Adrenal Disorders Flashcards
(100 cards)
1
Q
What are the adrenal glands?
A
Two pyramid-shaped organs located above the kidneys.
2
Q
Adrenal glands stimulated by
A
Stimulated by ACTH. Avg. size = 3x5x10cm
3
Q
Adrenal cortex weight
A
80% of gland’s wgt.
4
Q
What are the 3 layers of the Adrenal Glands?
A
Three Layers:
Zona glomerulosa
Zona fasciculata
Zona reticularis
5
Q
What does the Zona Glomerulosa regulate?
A
Mineralocorticoids
Na+, K+ Aldosterone
6
Q
Zona Glomerulosa regulated by
A
All and K+
7
Q
Zona Fasciculata is regulated by
A
ACTH
8
Q
Zona Fasciculata secretes
A
Glucocorticoids , Cortisol, Cortisone, Corticosterone
9
Q
Zona Reticularis is regulated by
A
ACT and unknown factors
10
Q
Zona Reticularis secretes
A
DHEA
DHEA sulfate
11
Q
DHEA
A
Precursor to testosterone
12
Q
Aldosterone on Na+ and K+ and H+
A
- Na+ retention
* K+ and H+ ion secretion
13
Q
What is the primary stimulant of aldosterone synthesis and secretion?
A
Angiotensin II
14
Q
What is renin activated by?
A
- ↓ Na+, ↓H2O
- ↓ blood volume
- ↑ K+
15
Q
Regulates Na+ and K+ balance
A
Aldosterone
16
Q
Where does Aldosterone act on the nephron?
A
Distal tubule
17
Q
Aldosterone regulated by
A
RAAS
18
Q
Cortisol action
A
↑ blood glucose in response to stress (↑gluconeogenesis,
↓insulin
19
Q
Cortisol Causes_________ and has _______, -________
A
protein breakdown
Has anti inflammatory, growth-suppressing effects
20
Q
Cortisol on the immune system
A
↓ immune response (eosinophils, neutrophils, lymphocytes) which increases likelihood for infection and poor wound healing
21
Q
ANDROGENS____
Converted by ___
A
DHEA
converted by peripheral tissues to stronger androgens
such as testosterone and estrogen
22
Q
What happens to the Conversion of androgens to estrogen?
A
increased in aging (post-menopause osteoporsis)
23
Q
Catecholamines : Name 3
A
Norepinephrine
Epinephrine
Dopamine
24
Q
What are catecholamines secreted by?
A
Secreted by chromaffin cells of medulla
25
Catecholamines are Synthesized from
phenylalanine
26
Catecholamines induce this response
“fight-or-flight” response
27
Catecholamines and blood glucose
Promote Hyperglycemia
28
Adrenergic Receptor Effects
| Blood Vessels: α1 & 2 =
vasoconstriction
29
Adrenergic Receptor Effects β2 =
vasodilation
30
At low doses of Epinephrine, which effects dominates
β
31
At high doses of Epinephrine, which effects dominates
α
32
β2 on bronchi =
Relax
33
Cholesterol
Leads to progesterone => Cortisol and aldosterone
34
Heart: β1&2 = action
↑ rate and contraction
35
Aldosterone tell kidneys to
Reabsorb sodium and K+ and H+ secretion
36
ADDISON DISEASE
(adrenal insufficiency)
37
Addison's Most often seen in adults
30-60
38
Addison's disease: when you see clinical manifestations
90% of gland destroyed before clinical manifestations = atrophy of adrenal gland
39
Gluconeogenesis
Produce glucose from non- carb sources
40
Addison disease caused by PSD
Due to:
Pituitary Failure(↓ACTH)
Suppression of HPA Axis
Damage to Adrenal Gland (Autoimmune)
41
Other causes of Addison (READ)
Other Causes:
Infections (***Tuberculosis, HIV, Fungal)
Infiltrative Ds. (Amyloidosis, Metastatic CA)
Assoc’d. w/ development of ***Autoimmune Disease
42
ADDISON DISEASE (adrenal insufficiency) hormone decrease
↓ Aldosterone, ↓ Cortisol
43
Addison Disease metabolic effects
Hyponatremia, Hypotension, Hyperkalemia,
| Hypoglycemia, Metabolic Acidosis
44
Signs and symptoms of Addison Disease
| WeSAV
```
Signs & Symptoms:
***Weakness/Fatigability
Eosinophilia
**** Skin Hyperpigmentation (or Vitiligo)
***** Anorexia
N/V
Diarrhea
***Vascular Collapse & Shock
```
45
Addison's Disease Treatment
Treatment: Hormone replacement
46
Anesthesia Considerations for adrenal insufficiency/Addison’s -->During surgery
Normal expectation is a rise in cortisol and
| aldosterone during anesthesia and surgery.
47
Pt.s with adrenal failure/Addison’s have
absence of steroid response resulting in hypotension, diminished response to vasopressors and low C.O.
48
Addison's May be exacerbated by
hyperkalemia.
49
Addison's Pre-op mgmt.
w/ fluid replacement, 0.9% NS and glucocorticoid replacement
50
CONN’S SYNDROME
| Due to:
↑ Aldosterone (Hyperaldosteronism)
Due to: Adrenal Adenoma (Primary)
↑ Renin/Angiotensin Angiotensin II (Secondary)
51
Conn's pseudohyperaldosteronism:
licorice, chewing tobacco)
52
What differentiates Primary vs Secondary Conn's syndrome?
Elevated Renin levels differentiate Secondary from
| Primary
53
CONN’S SYNDROME
| BP and K+ what happens
↑ Aldosterone
Hypertension, Hypokalemia (< 3.0 mEq/L)
Results in: Muscle Weakness, Cardiac Dysfunction
Hypervolemia
54
CONN's results in (acid base imbalance)
```
Metabolic Alkalosis
(K+ moves from intracellular to extracellular space in exchange for H+ ions. Also, ↑H+ excretion at the kidneys)
```
55
CONN's syndrome: Edema does not occur because of:
ANP release –↑ Na+ excretion
Pressure natriuresis- ↑ Renal hydrostatic pressure promotes Na+ excretion
Aldosterone escape – nephron compensates by
↑Na+excretion at proximal tubule
56
Conn's Tx
Treatment: with aldosterone receptor antagonist
| Spironolactone
57
Anesthesia Considerations for Conn’s Syndrome Pre-op
replacement of K+ and Mg++
58
Conn's disease: What should be avoided and why?
Hyperventilation should be avoided as respiratory alkalosis may worsen hypokalemia and preexisting metabolic
alkalosis
59
ANP is opposite
Aldosterone
60
ANP tell kidneys
Get rid of sodium
| Keep potassium
61
Cushing: Cortisol
In a normal individual there is circadian release pattern of Cortisol
Cushing pts. lack circadian pattern
62
Cushing syndrome is due to (2)
1) Due to: overproduction of ACTH from pituitary adenoma or less commonly adrenal tumor
2) High doses exogenous steroid
63
Cushing Signs & Symptoms:
```
Weight gain
Trunk Obesity, “Moon Face”,
“buffalo hump”
Muscle wasting (extremities)
Skin atrophy, Acne, Alopecia
Easy bruising
```
64
Cushing electrolytes and other abnormalities , BG
| CHOSH
↑ 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
Anesthesia Considerations for Cushing Syndrome
| Airway
Increased neck size secondary to facial changes may
| increase difficulty of intubation.
66
Anesthesia Considerations for Cushing Syndrome
| CV
Increased risk of Cardiovascular complications (CAD,
| heart failure, stroke).
67
Anesthesia Considerations for Cushing Syndrome
| Patient handling
Careful attention to handling/positioning of pt. to avoid
| risk of fracture secondary to osteoporosis.
68
Attention to aseptic technique if performing an epidural
| or spinal tap (immunosuppression).
Cushing
69
For Cushing--> If adrenalectomy performed laparoscopically,
be aware of risk of diaphragmatic injury and possible tension pneumothorax.
70
ANDROGEN IMBALANCE
Caused by tumors
| syndrome depends on the hormone, gender and age of patient
71
Androgen imbalance with high estrogen
causes feminization with development of female sex characteristics
72
↑ Androgens causes
virilization with development of male sex characteristics
73
Androgen imbalance Tx
Treatment for these conditions is surgical excision. No specific requirements for anesthesia in these patients.
74
Pheochromocytoma
↑ Norepi/Epi screted by chromaffin cell tumors of
| medulla
75
Pheochromocytoma population
Most common in pts. 40 – 60 yrs.
Men and women affected equally
Can be sustained or paroxysmal.
76
Pheochromocytoma Can be trigged by
| ARBY
ingestion of foods containing tyrosine (ex. Aged cheese, red wine, beer, yogurt).
77
“True” pheochromocytomas secreting epi/norepi arise from.
adrenal medulla
78
“Paraganglionomas” a.k.a. ________arise from
extra-adrenal pheochromocytomas secreting epi/norepi arise from the sympathetic chain.
79
↑ Norepi/Epi Signs/Symptoms: (5)
HHH , TPDS
```
HTN
Severe
HA
Tachycardia
Palpitations
Diaphoresis
Hyperglycemia
```
80
Pheochromocytoma : triad
At least one of a triad of diaphoresis, headaches and
| palpitations occurs in over 90% of these patients
81
Why does Hyperglycemia occurs with Pheochromocytoma?
via catecholamine induced inhibition of insulin
82
Treatment with pheochromocytama:
Phenoxybenzamine and/or surgical excision palpitations occurs in over 90% of these patients.
83
Pheochromocytoma Crisis Presents with:
```
Severe pounding HA
Sweating
Pallor
Palpitations
Anxiety
```
84
Ionized contrast media can precipitate
crisis
85
Catecholamine induced Cardiomyopathy
Notched P wave “P-mitrale” indication of left atrial hypertrophy left ventricular diastolic dysfunction.
Mitral valve stenosis may or may not be present.
86
Catecholamine induced Cardiomyopathy
| •CXR with
cardiac failure and pulmonary edema. This patient had ejection fraction of 24%.
87
Catecholamines and their oxidation products have
direct toxic effect on the myocardium.
88
•Cerebral ischemia and stroke may also occur with
cardiomyopathy.
89
Anesthesia Considerations in Pheochromocytoma
These tumors are very
Control HTN crisis with alpha blockers essential.
vascular, excision = significant blood loss.
90
Assessment of volume status difficult.
| As a guide, a difference in
Systolic pressure between peak inspiration and expiration >10mmHg suggests inadequate volume regardless of actual arterial pressure.
91
Phenoxybenzamine action
non-selective α-blocker forms irreversible bond with
| α-receptor.
92
Cannot be overcome during catecholamine surge.
Favored for pre-op hemodynamic control.
| High doses can result in post-op hypotension.
93
Anesthesia Considerations in Pheochromocytoma (CHAD)
Catecholamine-sensitizing anesthetics
Histamine-releasing agents
Anticholinergics
Droperinol
94
Anticholinergics to avoid in pheochromocytoma
Atropine
| Pancuronium
95
Histamine-releasing agents
```
Morphine
Fentanyl & Sufentanil on to use
Succinylcholine
Atracurium
Mivacurium, cisatracurium
```
96
How does droperidol act in pheochromocytoma
Inhibits catecholamine reuptake
97
Catecholamine-sensitizing anesthetics
Desflurane
| Halothane – rarely used now
98
Careful patient positioning essential -
Metastatic lesions have predilection for bone, particularly vertebral bodies and long bones – pathologic fractures common late in course of illness.
99
Pathway of steroid synthesisa
Cholesterol -> Pregnenalone --> Progesterone -->Aldosterone (CPREPROGA)
PREG->DEHYDROEPIAN(DHEA) -->Testosterone -->Estradiol
100
Endemic goiter caused by this deficiency
Iodine
