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Anesthesia Pharm Exam 3 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Pituitary Gland

A
  • master gland
  • attached to hypothalamus via pituitary stalk
  • sits in sella turcica
  • secretes 8 hormones that regulate organ function

- critical to survival!

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2
Q

Anterior Pituitary (Adenohypophysis)

A
  • arises from oral ectoderm
  • produces ACTH, TSH, GH, PRL, LH, FSH, and MSH
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3
Q

Hyperpituitarism

A
  • 2/2 anterior pituitary adenoma
  • often asymptomatic
  • presents in 3 distinct ways:
    1) hormonal hypersecretion
    2) local mass effects (including pituitary hypofunction 2/2 compression of normal gland - visual, sinus, or balance probs)
  • incidental discovery during imaging
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4
Q

Growth Hormone

A
  • secreted from anterior pituitary in pulsatile manner
  • under control of somatostatin and GH releasing hormone
  • high in childhood, max in puberty, dec w age
  • stimulates longitudinal growth of bones, bone density, condrocyte formation and increases muscle mass
  • acts on liver to stimulate gluconeogenesis and promote fat breakdown
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5
Q

Gigantism (childhood) and Acromegaly (adults)

A

2/2 hypersecretion of GH by ant pit

  • leads to increased production of IGH-1 by liver
  • gigantism due to growth plates (epiphyses) not closing
  • acromegaly inadulthood = cardiac dx, HTN, ventricular hypertrophy

- increased size of soft tissue, mouth, tongue, lips = OSA and upper airway obstruction

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6
Q

Giganitsm and Acromegaly Visual

A
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7
Q

Cushings 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% of patients

– Diabetes Mellitus occurs in 1/3 of patients

• Moon Facies

– High incidence of OSA~ Surprisingly despite this there is no association w/ more difficulty w/ intubation. Always be prepared!

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8
Q

Posterior Pituitary (Neurohypophysis)

A
  • Not a secretory gland. A collection of axon terminals – arise from supraoptic and paraventricular nuclei of the hypothalamus
  • Principal responsibility is secretion of Oxytocin and Vasopressin (ADH)
  • Primary stimulus for ADH secretion = Plasma Osmolarity

– Other factors include

• Left atrial distention, circulating blood volume, exercise, and certain emotional states

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9
Q

ADH

A
  • Controls water secretion and extracellular fluid osmolality

– more potent vasoconstrictor than angiotensin II

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10
Q

Oxytocin

A

– Promotes milk letdown and uterine smooth

muscle contraction

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11
Q

DI

A
  • absence of ADH secretion (commonly associated w pituitary surgery)
  • transient
  • symptoms: polyuria, thirst, polydipsia
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12
Q

SIADH

A
  • high levels of ADH
  • associated w CNS injury, trauma, lung CA
  • symptoms: hyponatremia (seizures)
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13
Q

SIADH vs DI Chart

A
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14
Q

Hormones of the Anterior Pituitary Chart

A
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15
Q

Vasopressin

A
  • posterior pituitary hormone
  • powerful vasoconstrictor
  • stimulates g-protein coupled receptors (V1) in VSM
  • acts on renal collecting ducts, increasing permeability to water (more concentrated urine) mediated by V2 receptors
  • V3 receptors found on anterior pituitary (2nd messenger system, have role in secreting ACTH)
  • desmopressin (DDAVP) is synthetic, long acting analogof vasopressin
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16
Q

Oxytocin

A
  • posterior pituitary hormone
  • synthesized in supraoptic and paraventricular nuclei of hypothalamus

– Transported down long axons into the posterior pituitary for release

– Physiologic functions of Oxytocin~ Stimulate cervical dilation and uterine contractions during labor

• Allows milk to be let down into the subareolar sinuses during lactation

– Adverse effects = water retention and hyponatremia

• IV admin causes vasodilation and subsequent hypotension w/ reflex tachycardia

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17
Q

Parathyroid Physiology

A

• 4 small glands (pea sized)

– Located posterior to thyroid gland

– Rich vascular supply

• Inferior thyroid artery

– Chief cells primarily secrete Parathyroid hormone (PTH) in response to hypocalcemia

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18
Q

PTH

A
  • plays chief role in bone remodeling and Calcium homeostasis

– Stims bone resorption which releases Ca into the blood stream

  • It also causes Ca reabsorption into the circulation and phosphate excretion via the kidney
  • PTH facilitates Vitamin D conversion to its activated form
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19
Q

What is the net result of interactions of PTH, Ca, Vit D and Calcitonin?

A

- maintenance of normal plasma Ca concentration!

– This helps maintain normal cell function, nerve transmission, membrane stability, bone integrity, coagulation and intracellular signaling

– Normal Calcium levels are 8.5 – 10.5 mg/dl (2.1-2.6 mM)

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20
Q

Primary Hyperparathyroidism

A

• Primary- Excess PTH production

– Most often d/t parathyroid gland hyperplasia or tumor

• This increases bone resorption and extracellular Ca

– Clinical Signs = Hypercalcemia, hypophosphatemia, nephroliathisis, osteoporosis, fatigue, weakness, and difficulties w/ cognition

• Treatment- Surgical excision of the parathyroid glands or tumor

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21
Q

Secondary Hyperparathyroidism

A

Generally a complication of chronic renal failure, but can be d/t any disease causing hypocalcemia

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22
Q

Anesthetic Considerations

A

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

– pre-op EKG

  • Show shortened PR and QT intervals (avoid zofran)
  • Potential for cardiac arrhythmias
  • Pts 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 recurrent laryngeal nerve, airway swelling and hematoma formation

– Can lead to devastating consequences!

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23
Q

Recurrent Laryngeal Nerve

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

Innervates ALL muscles of larynx except crycothyroid which is external laryngeal nerve.

If paralyzed, VC will be abducted causing strider and hoarseness.

If partially paralyzed, adducted, causing obstruction and lesion, possible aspiration risk

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24
Q

Recurrent Laryngeal Nerve Injury

A

• Can occur with intubation, neck surgery, stretching of neck

– Thyroid or cervical spine surgery

• Unilateral vs Bilateral

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

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25
Q

Hypoparathyroidism

A

• Generally associated w/ other endocrine disorders and as a result of surgical removal of parathyroid glands.

– Hypocalcemia is a major concern w/ 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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26
Q

Multiple Endocrine Neoplasma (MEN-1)

A

Rare, autosomal dominant syndrome, tumors develop in parathyroid glands. Pts present w hypoparathyroidism

– Parathyroid hyperplasia

– Pituitary adenoma

– Pancreatic neuroendocrine tumor

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27
Q

MEN-2A

A

– Autosomal dominant w/ incomplete penetrance and variable expression. Combo of medullary thyroid carcinoma (theo), usually a lack of parathyroid involvement

– Parathyroid hyperplasia

– Medullary thyroid cancer

– Pheochromocytoma

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28
Q

Thyroid Physiology

A

• Acinar gland positioned in neck, anterior to trachea

– Rich vascular supply from superior and inferior thyroid arteries

– Divided into right and left lobes by thyroid isthmus – Total gland weighs up to 25grams

• Made up of multiple types of cells

– Follicular cells, enothelial cells, parafollicular or C cells, fibroblasts, lymphocytes and adipocytes

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29
Q

Thyroid Hormones

A

• Play a major role in normal growth and development • Play a chief role in cellular energy metabolism

30
Q

Why do thyroid disease and dysfunction occur? (3 things)

A

– As a result of alterations in levels of thyroid hormones

– Impaired metabolism of those hormones

– Resistance to effects of thyroid hormones

31
Q

TSH

A
  • produced in hypothalamus
  • released in response to decreased free circulating thyroid hormone
32
Q

Iodide

A
  • required for thyroid hormone synthesis
  • body readily absorbs necessary iodine from dietary sources
33
Q

Hypothyroidism vs Hyperthyroidism Chart

A
34
Q

Primary Hypothyroidism

A

Disease at the level of thyroid gland

– Autoimmune disease, surgical excision or radioactive iodine therapy (iatrogenic causes)

  • thyroid hormone replacement therapy for life
35
Q

Secondary Hypothyroidism

A
  • Dysfunction outside the gland

– Most often dysfuction of hypothalamus or pituitary gland—decreased thyroid hormone release from thyroid gland

36
Q

Hypothyroid Medications

A

Lithium, amiodorone, iron, and others can cause iatrogenic causes of hypothyroidism

37
Q

Hypothyroidism S/S

A

Generally vague and nonspecific

– Fatigue, lethargy, joint pains, muscle aches, cold intolerance, constipation, change in voice (rough sounding), bradycardia (low voltage on ECG), and symptoms of heart failure

38
Q

Myxedema Coma

A
  • severe hypothyroidism

– Rare, may occur in postop period d/t triggers such as exposure to cold temp, infection, excessive sedation and analgesic medications

– Decreased mental status/coma, hypothermia, bradycardia, hyponatremia, heart failure and resp failure = High mortality

• Tx includes ICU care +/- mech vent, supportive therapy, rewarming, hydration, urgent IV admin of Levothyroxine and Hydrocortisone

39
Q

Hypothyroid Replacement Therapy

A

• Thyroid replacement is very common

– T4 (Thyroxine) is the hormone of choice for thyroid replacement • Consistent potency and duration of action • Absorbed in small intestine • Levothyroxine sodium most common tx. 75-150mcg/day

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

40
Q

Hyperthyroidism

A

Excessive thyroid hormone d/t an over producing / excessive function of thyroid gland.

– Causes increased metabolism and autonomic nervous system disturbances

41
Q

Graves Disease

A

–Most common cause of Hyperthyroidism in adults

– Other conditions include toxic nodular goiter, toxic adenomatous disease of thyroid, excessive admin of thyroid hormone, excessive iodine intake, thyroiditis and folllicular carcinoma and TSH producing tumor of pit gland

  • s/s = weight loss, tremor, heat intolerance, sweating, tachycardia, arrhythmias, afib, HF
42
Q

Hyperthyroidism Treatment

A
  • Antithyroid meds, Radioiodine and ultimately surgery are definitive tx for hyperthyroidism and tx of Graves Disease
  • Thioureylene Class

– Propylthiouracil (PTU), Methimazole and Carbimazole

  • Inhibits thyroid hormone synthesis
  • PTU inhibits peripheral conversion of T4-T3
43
Q

Thyroid Storm

A

• Severe form of Hyperthyroidism

– Can mimic MH in clinical environment

• Related to undiagnosed/untreated Hyperthyroidism

– Symptoms –Hyperpyrexia (+/- 41 degrees C), tachycardia, arrhythmias, weakness and delirium. Myocardial ischemia can also occur

– Treatment- Requires ICU – Supportive care!

• B blockers, multiple antithyroid meds, iodine, cooling measures, antithyroid meds (proylthiouracil)

– Must be given before iodine – which blocks the release of thyroid hormones.

44
Q

Sick Euthyroid Disorder

A

– Pt’s appear euthryoid clinically but have evidence of dysfunction on lab testing

  • effects pts w chronic non-thyroid issues
  • usually decreased T3 and T4
  • stress, surgical trauma, propranolol and amiodarone both impair conversion of T3 to T4
45
Q

Thyroiditis

A

– Inflammation of thyroid (acute or chronic)

  • Leads to abnormalities of thyroid function
  • Acute is very rare, but infectious
  • Chronic thyroiditis is Hashimoto’s thyroiditis

– An autoimmune condition of the thyroid gland

46
Q

Anesthetic Considerations for Hypo/Hyperthyroidism

A
  • Hypothyroid pt’s may be more sensitive to effects of anesthetic agents and can have prolonged recovery from anesthesia
  • In hyperthyroid pt’s you should understand their current status – Assess most current thyroid function tests. Inquire about symptoms of hyperthyroidism – tachycardia, afib, diarrhea, weight loss
  • Pt having thyroid sugery – remember the potential for a large gland and compression on tissues/structure – may be difficulty airway or cause obstruction.
47
Q

Postop Complications

A
  • Requires vigilance and quick treatment.
  • Airway obstuction d/t hemorrhage or swelling can be life threatening emergency!

– Neck wound may need to be opened to allow drainage

– Surgical re-exploration may be necessary. Must always be vigilant!!!!!!!!!!!!!!!!!!!!!

48
Q

Adrenal Gland Physiology

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 (HPA) stimulation

– Glucorticoids, mineralocorticoids, and androgens (cortisol, aldosterone, and dehydroepiandrosterone)

– Inner Medulla – neural crest cells

• Makes up 10% and synthesizes and releases catecholamines epi and norepi as a result of sympathetic stimulation

49
Q

Adrenal Medulla

A

• Inner most part of adrenal gland

– Highly vascular

• Made up of two types of Chromaffin cells

– Those that produce Epinephrine – Those that produce Norepinephrine

– Catecholamines such as Epi and Norepi are made from amino acid (Tyrosine) through enzymatic conversions:

• Tyrosine ⇒ L-DOPA (L-3,4-dihydroxyphenylalanine) ⇒ dopamine ⇒ norepinephrine ⇒ epinephrine. • Catecholamines released in direct response to SNS of adrenal medulla

50
Q

Catecholamine Reuptake and Degradation

A
  • Very Short half life – 10 seconds – 2 minutes
  • Undergo reuptake at extraneuronal sites
  • Degradation by Catechol-o-methyltransferase (COMT) or monoamine oxidase (MAO). – This degradation takes place mostly in liver
  • Produces the metabolite Vanillylmandelic acid (VMA)

– VMA is excreted in the urine and can be measured to assess cumulative catecholamine secretion!

51
Q

A vs B Adrenergic Receptor Stimulation

A
52
Q

Pheochromocytoma

A

• A tumor within the adrenal medulla (most often)

– Causes overproduction of catecholamines

• Signs and 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 extraadrenal in origin

– Very important to be identified early!

53
Q

Preop Eval for Pheo

A

• Focus on identification of pheo- 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 EKG, BP measurements and echocardiogram • Pts are usually hypovolemic w/ normal hematocrit

– MUST ALPHA BLOCK BEFORE BETA BLOCKADE!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

• Phenoxybenzamine, Metyrosine or Phentolamine are first line agents. Should start at least at least 10-14 days prior to scheduled surgery • Beta blockade can be added after successful initiation of alpa blockade

54
Q

IntraOp Mgmt of Pheo

A

• Standard ASA monitoring + A line !

– Rapid changes in BP – Potential for masive blood loss – Need for Volume resuscitation

• Place A line prior to induction?

– Central venous access ?

  • High likelihood for infusion of vasoactive medications and large volumes of fluid/blood
  • Smooth induction – Proceed carefully – Have drips made and ready!

– Ensure appropriate depth prior to laryngoscopy to avoid major swings in BP – Intraop HTN can be treated w/ Phentolamine, Nitroprusside, Nicardipine

• Avoid Ketamine, Ephedrine and Pancuronium • Once tumor is removed- Watch for hypotension

55
Q

Cortisol

A
  • adrenal hormone
  • 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 and gluconeogenesis, fatty acid mobilization, and prevention of muscle protein synthesis

56
Q

Glucocorticoid Effects Chart

A
57
Q

Aldosterone

A

• Synthesized and released from adrenal cortex (zona glomerulosa)

– Regulated by Renin-angiotensin-aldosterone system (NOT HPA axis)

  • Responsible for maintaining salt and water homeostasis
  • When intravascular volume and renal perfusion are decreased – Renin is released and through the angiotensin converting enzyme (ACE), angiotensin II is released and binds to g protein receptors and stimulates the release of aldosterone.

– Aldosterone increases Na and H20 absorption through the kidneys. Potassium is excreted.

– Potassium is also a stimulant for aldosterone release

58
Q

Aldosterone Secretion Stimulates

A

• Aldosterone secretion stimulates:

– Na+ Reabsorption in the distal renal tubule in exchange for K+ and H+ secretion

– Controls much of fluid & electrolyte balance for volume and acid/base homeostasis

– Net effect: expansion of extracellular fluid volume caused by fluid retention, a decrease in plasma potassium, and metabolic alkalosis

59
Q

Addison Disease

A

(glucocorticoid deficiency) (Hypoaldosteronism)

– Less common than Cushings

• 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 perioperative period. “Stress dose steroids” and maintenance

60
Q

Cushing Syndrome

A
  • glucocorticoid excess

– Occurs d/t variety of reasons: overproduction of cortisol by adrenal mass, excessive stim of normal adrenal gland to produce cortisol d/t excessive ACTH production by the pituitary gland and iatrogenic admin of glucocorticoids

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

61
Q

Corticosteroid Therapies

A

• Reactive airway disease

– Asthma, COPD – Inflammatory conditions

• Inhaled glucocorticoids agents of choice

– Reduce symptoms, improves quality of life, decreases exacerbations

• Neuro Critical Care

– Dexamethasone has clinical applications in patients with tumors, bacterial meningitis and prevention or tx of cerebral edema

  • Tumors- Initiated to reduce vasogenic edema.
  • Other uses- N/V prophylaxis, immunosuppression, tx of inflammatory conditions, airway edema, allergic reactions
62
Q

Hyperaldosteronism

A

• Excess aldosterone due to some sort of pathology

– Conn Syndrome – adrenal oversecretion of aldosterone by adrenal tumors (generally benign)

– Secondary Hyperaldosteronism results from pathologic state

• Reduced circulating blood volume (cirrhosis, CHF)

– This decreased circulating volume causes continuous stim of renin-angiotensin- aldosterone system 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 angio II and aldosterone
  • Anesthetic considerations:

– Correction of fluid and electrolyte abnormalities preop

• K sparring diuretics (Spironolactone)

– Helps manage hypokalemia and hypervolemia and controls hypertension

63
Q

Pancreas Physiology

A

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

– Located in retroperitoneal space, near duodenum – Most cells made up of exocrine cells

• Secrete an alkaline digestive fluid – Within pancreatic lobules are small clusters of endocrine cells – the islets of langerhans

– Arterial blood supply consists of branches from splenic artery and the superior and inferior pancreaticoduodenal arteries

64
Q

Insulin

A

• Synthesis begins w/ 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 releseased in response to increased blood glucose – Overall insulin has an anabolic effect on target organs • Increases synthesis of carbohydrates, fats, and proteins

65
Q

DM

A

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

– Type I (insulin dependent) and Type II (non insulin dependent)

• Type I – destruction of b cells – Required exogenous insulin to avoid ketoacidosis. Younger onset of age • Type II- More frequent – results from los of normal regulation of insulin secretion from pancreas and insulin sensitivity. Adult onset – obesity link

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

66
Q

DKA

A

An acute event characterized by increased blood glucose and ketone body formation along w/ anion gap metabolic acidosis. Lactic acidosis may also coexist.- May be d/t infection, stress, inadequate insulin. Treat aggressively w/ fluids and insulin. Replace electrolytes!

67
Q

Anesthetic Considerations for DM

A

• Thorough preop eval- what is baseline Hgb A1C?

– Is the patient compliant w/ treatment – What is treatment –OHAs only, insulin, combo?

• Normal hemoglobin A1C level is less than 6

– >8 % is considered to have poorly controlled DM

• These patients are at risk for postop complications

– Infection, delayed wound healing, MI

• Diabetics are higher risk for cardiovascular complications – 12 lead ekg should be obtained

– Diabetic autonomic dysfunction – Delayed gastric emptying

• Risk for aspiration

68
Q

Insulin

A

• Exogenous insulin is used to reduce blood sugar levels

– Hypoglycemic actions of Insulin include:

  • Liver- inhibits hepatic glucose production (decreases gluconeogenesis and glycogenolysis) ; Stimulates 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 amt compared to muscle) ; Inhibits flow of gluconeogenic precursors to liver (glycerol) and reduces energy substrate for hepatic gluconeogensis

– Has a plasma half life of 5-6 minutes when injected IV

  • Degraded in liver, kidney, muscle
  • Subq injection leads to slower release in to circulation and sustained pharmacological effect! –Recommended administration
69
Q

Clinical Application for DM

A
70
Q

OHAs

A
71
Q

Somatostatin Analogs

A

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

– 14 amino acid peptide somatostatin – 28 amino acid peptide and 12 amino acid peptide

  • Act as inhibitors of the release of TSH and Growth Hormone (GH) from pituitary, of insulin and glucagon from panceas, and vasoactive peptides from the GI tract.
  • Clinical Application- Somatostatin analogues (Octreotide and Lanreotide) are used in perioperative period to block hormone release in endocrine tumors. Most often given IV as continues infusion. Can be given sq. Can also be given in 50-100 mcg aliquots in response to hemodynamic instability related to vasoactive mediators
72
Q
A

Anesthesia Pharm Exam 3 (6 decks)

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