secondary to catecholamine release, acute onset after surgery manifest as stridor & apnea!!
Hypoparathyroidism
47
Contracture of facial muscle
Chvostek Sign
48
Contraction of fingers/wrist (BP cuff)
Trousseau Sign
49
Need symptoms under control before surgery. -Order ECG, Metabolic panel, ionized Ca level -Correct underlying causes (Ex: if r/t Mg depletion -> give Mg) -Electrolyte replacement fluid bolus, removal of phosphate from diet, etc. -Chronic: Ca supplements, VitD analogs -Acute: IV Ca, monitor Ca levels q2 hrs with clinical S&S, acute severe Ca (<7.5) is a life-threatening emergency!! (laryngospasm & seizures!!)
Management of Hypoparathyroidism
50
Autonomous secretion of PTH from solitary or multiple parathyroid adenomas -Decreased renal excretion of Ca, increased VitD activation → responsible for > 90% of hyperCa in population
Primary Hyperparathyroidism
51
Associated with renal failure -Low serum Ca, elevated PTH, impaired VitD metabolism, VitD deficiency & chronic lithium therapy, most often medically managed
Secondary Hyperparathyroidism
52
Occurs after successful renal transplantation -Autonomous secretion of PTH with hypercalcemia despite normal VitD metabolism (likely require parathyroidectomy)
Tertiary Hyperparathyroidism
53
Often asymptomatic: altered LOC, HTN, peptic ulcer dz, renal calculi, polyuria, pathologic fractures (positioning implications) -Typically order ECG & metabolic panel -Goal of mgmt: normal Ca levels (<12 is okay), correct hypovolemia (0.9 NS, loop diuretics, biphosphate therapy) -Ca > 14 requires hospitalization and fluid resuscitation
Hyperparathyroidism