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Pharmacology 2 > Endocrine, Thyroid, Hypoglycermics, and Steroids > Flashcards

Endocrine, Thyroid, Hypoglycermics, and Steroids Flashcards

1
Q

Endocrine Physiology

Body homeostasis is controlled by 2 major systems

A

Nervous System

Endocrine aka Hormonal System

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2
Q

Endocrine Physiology

The purpose of the Endocrine system is regulation…

A

The purpose of the Endocrine system is regulation of behavior, growth, metabolism, and fluid and electrolytes

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3
Q

Endocrine Physiology

Endocrine glands are mediated by hormones and secrete their hormones directly into…

A

Endocrine glands are mediated by hormones and secrete their hormones directly into “surrounding extracellular fluid”

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4
Q

Mechanism of Hormone action

Hormones bind to, what two?, receptors to trigger selective and diverse cellular responses.

A

Hormones bind to “membrane” and “nuclear” receptors to trigger selective and diverse cellular responses.

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5
Q

Mechanism of Hormone action

Membrane receptor binding (peptides and catecholamines) initiates signal transduction through enzymes such as…

A

Membrane receptor binding (peptides and catecholamines) initiates signal transduction through enzymes such as “adenylate cyclase, tyrosine kinase, and serine kinase.”

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6
Q

Mechanism of Hormone action

Receptor binding in the nucleus regulates gene expression in the BLANK and nucleus to produce what two things?.

A

Receptor binding in the nucleus (steroids and vitamin D) regulates gene expression in the “cytoplasm” and nucleus to produce “specific intracellular proteins and enzymes.”

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7
Q

Pituitary Gland

The Pituitary Gland is the size of a what?

A

The Pituitary Gland aka hypophysis

Size of a pea

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8
Q

Pituitary Gland

Connected to the hypothalamus by what?

A

Connected to the hypothalamus by pituitary stalk

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9
Q

Hypothalamus and pituitary gland

The hypothalamus is located where in relation to the thalamus, optic chiasm, and optic tracts?

A

The hypothalamus is below the thalamus behind the optic chiasm and between the optic tracts

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10
Q

Hypothalamus and pituitary gland

The pituitary gland and hypothalamus is there a BBB?

A

The pituitary gland & hypothalamus have NO BBB

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11
Q

Hypothalamus

Hypothalamus collects and integrates what four things?

A

Hypothalamus collects and integrates, pain emotions, energy, H2O balance, olfactory sensations and electrolyte sensations

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12
Q

Pituitary gland

The pituitary gland is divided what two structures?

A

The pituitary gland is divided anteriorly and posteriorly

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13
Q

What is the largest part of the pituitary gland?

A

Largest part of the pituitary gland, approx 80% of its weight

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14
Q

The anterior pituitary glad secretes what 6 major peptide hormones and 1 lipotropin?

A

GH/ Somatotropin

ACTH/ Corticotropin

Thyroid Stimulating Hormone/ TSH

Follicle Stimulating Hormone/ FSH

Luteinizing Hormone/ LH

Prolactin

The anterior pituitary also secretes β-lipotropin, which contains the amino acid sequences of several endorphins that bind to opioid receptors (Flood)

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15
Q

ACROMEGALY/ gigantismanterior Pituitary disorder

Is a hypersecretion of which hormone? which is usually caused by what?

A

Hypersecretion of GH usually caused by GH secreting pituitary adenoma 99% of the time

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16
Q

ACROMEGALY/ gigantismanterior Pituitary disorder

Caused by excessive action of, what what?, after adolescence leading to anatomical changes and metabolic dysfunction

A

Caused by excessive action of “GH and IGF-1” after adolescence leading to anatomical changes and metabolic dysfunction

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17
Q

GH hypersecretion prior to, what stage of life?, will cause the individual to grow 8-9 feet tall?

A

GH hypersecretion prior to “puberty” ie before closure of the growth plates can cause the individual to grow 8-9 feet tall

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18
Q

ACROMEGALY/ gigantismanterior Pituitary disorder

Common Features of Acromegaly?

A

Common Features of Acromegaly

  • Skeletal overgrowth- enlarged hands and feet, prognathic mandible
  • Soft tissue overgrowth- enlarged lips, tongue, epiglottis distorted facial features
  • Visceromegaly- enlarged liver, spleen, kidney and heart
  • Hypertension
  • Cardiomyopathy
  • Osteoarthritis
  • Glucose intolerance
  • Peripheral neuropathy
  • Skeletal muscle weakness
  • Extrasellar tumor extension- headache, visual field defects
  • Decreased life expectancy- cardiac and respiratory issues
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19
Q

Pharmacological treatment for Acromegaly?

A

-Octreotide or lanreotide (somatostatin receptor ligands)
Inhibits release of GH*
Long term use increase incidence of gallstones
Hyperglycemia and decreased glucose tolerance

  • Cabergoline- dopamine agonist
  • Pegvisomant GH receptor antagonist

-Stress dose of glucocorticoid therapy
Decrease synthesis of 1,25-dihydroxyvitamin D to decrease intestinal absorption of calcium increase renal excretion of calcium

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20
Q

Posterior pituitarysecretes what two Hormones?

A

Arginine Vasopressin (AVP)/ ADH

Oxytocin

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21
Q

What are the functions of AVP/ADH?***

A

Functions of Arginine Vasopressin (AVP)/ ADH

Vasoconstriction V1
Water retention V2
Corticotropin secretion V3

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22
Q

What stimulates the release of AVP/ADH?

A

Stimulates Arginine Vasopressin (AVP)/ ADH
release:

  • Decrease blood volume
  • Increase plasma osmolality
  • Decreased arterial pressure
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23
Q

What does Oxytocin do?

A

Stimulates uterine smooth muscle contraction during labor and decreases post partum bleeding

High boluses decrease SBP & DBP via direct effect on vascular smooth muscles (us giving it)

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24
Q

Oxytocin causes what to heart rate and what happens in high doses?

A
  • Reflex tachycardia & increased CO

- In high doses water intoxication, hyponatremia, neurologic dysfunction if excessive volume of fluid administered

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25
Q

What are the posterior pituitary drugs?

A

Vasopressin

Desomopressin DDAVP synthetic AVP- ( Nasal dose: Lypressin)

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26
Q

What is the recommended infusion rate for Tx of shock in adults with Vasopressin??**

A

Vasopressin

The recommended infusion rate in the Tx of shock in adults is 0.01-0.04 units/min**

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27
Q

Vasopressin is not recommended for what disorder?***

A

Not recommended for nephrogenic DI***

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28
Q

What is Vaopressin used to treat?

A
  • Tx AVP DI
  • Refractory hypotension
  • Uncontrolled hemorrhage esophageal varices- hepatic blood flow
  • Septic shock
  • Refractory cardiac arrest
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29
Q

Desomopressin DDAVP synthetic AVP- ( Nasal dose: Lypressin) is used to treat what?**

A

Treatment of AVP/ADH deficiency

Tx of central DI NOT recommended for nephrogenic DI**

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30
Q

Desomopressin DDAVP synthetic AVP

Increases levels of which clotting factors?

A

Increases levels of von Willebrand factor & factor VIII

Reverses coagulopathy associated with platelet adhesion defects including coagulopathy of renal failure

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31
Q

Diabetes insipidusinadequate secretion of???

A

Diabetes insipidusinadequate secretion of “ADH/AVP”

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32
Q

Destruction of neurons in or near the, what two structures?, of the hypothalamus may decrease vasopressin release to cause central diabetes insipidus.***

A

Destruction of neurons in or near the “supraoptic and paraventricular nuclei” of the hypothalamus from pituitary surgery, trauma, cerebral ischemia, or malignancy may decrease vasopressin release to cause central diabetes insipidus.***

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33
Q

What can cause damage to the neurons of the hypothalamus that may decrease vasopressin levels to cause ventral DI?**

A

Pituitary surgery, trauma, cerebral ischemia, or malignancy may decrease vasopressin release to cause central diabetes insipidus.***

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34
Q

If the posterior pituitary alone is damaged, however, the transected fibers of the pituitary stalk can still continue to secrete BLACK.

A

If the posterior pituitary alone is damaged, however, the transected fibers of the pituitary stalk can still continue to secrete “AVP.”

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35
Q

Diabetes insipidus from lack of vasopressin release during pituitary surgery is usually BLANK.

A

Diabetes insipidus from lack of vasopressin release during pituitary surgery is usually “transient.”

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36
Q

What are the hallmark signs of Diabetes Insipidus???**

A
  • Hallmark sign is polyuria which results in dehydration and HYPERnatremia ( Na > 145 mEq/L).
  • Serum osmolarity ( >290 mOsm/L)
  • Urine output greater than 2 mL/kg per hour
  • Urine osmolarity HYPOtonic relative to plasma**
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37
Q

What is the treatment for Diabetes insipidus?***

A

Treatment***

  • DDAVP or Vasopressin V2
  • Chlorpropamide (sulfonylurea hypoglycemic agent)
  • Carbmazepine (anticonvulsant)
  • Thiazide diuretics
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38
Q

What is syndrome of antidiuretic hormone?

A

Disorder characterized by high circulating vasopressin levels relative to plasma osmolarity & serum sodium concentration

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39
Q

What are the clinical features of syndrome of antidiuretic hormone

A
  • Water intoxication
  • Dilutional hyponatremia
  • Brain edema
  • Lethargy
  • Headache
  • Nausea
  • Mental confusion
  • Seizures
  • Coma
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40
Q

What are the hallmark signs of syndrome of antidiuretic hormone?**

A

Serum osmolarity less than 270 mOm/L
Serum sodium less than 130 mEq/L
Urine volume LOW
Urine osmolarity HYPERtonic relative to plasma*

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41
Q

What is the treatment for syndrome of antidiuretic hormone***

A

Treatment**

  • Fluid restriction 0.9% normal saline 800-1000 ml per day
  • If patient symptomatic of Na 115-120 mEq/L consider hypertonic saline
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42
Q

What are the hormones secreted from the thyroid?

A
  • T4 Thyroxine- 80% of body’s hormone production- prohormone synthesized from tyrosine
  • T3 Triiodothyronine 5x more active than T4 produced from tyrosine production

-Thyroid-stimulating hormone (TSH)
Stimulated by the ANTERIOR pituitary

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43
Q

What does the Thyroid do?

A
  • Maintains optimal metabolism for normal tissue function
  • Increases O2 consumption in nearly all tissues except the brain
  • Secretes calcitonin which is important for calcium ion use
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44
Q

Hypothyroid has a decrease concentrations of what? and increased levels of what?

A

Hypo-function with decreased circulating concentrations of T3 and T4 hormones

Increased levels of TSH

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45
Q

What is the most common thyroid disorder?

A

HypoThyroid

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46
Q

What is Hashimoto thyroiditis?

A

Autoimmune mediated hypothroidism

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47
Q

What are some Iatrogenic causes of Hypothroidism

A

Iatrogenic causes

Surgery, neck irradiation and radioiodine therapy

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48
Q

What two things are seen with hypothyroidism?

A

Iodine deficiency

Colloid goiter

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49
Q

What is the treatment for hypothroidism?

A

Treatment

  • Primary Tx is hormone replacement
  • TSH is monitored in Primary hypothyroidism
  • T4 is monitored in Secondary hypothyroidism TSH released is impaired
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50
Q

What can you use for thyroid hormone replacement for Hypothyroid?***

A

Synthetic Thyroxine Levothyroxine Sodium T4 (Tx of choice)*

Synthroid, Levoxyl*

  • Long ½ life 7- 10 days
  • Once a day dosing
  • Maintains physiologic levels of T3- active hormone
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51
Q

What are some side effects of hypothyroid hormone replacement?

A

Side effects

  • Patients with existing angina pectoris or underlying CAD requires careful monitoring
  • Myocardial O2 consumption is augmented by thyroid hormone
  • Patients with deficient coronary artery circulation may not tolerate full replacement dose
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52
Q

What is a long term treatment for Hypothyroid?***

A

Treatment ( Long term)

T3 formulations*

Liothyronine isomer of T3*

  • 2-3 times as potent as Levothyroxine
  • Rapid onset & short duration
  • Used for long term replacement
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53
Q

What are the goals of therapy for Hypothyroid?

A
  • Correction of hypothyroidism to euthyroid
  • Reduction in goiter
  • Prevention of Thyroid Ca recurrence
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54
Q

What is thyrotoxicosis?

What is the most common cause?

A

Defined as thyroid hormone excess

Most common cause of thyrotoxicosis is Graves Disease

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55
Q

What is Graves disease?

A

Autoimmune disease which TSH receptor antibodies bind & stimulate thyroid gland resulting in gland enlargement and excessive production of T3 and T4

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56
Q

Graves disease occurs most commonly in what population?

A

More common in women 40-60 years of age

3 fold increase incidence in post partum period

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57
Q

What are the potential risk associated with graves disease?

A

Potential risk cigarette smoking and stress

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58
Q

Other causes of Thyrotoxicosis, besides Graves disease?

A
  • Toxic Nodular Hyperthyroidism
  • Thyroiditis causes increased released hormones
  • Thyroid Cancer associated with euthyroid may cause hyper or hypo thyroidism
  • Iodine containing radiocontrast or angiography dyes
  • Amiodarone is iodine rich and may cause hyper or hypothyroid**
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59
Q

How do you determine Hyperthroid/thyrotoxicosis?

A

Diagnosis TSH levels and measurement of free T3 and T4.

Once steady state maintained you can measure TSH

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60
Q

What are the treatments for Hyperthyroid/thyrotoxicosis?

A

TREATMENT

  • Radioactive gland ablation
  • Surgery
  • Antithyroid medications
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61
Q

What is Methimazole?***

A

THIONAMIDES- Anti-thyroid medication

METHIMAZOLE ½ life 4-6 hours QD dosing

Crosses the placenta appears in breast milk*

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62
Q

What is Propylthiouracil (PTU)?**

A

THIONAMIDES- Anti-thyroid medication

PROPYLTHIOURACIL (PTU) ½ life 75 min dosed several times per day

Hepatic toxicity*

Preferred drug for parturient*

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63
Q

What are three Thionamides?

A

METHIMAZOLE

CARBIMAZOLE

PROPYLTHIOURACIL (PTU)

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64
Q

What is the MOA of Thionamides?

A
  • Inhibit thyroid hormone synthesis by interfering with in the incorporation of iodine to tyrosine residues of thyroglobulin
  • Euthyroid is obtained in 6-7 weeks
  • Agranulocytosis serious side effect of all drugs
65
Q

What are the SE of Thionamides?

A
  • Urticarial rash or macular skin rash 5% of patients
  • Arthralgia
  • GI discomfort
  • Granulocytopenia (rare SE)
  • Agranulocytosis (rare SE)
  • —Fever or pharyngitis earliest manifestation
  • —DC Med
66
Q

What are the treatments for Graves hyperthroid???????

A

Treatment

Iodine*
Saturated potassium

iodide solutions*

Potassium iodide-iodine ( Lugol’s Solution)*

  • Oldest available therapy
  • Inhibits thyroid hormone
  • Used before elective thyroid surgery
  • Recommended approach is potassium iodide and propranolol
  • Vascularity is decreased by the iodide
  • Chronic tx with iodide is associated with recurrence of previously suppressed thyroid gland
  • Allergic reactions with iodide
  • –Angioedema
  • –Laryngeal edema
67
Q

What is the treatment of choice for Grave’s hyperthyroidism?

A

Radioactive iodine*

  • Choice TX for Grave’s hyperthyroidism
  • Administered after the pt is euthyroid with thionamide therapy
  • Rapidly and efficiently trapped by thyroid gland & subsequently releases Beta rays which acts exclusively on the gland without incidence to surrounding tissues
  • Given orally
  • Works gradually over 2-3 months with excessive thyroid gland activity
  • ½ to 2/3 are cured from a single isotope the reminder required 1-2 additional doses
  • Contraindicated in parturient
68
Q

How many parathroids do we have and what does secrete and regulate?

A

4 Parathyroid glands secrete parathyroid hormone (PTH) which regulates calcium ions.
Major hormonal regulator of Calcium and Phosphate

69
Q

Secretion of PTH has what kind of relationship to plasma ionized calcium concentration?

A

Secretion of PTH is ““inversely related””” to plasma ionized calcium concentration. A decrease of calcium promotes release of PTH. An increase in phosphate stimulates PTH

70
Q

What does Parathyroid hormone (PTH) do?

A

Secretion of PTH

  • -Promotes bone calcium
  • -Converts Vitamin D to its active form 1,25-dihydroxycholecalciferol
  • -Increase GI absorption of Calcium
  • -Increases renal tubular Calcium
  • -Inhibits renal reabsorption of Phosphate to increase Calcium and to decrease Phosphate concentration in plasma
  • -Stimulates cAMP
71
Q

What are the clinical manifestations of Hypocalcemia?**

A

Clinical Manifestations of Hypocalcemia*****

  • -Laryngospasm
  • -Trousseau sign- latent- Inflation of BP cuff slightly above systolic level for 3 min. the ischemia enhances muscle irritability and causes flexion in the wrist and thumb w/ extension of the fingers
  • -Chvostek sign- latent- contracture/ twitching of ipsilateral facial muscles when facial nerve is tapped at the angle of the jaw
  • -Hyperreflexia
72
Q

What are the characteristics of Hypoparathyroidism?

A

-Characterized by low PTH levels & low Ca ( Ica <4.5 mg/dL and
total Ca <8.5 mg/dL)
-Can be inherited or acquired disorder
-Most common cause is inadvertent removal during surgery or damage to the blood supply of the gland during parathyroid surgery

73
Q

What is the treatment for Hypoparathyroidism?

A

Treatment

  • Vitamin D & Calcium supplement as well as Magnesium
  • Recombinant human PTH ( Natpara)
  • –Can decrease Vit D and Ca requirements however current recommendations restrict PTH to patients who Ca is not controlled with Vit D and Ca alone
74
Q

What are the treatments for HyperParathroidism?

A

Treatment

  • -Removal of the Parathyroid Gland
  • Once gland is removed Ca could drop 6 mg/dL, monitor for signs of hypocalcemia up to 24 hours post surgery
  • -Mild hypercalcemia can be managed with Saline 150 mL/hr
  • -Biphosphonates
  • Inhibit osteoclastic-mediated bone reabsorption
  • -Isotonic saline hydration and loop diuretics can rapidly decrease Ca by hemodilution, increased glomerular filtration and enhanced excretion
  • Lasix 40-80 mg IV every 2-4 hours
75
Q

What are the characteristics of HyperParathyroidism?

A

Elevated serum PTH despite high Ca levels > 12-14 mg/dL

Common causes parathyroid adenoma, gland hyperplasia or parathyroid cancer 90% of the cases

76
Q

The Adrenal Cortex secretes what 3 major classifications of corticosteroids?**

A

Mineralocorticoids (Aldosterone)

Glucocorticoids (Cortisol)

Androgens

The precursor of all steroids is cholesterol*****

77
Q

What are Mineralocorticoids (Aldosterone)?

A
  • Evokes distal renal tubular reabsorption of Na in exchange for K ions
  • Receptors present in distal renal tubules, colon salivary glands and hippocampus
78
Q

What are Glucocorticoids (Cortisol)?

A
  • Anti-inflammatory response
  • Receptor widely distributed and does not bind to aldosterone
  • Maintains homeostasis during severe stress at low levels
  • High levels exert anti-inflammatory and immunosuppressive effects
79
Q

What are the pharmacokinetics of Corticosteroids?

A
  • -Effective orally
  • -Antacids interfere with the oral absorption of corticosteroids
  • -Cortisol is released from the adrenal glands in an episodic manner and the frequency of pulses follows a circadian rhythm that is linked to the sleep-wake cycle.
  • -Maximal plasma concentrations of cortisol occur just before awakening and the lowest levels occur 8 to 10 hours later.
  • -Stress-induced changes in the plasma concentrations of cortisol are superimposed on the background baseline release of cortisol.
  • -Synthesis of cortisol is governed by adrenocorticotrophic hormone (ACTH) that is controlled by the hypothalamic hormones, corticotropin-releasing hormone and arginine vasopressin.
80
Q

What are the clinical uses for Corticosteroids?

A
  • -The only universally accepted use of corticosteroids & their synthetic derivatives is a replacement therapy for deficiency states
  • -In disease states the use is not curative although the anti-inflammatory response exerts an palliative effect
  • -Safe to administer a single large dose in life threatening situation without knowledge of adrenal or pituitary insufficiency
81
Q

What Corticosteroids is used most commonly for cerebral edema?**

A

Dexamethasone*

Commonly used for cerebral edema

82
Q

Which corticosteroid causes skeletal muscle weakness and mild diuresis?***

A

Triamcinolone*

  • Skeletal muscle weakness
  • Mild diuresis and Na loss
  • Edema in patients with low GFR
  • Does NOT increase urine K unless given in large dose
  • Anorexia
83
Q

What are examples of the Corticosteroids?

A 
Prednisolone
Prednisone
Methylprednisolone
Betamethasone
Dexamethasone* 
Triamcinolone*
84
Q

What are the side effects for Corticosteroids when used CHRONICly?**

A
  • -Suppression of HPA axis
  • -Electrolyte and metabolic changes
  • -Osteoporosis
  • -Peptic ulcer disease
  • -Skeletal myopathy
  • -Central nervous system dysfunction peripheral blood changes
  • -Inhibition of normal growth

-Systemic corticosteroid use for less than 7 days even at high doses are unlikely to evoke systemic effects*

85
Q

Adrenal cortex

Corticosteroids clinical uses

A
  • Deficiency states
  • Allergic therapy
  • Asthma
  • Antiemetic
  • Postoperative analgesia
  • Cerebral edema
  • Aspiration pneumonitis
  • Lumbar disc disease
  • Immunosuppression
  • Arthritis
  • Collagen diseases
  • Ocular inflammation cutaneous disorders
  • Post intubation laryngeal edema
  • Ulcerative colitis
  • Myasthenia gravis
  • Respiratory distress syndrome
  • Leukemia
  • Cardiac arrest
86
Q

Perioperative uses for corticosteroids,

Which patients would you suspect to have a suppressed HPA axis?*****

A

Patients taking greater than 20 mg per day of prednisone or its equivalent for more than 3 weeks have a suppressed HPA axis.* (will prob get stress dose)

87
Q

Perioperative uses for corticosteroids,

Which patients would you suspect to not have a suppressed HPA axis?*****

A

Patients taking less than 5 mg per day of prednisone or its equivalent can be considered not to have suppression of their HPA axis.* (prob not get a stress dose)

88
Q

Perioperative uses for corticosteroids considerations

A
  • Corticosteroid supplementation should be increased whenever the pt being tx for chronic hypoadenocorcorticism undergoes a surgical procedure.
  • These patients cannot release additional endogenous cortisol as a response to the stress of surgery
  • Patients taking 5 to 20 mg per day of prednisone or its equivalent for more than 3 weeks may or may not have suppression of the HPA axis.
89
Q

Steroid replacement in perioperative period

A
  • Avoid steroid supplementation in patients who do not have a suppressed HPA axis (patients taking any dose of glucocorticoids for less than 3 weeks or a daily dose of prednisone <5 mg).
  • HPA axis should be further assessed
  • For patients with a suppressed HPA axis (patients taking >20 mg prednisone per day for more than 3 weeks), glucocorticoid supplementation should consider the stress of surgery.
90
Q

corticosteroids perioperative replacement guideline for Minor Surgical Stress

A

Glucocorticoid replacement dose of 25 mg of hydrocortisone or 5 mg of methylprednisolone is sufficient

If the postoperative course is uncomplicated, the patient can be returned the next day to the prior glucocorticoid maintenance dose.

Ie inguinal hernia

91
Q

corticosteroids perioperative replacement guideline for Moderate Surgical Stress

A

The glucocorticoid requirement is about 50 to 75 mg daily of hydrocortisone for 1 to 2 days.

Ie open chole, bowel resection, THR

92
Q

corticosteroids perioperative replacement guideline for Major Surgical Stress

A
  • The glucocorticoid dose should be 100 to 150 mg of hydrocortisone daily for 2 to 3 days
  • Even with this coverage, vascular collapse has been described in a patient experiencing massive hemorrhage during surgery.
  • Burns or sepsis could exaggerate the need for exogenous corticosteroid supplementation, the continuous infusion of cortisol, 100 mg every 12 hours, should be sufficient.

Ie CABG, Pancreadueodenctomy, esophagectomy

93
Q

What do Mineralocorticoids do?

A

Regulates extracellular Na, K and total body fluid balance

94
Q

What does Aldosterone do?

A

Aldosterone

  • Protects volume status
  • Renin-angiotensin-aldosterone system
  • –Renin acts on angiotensin to form angiotensin I to form angiotensin converting enzyme to form angiotensin II- a powerful vasoconstrictor and a potent stimulus of aldosterone synthesis and release.
  • Released by the kidney in response to hypovolemia, SNS, hypotension and hyponatremia.
95
Q

What is the MOA of Cortisol (hyrocortisone)?

A

Glucocorticoid: Cortisol (Hydrocortisone)
MOA
–Intracrine hormones that interact with intracellular receptors
–Stimulates DNA dependent synthesis of mRNA in the nuclei of responsive cells leading to the synthesis of necessary enzymes

96
Q

What are the physiological effects of Cortisol (Hydrocortisone)?

A

Physiological effects

  • Increases gluconeogenesis
  • —Adrenal diabetes by increased gluconeogenesis & decrease glucose
  • Breaks down protein causing skeletal weakness
  • Mobilizes fatty acid causing excess fat in neck and chest causing buffalo like torso
  • —Anti-inflammatory effects
  • Can be used in allergic reactions, RA, acute glomerulonephritis, assist with transplant rejection
97
Q

What is a key feature of HPA?**

A

A key feature of hypothalamic-pituitary-adrenal (HPA) physiology is negative feedback that suppresses release of ACTH by the pituitary by high levels of endogenous or exogenous glucocorticoids*

98
Q

Pre-op stress and surgery stimulates ACTH and Cortisol, when does plasma cortisol levels usually return?

A
  • -Pre-op stress and surgery stimulates ACTH and Cortisol

- -Plasma cortisol usually returns 24 hours post-op but can remain elevated for as long as 72 hours

99
Q

How do Opioids, Etomidate, and Volatile anesthetics interact with cortisol?

A
  • Large doses of Opioids may increase cortisol response to surgical stimulation
  • Etomidate inhibits cortisol synthesis even in the absence of surgical stimulation
  • Volatile anesthetics do not suppress the stress-induced endocrine response as much
100
Q

Suppression of the hypothalamic-pituitary axis by regular administration of corticosteroids prevents what??

A

Suppression of the hypothalamic-pituitary axis by regular administration of corticosteroids prevents the release of cortisol in response to stressful stimuli.

101
Q

What is Conn Syndrome?*****

A 
Conn Syndrome (J.W. Conn)
HYPERsecretion of aldosterone from an adrenal adenoma independent of stimulus*
102
Q

What are manifestations of Primary Aldosteronism?

A

Manifestations include

Systemic HTN with coexisting HYPOkalemia

103
Q

What are the treatments for Conn Syndrome?

A

Treatment

  • Surgical removal of adenoma
  • Medical Management
  • K supplement
  • HTN drugs
104
Q

What are the Anesthesia management for Primary Aldosteronism?

A

Anesthesia management
-Correction of electrolytes K (depletion show U on EKG)
-Restoring intravascular fluid
-Management of HTN
-Sodium restriction
-Spironolactone (aldosterone antagonist) 25-100mg Q8H
(dont need to know the dose)

105
Q

What is Cushing Syndrome?

A

–Excess glucocorticoid hormones (Cortisol) from overproduction of adrenal cortex or exogenously administered

–ACTH dependent causes pituitary adenoma and ectopic secretion of ACTH non pituitary tumor

–ACTH independent causes adrenal tumor, adrenal carcinoma

–Iatrogenic causes supraphysiologic doses of glucocorticoids for arthritis, allergies and asthma- most common cause

106
Q

What is the Anesthesia Management for Cushing syndrome/ glucocorticoid excess?

A
  • -Normalizing blood pressure
  • -Normalizing blood glucose
  • -Normalizing intravascular fluid volume
  • -Normalizing electrolyte concentrations
  • -Osteopenia and pathologic fractures
  • -Positioning fractures and buffalo hump
  • -Osa
  • -Skin risk of tearing and infection
107
Q

Adrenal resection will require glucocorticoid administration for maximum stress with cushing syndrome, what would you give?*****

A

Adrenal resection will require glucocorticoid administration for maximum stress
Hydrocortisone 100mg IV over 24 hours**

108
Q

Addison Disease is characterized by what symptoms?

A

Characterized by skin wasting, skin hyperpigmentation and destruction of the adrenal gland. Rare clinical syndrome.

109
Q

Most common causes of Addison Disease is what?

A

Most common causes is TB, AIDS, and fungal infections.

110
Q

What dose Addison Disease?

A

Destructs all cortical zones adrenal androgen, glucocorticoid and mineralocorticoid deficiency

Autoimmune causes Thyroid disease

Becomes apparent when 90% of the gland is diseased

111
Q

What is the treatment for Primary adrenocortical insufficiency?***

A

Replacement of glucocorticoid(anti-inflammatory) & mineralocorticoid (salt) deficiency
Replacement therapy
-Hydrocortisone 15-20 mg on awakening*
-Hydrocortisone 5-10mg early afternoon*
-Mineralocorticoid replacement Fludrocortisone 0.1mg/day*

These patients also will require stress dose replacement if going to surgery

112
Q

Secondary Adrenocortical insufficiency

is Caused by what 2 primary etiologies?

A
  1. ACTH deficiency by iatrogenic HPA axis suppression after exogenous glucocorticoid therapy
  2. ACTH deficiency secondary to hypothalamic or pituitary gland dysfunction ie tumor, infection, surgical, radiologic ablation

Secondary, something we caused, primary is the glad itself

113
Q

What are Clinical Manifestations of Secondary Adrenocortical insufficiency?

A

Clinical Manifestations

  • -Less likely associated with severe hypovolemia, hyperkalemia, hyponatremia because renin-angiotensin-aldosterone system intact & mineral corticoid secretion is preserved
  • -NO hyperpigmentation ACTH levels are low
114
Q

What are two Inhibitors of Corticosteroid Synthesis?

A

Metyrapone**

Aminoglutethimide**

115
Q

MoA of Metyrapone**

A
  • -Decreases cortisol synthesis by inhibition of the 11-β-hydroxylation reaction, resulting in accumulation of 11-deoxycortisol
  • -May induce acute adrenal insufficiency in patients with decreased adrenocortical function.

Clinical Uses
Diagnosis of adrenal insufficiency and treatment of excessive adrenocortical function that results from adrenal neoplasms that function autonomously or as a result of ectopic production of ACTH by tumors.

116
Q

MoA Aminoglutethimide**

A
  • -Inhibits the conversion of cholesterol to 20-α-hydroxycholesterol, which interrupts production of both cortisol and aldosterone
  • -Effective in decreasing the excessive secretion of cortisol in autonomously functioning adrenal tumors and in hypersecretion resulting from ectopic production of ACTH
117
Q

What are the islets of Langerhans?

A

The islets of Langerhans are organized endocrine cells that secrete four hormones (insulin, glucagon, somatostatin, and pancreatic polypeptide) into the systemic circulation.

The pancreas contains 1 to 2 million islets, which, based on staining characteristics and morphology, are classified as α, β, δ, and pancreatic polypeptide cells.

Each islet receives a generous blood supply, which unlike any other endocrine organ, drains into the portal vein.

118
Q

What do the beta and alpha cells do in the pancreas?*****

A
  • –β cells account for about 60% of the islet cells and are the site of insulin production. *
  • –The α cells account for 25% of islet cells and produce glucagon. *
119
Q

What is insulin?

A
  • Insulin is a 51-amino acid peptide hormone synthesized in the β cells of the islets of Langerhans as a single polypeptide proinsulin, which is the precursor molecule to insulin
  • Insulin is an anabolic hormone promoting the storage of glucose, fatty acids, & amino acids.
120
Q

How much of insulin is secreted daily?

A

The amount of insulin secreted daily is equivalent to approximately 40 units.

121
Q

What is the systemic circulation, elimination half-time for insulin?

A

In the systemic circulation, insulin has an elimination half-time of approximately 5 minutes, with greater than 80% degraded in the liver & kidneys.

122
Q

What stimulates the release of insulin (sympathetic)?

What Inhibits the release of insulin?

A
  • –Insulin is released in response to β-adrenergic stimulation or to acetylcholine.
  • –α-adrenergic stimulation or β-adrenergic blockade inhibits insulin release.
123
Q

What is DM type I?

A
  • –Result of autoimmune-mediated destruction of pancreatic Beta Cells
  • -Younger age onset
  • -Sensitivity to insulin is normal
  • -Lack of insulin my precipitate diabetic ketoacidosis
  • -These pt do not produce insulin and need it to survive
124
Q

What is DM type II?

A
  • Peripheral insulin resistance
  • Failure to secrete insulin due to dysfunctional pancreatic Beta cell
  • Oral hypoglycemics are alternatives to insulin with type II DM, if this fails then these patients must get insulin
125
Q

How is insulin metabolized?

A

Metabolized in kidney and liver by proteolytic enzyme

126
Q

How do you gain adequate glycemic control in type 1 diabetes?

A

To gain adequate glycemic control in type 1 diabetes, at least two daily subcutaneous injections of intermediate- or long-acting insulin combined with rapid-acting insulin are nearly always required.

127
Q

What is the pharmacologic effect of insulin?

A

Pharmacologic effect lasts for 30-60 min because it is tightly bound to tissue receptors

128
Q

The total daily exogenous dose of insulin for treatment of type 1 diabetes mellitus is usually in the range is what?

A

The total daily exogenous dose of insulin for treatment of type 1 diabetes mellitus is usually in the range of 0.5 to 1 U/kg/day.

129
Q

This insulin requirement, however, may be increased dramatically by stress associated with what two things?

A

This insulin requirement, however, may be increased dramatically by stress associated with sepsis or trauma.

130
Q

Continuous subcutaneous insulin infusion (CSII) through an external pump delivers basal insulin (what dose?) and bolus doses before meals.

A

Continuous subcutaneous insulin infusion (CSII) through an external pump delivers basal insulin (0.01 to 0.015 U/kg/hour) and bolus doses before meals.

131
Q

What are the only preparations used for CSII delivery pumps?

A

Short-acting insulin (regular) and ultra rapid–acting insulins (lispro, aspart, and glulisine) are the only preparations used for CSII delivery pumps.

132
Q

With the continuous subcutaneous insulin infusion, infusions can be altered during what?

A

Infusions can be altered during exercise, and doses can be calculated via algorithms of previous glucose values and insulin delivery

133
Q

What is an important benefit of lispro?

A

Lispro

  • Short acting
  • Must be administered 30-60 min prior to eating to limit post prandial hyperglycemia
  • An important benefit of lispro is a decrease in postprandial hyperglycemia & less risk of hypoglycemia, which may follow injection of regular insulin.
134
Q

Which insulin contains protamine?***

A

Neutral Protamine Hagedorn (NPH)

This insulin preparation contains 0.005 mg protamine/U of insulin.**

135
Q

What is the preferred treatment for abrupt onset of hyperglycemia or ketoacidosis?

A

Regular insulin

Fast acting

Only insulin that can be given IV or Sub Q

136
Q

Why is the sub Q injection delayed with NPH?

A

Neutral Protamine Hagedorn (NPH)

Sub Q injection site is delayed because insulin is conjugated with protamine

137
Q

Side effects of Insulin?

A 
=Hypoglycemia 
-Most serious side effect
=Allergic reactions
=Lipodystrophy
=Insulin resistance 
=Drug interactions
138
Q

What are the first symptoms of hypoglycemia?

A

-The first symptoms of hypoglycemia are the compensatory effects of increased epinephrine secretion: diaphoresis, tachycardia, and hypertension.

139
Q

Rebound hyperglycemia caused by (BLANK) activity in response to hypoglycemia (Somogyi effect) may mask the correct diagnosis.

A

Rebound hyperglycemia caused by SYMPATHETIC NERVOUS SYSTEM activity in response to hypoglycemia (Somogyi effect) may mask the correct diagnosis.

140
Q

Symptoms of hypoglycemia involving the central nervous system (CNS) include what?

A

Symptoms of hypoglycemia involving the central nervous system (CNS) include mental confusion progressing to seizures and coma.

The CNS effects are intense because the brain depends on glucose as a selective substrate for oxidative metabolism.

141
Q

A prolonged period of hypoglycemia may result in what??

A

A prolonged period of hypoglycemia may result in irreversible brain damage.

142
Q

What does Metformin do?

A

Decreases blood glucose concentrations in both the fasting & postprandial state and rarely causes hypoglycemia.

143
Q

What can be used in combination with other medications such as insulin and sulfonylureas?

A

Metformin can be used in combination with other medications such as insulin and sulfonylureas.

144
Q

Metformin should not be prescribed for patients with what?

A

Metformin should not be prescribed for patients with lactic acidosis, acute kidney injury, gastrointestinal intolerance, or acute hepatic disease.

145
Q

The most common side effects of metformin include?

A

The most common side effects of metformin are anorexia, nausea, & diarrhea, which are dose related.

146
Q

What is a possible side effect associated with metformin that has been described during the intraoperative period?

A

Lactic acidosis is a possible side effect associated with metformin that has been described during the intraoperative period.

For this reason, some have recommended discontinuing metformin 48 hours or longer before elective operations

147
Q

MOA of Metformin?

A

MOA

  • —Metformin activates adenosine monophosphate–activated protein kinase to suppress hepatic glucose production by decreasing gluconeogenesis and glycogenolysis and to enhance postprandial insulin suppression of hepatic glucose production.
  • -Metformin also regulates glucose levels by decreasing gastrointestinal glucose absorption, increasing insulin sensitivity in peripheral tissues, and enhancing synthesis of glucagon-like peptide-1 (GLP-1) in the ileum.
148
Q

Pharmacokinetics of Metformin?

A

Pharmacokinetics

  • –It is eliminated by the kidneys, with 90% of an oral dose excreted in approximately 12 hours.
  • –Peak plasma concentrations of metformin occur approximately 2 hours after oral administration.
  • –The drug has an elimination half-time of 2 to 4 hours, which means that it is taken up to three times a day (500 to 1,000 mg with meals).
  • –In view of its dependence on renal clearance, metformin is prescribed with caution, if at all, to patients with renal dysfunction.
149
Q

Which oral insulin does not cause hypoglycemia?

A

Metformin Does NOT cause hypoglycemia

150
Q

Metformin Side effects?

A 
Metformin
Side effects- dose related
Anorexia
Nausea
Diarrhea
151
Q

Serious SE of Metformin?

A

Serious SE Lactic acidosis

152
Q

Metformin needs to be taper off because?

A

15% of patients get SE from withdrawal of the drug

153
Q

Sulfonyureas are capable of what?

A

Sulfonyureas

=Capable of lowering glucose concentrations to hypoglycemic levels

154
Q

Most patients are unsuccessful with which oral insulin therapy?

A

Sulfonyureas

155
Q

Can sulfonyureas be used with Type I DM?

A

NO

156
Q

Which Oral insulin is associated with decreased hepatic production of very low density lipoproteins?

A

Sulgonyureas are associated with decreased hepatic production of very low density lipoproteins as well as melioration of hypertriglyceridemia

157
Q

Does Sulfonyureas have antibacterial actions?

A

No antibacterial actions

Should not be administered with patients with SULFA allergy

158
Q

What is the MOA of Sulfonylurea?

A

=Sulfonylurea receptors are found on pancreatic & cardiac cells.
=These drugs inhibit adenosine triphosphate–sensitive potassium ion channels (now known as thesulfonylurea receptor-1) on pancreatic β cells.
=As a result, there is an influx of calcium and stimulation of exocytosis (release) of insulin storage granules.
=Although sulfonylureas decrease insulin resistance, this effect is minor, if at all, in decreasing blood glucose concentrations.

159
Q

What are the side effects of Sulfonyureas?

A

Side Effects
=Hypoglycemia
=Greatest risk with drugs with longest elimination half-times ie glyburide and chlorpropamide
=May act up to 7 days
=If hypoglycemia occurs the effect is more severe than insulin

Pharmacology 2 (11 decks)

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