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Concepts 3 > Endocrine Physiology (Lea) > Flashcards

Endocrine Physiology (Lea) Flashcards

1
Q

Homeostasis is controlled by what two systems?

A

Nervous System
Endocrine System

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2
Q

Functions of both the nervous and endocrine system

A

1) communicate, 2) integrate, and 3) organize the body’s response to a changing internal or external environment

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3
Q

With the endocrine system, messengers are ___.

A

hormones

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4
Q

With the endocrine system, messengers travel through ___.

A

ECF

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5
Q

With the endocrine system, responses are ___.

A

slow and widespread

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6
Q

With the endocrine system, duration of action is ___.

A

long

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7
Q

With the nervous system, messengers are ___.

A

neurotransmitters

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8
Q

With the nervous system, messengers travel through ___.

A

chemicals or electric pathways

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9
Q

With the nervous system, responses are ___.

A

fast, precise, and specific

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10
Q

With the nervous system, duration of action is ___.

A

short

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11
Q

The purpose of the endocrine system is to ___

A

regulate behavior, growth, metabolism, fluid status, development and reproduction

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12
Q

Endocrine function is mediated by ___

A

hormones

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13
Q

Hormones are _____

A

messengers that transport information from one set of cells to another

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14
Q

Endocrine Function – target site is ____

A

a distant cell
Ex: Adrenal Gland

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15
Q

Paracrine Function – target site is ___

A

a neighboring cell of a different type
Ex: pancreatic alpha cells influencing pancreatic beta cells

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16
Q

Autocrine Function – target site is ____

A

on the secreting cell itself and/or an identical neighboring cell

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17
Q

Peptide or Protein Hormones

A

The majority of hormones
Prehormones and prohormones are synthesized in endocrine cells
Stored in secretory granules within endocrine glands
Secreted out of the endocrine gland via exocytosis into ECF
Includes insulin, growth hormone, vasopressin, angiotensin, prolactin, erythropoietin, calcitonin, somatostatin, adrenocorticotropic hormone, oxytocin, glucagon, and parathyroid hormone

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18
Q

Amine or Amino Acid-Derivative Hormones

A

Includes serotonin, thyroid hormones and catecholamines

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19
Q

Serotonin is synthesized from ___

A

tryptophan

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20
Q

Thyroid hormones and catecholamines (epinephrine, norepinephrine, dopamine) are derived from ______

A

tyrosine

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21
Q

Steroid Hormones
(derived from, duration, examples)

A

Either Derived from cholesterol or are like cholesterol in chemical structure
Compartmentalized in the endocrine cell (not in secretory granules)
Released via simple diffusion (not exocytosis)
Circulating steroid hormones are bound to transport proteins to protect from metabolism andrenal clearance
Long duration of action
Includes cortisol, aldosterone, estrogen, progesterone, testosterone and active metabolites of Vitamin D

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22
Q

Hormone Receptor Activation (how does it work)

A

Hormone receptors are located either on the surface of cells or inside
The activation of hormone receptors on the cell membrane triggers an enzyme system that generates an intracellular signal, also known as a second messenger

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23
Q

Examples of second messengers includes the cyclic adenosine monophosphate (cAMP) system (steps of how it works)

A

Hormone receptor occupation activates the plasma membrane enzyme adenyl cyclase
Adenyl cyclase catalyzes adenosine triphosphate (ATP) to cAMP
cAMP acts as second messenger
cAMP may activate intracellular enzymes, modify cell-membrane permeability or transport, or alter gene expression
Ex: TSH, vasopressin, parathyroid hormone, glucagon, FSH, and luteinizing hormone

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24
Q

Other examples of second messenger systems include ____

A

calcium and cyclic guanosine monophosphate

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25
Q

Thyroid and steroid hormones
(how do they produce their effects)

A
  • Thyroid and steroid hormones produce the desired target cell response by interacting with specific intracellular hormone receptors
  • Thyroid and steroid hormones are lipophilic and enter target cells via simple diffusion and/or special transport mechanism
  • Thyroid and steroid hormones interact with DNA to suppress or enhance gene transcription/translation
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26
Q

Simple Steps of the Second Messenger System

A
  1. Agonist activates membrane bound receptor
  2. G-protein is activated and produces effector
  3. Effector stimulates second messenger synthesis
  4. SEcond messenger activates intercellular process
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27
Q

Hormone receptors are constantly being ___

A

destroyed and created

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28
Q

The quantity of hormone receptors present is often inversely related to ___

A

the concentration of circulating hormone

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29
Q

Downregulation =

A

a sustained elevated plasma concentration of a given hormone results in a decrease in receptors per cell on the target site

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30
Q

Upregulation

A

a sustained low plasma concentration of a given hormone results in an increase in receptors per cell on the target site

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31
Q

The synthesis and secretion of hormones are regulated by _____.

A

neural controls, biorhythms and feedback mechanisms

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32
Q

Neural controls = ___

A

Stress, emotions and senses may influence the release of hormones

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33
Q

Biorhythms = __

A

hormonal release may be circadian, weekly, or seasonal

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34
Q

Negative Feedback control

A

virtually all hormones are controlled by negative feedback loops
Negative feedback acts to limit or terminate the production and secretion of a given hormone once the appropriate response has occurred
Ex: Parathyroid hormone is controlled by calcium; insulin and glucagon are controlled by blood glucose
​

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35
Q

Positive feedback loop

A

Positive feedback is when a given hormone response initiates signals amplifying hormone release
Ex: Luteinizing hormone that precedes ovulation is stimulated by LH

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36
Q

PITUITARY GLAND

A

AKA the hypophysis
Master endocrine gland
Pea-sized
Resides in the sella turcica of the sphenoid bone
Connected to the hypothalamus via the hypophyseal stalk

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37
Q

HYPOTHALAMUS

A

An important regulator of the pituitary gland
Influences the pituitary gland based on integrates information from pain, emotions, energy needs, water balance, olfactory, and electrolyte levels

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38
Q

Image of Pituitary Gland

A
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39
Q

Anterior Pituitary Lobe is AKA ____ and releases which hormones?

A

Adenohypophysis
Releases: follice-stimulating hormone, luteinizing hormone, adrenocorticotropic hormone, thyroid stimulating hormone, prolactin, and growth hormone
*think of the pneumonic “FLAT PIG”

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40
Q

Function of Follicle-Stimulating hormone

A

stimulates ovarian follicle development in females and spermatogenesis in males

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41
Q

Function of Luteinizing Hormone

A

induces ovulation and corpus luteum development in females and stimulates the testes to produce testosterone

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42
Q

Function of Adrenocorticotropic Hormone

A

regulates the growth of the adrenal cortex and the release of cortisol and androgenic hormones of the adrenal gland

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43
Q

Function of Thyroid Stimulating Hormone

A

controls the growth and metabolism of the thyroid gland and the secretion of thyroid hormone

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44
Q

Function of Prolactin

A

promotes mammary gland development and milk production by the breasts. Also, inhibits the secretion of LH and FSH

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45
Q

Function of Growth Hormone

A

promotes skeletal development and body growth and regulates protein and carbohydrate metabolism

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46
Q

Thyrotropin-releasing hormone comes from the ____ and corresponds with _____ at what site?

A

Hypothalamus and corresponds with thyroid-stimulating hormone (TSH, thyrotropin) at the anterior pituitary with its target site being the thyroid gland

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47
Q

Corticotropin-releasing hormone comes from the ____ and corresponds with _____ at what site?

A

Hypothalamus and corresponds with adrenocorticotropic hormone (ACTH, cotricotropin) at the anterior pitutary with its target site being the adrenal gland

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48
Q

Gonadotropin releasing hormone comes from the ____ and corresponds with _____ at what site?

A

Hypothalamus and corresponds with follicle stimulating hormone and luteinizing hormone at the anterior pituitary with their target sites being the Gonads (testes/ovaries)

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49
Q

Prolactin releasing factor comes from the ____ and corresponds with _____ at what site?

A

Hypothalamus and corresponds with Prolactin at the Anterior Pitutary with its target site being the breast

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50
Q

Both Growth hormone-releasing hormone and Growth hormone-inhibitoing hormone come from the ____ and corresponds with ___ at which target site?

A

Hypothalamus and corresponds with growth hormone at the anterior pitutary with its target site being all tissues

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51
Q

What is the etiology of hyposecretion at the anterior pituitary lobe?

A

Pituitary tumors, Sheehan syndrome, trauma, radiation

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52
Q

What will we see clinically with a patient with Panhypopituitarism?

A

Decrease thyroid function
Depression of glucocorticoid production
Suppression of sexual development
Macroadenomas may cause compression of adjacent structures and result in diplopia, visual loss, facial numbness

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53
Q

Sheehan’s Syndrome

A

AKA postpartum pituitary gland necrosis, is hypopituitarism caused by ischemic necrosis due to blood loss and hypovolemic shock after giving birth.

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54
Q

For patients who are having hyposecretion due to a mass near the pituitary gland, what is the treatment option?

A

Surgical intervention to control bleeding, decompression or removal of tumor may be warranted
Transsphenoidal approach a common route

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55
Q

Most problems with the anterior pituatary gland = ___

A

hypersecretion
Most pituitary tumors are hypersecreting adenomas
Prolactin, ACTH and GH are the most common hormones hypersecreted

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56
Q

Discuss the deviations from normal function with growth hormone.

A

Hyposecretion
Dwarfism – deficient GH during childhood
Hypersecretion
Gigantism – increased and sustained hypersecretion of GH during childhood (before closure of growth plates) and thereafter
Acromegaly – sustained hypersecretion of GH after adolescence

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57
Q

What is acromegaly?

A

Skeletal overgrowth (enlarged hand and feet, prominentprognathic mandible)
Soft-tissue overgrowth (enlarged lips, tongue, and epiglottis)
Overgrowth of internal organs
Glucose intolerance
Surgical Treatment
Microsurgical removal of pituitary tumor (transsphenoidal route)

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58
Q

Anesthetic Considerations for the patient with Acromegaly

A

VAE precautions
Identify appropriate fitting mask
Challenging airway r/t macroglossia , hypertrophy of epiglottis, obstructive teeth, enlarged thyroid gland
Smaller ETT r/t subglottic narrowing
Challenging nasal intubation r/t enlarged turbinate
Thorough cardiac evaluation r/t cardiomyopathy, dysrhythmias and htn
r/f entrapment neuropathies (e.g. carpal tunnel syndrome)
Confirm ulnar artery flow prior to catheterization of radial artery related

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59
Q

Anesthetic Considerations for a transphenoidal approach

A

Semi-sitting position
Venous air embolism precautions (precordial doppler, end-tidal CO2, avoid nitrous oxide)
Use of epinephrine for vasoconstriction
Accumulation of tissue debris, in the pharynx and stomach
N/V related to post-nasal bleeding
Smooth extubation
Difficult mask s/p extubation r/t surgical site
Rapid neurological assessment
Patients may require thyroid hormone and corticosteroid coverage perioperatively
Vasopressin should be available to treat DI s/p surgical removal
Minimal blood loss

60
Q

Posterior pituitary AKA _____

A

neurohypophysis

61
Q

The posterior pituitary lobe communicates with ___.
Which hormones are found in this area?

A

communicates with the hypothalamus via a neural pathway
ADH and Oxytocin

62
Q

Function of antidiuretic hormone and where is it synthesized

A

controls water excretion andreabsorption in the kidney and is a major regulator ofserum osmolarity

ADH is synthesized in the supraoptic nucleus

63
Q

Function of Oxytocin and where is it synthesized?

A

stimulates breast milk ejection during lactationand is stimulates uterine contraction

Oxytocin is synthesized in the paraventricular nucleus

64
Q

What causes the release of antidiuretic hormone?

A
  • increased plasma sodium ion concentration
  • increased serum osmolarity
  • decreased blood pressure or blood volume
  • Pain, stress, nausea
  • Medications: chlorpropamide, clofibrate, thiazide diuretics, carbamazepine, nicotine, cyclophosphamide, vincristine
  • Angiotensin II
  • Positive Pressure Ventilation
65
Q

What is the osmotic threshold for ADH release?

A

284 mOsm/L

66
Q

What amount of blood loss needs to occur for ADH to be release and how is it sensed?

A

5-10% decrease in blood volume or blood pressure (sensed in peripheral baroreceptors and atrial stretch receptors and transmitted afferent signals from the vagus and glosspharyngeal nerves to the hypothalamus)

67
Q

What is neurogenic diabetes insipidus? Eitology?

A

inadequate ADH secretion from the posterior pituitary lobe

Etiology: head trauma, infiltrating pituitary tumors, and neurosurgical procedures
Neurogenic DI s/p neurosurgical procedures is usually transient and resolves in 5-7 days

68
Q

What is nephrogenic diabetes insipidus? Etiology?

A

inability of the renal collecting duct receptors to respond to ADH

Etiology: nephrotoxic mediations, x-linked genetic mutation, hypercalcemia and hypokalemia

69
Q

Signs and Symptoms of Diabetes Insipidus

A
  1. polydipsia
  2. polyuria- high output of dilute (hypo osmotic) urine- so there’s a lot of really dilute urine.
  3. hypernatreamia(>145 mEq/L)
  4. hypovolemia
  5. hypotension
  6. high serum osmolarity (> 290 mOsm/L)
70
Q

Treatment of Diabetes Insipidus

A

Intravascular volume repletion
Correct hemodynamic instability
Correct serum NA over 36-48 hours - Reduce by 1meq/L every 2 hours
DDAVP or vasopressin

71
Q

What is SIADH? What are signs and symptoms?

A

High circulating vasopressin levels

Signs and Symptoms
Serum OSM low; Urine OSM high
Serum osmolarity <130
Low urine volume but the urine is highly concentrated
Low serum sodium levels
Dilutional Hyponatremia
Brain edema (Na+ < 110 mEq/L)
Lethargy – HA – Nausea
Mental confusion (<250mOsm/L)

72
Q

Etiology of SIADH

A

TBI (most common)
Neoplasia
Non CancerousPulmonary disease
Carbamazepine (medication for seizures called Tegretol)

73
Q

Managment of SIADH

A

Fluid restriction (500-800mL/d)
IV hypertonic (3%) saline if sodium level <120
Furosemide
Demeclocycline: decreases the responsiveness to ADH

74
Q

Thyroid Gland anatomy

A

Located anterior to the trachea between the cricoid cartilage and suprasternal notch
Receives blood supply from the superior and inferior thyroid arteries
Highly perfused organ
Gland consists of two lobes and an isthmus
The recurrent laryngeal nerve runs along the lateral borders of each lobe

75
Q

Thyroid hormone production and release is under the control of ____

A

TSH which is secreted by the anterior pituitary lobe

Circulating thyroid hormones inhibit the secretion of TSH and TRH through negative feedback

76
Q

Function of thyroid hormone

A

Thyroid hormone initiates proteinformation in most cells
Thyroid hormone stimulatesmetabolic activity, heatproduction and oxygenconsumption
Increases number of beta adrenergic receptors
Increases rate of hormone secretions, specifically the pancreas

77
Q

___ is cleaved from thyroglobulin

A

Thyroxine (T4) and 3,5,3-triiodothyronine (T3) are cleaved from thyroglobulin

78
Q

How much of thyroid hormone is T4?

A

90% of thyroid hormone is T4 and 10% is T3
At the tissues, most T4 is deiodinated to T3
Thus, T4 is highest in blood and T3 is in the tissues
T3 is a more potent and active form compared to T4
T4 has a 7 day half life, T3 has a 1 day half life
Tests of thyroid function
T3, T4, measure total (bound and free)hormone
TSH: most sensitive to mildhypothyroidism

79
Q

Thyroid horomone effects: CV, Resp and ANS

A

CV Increased chronotropy, contractility, and decrease SVR

Respiratory: Increased BMR, Increased CO2 production, Increased minute ventilation

ANS: Increased number and sensitivity of beta receptors and decreased number of cardiac muscarinic receptors

80
Q

Thyroid hormone effects on anesthesia

A

MAC is not affected by hyper or hypothyroid

Increased CO increases the anesthetic uptake into the blood and decreases the rate of rise of FA/FI (slows induction)

81
Q

Thyroid hormone: effects on GI system

A

GI intestinal hypermobility – diarrhea

Increased catabolism, increased utilization of fat stores, vasodilatation (heat loss), increased insulin, increased glucose uptake and increase gluconeogenesis

82
Q

Hyerthyroidism

A

Thyrotoxicosis is a state of thyroid hormone excess
* Graves disease is most common cause of thyrotoxicosis in the US
Autoimmune disorder in which TSH-receptor antibodies bind to and stimulate the thyroid gland
* More common in women ages 20 to 50 years old
* Alternative etiologies for thyrotoxicosis includes follicular adenomas,exogenous iodine excess (amiodarone), thyroid Ca,TSH-secreting pituitary tumors

83
Q

Clinical Signs and Symptoms of Graves Disease

A

Clinical signs/symptoms
Nervousness, palpitations, fatigue, weakness, fine tremor, DOE, insomnia, weight loss, diarrhea, heat intolerance
Tachycardia, arrhythmia (AF), hypertension
Ocular changes
* Exophthalmos
* Lid retraction
* Lid lag
* Infrequent blinking

84
Q

How is Grave’s Disease diagnosed?

A

Abnormally high total and unbound serum T4 assay and depressed TSH levels

85
Q

For patients with undiagnosed hyperthyroidism, the first symptom can often be _____

A

atrial fibrillation

86
Q

Treatment of Grave’s Disease

A

Radioactive Iodine - ablation of the thyroid gland with radioactive iodine for 2-4 months, often results in hypothyroidism, contraindicated in pregnant patients

Antithyroid drugs and beta adrenergic receptor blockade
Thionamides: Methimazole, Carbimazole & Propylthiouracil (PTU)
Inhibit thyroid synthesis by blocking iodine addition to tyrosine, PTU also inhibits peripheral conversion of T4 to T3
Requires 6-7 weeks to achieve euthyroid
Propanolol is prescribed to reduce cardiovascular symptoms and peripheral conversion of T4 to T3

87
Q

Surgical Treatment of Grave’s Disease = ___

A

Subtotal Thyroidectomy – surgical option is exercised for somepatients (antithyroid drugs ineffective,large goiter,refused radioidine treatment, or pregnant)
Complications include damage to the recurrent laryngeal nerve, hypoparathyroidism and neck hematoma

88
Q

What is thyroid storm? Treatment?

A

Thyroid storm is a surge of thyroid hormone and is a medical emergency. It can occur in hyperthyroid or euthyroid patients, most commonly 6 -18 hours after surgery
Clinical manifestations of a thyroid storm is confusion and agitation, N/V, abnormal LFTS, tachycardia, dysrhythmias hypertension, CHF
Mortality rates are as high as 30% even with early diagnosis
Treatment includes beta adrenergic blockade, potassium iodide, antithyroid drugs (PTU or methimazole).

89
Q

Anesthetic Management of Pt with hyperthyroidism

A

Normalize thyroid function prior to surgery, medical management can take up to 6-8 weeks
Emergency surgery requires beta blocker, potassium iodine glucocorticoid and PTU.
Induction agent thiopental reduces T4-T3 conversion
Avoid sympathomimetics, anticholinergics, ketamine and pancuronium
Atrial fibrillation is present in 10-20% of patients
Exophthalmos increases risk of corneal abrasion
Assessment of fluid and electrolyte balance
Airway assessment
Substernal goiters - Tracheoesophageal compression
**On boards goiter equals awake intubation or a technique that maintains spontaneous respiration**

90
Q

Maintenance of Anesthesia for pt with hyperthyroidism

A

Isoflurane or sevoflurane with N2O (helps offset the sympathetic nervous system response)

Increased CO decreases the uptake of inhale agents
Anesthetic requirements increase with coexisting hyperthermia
Beware of NMB dose with co-existing muscle weakness– increased incidence of myasthenia gravis and myopathy
Careful positioning-–increased bone turnover-–increase risk of osteoporosis
Hypoxia and hypercarbia stimulate the SNS

91
Q

Hypothyroidism: general info

A

Tenfold > incidence in women
Pediatric (cretinism)
Decreased concentration of circulating T3 & T4
Increased concentration of circulating TSH in primary
Pathology
Hashimoto’s Thyroiditis (autoimmune and most common)
Iatrogenic (post surgery or ablation)
Inadequate hormone replacement
Dietary: inadequate iodine leading to TSH stimulation leading to hypertrophy and goiter
Secondary: pituitary hypofunction or tumor

92
Q

Primary vs. Secondary Hypothyroidism

A

Primary: thyroid can’t produce amount of hormones pituitary calls for
Secondary: thyroid isn’t being stimulated by pituitary to produce hormones

93
Q

Signs and Symptoms of Hypothyroidism

A

Goiter, weight gain
Muscle fatigue, lethargy
Constipation
Hoarseness
Cold intolerance -Hypothermia
Dry, thick skin, Hair loss
Periorbital edema
Bradycardia
Slow deep tendon reflexes

94
Q

Effect of Hypothyroidism on body systems head to toe

A

CV– cardiomyopathy (CO may be REDUCED by 40%)
Pericardial effusions
Bradycardia - decreased stroke volume – decreased contractility- CHF
decreased blood volume (10-24%)
Peripheral vasoconstriction
Respiratory
Pleural effusions
Decreased minute ventilation
Impaired response to hypoxia and hypercarbia
Neurologic changes
GI: Slow hepatic metabolism and renal excretion
Affiliated adrenal insufficiency
Ileus & gastroparesis

95
Q

Anesthetic Management of the Patient with Hypothyroidism

A

**Airway evaluation!! **Again goiter means awake or keep spontaneous respirations on boards, and possible airway obstruction due to large tongue and smaller vocal cords
**Very sensitive to depressant drugs, slowed drug metabolism (esp. opiates) **
Decreased intravascular volume and decreased cardiac output and cardiac reserve
Minimal baroreceptor reflexes
Blunted ventilatory drive to hypoxia and hypercarbia
Consider RSI d/t delayed gastric emptying
Decreased free-water clearance (Hyponatremia)

96
Q

Anesthetic Maintenance in the patient with hypothyroidism

A

Minimize use of volatile anesthetics
MAC is unchanged, Decreased cardiac output- Inhalation induction is faster
Avoid hypothermia, hypoglycemia
Postoperative respiratory depression
Consider adrenal insufficiency in refractory hypotension - treat with corticoid steroids
Hemodynamic support is best provided by sympathomimetic drugs that improve cardiac performance, NOT Phenylephrine

97
Q

Myxedema Coma

A

**Severe hypothyroidism ** occurs with end stage hypothyroidism, coma is a consequence of severely impaired thyroid function
Loss of deep tendon reflexes
Hypothermic – 80° F
Hypoventilation
Hyponatremia
Hypoglycemic
Cardiovascular collapse
Coma and death

98
Q

Treatment of Myxedema Coma

A

IV T3 –
L-thyroxine 300 - 500μg loading – 200μg/day
Hydrocortisone 100 – 300 mg/day
Fluid replacement
Glucose containing solutions

99
Q

Compare the cardiac effects of pts with hyper and hypo thyroid

A

Generally speaking, cardiac #s are increased with hyperthyroidism and decreased with hypothroidism EXCEPT for SVR.

Pts with hyperthyroid have DECREASED SVR and vice versa.

100
Q

Surgical Complications of Thyroidectomy

A

Recurrent laryngeal nerve palsy
Stridor
Hoarseness
Aphonia
Hematoma
Hypoparathyroidism
Hypocalcemia @ 6-12 hours after surgery

101
Q

Parathyroid Glands (general info)

A

Small oval bodies located on the posterior surface of the thyroid gland
Usually four but can be anywhere from 1-12.
Blood supply via the inferior thyroid arteries
Mediator of calcium metabolism in bone, gut and kidney

102
Q

Parathyroid Hormone

A

Secreted from chief cells
Secreted in response to low serum ionized Ca++
Other stimulants for PTH secretion
Hyperphosphatemia
Hypomagnesemia

103
Q

_____ results from resection of parathyroid glands.
& S&S

A

**Hypocalcemia **results from resection of parathyroid glands without reimplantation and occurs at least 6-12 hours after surgery

S/S of increased nerve and muscle irritability, muscle spasms-tetany, laryngospasm, hypotension, paresthesia’s and prolonged QT
Facial nerve (Chvostek’s)
Carpopedal spasm (Trousseau’s)
Chronic - Fatigue & Muscular cramps

104
Q

Treatment of Hypocalcemia

A

Treatment IV calcium: Calcium gluconate has less calcium and carries a lower risk of necrosis if infiltrated than calcium chloride

105
Q

Blood passing through the adrenal gland

A

Arterial blood supply
Abdominal aorta
Renal arteries
Phrenic arteries

Venous drainage
Left gland: renal vein
Right gland: inferior vena cava

106
Q

Three Zones of the Adrenal Cortex

A

ZONA GLOMERULOSA SECRETES THE MINERALOCORTICOIDS = ALDOSTERONE = REABSORTION OF SODIUM AND WATER AND EXCRETION OF POTASSIUM AND HYDROGEN IONS( H+)

ZONA FACICULATA SECRETES GLUCOCORTICOIDS = CORTISOL

ZONA RETICULARIS SECRETES ANDROGENS

MEDULLA SECRETES CATECHOLAMINES = EPINEPHRINE (80%) AND NOREPINEPHEINE (20%)

remember this: from outside to inside its “GFR”

107
Q

In response to decreased renal perfusion, what happens?

A

renin release in kidneys which converts angiotensinogen converted to angiotensin I which is then converted to ACE –Angiotensin II –Aldosterone

108
Q

Aldosterone function

A

Enhances sodium reabsorption in exchange for potassium and hydrogen ions. Fluid retention and expansion of the extracellular space and decreased K+ and decreased metabolic alkalosis.

109
Q

An excess of aldosterone = ____

A

Hyperaldosteronism AKA Conn’s Syndrome

110
Q

What is the etiology of Conn’s Syndrome?
How do we diagnose it?

A

Etiology
Hypersecretion of aldosterone by the adrenal gland with normal renin is primary hyperaldosteronism. Increase aldosterone from external adrenal sources like renal hypertension and high renin activity
Adrenocortical adenoma - Bilateral adrenocortical hyperplasia - Adrenal carcinoma (rare)
Diagnosis
Hypertension - Hypokalemic (no diuretic therapy)

111
Q

What is the treatment for Conn’s Syndrome?

A

Unilateral adrenalectomy for adenomas –
Anti-mineralocorticoid therapy Spironolactone – eplerone
K+ supplementation and Na++ restriction

112
Q

Mineralocorticoid Excess Anesthesia Implications

A

Plasma renin activity is suppressed in primary hyperaldosteronism and renin activity is high in secondary hyperaldosteronism
Hypokalemia = - Muscular weakness - Cardiac irritability and arrhythmias increased sensitivity to neuromuscular blocking drugs U wave on EKG.
* Correct hypokalemia. Treat hypertension
* Inadvertent hyperventilation may ↓ K
* Plasma electrolytes and acid base balance should be assessed

113
Q

Mineralocorticoid Deficiency AKA ____

A

Hypoaldosteronism
Atrophy or destruction of both adrenal glands results in a combined deficiency of both mineralocorticoids and glucocorticoids
Isolated deficiency of mineralocorticoid activity almost never occurs.

114
Q

What would happen with a mineralocorticoid deficit?

A

death would ensue within 3 days to 2 weeks
Potassium ion concentration increases greatly
Sodium and chloride concentration decreases
Blood volume and CO become greatly reduced
Shock like state followed by death

115
Q

INCREASE HORMONE SECRETION FROM ADRENAL CORTEX = _____

A

Cushing’s Syndrome

116
Q

Cortisol Function

A

Responsible for utilization of proteins, CHO and fats
Stimulates gluconeogenesis
Helps block inflammation process
Stabilizes lysosome membranes decreases cytokine release
Decreases capillary permeability
Decreased lymphocytic production (eosinophils and lymphocytes)
Enhances SVR responses to endogenous vasoconstrictors, improves myocardial performance by increasing the sensitivity of beta receptors

117
Q

Causes of Cushing’s Syndrome

A

Exogenous administration OR

Endogenous causes:
* Hypersecretion by a pituitary adenoma (Cushing’s Disease) and referred to as ACTH dependent
* Intrinsic hyperfunction of the adrenal cortex (adenoma) which is ACTH independent

118
Q

Clinical Features of Cushing’s Syndrome

A

Related to cortisol glucocorticoid, mineralocorticoid and androgenic effects

Glucocorticoid:
Hyperglycemia, weight gain (central obesity), increased risk of infection, osteoporosis muscle weakness and mood disorder
Mineralocorticoid:
Hypertension, hypokalemia and metabolic alkalosis
Androgenic:
Women facial hair and amenorrhea Men: gynecomastia impotence

119
Q

Treatment of Cushing’s Syndrome

A

Transphenoidal Pituitary surgery
Pituitary radiation
Bilateral adrenalectomy (if adrenal tumor)

120
Q

Anesthetic Management of a pt with Cushing’s Syndrome

A

Special attention to aseptic technique
Careful positioning to decrease skin and bone injury
Consider post op steroid supplementation
Diabetes Insipidus is transient post pituitary resection
All considerations of hyperaldosteronism stated previously

121
Q

DECREASE HORMONE SECRETION FROM ADRENAL CORTEX = ____

A

Addison’s Disease

122
Q

What is Addison’s Disease

A

Primary adrenal insufficiency is Addison’s Disease caused by autoimmune destruction of the adrenal gland (most common) HIV, TB
Usually have both glucocorticoid and mineralocorticoid deficiency

123
Q

Clinical Manifestations of Addison’s Disease

A

Decrease Aldosterone; hyponatremia, hyperkalemia, hypovolemia, hypotension, and metabolic acidosis.
Cortisol: weakness fatigue, hypoglycemia, hypotension and weight loss.

124
Q

Secondary Adrenal Insufficiency

A

Inadequate secretion of ACTH from the pituitary
**The most common cause is iatrogenic from administration of exogenous glucocorticoids **
Mineralocorticoid secretion is not affected-fluid and electrolyte alterations are not present
Acute adrenal insufficiency can be triggered during periods of stress-infection, trauma, surgery
Acute adrenal insufficiency=Addisonian Crisis

125
Q

Addisonian Crisis

A

Insufficient hormone to respond to stress
Cessation of exogenous steroid
Clinical presentation
Shock unresponsive to volume or vasopressors
Precipitating event
Hemodynamically unstable, circulatory collapse, fever, hypoglycemia, and impaired mental status

126
Q

Treatment of Addisonian Crisis

A

Adrenal insufficiency: Steroid replacement 15-30 mg cortisol equivalent per day
Acute Crisis: Steroid replacement 100 mg IV and 100-200 mg every 24 hours
ECF volume expansion with D5NS and hemodynamic support

127
Q

Describe HPA axis suppression

A

Exogenous steroids suppress ACTH release from the anterior pituitary gland. Chronic high dose steroids prevent cortisol response to stress

128
Q

What are some risks for HPA Axis suppression? In what scenarios would you give the stress dose?

A

Risks of HPA suppression:
>20mg/day > three weeks= give stress dose
5-20mg/day > three weeks=give stress dose
<5mg/day for any time period=no stress dose
Any dose less than three weeks=no stress dose

129
Q

For superficial surgery, what is the hydrocortisone dose?

A

no dose

130
Q

For minor surgery (like a hernia or colonoscopy), what is the hydrocortisone dose?

A

25 mg IV

131
Q

For moderate surgery (like colon resection, total joint, TAH), what is the hydrocortisone dose?

A

50-75mg IV
Taper over 1-2 days

132
Q

For major surgery (like cardiovascular, thoracic, liver), what is the hydrocortisone dose?

A

100-150mg IV
Taper over 1-2 days

133
Q

Hormone therapies for male to female

A
  • androgen supression
  • Medroxyprogesterone acetate (IM)
  • Spironolactone (oral)
  • Finesteride (oral)
  • Histrelin (SQ implant)
  • Progesterone (oral)
  • Estrogen
  • Estradiol (oral, IM, SQ, transdermal)
134
Q

Hormone therapies for female to male (& considerations)

A
  • think about getting an HCG during pre-op because they are likely holding their testosterone and are more fertile during this time
  • testosterone or testosterone gel
  • Testopel (SQ implant)
135
Q

Labs that will be increased with Transwomen

A

HDL, LDL, Total cholesterol, and Triglycerides

136
Q

Labs that will be increased in Transmen

A
  • Hematocrit, Hemoglobin
  • RBC
  • ALT, AST
  • Creatinine, cholesterol, triglycerides
  • HDL
137
Q

Transgender patients s/p gender affirming surgeries involving the urethra (e.g. vaginoplasty, phalloplasty, metoidplasty with urethral lengthening) may require _____.

A

a smaller urinary catheter and perhaps placed by a practitioner experienced with transgender anatomy

138
Q

Transgender women s/p laryngoplasty and/or chondroplasty to alter voice pitch are at increased risk for ____.

A

vocal cord damage, tracheal stenosis, dysphagia or tracheal perforation and requires caution during intubation.

139
Q

Transgender men many wear breast binders or chest wraps. A discussion should occur that these devices may influence ____.

A

respiratory function and will be removed for the intraoperative and postoperative period.

140
Q

What is a pheochromocytoma? Classic presentation?

A

Catecholamine secreting tumors mostly release norepinephrine that originates from the chromaffin tissue in the adrenal gland
90% from adrenal medullary chromaffin cells
< 10% malignancy
Classic presentation reflects excessive SNS stimulation: headache, diaphoresis, hypertension and tachycardia

141
Q

How is a pheochromocytoma diagnosed?

A

Measurement of 24 hr urine for free catecholamines
Norepinephrine, epinephrine and dopamine
Vanillomandelic acid (VMA)
Total metanephrines
Symptoms for diagnosis
Hypertension, Diaphoresis, tachycardia & H/A
Other S&S = Arrhythmias - palpitations - Diaphoresis, pallor - nausea & vomiting - wt. loss - tremors - nervousness – anxiety – weakness - exhaustion

142
Q

What is the pathophysiology behind the hypertension response from a pheochromocytoma

A

Alpha1 mediated vasoconstriction
Beta1 receptor
increase cardiac output
increase renin release with increase circulating levels of angiotensin 2
Chronic vasoconstriction of arterial and venous beds
Chronic elevated catecholamine levels
Sudden release of catecholamines during surgery or obstetric deliveries may prove fatal

143
Q

Treatment of Pheochromocytoma

A

Surgical excision –
Preoperative Preperation:
Alpha 1 non-selective:
Phenoxybenzamine .5-1 mg/kg/day in divided doses 2
Metyrosine (catecholamine synthesis blocker)
Expand the intravascular volume
Normalize myocardial performance
May use competitive antagonist (Alpha 1 selective)
Prazosin, doxazocin

144
Q

What do you give first in a pheo patient: beta or alpha blockade?

A

Give alpha blockade first

If tachycardia develops after the institution of alpha-adrenergic blockade - beta blockade may be used
Beta blockade prior to alpha blockade may depress the heart
Beta 2 blockade inhibits skeletal muscle vasodilatation and increases SVR
Beta 1 blockade reduces inotropy and can cause CHF in the setting of high SVR

145
Q

Anesthetic management of a pheochromocytoma patient

A

Preoperative medication
Avoid sympathetic stimulation
Intubation of trachea
Surgical manipulation of tumor
After ligation of the tumor’s venous drainage
Continue alpha blockade
After tumor resection all catecholamines go too, prepare to treat hypotension and hypoglycemia

Concepts 3 (12 decks)

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