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SRNA3AdvancedPatho2 > Adrenal Disorders > Flashcards

Adrenal Disorders Flashcards

1
Q

What are the adrenal glands?

A

Two pyramid-shaped organs located above the kidneys.

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2
Q

Adrenal glands stimulated by

A

Stimulated by ACTH. Avg. size = 3x5x10cm

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3
Q

Adrenal cortex weight

A

80% of gland’s wgt.

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4
Q

What are the 3 layers of the Adrenal Glands?

A

Three Layers:
Zona glomerulosa
Zona fasciculata
Zona reticularis

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5
Q

What does the Zona Glomerulosa regulate?

A

Mineralocorticoids

Na+, K+ Aldosterone

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6
Q

Zona Glomerulosa regulated by

A

All and K+

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7
Q

Zona Fasciculata is regulated by

A

ACTH

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8
Q

Zona Fasciculata secretes

A

Glucocorticoids , Cortisol, Cortisone, Corticosterone

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9
Q

Zona Reticularis is regulated by

A

ACT and unknown factors

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10
Q

Zona Reticularis secretes

A

DHEA

DHEA sulfate

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11
Q

DHEA

A

Precursor to testosterone

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12
Q

Aldosterone on Na+ and K+ and H+

A
  • Na+ retention

* K+ and H+ ion secretion

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13
Q

What is the primary stimulant of aldosterone synthesis and secretion?

A

Angiotensin II

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14
Q

What is renin activated by?

A
  • ↓ Na+, ↓H2O
  • ↓ blood volume
  • ↑ K+
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15
Q

Regulates Na+ and K+ balance

A

Aldosterone

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16
Q

Where does Aldosterone act on the nephron?

A

Distal tubule

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17
Q

Aldosterone regulated by

A

RAAS

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18
Q

Cortisol action

A

↑ blood glucose in response to stress (↑gluconeogenesis,

↓insulin

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19
Q

Cortisol Causes_________ and has _______, -________

A

protein breakdown

Has anti inflammatory, growth-suppressing effects

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20
Q

Cortisol on the immune system

A

↓ immune response (eosinophils, neutrophils, lymphocytes) which increases likelihood for infection and poor wound healing

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21
Q

ANDROGENS____

Converted by ___

A

DHEA
converted by peripheral tissues to stronger androgens
such as testosterone and estrogen

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22
Q

What happens to the Conversion of androgens to estrogen?

A

increased in aging (post-menopause osteoporsis)

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23
Q

Catecholamines : Name 3

A

Norepinephrine
Epinephrine
Dopamine

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24
Q

What are catecholamines secreted by?

A

Secreted by chromaffin cells of medulla

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25
Q

Catecholamines are Synthesized from

A

phenylalanine

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26
Q

Catecholamines induce this response

A

“fight-or-flight” response

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27
Q

Catecholamines and blood glucose

A

Promote Hyperglycemia

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28
Q

Adrenergic Receptor Effects

Blood Vessels: α1 & 2 =

A

vasoconstriction

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29
Q

Adrenergic Receptor Effects β2 =

A

vasodilation

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30
Q

At low doses of Epinephrine, which effects dominates

A

β

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31
Q

At high doses of Epinephrine, which effects dominates

A

α

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32
Q

β2 on bronchi =

A

Relax

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33
Q

Cholesterol

A

Leads to progesterone => Cortisol and aldosterone

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34
Q

Heart: β1&2 = action

A

↑ rate and contraction

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35
Q

Aldosterone tell kidneys to

A

Reabsorb sodium and K+ and H+ secretion

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36
Q

ADDISON DISEASE

A

(adrenal insufficiency)

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37
Q

Addison’s Most often seen in adults

A

30-60

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38
Q

Addison’s disease: when you see clinical manifestations

A

90% of gland destroyed before clinical manifestations = atrophy of adrenal gland

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39
Q

Gluconeogenesis

A

Produce glucose from non- carb sources

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40
Q

Addison disease caused by PSD

A

Due to:
Pituitary Failure(↓ACTH)
Suppression of HPA Axis
Damage to Adrenal Gland (Autoimmune)

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41
Q

Other causes of Addison (READ)

A

Other Causes:
Infections (**Tuberculosis, HIV, Fungal)
Infiltrative Ds. (Amyloidosis, Metastatic CA)
Assoc’d. w/ development of **Autoimmune Disease

42
Q

ADDISON DISEASE (adrenal insufficiency) hormone decrease

A

↓ Aldosterone, ↓ Cortisol

43
Q

Addison Disease metabolic effects

A

Hyponatremia, Hypotension, Hyperkalemia,

Hypoglycemia, Metabolic Acidosis

44
Q

Signs and symptoms of Addison Disease

WeSAV

A 
Signs & Symptoms:
 ***Weakness/Fatigability
 Eosinophilia
**** Skin Hyperpigmentation (or Vitiligo)
***** Anorexia
 N/V
 Diarrhea
 ***Vascular Collapse & Shock
45
Q

Addison’s Disease Treatment

A

Treatment: Hormone replacement

46
Q

Anesthesia Considerations for adrenal insufficiency/Addison’s –>During surgery

A

Normal expectation is a rise in cortisol and

aldosterone during anesthesia and surgery.

47
Q

Pt.s with adrenal failure/Addison’s have

A

absence of steroid response resulting in hypotension, diminished response to vasopressors and low C.O.

48
Q

Addison’s May be exacerbated by

A

hyperkalemia.

49
Q

Addison’s Pre-op mgmt.

A

w/ fluid replacement, 0.9% NS and glucocorticoid replacement

50
Q

CONN’S SYNDROME

Due to:

A

↑ Aldosterone (Hyperaldosteronism)
Due to: Adrenal Adenoma (Primary)
↑ Renin/Angiotensin Angiotensin II (Secondary)

51
Q

Conn’s pseudohyperaldosteronism:

A

licorice, chewing tobacco)

52
Q

What differentiates Primary vs Secondary Conn’s syndrome?

A

Elevated Renin levels differentiate Secondary from

Primary

53
Q

CONN’S SYNDROME

BP and K+ what happens

A

↑ Aldosterone
Hypertension, Hypokalemia (< 3.0 mEq/L)
Results in: Muscle Weakness, Cardiac Dysfunction
Hypervolemia

54
Q

CONN’s results in (acid base imbalance)

A 
Metabolic Alkalosis
(K+ moves from intracellular to extracellular space in exchange for H+ ions. Also, ↑H+ excretion at the kidneys)
55
Q

CONN’s syndrome: Edema does not occur because of:

A

ANP release –↑ Na+ excretion
Pressure natriuresis- ↑ Renal hydrostatic pressure promotes Na+ excretion
Aldosterone escape – nephron compensates by
↑Na+excretion at proximal tubule

56
Q

Conn’s Tx

A

Treatment: with aldosterone receptor antagonist

Spironolactone

57
Q

Anesthesia Considerations for Conn’s Syndrome Pre-op

A

replacement of K+ and Mg++

58
Q

Conn’s disease: What should be avoided and why?

A

Hyperventilation should be avoided as respiratory alkalosis may worsen hypokalemia and preexisting metabolic
alkalosis

59
Q

ANP is opposite

A

Aldosterone

60
Q

ANP tell kidneys

A

Get rid of sodium

Keep potassium

61
Q

Cushing: Cortisol

A

In a normal individual there is circadian release pattern of Cortisol
Cushing pts. lack circadian pattern

62
Q

Cushing syndrome is due to (2)

A

1) Due to: overproduction of ACTH from pituitary adenoma or less commonly adrenal tumor
2) High doses exogenous steroid

63
Q

Cushing Signs & Symptoms:

A 
Weight gain
Trunk Obesity, “Moon Face”,
“buffalo hump”
Muscle wasting (extremities)
Skin atrophy, Acne, Alopecia
Easy bruising
64
Q

Cushing electrolytes and other abnormalities , BG

CHOSH

A

↑ Cortisol
Hyperglycemia (insulin resistance & ↑ gluconeogensis)
Suppressed Immunity (susceptible to infx. & poor healing)
HTN (↑ Cortisol = ↑vascular sensitivity to catecholamines =
↑vasoconstriction)
Osteoporosis (pathologic fractures & renal calculi)

65
Q

Anesthesia Considerations for Cushing Syndrome

Airway

A

Increased neck size secondary to facial changes may

increase difficulty of intubation.

66
Q

Anesthesia Considerations for Cushing Syndrome

CV

A

Increased risk of Cardiovascular complications (CAD,

heart failure, stroke).

67
Q

Anesthesia Considerations for Cushing Syndrome

Patient handling

A

Careful attention to handling/positioning of pt. to avoid

risk of fracture secondary to osteoporosis.

68
Q

Attention to aseptic technique if performing an epidural

or spinal tap (immunosuppression).

A

Cushing

69
Q

For Cushing–> If adrenalectomy performed laparoscopically,

A

be aware of risk of diaphragmatic injury and possible tension pneumothorax.

70
Q

ANDROGEN IMBALANCE

A

Caused by tumors

syndrome depends on the hormone, gender and age of patient

71
Q

Androgen imbalance with high estrogen

A

causes feminization with development of female sex characteristics

72
Q

↑ Androgens causes

A

virilization with development of male sex characteristics

73
Q

Androgen imbalance Tx

A

Treatment for these conditions is surgical excision. No specific requirements for anesthesia in these patients.

74
Q

Pheochromocytoma

A

↑ Norepi/Epi screted by chromaffin cell tumors of

medulla

75
Q

Pheochromocytoma population

A

Most common in pts. 40 – 60 yrs.
Men and women affected equally
Can be sustained or paroxysmal.

76
Q

Pheochromocytoma Can be trigged by

ARBY

A

ingestion of foods containing tyrosine (ex. Aged cheese, red wine, beer, yogurt).

77
Q

“True” pheochromocytomas secreting epi/norepi arise from.

A

adrenal medulla

78
Q

“Paraganglionomas” a.k.a. ________arise from

A

extra-adrenal pheochromocytomas secreting epi/norepi arise from the sympathetic chain.

79
Q

↑ Norepi/Epi Signs/Symptoms: (5)

HHH , TPDS

A 
HTN 
Severe 
HA 
Tachycardia 
Palpitations
Diaphoresis 
Hyperglycemia
80
Q

Pheochromocytoma : triad

A

At least one of a triad of diaphoresis, headaches and

palpitations occurs in over 90% of these patients

81
Q

Why does Hyperglycemia occurs with Pheochromocytoma?

A

via catecholamine induced inhibition of insulin

82
Q

Treatment with pheochromocytama:

A

Phenoxybenzamine and/or surgical excision palpitations occurs in over 90% of these patients.

83
Q

Pheochromocytoma Crisis Presents with:

A 
Severe pounding HA
 Sweating
 Pallor
 Palpitations
 Anxiety
84
Q

Ionized contrast media can precipitate

A

crisis

85
Q

Catecholamine induced Cardiomyopathy

A

Notched P wave “P-mitrale” indication of left atrial hypertrophy left ventricular diastolic dysfunction.
Mitral valve stenosis may or may not be present.

86
Q

Catecholamine induced Cardiomyopathy

•CXR with

A

cardiac failure and pulmonary edema. This patient had ejection fraction of 24%.

87
Q

Catecholamines and their oxidation products have

A

direct toxic effect on the myocardium.

88
Q

•Cerebral ischemia and stroke may also occur with

A

cardiomyopathy.

89
Q

Anesthesia Considerations in Pheochromocytoma
These tumors are very
Control HTN crisis with alpha blockers essential.

A

vascular, excision = significant blood loss.

90
Q

Assessment of volume status difficult.

As a guide, a difference in

A

Systolic pressure between peak inspiration and expiration >10mmHg suggests inadequate volume regardless of actual arterial pressure.

91
Q

Phenoxybenzamine action

A

non-selective α-blocker forms irreversible bond with

α-receptor.

92
Q

Cannot be overcome during catecholamine surge.

A

Favored for pre-op hemodynamic control.

High doses can result in post-op hypotension.

93
Q

Anesthesia Considerations in Pheochromocytoma (CHAD)

A

Catecholamine-sensitizing anesthetics
Histamine-releasing agents
Anticholinergics
Droperinol

94
Q

Anticholinergics to avoid in pheochromocytoma

A

Atropine

Pancuronium

95
Q

Histamine-releasing agents

A 
Morphine
Fentanyl &amp; Sufentanil on to use 
Succinylcholine
Atracurium
Mivacurium, cisatracurium
96
Q

How does droperidol act in pheochromocytoma

A

Inhibits catecholamine reuptake

97
Q

Catecholamine-sensitizing anesthetics

A

Desflurane

Halothane – rarely used now

98
Q

Careful patient positioning essential -

A

Metastatic lesions have predilection for bone, particularly vertebral bodies and long bones – pathologic fractures common late in course of illness.

99
Q

Pathway of steroid synthesisa

A

Cholesterol -> Pregnenalone –> Progesterone –>Aldosterone (CPREPROGA)
PREG->DEHYDROEPIAN(DHEA) –>Testosterone –>Estradiol

100
Q

Endemic goiter caused by this deficiency

A

Iodine

SRNA3AdvancedPatho2 (15 decks)

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