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Advanced Principles of Anesthesia > Week 11 - Endocrine > Flashcards

Week 11 - Endocrine Flashcards

1
Q

Where is the Pituitary Gland and what does it do?

A

It is attached to the Hypothalamus via pituitary stalk (Infundibulum) and is located in the Sella Turcica of the sphenoid bone

“Master Gland” – secretes at least 8 hormones that regulate organ function
*Critical to survival

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2
Q

What hormones does the Anterior Pituitary Gland produce?

A

ACTH (Adrenocorticotropic Hormone)

TSH (Thyroid-Stimulating Hormone)

GH (Growth Hormone)

PRL (Prolactin)

LH (Luteinizing Hormone)

FSH (Follicle-Stimulating Hormone)

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3
Q

What is the releasing factor (from hypothalamus), inhibiting factors, effect, and target of ACTH (adrenocorticotropic hormone)?

A

Released via Corticotropin-releasing hormone

Inhibited via glucocorticoids (cortisol)

Target = Adrenal Gland

Effect = secretion of the adrenal cortex (especially glucocorticoids - cortisol), formation of cholesterol in adrenal cortex

*ACTH levels are high in the mornings and low in the evening

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4
Q

What is the releasing factor (from hypothalamus), inhibiting factors, effect, and target of TSH?

A

Released via thyrotropin-releasing hormone

Inhibited via T3 and T4

Target = Thyroid gland

Effect = secretion of thyroid hormones
*SNS stimulation and corticosteroids suppress secretion of TSH

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5
Q

What is the releasing factor (from hypothalamus), inhibiting factors, effect, and target of GH (growth hormone)?

A

Released via growth hormone-releasing hormone

Inhibited via somatostatin, growth hormone, insulin-like growth factor-1,

Target = Liver, adipose tissue

Effects = growth of all tissues, increased rates of protein synthesis (anabolic effect), promotes lipid and carbohydrate metabolism, sodium and water retention
*most striking and specific effect is stimulation of linear bone growth

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6
Q

What is the releasing factor (from hypothalamus), inhibiting factors, effect, and target of prolactin (PRL)?

A

Released during pregnancy

Inhibited via dopamine

Target = ovaries, mammary glands

Effects = milk production (growth and development of breast in preparation for breast feeding), lipid and carbohydrate metabolism
*little metabolic activity

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7
Q

What is the releasing factor (from hypothalamus), inhibiting factors, effect, and target of LH and FSH?

A

Released via gonadotropin-releasing hormone

Inhibited via estrogen, testosterone

Target = gonads

Effects = sex hormone production and pubertal maturation

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8
Q

What are the 3 ways hyperpituitarism presents?

A
  • Hormonal Hypersecretion
  • Local mass effects (including pituitary hypofunction due to compression of normal gland)
  • Incidental discovery during cranial imaging for unrelated condition
  • Almost always related to pituitary adenoma – 10% of brain neoplasms
  • Very often asymptomatic
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9
Q

What does growth hormone sitmulate?

A
  • Longitudinal growth of bones, bone density, stimulates chondrocyte formation and increases muscle mass
  • Acts on liver to stimulate gluconeogenesis and promote fat breakdown
  • Increased mobilization of free fatty acids (ketogenic effect)

*high in childhood, maximal at puberty and decreases with age

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10
Q

What causes gigantism and acromegaly? What are their characteristics?

A

Hypersecretion of growth hormone by the anterior pituitary

  • Gigantism: during childhood when growth plates are not closed
  • Acromegaly: in adults – causes increased size of soft tissue in nose, mouth, tongue, and lips – develop cardiac disease, HTN, ventricular hypertrophy, OSA/airway obstruction

-leads to increased production of insulin like growth factor (IFG-1) by the liver

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11
Q

What is Cushing’s Disease?

A

Unregulated hypersecretion of ACTH by Pituitary adenoma

Hypercortisolism

  • systemic HTN is most common manifestation (secondary to LV hypertrophy – concentric remodeling of heart)
  • glucose intolerance occurs ~>60% (DM occurs in 1/3 of patients)
  • moon facies (high incidence of OSA - no association w/ more difficulty w/ intubation)
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12
Q

Difference between the anterior pituitary and posterior pituitary

A

Anterior Pituitary = glandular secretory organ responsible for producing many hormones

Posterior Pituitary = a collection of axon terminals that arise from supraoptic and paraventricular nuclei of the hypothalamus responsible for secreting Oxytocin and Vasopressin

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13
Q

What is the primary stimulus for ADH secretion?

A

Increased Plasma Osmolarity

*other factors include: left atrial distention, decreased circulating blood volume, decreased arterial pressure, exercise, and certain emotional states

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14
Q

What is the function of both ADH and Oxytocin?

A

ADH - controls water secretion and extracellular fluid osmolality (controversially more potent vasoconstrictor than angiotensin II)

Oxytocin - promotes milk letdown and uterine smooth muscle contraction
*one of the few hormones with a positive feedback loop

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15
Q

Diabetes Insipidus vs Syndrome of Inappropriate ADH (SIADH)

A

Diabetes Insipidus = absence of ADH secretion

  • most commonly associated with pituitary surgery (commonly transient)
  • symptoms: abrupt onset of polyuria, thirst, and polydipsia (excessive water loss, hypernatremia)

SIADH = inappropriately high levels of ADH

  • most commonly associated with CNS injury, trauma, and cancer (especially lung CA)
  • symptoms: hyponatremia and sequella related to it
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16
Q

What action does vasopressin have on V1, V2, and V3 receptors?

A

V1: Stimulates V1 receptors in the vasculature to promote vasoconstriction

V2: Acts on renal collecting ducts – increases permeability to water (increases reabsorption of water) = more concentrated urine

V3 receptors are found on anterior pituitary - coupled with second messenger system – have a role in secretion of ACTH

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17
Q

What is the physiologic function of Oxytocin? What are the adverse effects when administered?

A

Stimulate cervical dilation and uterine contractions during labor
Allow milk to be let down into the subareolar sinuses during lactation

AE: water retention and hyponatremia
-IV admin causes vasodilation and subsequent hypotension with reflex tachycardia

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18
Q

What is the role of Parathyroid hormone?

A

Plays chief role in bone remodeling and Calcium homeostasis — secreted by Chief cells in the Parathyroid in response to hypocalcemia and elevated phosphorous levels

  • stimulates bone resorption which releases Ca++ into the blood stream
  • causes Ca++ reabsorption into circulation and phosphate excretion via the kidney
  • facilitates Vitamin D conversion to its activated form to increase GI absorption of Calcium

*Net result of interactions of PTH, Ca, Vit D, and Calcitonin is maintenance of normal plasma Ca++ concentration — helps maintain normal cell function, nerve transmission, membrane stability, bone integrity, coagulation and intracellular signaling

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19
Q

What are the types of Hyperparathyroidism?

A

Primary – Excess PTH production

  • most often due to parathyroid gland hyperplasia or tumor (this increases bone resorption and extracellular Ca++)
  • Clinical signs = hypercalcemia, hypophosphatemia, nephrolithiasis, osteoporosis, fatigue, weakness, difficulties w/ cognition
  • Treatment = surgical excision of parathyroid glands or tumor

Secondary – Generally a complication of chronic renal failure, but can be due to any disease causing hypocalcemia

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20
Q

What are the anesthetic considerations with Hyperparathyroidism?

A

Thorough preop eval to focus on effects of hypercalcemia and the degree of CV and/or renal complications

  • ECG may be warranted (show shortened PR and QT intervals, potential for cardiac arrhythmias, pt may be hypertensive and hypovolemic - severe hypercalcemia)
  • Focus should be on emergence in terms of potential concerns — surgery on thyroid or parathyroid glands can result in damage to the recurrent laryngeal nerve, airway swelling and hematoma formation
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21
Q

What does the Recurrent Laryngeal Nerve innervate and when can injury occur and what does it cause?

A
  • Sensory innervation below true cords and into upper trachea
  • Motor innervation to all intrinsic laryngeal muscles except cricothyroid and external branch of superior laryngeal nerve

Injury can occur with intubation, neck surgery, stretching of neck

  • Unilateral Injury causes cord on injured side to assume midline position = hoarseness
  • Bilateral Injury causes both cords to close to midline (adducted) position = aphonia and airway obstruction occurs ***airway emergency
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22
Q

What is hypoparathyroidism associated with and what is a major concern with it?

A

Generally associated with other endocrine disorders and as a result of surgical removal of parathyroid glands

  • hypocalcemia is a major concern with inadvertent removal of parathyroid glands
  • tetany related to hypocalcemia results in painful muscle spasms of facial muscles and extremities. also laryngeal muscle spasm and upper airway obstruction are possible
  • ECG changes include prolonged QT and possible heart block
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23
Q

What are the different types of Multiple Endocrine Neoplasia?

A

MEN-1: rare, autosomal dominant syndrome

  • parathyroid hyperplasia
  • pituitary adenoma
  • pancreatic neuroendocrine tumor

MEN-2A: autosomal dominant with incomplete penetrance and variable expression

  • parathyroid hyperplasia
  • medullary thyroid cancer
  • pheochromocytoma
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24
Q

What is the physiology of the Thyroid gland?

A

Acinar gland positioned in the neck, anterior to the trachea

Rich vascular supply from superior and inferior thyroid arteries

Innervation from ANS

Divided into right and left lobes by thyroid isthmus
*made up of multiple types of cells – follicular cells, endothelial cells, para-follicular or C cells, fibroblasts, lymphocytes and adipocytes

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25
Q

What is the role of thyroid hormones?

A

Play a major role in normal growth and development

Play a chief role in cellular energy metabolism – stimulate carbohydrate metabolism and facilitate mobilization of free fatty acids

Increase oxygen consumption in nearly all tissues, expect the brain

  • Thyrotropin releasing hormone (TSH) is produced in the hypothalamus and released in response to decreased free circulating thyroid hormone
  • Iodide is required for thyroid hormone synthesis – body readily absorbs necessary iodine from dietary sources

*Thyroid gland also secretes calcitonin - important for calcium ion use

26
Q

What are the three reasons thyroid disease and dysfunction occur?

A

As a result of alterations in levels of thyroid hormones

Impaired metabolism of those hormones

Resistance to effects of thyroid hormones

27
Q

What are the two types of hypothyroidism?

A

Primary - Disease at the level of the thyroid gland (destruction of actual thyroid gland) – increased TSH levels, low thyroid hormones
*autoimmune disease, surgical excision or radioactive iodine therapy (iatrogenic causes)

Secondary - Dysfunction outside the gland – low TSH and thyroid hormone
*most often dysfunction of hypothalamus or pituitary gland – decreased thyroid hormone released from thyroid gland

*Lithium, amiodarone, iron and other medications can cause iatrogenic causes of hypothyroidism

28
Q

What are the signs and symptoms of hypothyroidism?

A

Generally vague and nonspecific:

  • Fatigue
  • Lethargy
  • Joint pains
  • Muscle aches
  • Cold intolerance
  • Constipation
  • Change in voice (rough sounding)
  • Bradycardia (low voltage on ECG)
  • Symptoms of heart failure

*absence of thyroid gland hormones decreases minute oxygen consumption to approx 40% less than normal

29
Q

What is Myxedema Coma?

A

Severe Hypothyroidism

  • rare, may occur in postop period due to triggers such as exposure to cold temp, infection, excessive sedation and analgesic medications
  • decreased mental status/coma, hypothermia, bradycardia, hyponatremia, HF, and respiratory failure

Treatment = ICU care +/- mechanical ventilation, supportive therapy, rewarming, hydration, urgent IV admin of Levothyroxine and Hydrocortisone

*High Mortality

30
Q

What is used to treat hypothyroidism?

A

Thyroid replacement therapy:

T4 (Thyroxine) = hormone of choice for thyroid replacement

  • consistent potency and duration of action
  • absorbed in small intestine
  • Levothyroxine sodium most common – 50-200 mcg/day

T3 (Liothyronine sodium) = salt of triiodothyronine is also used and available in tablet and injection – 50-75 mcg/day
*recombinant TSH

31
Q

What is Hyperthyroidism and the different causes?

A

Excessive thyroid hormone due to an over producing/excessive function of thyroid gland – causes increased metabolism and autonomic nervous system disturbances

Graves Disease = Most common cause

  • other conditions include: toxic nodular goiter, toxic adenomatous disease of thyroid, excessive admin of thyroid hormone, excessive iodine intake, thyroiditis and follicular carcinoma and TSH producing tumor of pituitary gland
  • excess thyroid hormones can expand oxygen consumption as much as 100% more than normal
32
Q

What is the treatment for hyperthyroidism?

A

Anti-thyroid medications

Radioiodine – therapy of choice for Graves’ hyperthyroidism

Surgery

  • Thioureylene Class: Propylthiouracil (PTU), Methimazole, and Carbimazole — inhibits thyroid hormone synthesis
  • PTU inhibits peripheral conversion of T4-T3
  • Iodine = oldest available treatment for hyperthyroid
33
Q

What is a Thyroid Storm?

A

Severe form of Hyperthyroidism
-can mimic MH in clinical environment (related to undiagnosed/untreated hyperthyroidism)

Symptoms = hyperpyrexia (+/- 41*C), tachycardia, arrhythmias, weakness, and delirium… MI can also occur

Treatment = requires ICU supportive care

  • Beta blockers, multiple anti-thyroid meds, iodine, cooling measures
  • anti-thyroid meds (PTU) must be given before iodine which blocks the release of thyroid hormones
34
Q

What is Sick Euthyroid Syndrome?

A

Thyroid Disorder where patient appear euthyroid clinically but have evidence of dysfunction on lab testing

35
Q

What is Thyroiditis?

A

Inflammation of the thyroid (acute or chronic)

  • leads to abnormalities of thyroid function
  • acute is very rare but infectious
  • chronic thyroiditis is Hashimoto’s thyroiditis (autoimmune condition of thyroid gland)
36
Q

What are the anesthetic considerations for thyroid dysfunctions?

A

Hypothyroid patients may be more sensitive to effects of anesthetic agents and can have prolonged recovery from anesthesia

Hyperthyroid patients – you should understand their current status - assess most current thyroid function tests, inquire about symptoms of hyperthyroidism (tachy, a-fib, diarrhea, weight loss)

Patients having thyroid surgery – remember the potential for a large gland and compression on tissue/structure - may be difficult airway or cause obstruction

37
Q

What are possible post-op complications after thyroid surgery?

A

Airway obstruction due to hemorrhage or swelling

**can be life threatening emergency – neck wound may need to be opened to allow drainage – surgical re-exploration may be necessary

**Requires vigilance and quick treatment

38
Q

What is the physiology of the adrenal gland?

A

Small glands located superior to each kidney

Outer Adrenal Cortex - mesodermal tissue
-makes up 90% of adrenal mass and produces steroid hormones as a result of hypothalamic pituitary adrenal simulation (Glucocorticoids, mineralocorticoids, and androgens)

Inner Medulla - neural crest cells
-makes up 10% and synthesizes and releases catecholamines epi and norepi as a result of sympathetic stimulation

39
Q

How does the Hypothalamic Pituitary Adrenal Axis (HPA) regulate adrenal output of Glucocorticoids (Cortisol)?

A
  • Hypothalamus releases Corticotrophin Releasing Hormone (CRH)
  • CRH stimulates the anterior pituitary to produce Adrenocorticotrophic Hormone (ACTH)
  • ACTH stimulates the middle adrenal cortex (zona fasciculata) to produce cortisol
  • Cortisol completes the cycle by providing negative feedback for CRH and ACTH release
40
Q

How is the Hypothalamic Pituitary Adrenal Axis stimulated?

A

By stressors such as:

  • Surgery
  • Trauma
  • Burns
  • Exercise
  • Psychologic trauma

Normal cortisol endogenous production in non-stressed conditions is 20-30 mg/day — Cortisol output amplifies proportionate to degree of stress up to 150 mg/day

41
Q

What are the actions of Hypothalamic Pituitary Adrenal Axis ?

A
  • Conversion of NE to Epi and inhibits PGI2 (responsible for vasodilation) — cortisol required for vascular and smooth muscle to be responsive to catecholamines – cortisol deficiency results in vasodilated state
  • Retention of Na+ and excretion of K+ (similar structure to aldosterone leads to promoting sodium retention and potassium excretion)
  • Enhances gluconeogenesis
  • Inhibits peripheral glucose utilization
  • Anti-inflammatory and anti-allergic effects
42
Q

How are the catecholamines Epi and Norepi made?

A

In the adrenal medulla

Made from amino acid (Tyrosine) through enzymatic conversions:
-Tyrosine –> L-DOPA –> Dopamine –> Norepi –> Epi

Released in direct response to SNS of adrenal medulla

43
Q

Where do catecholamines undergo reuptake degradation?

A

Undergo reuptake at extra-neuronal sites

Degradation by COMT or MAO taking place mostly in the liver
*produces the metabolite VMA which is excreted in the urine and can be measured to assess cumulative catecholamine secretion

*Very short T1/2 – 10 seconds to 2 minutes

44
Q

What is a Pheochromocytoma?

A

Tumor within the adrenal medulla (most often) —causes overproduction of catecholamines

Signs/Symptoms = severe and sustained HTN, headaches, sweating, palpitations

Most often benign and usually isolated to one adrenal gland – 10% are malignant and 10% are bilateral or extra-adrenal

**Very important to be identified early

45
Q

What are preop considerations for a Pheochromocytoma?

A

Focus on identification of pheochromocytoma – classic diagnostic sign is high metanephrine levels on blood tests

Once determined then focus on treatment = Alpha Adrenergic Blockade and volume replacement

  • determine severity based on ECG, BP, and Echo-
  • patients are usually hypovolemic with normal hematocrit
  • must alpha block BEFORE beta blockade – or else you will get an unopposed alpha agonism
  • Phenoxybenzamine, Metyrosine, or Phentolamine are 1st line agents – block the catecholamine effects (should start at least 10-14 days prior to surgery)
  • Beta blockade can be added after successful initiation of alpha blockade
46
Q

What is the intraop management of Phenochromocytoma?

A

Standard ASA monitoring plus an A-line

  • rapid changes in BP
  • potential for massive blood loss
  • need for volume resuscitation
  • central venous access?

Smooth induction - proceed carefully - have drips made ready

  • ensure appropriate depth prior to laryngoscopy to avoid major swings in BP
  • intraop HTN can be treated with Phentolamine Nitroprusside, Nicardipine
  • Avoid ketamine, ephedrine, and pancuronium
  • Watch for hypotension once tumor is removed
47
Q

What is Cortisol and its actions?

A

A glucocorticoid that is released from the adrenal cortex in a pulsatile fashion – follows circadian rhythm (light, sleep, stress, and disease)

  • Bound to carrier called transcortin, some bound to albumin and some remains unbound (this is the biologically active portion)
  • Actions include protein breakdown, increases gluconeogenesis, fatty acid mobilization, and prevention of muscle protein synthesis, anti-inflammatory effects
48
Q

Where is aldosterone synthesized and what is it regulated by?

A

Synthesized and released from adrenal cortex (zona glomerulosa) – Accumulation of potassium in plasma is the most important stimulus for secretion

Regulated by Renin-Angiotensin-Aldosterone system (NOT HPA axis)

  • responsible for maintaining salt/water homeostasis
  • when intravascular volume and renal perfusion are decreased – renin is released and through the angiotensin converting enzyme, angiotensin II is released and binds to G-protein receptors and stimulates the release of aldosterone

*Increases Na+ and H2O absorption through the kidneys – K+ is excreted

49
Q

What does aldosterone secretion stimulate?

A
  • Na+ reabsorption in the distal renal tubule in exchange for K+ and H+ secretion
  • Controls much of fluid and electrolyte balance for volume and acid/base homeostasis

Net Effect = expansion of extracellular fluid volume causes by fluid retention, a decrease in plasma potassium, and metabolic alkalosis

*in a hypovolemic pt: renin released –> angiotensin activated –> aldosterone released –> Na/K/H pump starts working –> leads to Na and H2O reabsorption –> increases blood volume and compensation for hypovolemic problem

50
Q

What is Addison Disease? Its clinical manifestations and anesthetic considerations?

A

Glucocorticoid Deficiency — Hypoaldosteronism

Results from:

  • dysfunction of adrenal gland (primary deficiency)
  • lack of ACTH stimulation of adrenal glucocorticoid production (secondary deficiency)

Clinical Manifestations: weakness, fatigue, hypoglycemia, hypotension, weight loss

Anesthetic considerations: steroid replacement therapy during periop period.. “stress dose steroids” and maintance

51
Q

What is Cushing Syndrome?

A

Glucocorticoid Excess

Occurs due to variety of reasons:

  • overproduction of cortisol by adrenal mass
  • excessive stimulation of normal adrenal gland to produce cortisol due to excessive ACTH production by the pituitary gland
  • iatrogenic admin of glucocorticoids

Manifests by large weight increase – central abdomen, moon facies, buffalo hump

52
Q

What are the uses of corticosteroid therapies?

A

-Deficiency states (adrenal insufficiency)

  • Reactive airway disease: asthma, COPD (inflammatory conditions)
  • inhaled glucocorticoids agent of choice – reduces symptoms, improves quality of life, decreases exacerbations

-Neuo Critical Care: dexamethasone has clinical applications in pts with tumors, bacterial meningitis and prevention or tx of cerebral edema

Other uses: N/V prophylaxis, immunosuppression, tx of inflammatory conditions, airway edema, allergic reactions (topical)

53
Q

What are the types of hyperaldosteronism?

A

Conn Syndrome: adrenal over secretion of aldosterone by adrenal tumors (usually benign)

Secondary Hyperaldosteronism results from pathologic state
-reduced circulating blood volume (cirrhosis, CHF) – this decreases circulating volume causes continuous stimulation of RAAS and overproduction of aldosterone

Tertiary (Bartter Syndrome): Renal Disorder
-leads to increased renin release in order to compensate for excessive Na loss – causes excess production of angiotensin II and aldosterone

54
Q

What are the anesthetic considerations for hyperaldosteronism?

A

Correction of fluid and electrolyte abnormalities preop

-Potassium sparring diuretics help manage hypokalemia and hypervolemia and control HTN

55
Q

What is the role of the pancreas?

A

Plays key role in digestion and metabolism as well as storage of energy

  • most cells made up of exocrine cells (secrete an alkaline digestive fluid into the duodenum)
  • within pancreatic lobules are small clusters of endocrine cells (the islets of langerhans) that secrete insulin, glucagon, somatostatin, and pancreatic polypeptide
  • arterial blood supply consists of branches from splenic artery and superior/inferior pancreaticoduodenal arteries
56
Q

How is insulin synthesized? Where is it stored?

A

Begins with inactive protein, pre-proinsulin

This gets cleaved to proinsulin and then to insulin
*made up of two amino acid peptides a and b (linked by a disulfide bond)

Insulin and C peptide make up secretory granules — stored in beta cells of islets of langerhans and released in response to increased blood glucose

*overall insulin has an anabolic effect on target organs – increases synthesis/storage of carbohydrates, fats and proteins

57
Q

What does diabetes mellitus result from? What’s the difference between the two types?

A

Results from impaired secretion of insulin from pancreas and/or reduced tissue sensitivity

Type I (insulin deficiency): autoimmune mediated destruction of beta cells – dependent on exogenous insulin to regulate metabolism and avoid ketoacidosis

  • younger age of onset
  • sensitivity to insulin is normal

Type II (peripheral insulin resistance): results from loss of normal regulation of insulin secretion from pancreas and insulin sensitivity — peripheral insulin resistance coupled with failure to secrete insulin because of pancreatic beta cell dysfunction

  • oral hypoglycemic drugs are alternatives to exogenous admin of insulin
  • more frequent – adult onset

Diagnosis = fasting serum glucose >126 mg/dL or random serum glucose >200 mg/dL with symptoms like polydipsia, polyuria, polyphagia

  • DKA = increased blood glucose and ketone body formation along with anion gap metabolic acidosis
  • Type 1 to Type 2 ratio is 1:9
58
Q

What are the anesthetic considerations with Diabetes Mellitus?

A

-Thorough preop eval – what is baseline Hbg A1C? is patient compliant with treatment? what is their treatment (oral, insulin, combo)?

  • Normal hbg A1C level is less than 6 – >8% is considered to have poorly controlled DM
  • these pts are at risk for postop complications – infection, delayed wound healing, MI
  • Diabetics are higher risk for CV complications – 12 lead ekg should be obtained
  • diabetic autonomic dysfunction – delayed gastric emptying (risk for aspiration)
59
Q

What are the hypoglycemic actions of Insulin in the liver, muscle, and adipose tissue?

A

Liver: inhibits hepatic glucose production (decreases gluconeogenesis and glycogenolysis), stimulated hepatic glucose uptake

Muscle: stimulates glucose uptake, inhibits flow of gluconeogenic precursors to the liver (alanine, pyruvate and lactate)

Adipose Tissue: stimulates glucose uptake (small amount compare to muscle), inhibits flow of gluconeogenic precursors to liver (glycerol) and reduces energy substrate for hepatic gluconeogenesis

  • plasma half-life of 5-6 minutes when IV – SubQ leads to slower release into circulation and sustained pharmacological effect
  • degraded in liver, kidney, muscle
60
Q

What are the goals for therapy for DM by American Diabetes Association?

A

Hemoglobin A1c <7%

Pre-prandial glucose 70-130 mg/dL

Peak post-prandial plasma glucose <180 mg/dL

*variety of insulin regimens may be used to achieve glycemia targets

61
Q

What are the classes of oral hypoglycemic agents?

A

Sulfonylureas: act by increasing insulin secretion by stimulating beta cells (decrease hepatic clearance of insulin)

Biguanides (Metformin): decrease serum glucose by decreasing hepatic output (decreasing gluconeogenesis) and sensitizing peripheral tissues to effects of insulin

Thiazolidinediones: act on extra-pancreatic sites to increase insulin sensitivity and decrease hepatic glucose production

62
Q

What are somatostatin analogues?

A

A group of related peptides (released from pancreatic islets - delta cells) in CNS and GI system

Act as inhibitors of the release of TSH and Growth Hormone from pituitary, of insulin and glucagon from pancreas and vasoactive peptides from the GI tract

*Might use to block hormone release in endocrine tumors – given prop

Advanced Principles of Anesthesia (31 decks)

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