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*Endocrine > Endocrine Apex > Flashcards

Endocrine Apex Flashcards

1
Q

What describes a cell that releases a substance and travels through the bloodstream before it acts on different cells?

A

Endocrine

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2
Q

What describes a cell that releases a substance that works on adjacent cells?

A

Paracrine

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3
Q

What describes a cell that releases a substance that works on the surface of that exact same cell?

A

Autocrine

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4
Q

What 2 substances does the posterior pituitary release?

A
  1. Vasopressin (ADH)

2. Oxytocin

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5
Q

What 6 hormones does that anterior pituitary release? (mnemonic)

A

FLAT PiG

Follicle stimulating hormone
Luteinizing hormone
Adrenocorticotropin
Thyroid-stimulating hormone

Prolactin
ignore
Growth hormone

(Sex + growth hormones)

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6
Q

The other name for the anterior pituitary gland vs posterior pituitary gland

A

Adenohypophysis (Anterior) (A-Adeno)

Neurophypophysis (Posterior)

(Posterior releases ADH, causes of ADH can be NEUROlogic in nature)

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7
Q

What is follicle-stimulating responsible for?

A

Germ-cell maturation + ovarian follicle growth (females)

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8
Q

What is LH (luteinizing hormone) responsible for?

A 
Testosterone production (males)
Ovulation (females)
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9
Q

What is adrenocorticotropin responsible for?

A

Adrenal hormone release

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10
Q

What is TSH (thyroid stimulating hormone) responsible for?

A

Thyroid hormone release

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11
Q

What is prolactin responsible for?

A

Lactation

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12
Q

What is growth hormone responsible for?

A

Cell growth

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13
Q

What is antidiuretic hormone responsible for?

A

Water retention

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14
Q

What is oxytocin responsible for?

A

Uterine contraction & breast feeding

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15
Q

Does the hypothalamus reside inside or outside of the blood-brain barrier?

A

Outside - that’s how it’s able to secrete these substances into the bloodstream

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16
Q

Where is ADH formed?

A

In the supraoptic nuclei of the hypothalamus.

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17
Q

Where is oxytocin formed?

A

In the paraventricular nuclei of the hypothalamus

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18
Q

Which pituitary gland is always bigger?

A

Anterior

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19
Q

Which sits higher, the supraoptic or paraventricular nuclei of the hypothalamus?

A

The paraventricular

(Think the supraoptic sits closer to the eye and the paraventricular sits closer to the ventricles of the brain which are higher up)

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20
Q

What additional hormone does Luteinizing hormone-releasing hormone increase other than Luteinizing hormone?

A

Follicle-Stimulating hormone

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21
Q

T/F - Follicle-Stimulating releasing hormone increases the amount of follicle-stimulating hormone (FSH)

A

False! - Luteinizing releasing hormone increases FSH secretion.

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22
Q

What does corticotropin-releasing hormone cause?

A

increased adrenocorticotropin hormone (ACTH) from the anterior pituitary.

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23
Q

Which hormone released from the hypothalamus results in increased secretion of thyroid-stimulating hormone from the anterior pituitary?

A

Thyrotropin-releasing hormone

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24
Q

Where does that pituitary gland reside?

A

In the Sella Turcica

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25
Q

What connects the pituitary gland to the hypothalamus?

A

The pituitary stalk

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26
Q

What hormone stimulates germ cell maturation in males and females?

A

FSH

follicle-stimulating hormone
-Anterior Pituitary

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27
Q

What hormone stimulates ovarian follicle growth in females?

A

FSH

follicle-stimulating hormone
-Anterior Pitutiary

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28
Q

What hormone stimulates testosterone production in males?

A

LH

Luteinizing hormone
-Anterior pituitary

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29
Q

What hormone stimulates ovulation in females?

A

LH

Luteinizing hormone
-Anterior pituitary

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30
Q

What hormone stimulates adrenal hormone release?

A

ACTH

Adrenocorticotropic hormone
-from the anterior pituitary

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31
Q

What hormone stimulates the release of thyroid hormone?

A

Thyroid-stimulating hormone (TSH)

-from the anterior pituitary

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32
Q

What hormone stimulates lactation?

A

Prolactin

-from the anterior pituitary

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33
Q

What hormone stimulates cell growth?

A

Growth hormone

-from the anterior pitutary

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34
Q

Hypersecretion of what 2 hormones from the anterior pit can result in early puberty?

A
  1. FSH
  2. LH

(1. germ cell maturation and ovarian follicle growth
2. testosterone production and ovulation)

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35
Q

HYPOsecretio of what 2 hormones from the anterior pit can result in infertility?

A
  1. FSH
  2. LH

(1. germ cell maturation and ovarian follicle growth
2. testosterone production and ovulation)

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36
Q

(Hyper/Hypo)secretion of ATCH leads to (Cushings/Addisons) disease

A

Hypersecretion ACTH > cushings
Hyposecretion of ACTH > addisons

(adrenal hormone release)

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37
Q

(Hyper/Hypo)secretion of TSH leads to (hyper/hypo)thyroidism

A

Hypersecretion TSH > hyperthyroid

Hyposecretion of TSH > hypothyroid/cretinism

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38
Q

HYPERsecretion of which hormone from the anterior pit can result in infertility?

A

Prolactin

if your lactating all the time, ain’t no one gonna wanna get you pregnant there for you will be infertile

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39
Q

Hypersecretion of growth hormone results in what 2 conditions?

A

Acromegaly

Gigantism

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40
Q

Hyposecretion of growth hormone results in what condition?

A

Dwarfism

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41
Q

(Hyper/hypo) secretion of ADH results in (SIADH/DI)

A

hypersecretion of ADH = SIADH

hyposecretion of ADH = DI

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42
Q

Which endocrine hormone is a function of a positive feedback loop?

A

Oxytocin (birth/contractions)

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43
Q

What regulates the release of corticotropin-releasing hormone (CRH)?

A

cortisol >CRH > ACTH

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44
Q

What regulates the release of thyrotropin-releasing hormone (TRH)?

A

Triiodothyronine (T3) > TRH > TSH

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45
Q

What regulates the release of luteinizing hormone-releasing hormone (LHRH)?

A

Testosterone, Estrogen, Progesterone

> LHRH > FSH & LH

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46
Q

What regulates the release of growth hormone-releasing hormone (GHRH) and Growth hormone-inhibiting hormone (GHIH)? (2)

A

Growth hormone &

Insulin growth factor-1

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47
Q

Why do dopamine antagonists, such as metoclopramide cause hyperlactatinemia?

A

Prolactin is under neuronal control.
Normally Dopamine decreases prolactin.
So if it is inhibited, prolactin will accumulate

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48
Q

What is the most common cause of DI?

What about SIADH?

A

Pituitary surgery - DI

TBI - SIADH

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49
Q

Treatment for DI?

A

DDAVP (or vasopressin)

SC: 0.5-2mcg BID

Nasal: 5-40mcg QD

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50
Q

What syndrome does excess ADH in the blood create? what about too little?

A

SIADH - too much (si, ADH, too much, si)

DI - too little

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51
Q

What does the treatment of SIADH consist of? (3)

A
  1. Fluid restriction
  2. Demeclocycline
  3. Hypertonic saline (if severely hyponatremic)
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52
Q

What 4 airway challenges can present in a kid with acromegaly?

A
  1. difficult seal with BMV > distorted facial features
  2. difficult laryngoscopy > Large tongue, teeth, and epiglottis
  3. difficult ETT placement > subglottic narrowing and vocal cord enlargement
  4. Risk of epistaxis > enlarged turbinates
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53
Q

5 conditions associated with acromegaly

A
  1. OSA
  2. CAD (risk for rhythm disturbances and htn)
  3. Glucose intolerance
  4. skeletal muscle weakness
  5. entrapment neuropathies
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54
Q

5 causes of SIADH

A
  1. TBI (most common)
  2. small cell lung CA
  3. noncancerous lung disease
  4. Carbamazepine
  5. Hypothyroidism
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55
Q

4 Causes of DI

A
  1. Pituitary surgery (most common)
  2. Pituitary tumor
  3. TBI
  4. SAH
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56
Q

Presentation of SIADH

A

hyponatremia

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57
Q

presentation of DI

A

polyuria

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58
Q

SIADH vs DI plasma and urine osmolarity

A

Plasma Os:
SIADH: hypotonic <275mOsm/L
DI: hypertonic >290mOsm/L

Urine Os:
SIADH: higher than plasma os
DI: lower than plasma os

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59
Q

How does demeclocycline work?

A

It decreases the responsiveness to ADH

given to treat SIADH/excess ADH

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60
Q

When should you treat SIADH with hypertonic saline?

A

if they are symptomatic with their hyponatremia or if <120

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61
Q

How fast should you correct hyponatremia?

A

no more than 1meq/L/hr

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62
Q

What is another name for growth hormone?

A

Somatotropin

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63
Q

What condition results from oversecretion of growth hormone AFTER adolescence?

What is this most often caused by?

A

Acromegaly

-a pituitary adenoma

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64
Q

What condition results from oversecretion of growth hormone BEFORE puberty?

A

Gigantism

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65
Q

Why should you use a smaller ETT in a patient with acromegaly?

A

Bc of subglottic narrowing and vocal cord enlargement

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66
Q

What is thyroxine?

A

T4

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67
Q

What is triiodothyronine?

A

T3

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68
Q

The thyroid gland stores and secretes what 3 hormones?

A

thyroxine (T4)
triiodothyronine (T3)
Calcitonin (reduces serum CA)

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69
Q

What does calcitonin result in?

A

Reduced serum calcium/Hypocalcemia

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70
Q

What does the thyroid need to synthesize T3 & T4?

A

Iodine

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71
Q

What nerve is at risk during thyroid and parathyroid surgery and why?

A

Recurrent laryngeal nerve

> it runs along the lateral border of each thyroid lobe

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72
Q

What are the right and left thyroid glands attached by?

A

The thyroid isthmus

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73
Q

The thyroid gland lays:
Anterior to ___________
Inferior to______________
Superior to _____________

A

Anterior to the trachea
Inferior to the cricoid cartilage
Superior to the suprasternal notch

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74
Q

Which one is more potent : T3 or T4

A

T3 (active form)

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75
Q

Which one is more protein bound: T3 or T4

A

T4 (travels in blood)

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76
Q

Which one is directly released from thyroid: T3 or T4

A

T4

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77
Q

Where is T4 converted to T3 and what does this require?

A

In the target cell

-requires iodine

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78
Q

Which is the active form: T3 or T4?

A

T3

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79
Q

Half life of T3 vs T4

A 
T3 = 1 day (short and potent)
T4 = 7 days (long car drive, less potent)
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80
Q

Why does a hypothyroid patient have ELEVATED TSH?

A

Because the anterior pitutiary is releasing TSH to stimulate the thyroid to release T3/T4

> if the thyroid is hypoactive, it doesn’t secrete enough T3/T4 to tell the anterior pituitary to stop secreting TSH (negative feedback)
so anterior pituitary continues to sense these low levels of T3/T4 and keeps secreting TSH to try and boost them

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81
Q

Why does increased thyroid hormone result in vasodilation?

A

because increased BMR leads to increased O2 consumption. The vessels vasodilate in attempt to get more o2 supply to match the demand.

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82
Q

Why does excess thyroid hormone result in increased minute ventilation?

A

increased basal metabolic rate = increase end products of metabolism (CO2) - increased minute ventilation to blow off that CO2

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83
Q

What is the most common cause of hyperthyroidism?

A

Graves disease

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84
Q

What is the most common cause of hypothyroidism?

A

Hashimotos Thyroiditis

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85
Q

Why doesn’t hyper/hypothyroidism affect MAC?

A

because it alters o2 consumption in all tissues EXCEPT the CNS

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86
Q

How does hyperthyroidism affect MAC?

A

It doesn’t
-it does increase cardiac output though which increases anesthetic uptake into the blood
>decreases the rate of rise FA/FI (slower induction)

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87
Q

7 causes of hyperthyroidism

A
  1. Graves disease (most common) : autoimmune
  2. Myasthenia gravis (autoimmune)
  3. Multinodal goiter
  4. Carcinoma
  5. Preganancy
  6. Pituitary adenoma
  7. Amiodarone (less common)
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88
Q

6 causes of hypothyroidism

A
  1. Hashimotos thyroiditis (most common): autoimmune
  2. Iodine deficiency
  3. Hypothalamic-pituitary dysfunction
  4. Neck radiation
  5. Thyroidectomy
  6. Amiodarone (more common)
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89
Q

Is amiodarone more likely to cause hyper or hypothyroidism?

A

hypothyroidsm

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90
Q

Diagnosis of hyperthyroidism

A

Low TSH

High T3, T4

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91
Q

Diagnosis of hypothyroidism

A

High TSH

Low T3, T4

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92
Q

What is thyroid storm?

Does it occur in patients with hyper or hypothyroidism?

What time frame is it seen?

A

When periods of increased stress (surgical), the thyroid gland increases thyroid hormone output.

Hyperthyroidism and can occur in euthyroid patients too.

6-18 hours AFTER surgery

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93
Q

What is myxedema coma?

A

A complication/consequence of severe hypothyroidism (not a cause of it!)

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94
Q

What does cretinism lead to?

A

Impaired physical and mental development

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95
Q

Which betablocker inhibits the conversion of T4 to T3?

A

Propanolol

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96
Q

4 classes of drugs to manage hyperthyroidism

A
  1. Thionamides (PTU, methimazole, carbimazole)
  2. Betablockers (Esmolol, Propanolol)
  3. Potassium Iodine
  4. Radioactive Iodine
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97
Q

What are the 3 thionamides and how do they work?

2 main side effects

A

Propylthiouracil (PTU), methimazole, carbimazole

-block thyroid synthesis by blocking further iodine on the tyrosine residues of thyroglobulin

  1. Hepatitis
  2. Agranulocytosis
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98
Q

What 2 drugs inhibit the peripheral conversion of T4 to T3?

A

Propylthiouracil (PTU) and propanolol

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99
Q

How does potassium iodine treat hyperthyroidism and how many days should it be administered before surgery?

A

It decreases thyroid hormone synthesis & release

*10 days prior to surgery

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100
Q

How does radioactive iodine treat hyperparathyroidism?

2 contraindications

A

It destroys thyroid tissue

No preggos or breastfeeding mamas

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101
Q

4 Complications that may occur secondary to subtotal or total thyroidectomy

A
  1. hypothyroidism
  2. hemorrhage > tracheal compression
  3. RLN injury
  4. Hypocalcemia
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102
Q

How do you manage a hyperthyroid patient presenting for an elective surgery?

A

cancel!

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103
Q

How should you manage a hyperthyroid patient presenting for emergency surgery?

A

-Betablockers, potassium iodine, glucocorticoids and start PTU.

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104
Q

What are your concerns with a goiter?

A

It can cause tracheal deviation or tracheomalacia

AWAKE INTUBATION (First choice)
2nd choice- a technique that maintains spontaneous ventilation

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105
Q

What 3 drugs should be avoided in patients with hyperthyroidism?

A
  1. Anticholinergics
  2. Ketamine
  3. Pancuronium (who even has that shit)
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3
4
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106
Q

Why would the hyperthyroid patient be at risk for corneal abrasion?

A

If they have exophthalmos

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107
Q

When you have a patient presenting for an elective thyroidectomy d/t hyperthyroidism, what are your main concerns? (7)

A 
1. Complications 
>hypothyroid >prolonged wakeup from decreased CO
>hemorrhage > tracheal compression
>RLN injury > bilateral = emergency 
>hypocalcemia> muscle weakness
  1. Ensure they are euthyroid
  2. Goiters
    >tracheal deviation? tracheomalacia
    >poss awake intubation (glide) or keep spontaneous resps
  3. Are they exophthalmic?
    >increased risk of corneal abrasion
  4. Caution with NMB
    >what’s the cause of the hyperthyroidism? it could be myasthenia gravis
  5. Careful positioning
    >increased bone turnover = increased risk of osteoporosis and risk of fractures
  6. Consider DL prior to extubation to assess vocal cords and for any glottic edema
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108
Q

What does the RLN innervate?

A

All the intrinsic laryngeal muscles except the cricothyroid muscle which is innervated by the SLN.

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109
Q

What would you see on DL if there was unilateral RLN injury?

How would this patient present after extubation?

How would you best assess this?

A

The ipsilateral (same side) vocal cord would stay midline on inspiration

hoaRsNess (RNL)

Ask the patient to say “E” or “moon”

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110
Q

What would you see on DL if there was BILATERAL RLN injury?

How would this patient present after extubation?

A

Both cords would stay midline on inspiration

Complete airway obstruction!

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111
Q

Which is the emergency - B/L SLN or B/L RLN injury?

A

B/L RLN injury

  • Complete airway obstruction
  • RuNNNNNN!
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112
Q

T/F : hypocalcemia resulting from parathyroid resection can put your patient at increased risk for layngospasm in the immediate postop period

A

False - the hypocalcemia usually results in 24-48hrs after surgery.

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113
Q

8 s/s hypocalcemia

A
  • Muscle spasm –> tetany
  • Laryngospasm
  • Chvostek’s sign
  • Trousseau’s sign
  • Mental status changes
  • Parasthesias
  • Hypotension
  • Prolonged QT
114
Q

What is chvosteks sign and what does it indicate?

A

tapping on the angle of the jaw (facial nerve/masseter muscle) causes ipsilateral facial contraction

-hypocalcemia

115
Q

How to assess for Trousseau’s sign.

What does it indicate?

A

inflate upper extremity BP cuff x 3 mins
>decreased blood flow should accentuate neuromuscular irritability
>muscle spasms of hand and forearm

116
Q

What contains more elemental calcium…. chloride or gluconate?

A

calcium chloride

gluconate usually used bc less risk of necrosis if infiltrate occurs

117
Q

What is thyroid storm typically triggered by, who is affected, and when?

A

triggered by: stressful events: surgery, infection, ect.

who: hyperthyroid AND euthyroid patients
when: 6-18 hours AFTER surgery

118
Q

7 s/s of thyroid storm

A
  1. Fever > 38.5
  2. Tachy
  3. HTN
  4. CHF
  5. Shock
  6. Confusion/Agitation
  7. N/V
119
Q

What 4 things can thyroid storm mimic under GA?

A
  1. MH
  2. Pheo
  3. NMS
  4. Light anesthesia
120
Q

What are the 4 B’s in treating thyroid storm?

A

Block synthesis (methimazole, PTU, carbimazole, potassium iodine)

Block release (potassium iodine, radioactive iodine)

Block T4-T3 conversion (PTU, propanolol, gluticocorticoids)

Block beta (propanolol and esmolol)

121
Q

What drugs block the synthesis of thyroid hormone? (4)

A
  1. Methimazole
  2. PTU
  3. carbimazole
  4. potassium iodine
122
Q

What drugs block the release of thyroid hormone (2)?

A

Potassium iodine and radioactive iodine

123
Q

What drugs block the conversion of T4 to T3? (3)

A

PTU
Propanolol
glucocorticoids

124
Q

Betablockers for hyperthyroidism or thyroid storm

A

propanolol

esmolol

125
Q

Why shouldn’t you give aspirin to someone with hyperthyroidism or thyroid storm?

A

Because aspirin can dislodge T4 from plasma proteins
>increased free fraction of T4
>worsening situation

126
Q

Those with hyperthyroidism have increased resistance to depolarizing or nondepolarizing NMB?

A

depolarizing

(hypocalcemia = more irritable muscles, will take more to relax them) - my thoughts at least idk

127
Q

What sympathomimetic agent should you avoid when treating hypotension in a hypothyroid patient?

A

phenylephrine (want to enhance myocardial performance, not slow the rate)

128
Q

In a hypothyroid patient whose BP is unresponsive to catecholamines, what would be the next agent to try?

-why?

A

Corticosteroids

-these patients often have decreased adrenal function

129
Q

Your main thoughts when anesthetizing a patient with mild-moderate hypothyroidism (9)

A
  1. They’re probably going to obstruct on me
    >big tongue, swollen VC, goiter
  2. Risk of aspiration
    >decreased gastric emptying
  3. FASTER inhalation induction
  4. No change in MAC
  5. Avoid phenylephrine (don’t want to further depress cardiac rate)
  6. Refractory hypotension
    >tx with corticosteroids (these pts often have decreased adrenal function)
  7. If lethargic, they will prob be very sensitive to anesthetics
  8. Increased sensitivity to NDMRs
  9. Slowed hepatic metabolism and renal excretion can prolong drug effects
130
Q

What two hormones act antagonistically to regulate the ionized calcium level?

A

Calcitonin & PTH

131
Q

Where is calcitonin produced and what does it do?

A

It’s produced in C-Cells (Calcitonin) of the thyroid gland

> decreases ionized calcium
increases serum phos

132
Q

Where is PTH produced and what does it do?

A

It’s produced in the chief cells of the Parathyroid

> it increases ionized calcium
decreases serum phos

133
Q

What is the most common cause of hypercalcemia?

A

Primary hyperparathyroidism

134
Q

What is the most common cause of primary hyperparathyroidism and how is it treated?

A

Parathyroid adenoma > primary hyperparathyroidism > hypercalcemia

*tx- surgical resection of the parathyroid glands

135
Q

What is secondary hyperparathyroidism?

*most common cause?

A

Hyperparathyroidism that is caused by something that stimulates the parathyroid glands to increase PTH output

(the glands themselves are normal)

*CKD

136
Q

T/F hypoparathyroidism causes hypocalcemia

A

True

137
Q

What is the most common cause of primary hypoparathyroidism?

*treatment

A

iatrogenic gland removal during thyroidectomy

*Tx- Calcium, vitamin D, and Mag supplements

138
Q

What are osteoblasts?

A

they are bone cells that add calcium to the bone

*this decreases CA+ concentration in the blood

(Blast calcium into the bone)

139
Q

What are osteoclasts?

A

bone cells that remove calcium from bone and increase ionized ca++ levels in the blood

140
Q

What bone cells promote bone deposition?

A

Osteoblasts (blast calcium into the bone)

141
Q

What bone cells promote bone resorption?

A

Osteoclasts

142
Q

Difference between calcitocin and calcitrol

A

Calcitonin decreases ionized CA and increases serum phos

Calcitrol is the active form of vitamin D

143
Q

What functions as a resovior for calcium in our bodies?

*what is it stored as?

A

Bones

*Hydroxyapatite

144
Q

What is ionized calcium?

A

The amount of free calcium not bound to plasma proteins

145
Q

Calcitonin and PTH regulate calcium in what parts of the body (3)?

A

bones, kidneys, and intenstines

146
Q

Normal Calcium level

A

8.5-10.5mg/dL

147
Q

Normal ionized calcium level

A

4.5-5.5mg/l

(2.2-2.6meq/l)

148
Q

What happens when an increased calcium level is detected?

A

Thyroid gland releases CALCITONIN which:

  1. Inhibits osteoclast activity
  2. decreases calcium resorption in the kidneys
149
Q

What happens when a decreased calcium level is detected?

A

Parathyroid glands release PTH, which:

  1. stimulates osteoclast activity (calcium release from bone into blood)
  2. Calcium is reabsorbed in the kidney (reabsorbs it into the blood)
  3. Vitamin D synthesizes absorption of calcium from the small intestines
150
Q

T/F: only the ionized portion of calcium exerts physiologic effects

A

True

151
Q

What is the term for bone disease caused by hyperparathyroidism secondary to CKD?

A

Renal osteodystrophy

152
Q

The adrenal gland is composed of what 2 things?

A 
Adrenal cortex (outer region)
Adrenal medulla
153
Q

Where are mineralocorticoids secreted from specifically?

Example of a mineralocorticoid

A

Zona-gloMerulosa of the adrenal cortex

  • Aldosterone
  • Salt
154
Q

Where are corticosteroids produced specifically?

-Example of a corticosteroid

A

Zona- Fasiculata of the adrenal cortex

  • Cortisol
  • Sugar

(cortisol is Fascinating)

155
Q

What is produced by the Zona Reticularis of the adrenal cortex?

A
  • Androgens (Sex hormones)

(dehydro-epi-andosterone)

(Androgens are Ridiculous, zona Reticularis)

156
Q

What 3 things cause the release of aldosterone?

A
  1. RAAS activation
  2. Hyperkalemia
  3. Hyponatremia

(holds onto sodium, releases K)

157
Q

What stimulates the kidney to conserve sodium & water and to excrete potassium and hydrogen?

A

Aldosterone

158
Q

T/F aldosterone regulates sodium concentration and osmolarity

A

False (ADH does this)

159
Q

What increases cortisol production?

A

Stress

160
Q

By what 3 methods does cortisol increases glucose?

A
  1. Gluconeogenesis
    >liver converts aminoacids to glucose
  2. Protein catabolism
    >muscle breakdown to increase amount of aminoacids available for the liver to convert to glucose
  3. Fatty acid mobilization
    >increased fatty acid oxidation
    >body able to use fat for energy instead of glucose
161
Q

How does cortisol mitigate the inflammatory cascasde?

A

By stabilizing lysosomal membranes & decreasing cytokine release

162
Q

3 catagories of steroids synthesized and released from the adrenal cortex

A
  1. Mineralocorticoids (aldosterone) (G) (salt)
  2. Corticosteroids (cortisol) (F) (sugar)
  3. Androgens (sex hormones) (R) (sex)
163
Q

What steroid is required for the vasculature to respond to the vasoconstriction effects of catecholamines?

A

Cortisol

164
Q

T/F- decreased levels of ACTH cause hypoaldosteronism

A

False- ACTH only has a minor influence on aldosterone release

165
Q

What receptors on the cell membrane does cortisol bind to?

A

None- it diffuses through the lipid bilayer & binds with INTRACELLULAR steroid receptors

(process requires time, which is why there is a longer onset with steroids)

166
Q

Normal cortisol production/day

A

15-30mg/day

167
Q

Normal cortisol level

A

12mcg/dL

168
Q

T/F - cortisol reduces histamine

A

false

169
Q

Which endogenous steroid has equal glucocorticoid and mineralocorticoid effects?

A

Cortisol

170
Q

T/F aldosterone has some glucocorticoid (anti-inflammatory) effects

A

False!

171
Q

What should you think of when differentiating the effects of glucocorticoids and mineralocorticoids?

A 
glucocortiocid = anti-inflammatory effects
mineralcorticoid = sodium-retaining effects
172
Q

Adrenocortical insufficiency is known as….

A

Addison’s disease

173
Q

What is a good choice to treat adrenocortical insufficiency ( _________ disease) and why?

A

Addison’s disease

-Prednisone - bc it’s an analog of cortisol (meaning it most closely resembles cortisol of all the exogenous steroids)

174
Q

Which exogenous steroids have no mineralocorticoid effects? (3)

A
  1. Dexamethasone
  2. Bexamethasone
  3. Triamcinolone
175
Q

What is the name of the steroid commonly injected into the epidural space to treat lumbar disc disease?

A

Triamcinolone

176
Q

3 things that make triamcinolone unique?

A
  1. Higher incidence of skeletal muscle weakness
  2. Can cause sedation rather than euphoria
  3. Anorexia rather than increased appetite
177
Q

3 endogenous steroids

A
  1. Cortisol
  2. cortisone
  3. Aldosterone
178
Q

Which disease states:

  • insufficient cortisol
  • excess cortisol
  • excess aldosterone
A
  • insufficient cortisol = Addison’s (need to ADD some cortisol)
  • excess cortisol = Cushing’s (cush balls are so extra)
  • excess aldosterone = Conn’s (aldosterone = the con man, cons off sodium for potassium) - extra conning going on
179
Q

Another name for primary hyperaldosteronism

A

Conn’s Syndrome

180
Q

3 Causes of Conn’s Syndrome

A
  1. Aldosteroma
  2. Pheo
  3. Primary Hyperthyroidism
181
Q

Long-term licorice ingestion ( ________ acid) contributes to a syndrome that highly resembles what?

A

Hyperaldosteronism (Conn’s Syndrome)

-Glycyrrhizic Acid

182
Q

3 Clinical features of hyperaldosteronism (Conn’s Syndrome)

A
  1. Hypertension (sodium and water retention)
  2. Hypokalemia (K+ excretion)
  3. Metabolic Alkalosis (H+ wasting)
183
Q

Why would you want to avoid hyperventilating someone with Conn’s syndrome?

A

Bc hyperventilation activates the H+/K+ and will make hypokalemia and alkalosis worse

184
Q

What results from when the anterior pituitary releases too much ACTH which then triggers the increased cortisol release from the zona fasciculata of the adrenal cortex?

A

Cushing’s syndrome

185
Q

T/F - cortisol has glucocorticoid, mineralocorticoid, AND androgenic effects

A

True

*Cushing’s disease affects all these areas

186
Q

What disease is caused by excess ACTH?

A

Cushing’s syndrome

187
Q

Causes of Cushing’s syndrome

A
  1. Pituitary tumor > “Cushing’s disease”
  2. Adrenal tumor
  3. Other
188
Q

Difference between Cushing’s syndrome and Cushing’s disease

A

Cushing’s disease causes Cushing’s syndrome

Cushing’s disease = oversecretion of ACTH from pituitary tumor > increased cortisol release from adrenal cortex

189
Q

What does the destruction of all 3 zones of the adrenal cortex result in?

A

Adrenal insufficiency

190
Q

What are your concerns with someone who has adrenal insufficiency?

A

That it can turn into an adrenal crisis which is triggered by additional stress on the body (surgery, pain, infection, sepsis

191
Q

How does Etomidate cause dose-dependent adrenocortical suppression?

A

By inhibiting 11-Beta hydroxylase

192
Q

What happens with primary adrenal insufficiency (Addison’s disease)

A

ADrenal glands don’t secrete enough steroid hormone (cortisol)

Anterior pituitary will increase ACTH secretion in attempt to stimulate the failing gland

193
Q

Most common caue of primary adrenal insufficiency (Addison’s disease) in the US vs worldwide

A

US- autoimmune destruction of both glands
WW- TB

(HIV also a cuase)

194
Q

What happens with secondary adrenal insufficency?

A

There is decreased cortisol-releasing hormone or decreased ACTH release which results in decrease stimulation of the adrenal gland and decreased cortisol release

195
Q

Most common cause of secondary adrenal insufficency?

A

Exogenous steroid administration

or HPA disease from tumor, infection, surgery, or radiation

196
Q

Clinical features of adrenal insufficiency (8)

A

Muscle weakness/fatigue
Hypotension
Hypoglycemia
Hyponatremia, Hyperkalemia, Metabolic Acidosis
N/V
Hyperpigmentation of knees, elbows, knuckles, lips, and buccal mucosa (Primary adrenal insufficiency)

197
Q

Treatment for adrenal insufficiency

A

Steroid replacement therapy

15-30mg cortisol equivilent/day

198
Q

4 S/S of adrenal crisis

A
  1. Hemodynamic instability (collapse)
  2. Fever
  3. Hypoglycemia
  4. . Change in MS
199
Q

Treatment for Adrenal Crisis (3)

A
  1. Hydrocortisone 100mg + 100-200mg/day
  2. ECF volume expansion with D5NS
  3. Support hemodynamics
200
Q

How does exogenous steroid supplementation work?

A

It decreases ACTH release from the anterior pituitary

> decreased ACTH = decreased cortisol (pt’s wont be able to increase cortisol in response to surgical stress)

201
Q

What dose/duration of prednisone poses the following risks of HPA suppression?

  • Yes:
  • Maybe:
  • No:

Which require stress- dose steroids?

A

Yes: >20mg/day for > 3 weeks *Stress dose

Maybe: 5-20mg/day for >3 weeks *Stress dose

No: <5mg/day for any period of time
or any dose for < 3 weeks !

202
Q

Pre-op hydrocortisone dose for superficial procedures such as dental work and biopsies? Taper?

A

None

203
Q

Pre-op hydrocortisone dose for minor surgical procedures such as inguinal hernia repairs and colonoscopy. Taper?

A

25mg IV

-no taper

204
Q

Pre-op hydrocortisone dose for moderate surgical procedures such as: Colon resection, TJR, total abdominal hysterectomy? Taper?

A

50-75mg IV

-taper over 1-2days

205
Q

Pre-op hydrocortisone dose for major surgical procedures such as CV, whipple, thoracic, liver? Taper?

A

100mg-150mg IV

-taper over 1-2 days

206
Q

How long does the adrenocortical supression effects of etomidate last after a single induction dose?

A

5-8 hours (some sources say up to 24)

207
Q

In addition to etomidate, what other drug can inhibit cortisol synthesis?

A

Ketoconazole (an antifungal)

208
Q

What are the 2 broad groups of hormones secreted by the pancreas, where are they secreted, and what are they produced by?

A
  1. Endocrine > released into the duodenum for digestion > Acini tissue
  2. Exocrine > released into circulation for metabolism > islets of Langerhans
209
Q

What cells are glucagon secreted from and what does it do?

A

Alpha cells > increase blood glucose

210
Q

What cells are insulin secreted from and what does it do?

A

Beta cells > reduce blood glucose

211
Q

What cells are somatostatin secreted from and what does it do?

A

Delta cells > inhibits insulin and glucagon; inhibits splanchnic blood flow, gastric acid secretion, and gastric motility, and GB contraction

212
Q

What inhibits pancreatic exocrine secretion, GB contraction, gastric acid secretion, and gastric motility?

A

Pancreatic Polypeptide

213
Q

What is the primary stimulator of insulin release from the pancreatic beta cells?

A

Glucose

therefore anything that increases serum glucose will increase insulin release

214
Q

Cerebral function steadily declines with glucose levels are less than what?

A

< 50mg/dL

215
Q

How does glucagon increase cardiac contractility, HR and AV conduction?

A

By increasing intracellular cAMP (occurs independently of the ANS)

1-5mg

216
Q

How does insulin lower potassium levels?

A

Because it stimulates the NA/K ATPase pump
>3 sodium out of cell, 2 potassium into cell

-D50 is given to prevent hypoglycemia

217
Q

What is the physiologic antagonist to insulin?

A

Glucagon

218
Q

What are key side effects of glucagon?

A

N/V!

219
Q

When might glucagon be used? (5)

A
  1. Betablocker overdose
  2. CHF
  3. Low cardiac output after MI or CPB
  4. Improving map during anaphylaxis
  5. Relax the biliary sphincter during ERCP
220
Q

Somatostatin vs Somatotropin

A

Somatotropin = Growth hormone (Your TROPS grow after cardiac ischemia)

Somatostatin = Growth hormone-inhibiting hormone (Statins inhibit cholesterol)

221
Q

Which type of diabetes is due to beta cell destruction?

A

Type 1 (lack of insulin production)

222
Q

Which type of diabetes is characterized by insulin resistance and a relative lack of insulin

A

Type 2

223
Q

What describes a group of characteristics that are common do diabetics or those at risk for developing diabetes?

A

Metabolic syndrome

224
Q

What are the 5 criteria for metabolic syndrome and how many of them do you need?

A

Fasting glucose > 110mg/dL
Abdominal obesity (waist > 40” in men, >35 in females)
Triglycerides > 150mg/dL
Serum HDL <40mg/dL in men and <50 in females
BP 130/85mmHg

225
Q

Type 1 and 2 diabetes, which one for DKA and which one for Hyperglycemic Hyperosmolar state

A

1- DKA

2- HH

226
Q

The usual cause of DKA and treatment

A
  • infection

tx: volume resuscitation, insulin, and potassium once acidosis subsides

227
Q

is metabolic acidosis worse in DKA or HH?

A

DKA

may not even be acidotic in HH

228
Q

Diagnostic criteria for diabetes mellitus (4)

A
  1. Fasting glucose > 126mg/dL
  2. Random glucose > 200mg/dL + classic sx
  3. 2Hr plasma glucose >200mg/dL during an oral glucose tolerance test
  4. Hgb A1C > 6.5%
229
Q

What causes fruity-smelling breath in diabetics?

A

Acetone

230
Q

What causes kussmauls respirations?

A

Metabolic Acidosis

231
Q

Which type of diuretics increase serum glucose?

List 3 examples

A

Thiazide diuretics

HCTZ, metalozone [zaroxolyn], indapamide

232
Q

Why should LR be avoided in diabetics?

A

Because the lactate can be converted to glucose and contribute to hyperglycemia

233
Q

Which oral diabetic agent carries a risk of lactic acidosis? How long is it recommended to be held before surgery?

A

Metformin

-Hold 24hr before surgery

234
Q

How does metformin work?

A

It disrupts mitochondrial function
>decreases intracellular levels of ATP

Pyruvate is the final product of glycolysis
>if mitochondrial are dysfunctional, the cell shits to anaerobic metabolism and produces lactate

235
Q

Which class of oral hypoglycemic agents shouldn’t be used in someone with a sulfa allergy?

A

Sulfonylureas (Glyburide)

-dont know why I have to know this shit, I’m not going to be prescribing oral hypoglycemic agents

236
Q

Which class of oral hypoglycemic agents is contraindicated in pts with liver failure?

A

Thiazolidinediones (Rostiglitazone)

237
Q

MOA of Biguanides

Example (1)

A
  1. Inhibits gluconeogenesis and glycogenolysis in the liver
  2. Decreases peripheral insulin resistance

(inhibits body from making more glucose and allows insulin to act on cells in order to get glucose into them)

Metformin

238
Q

MOA of Sulfonylureas

Example (6)

A

Stimulate insulin secretion from pancreatic beta cells

Glyburide (-ride)
Gliimepiride (-ride)
Glipizide (-zide)
Gliclazide (-zide)
Chlorpropamide (-mide)
Acetohexamide (-mide)

Tolbutamine (-mine)

239
Q

MOA of Megalitinides

Examples (2)

A

Stimulate insulin secretion from the pancreatic beta cells

Repa-glinide
Nate-glinide

Nate and Repa are so mega

240
Q

MOA of Thiazolidinediones

Examples (2)

A

Decrease peripheral insulin resistance and increase hepatic glucose utilization

Rosi-glitazone
Pio-glitazone

-glitazone

241
Q

Drug class ending in “-glitazone”

A

Thiazolidinediones

242
Q

Drug class ending in “-glinide”

A

Megalitinides

243
Q

Which class of oral hypoglycemic agents may cause vitamin B12 deficiency?

A

Biguanides (Metformin)

244
Q

How should you treat lactic acidosis from metformin? (3)

A

Hemodialysis, sodium bicarb, CV support

245
Q

Which class of oral hypoglycemic agents is often used for polycystic ovarian disease?

A

Biguanides (Metofrmin)

246
Q

In what patient populations should metformin be avoided in due to accumulation of drug increasing the risk of lactic acidosis? (5)

A

Liver disease, Renal disease, Acute MI, CHF, Iodinated Contrast Media

247
Q

Which oral hypoglycemic drug class expands ECF and can lead to edema?

A

Thiazolidinediones

> Rosi-glitazone & Pio-glitazone

248
Q

MOA of alpha-Glucosidase inhibitors

2 examples

A

slow digestion and absorption of carbs from the GI tract

-Acarbose and miglitol

249
Q

MOA of Glucagon-Like Peptide-1 Receptor Agonists

2 examples

A
  • Increase insulin release from pancreatic beta cells
  • decrease glucagon release from alpha cells
  • prolong gastric emptying

ExenaTIDE, LiragluTIDE

250
Q

MOA of Dipeptidyl-Peptidase-4 Inhibitors

Suffix of these drugs

A

Increase insulin release from pancreatic beta cells
-decrease glucagon release from alpha cells

“-leptin”

251
Q

MOA of Amylin Agonists

1 example

A

Inhibit glucagon release from the pancreatic alpha cells
-decrease gastric emptying

Pramlintide

252
Q

Out of the oral hypoglycemic drug classes, which ones do NOT cause hypoglycemia? (3)

A

Biguanides (Metformin)
Thiazolidinediones (-“glitazone)
Alpha-Glucosidase inhibitors (Acarbose/Miglitol)

253
Q

Which oral hypoglycemic drug class poses a risk of hypoglycemia when used with insulin?

A

Amylin agonists (Pramlintide)

254
Q

Which oral hypoglycemic drug class may cause N/V

A

Amylin agonist (Pramlintide)

255
Q

What kind of insulin is the only kind that can be administered IV?

A

Regular insulin (Rapid-Acting)

256
Q

Which receptors stimulate and inhibit insulin secretion?

A

Beta-2 –> Stimulate insulin secretion

Alpha 2 –> inhibit insulin secretions

257
Q

What organ secretes insulin?

A

The pancreas

258
Q

Onsets for Insulins:

  • Ultra-Rapid-Acting:
  • Rapid-acting:
  • Intermediate acting:
  • Long-Acting
  • Ultra-long-acting:
A
  • Ultra-Rapid-Acting: 5-15 mins
  • Rapid-acting: 30 mins
  • Intermediate acting: 2 hours
  • Long-Acting: 2 hours
  • Ultra-long-acting: 2 hours
259
Q

Peaks for insulins:

  • Ultra-Rapid-Acting:
  • Rapid-acting:
  • Intermediate acting:
  • Long-Acting
  • Ultra-long-acting:
A
  • Ultra-Rapid-Acting: 1 hour (45-75 minutes)
  • Rapid-acting: 2-4 hours
  • Intermediate acting: 4-12 hours
  • Long-Acting: 3-9 hours (glargine no peak)
  • Ultra-long-acting: none
260
Q

Durations for insulins:

  • Ultra-Rapid-Acting:
  • Rapid-acting:
  • Intermediate acting:
  • Long-Acting
  • Ultra-long-acting:
A
  • Ultra-Rapid-Acting: 2-4 hours
  • Rapid-acting: 6-8 hours
  • Intermediate acting: 24 hours (18-28hrs)
  • Long-Acting: 6-24 hrs detrimir; 24hrs gargline
  • Ultra-long-acting: 48 hours (40+hrs)
261
Q

What are the 3 ultra-rapid-acting insulins?

A

Lispro
Insulin Aspart (Novolog)
Glulisine

262
Q

Goals of insulin therapy:
AIC < ____%
Blood glucose before a meal: ______-_______
Blood glucose after a meal:

A

AIC < 7%
Blood glucose before a meal: 70-130
Blood glucose after a meal: <180

263
Q

S/E of hypoglycemia (3) under anesthesia

A

SNS stimulation: increased HR, BP, and diaphoresis
>difficult to detect if beta blocked!

(the brain needs glucose: confusion, seizures, coma, death)

264
Q

3 drugs that counter the hypoglycemic effect of insulin

A
  1. Epi
  2. Glucagon
  3. ACTH
265
Q

3 drugs that extend or enhance the hypoglycemic effects of insulin

A
  1. MAOis
  2. Salicylates
  3. Tetracycline
266
Q

What syndrome is associated with secretion of vasoactive substances from the enterochromaffin cells?

A

Carcinoid syndrome

> usally associated with tumors found in the GI tract but can arise outside GI tract as well

267
Q

Two categories of drugs to avoid in pts with carcinoid syndrome

A
  1. Histamine releasing drugs:
    Morphine, meperidine, atracurium, sux, thiopental
    *fasciculations from sux can also stimulate secretions from tumors

(meperidine, atracurium, thiopental)

  1. Sympathomimetics
    Ketamine, ephedrine, NE
268
Q

what drugs to tx hypotension in a patient with carcinoid syndrome?

A

Neo & Vasopressin

269
Q

Treatment for carcinoid syndrome (4)

A
  1. Somatostatin
    >Octreotide or Lanreotide
    >inhibit the release of vasoactive substance from carcinoid tumors, improving hemodynamic stability
  2. Antihistamines (H1 + H2 blocker):
    >diphenhydramine +
    >ranitidine or cimetidine
  3. Steroids
  4. 5-HT3 antagonists (Zofran)
270
Q

2 most common signs of carcinoid syndome

A

Hypotension & Flushing

bronchoconstriction, h/a, abdominal pain

271
Q

3 groups of hormones released with carcinoid syndrome

A
  1. Histamine
  2. Kinins & Killikrean
  3. Serotonin
272
Q

What two cardiac conditions are often co-exisiting in someone with carcinoid syndrome

A

Pulmonic stenoisis and TR

273
Q

5 s/s of carcionid crisis

A
  1. Tachycardia
  2. Hyper or hypotension
  3. Abdominal Pain
  4. Diarrhea
  5. Intense Flushing
274
Q

Exogenous somatostatin (2)

A

Octreotide & Lanreotide

275
Q

5 Drugs at your disposal that cause histamine release (Acronym)

A

MMAST (mast cells release histamine)

Morphine
Meperidine 
Atracurium 
Sux
Thiopental
276
Q

Normal Phosphate level

A

2.5-4.5mg/dL

277
Q

Suffix “-tropin”

A

a substance that is going to travel to another part of the body to tell it to release another hormone

278
Q

What is the cortex? What does it secrete?

A

The outer portion of the adrenal gland
>aldosterone (mineralocorticoid/salt/Glomerulosa)
>cortisol (glucocorticoid/sugar/Fasiculata)
>androgens (sex/Reticularis)

279
Q

What is the medulla?

A

The inner portion of the adrenal gland

280
Q

What is erythropoietin, where is it produced, and why?

A

It increases RBC production
>produced in the kidneys
>to maintain it’s own o2 rich blood supply

(kidneys will increase RBC production in response to hypoxia, or venous congestion)

*Endocrine (2 decks)

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