Anesthesia And Endocrine Disorders Part Ii

Front 1

what test must be done prior to radial artery catheter placement in a pt with acromegaly? Why?

Back 1

Allens test- carpal ligament enlargement may cause inadequate ulnar artery flow

Front 2

Pre-op workup of acromegalic patient reveals impairment of adrenal and/or thyroid axis. What should be implemented in perioperative period?

Back 2

stress-level glucocorticoid therapy ; thyroid replacement

Front 3

What two important peptide hormones does the posterior pituitary hormone secrete?

Back 3

ADH (Vasopressin)
Oxytocin

Front 4

What is the function of ADH?

Back 4

ADH controls water excretion and reabsorption in the kidney and is a majorregulator of serumk osmolarity

Front 5

What effect does ADH have on renal collecting ducts?

Back 5

Decreases permeability

Front 6

What stimulates the release of ADH?

Back 6

Na and plasma osmolality

Front 7

What effect does ADH have on the vasculature?

Back 7

Potent vasoconstriction

Front 8

What effect does ADH have on blood volume?

Back 8

Increases

Front 9

How does ADH affect hemostasis?

Back 9

promotes hemostasis by increasing vWF and FVIII

Front 10

Will ADH release be increased, decreased or unchanged in the perioperative period?

Back 10

Increased D/T stress, hemmorrhage, anemia, medications, hypotension

Front 11

What is diabetes insipidus? (DI)
what are the two types?

Back 11

Neurogenic DI-Inadequate ADH secretion from the posterior pituitary
Nephrogenic DI-inability of renal collecting duct tubule receptors to respond to ADH

Front 12

What are causes of DI?

Back 12

genetic,
hypercalcemia
hypokalemia
medication-induced nephrotoxicity
ETOH

Front 13

What perioperative management will be taken with DI?

Back 13

electrolyte evaluation
volume status-SLOW restoration of volume pre-op (24-48 hrs)

Front 14

What is SIADH?

Back 14

High vasopressin level despite hyponatremia and plasma hypotonicity

Front 15

What are clinical manifestations of SIADH?

Back 15

cerebral edema->lethargy, H/A, N/V, seizures coma

Front 16

How is SIADH managed?

Back 16

Mild SIADH: fluid restriction
Na<115: SLOW IV infusion of hypertonic saline (no more than 5-7mEq/hr)

Front 17

What negative sequelae may result from rapid infusion of hypertonic saline?

Back 17

Central Pontine Demyelination Syndrome-permanent neurologic damage

Front 18

What % of body Ca++ exists in the bone?

Back 18

99%

Front 19

In what three forms does serum CA++ exist, and in what percentage each?

Back 19

Plasma protein bound -40%
Nonionized (bound to anion)-10%
Ionized Ca++-50% (only part that counts!)

Front 20

What is the effect of alkalosis on Ca++?

Back 20

Alkalosis (think hyperventilation) reduces ionized Ca++ by allowing more to bind with proteins

Front 21

What three hormones work in concert to regulate the plasma concentratin of calcium?

Back 21

Vit D
Parathyroid Hormone (PTH)
Calcitonin

Front 22

What effect does decreased PTH have on CA++?

Back 22

decreases CA++

Front 23

How does a decreased PTH affect nerve function?

Back 23

decreased Ca++ -> lowered threshold potential->neuromuscular excitability->muscle spasm and tetany

Front 24

What sx will be seen in hypocalcemia?

Back 24

variable severity: cramps, perioral perissthesias, numbness in feet or toes, hyperactive deep tendon reflexes
Acute laryngeal muscle spasm->stridor

Front 25

What are two classic manifestations of latent hypocalcemia?

Back 25

Chvostek's sign-ipsilateral twitching when facial nerve is tapped at angle of jaw
Trousseau's Sign-inflation of BP cuff->aggravation of muscle yielding irritability and spasm at the wrist

Front 26

following parathyroid surgery for hyperparathyroidism, the anesthetist would be alert for ...?

Back 26

Transient (1-2 day) hypocalcemia D/T "bone hunger"
Monitor Ca++ level regularly

Front 27

What mainifestations of neuromuscular compromise secondary to hypocalcemia may be seen s/p parathyroid surgery?

Back 27

Laryngeal spasm (unilateral or bilateral)
Prolonged QT interval -> hypotension, decreased contractility

Front 28

What interventions may cause an abrupt decline in levels of ionized calcium?

Back 28

Hyperventilation
NaHCO3 administration
Blood transfusion

Front 29

What affect does hypocalcemia have on NDMR?

Back 29

Altered response-consider shorter acting NDMR

Front 30

How is the QT interval measured?

Back 30

Begins with the start of the Q wave , lasts thru the QT interval and ends with the end of the T wave, and is corrected for heart rate

Front 31

what is the primary cause of hyperparathyroidism?

Back 31

Increased PTH despite high serum Ca++ levels
90% from parathyroid adenoma

Front 32

When will sx of hyperparathyroidism be seen?

Back 32

Asymptomatic until Ca++ =11-12 mg/dL
"Stones, Bones and Groans"- stones, bone damage, pain weakness, confusion, pathologic fx

Front 33

What is a significant diagnostic feature of hyperparathyroidism?
Why does this occur?

Back 33

Elevated alkaline phosphatase (secreted by osteoblasts as they try to rebuild bone destroyed by osteoclast exagerated activity in response to PTH)
(Rich had this wrong in the notes, see N&Z pg 749)

Front 34

What are sx of hyperparathyroidism?

Back 34

1)"Stones, Bones and Groans"- stones, bone damage, pain weakness, confusion, pathologic fx

Front 35

Distinguish clinical features of hyper vs hypo poarathyroidism

Back 35

CV
HYPER=HTN, conduction disturbances, shortened QT
HYPO=hypotension, decreased contractility,prolonged QT

MUSCULOSKELETAL
HYPER=bone pain, pathologic fx, muscle weakness, &atrophy
HYPO=NM excitability

NEUROLOGIC
HYPER=somnolence, cognitive impairment, depression, hypotonia
HYPO=tetany, paresthesias, numbness in fingers/toes, seizures

GI
HYPER=anorexia, N?V, constipation, abd pain, pancreatitis , peptic ulcer
HYPO=None

RENAL
HYPER=tubular resorption defects, dim renal function, kidney stones, polyuria
HYPO=None

Front 36

What is the surgical treatment for hyperparathyroidism?

Back 36

Removal of abnormal thyroid tissue

Front 37

Is nerve monitoring required for parathyroid surgery?

Back 37

No

Front 38

What type of blood loss is anticipated with parathyroid surgery?

Back 38

minimal

Front 39

Anesthetic medication doseages and selection may be affected by impairments in which system of a pt undergoing parathyroid surgery for secondary hyperparathyroidism?

Back 39

Renal impairment-> volume overload, anemia, electrolyte derangements

Front 40

In a hyperparathyroid pt, how is severe hypercalcemia (>14mg/dL) treated perioperatively?

Back 40

isotonic salione and loop diuretics

Front 41

What CV effects does hypercalcemia have?

Back 41

HTN,arrhythmias, short QT interval

Front 42

Why might the hypercalcemic pt be dehydrated?

Back 42

N/V, anorexia

Front 43

In the hyperparathyroid pt who is hypercalcemic, what considerations are there regarding sedation and NMB?

Back 43

Avoid pre-op sedative in lethargic/confused pt. NDMR may be prolonged due to muscle wekness

Front 44

Where are the adrenal glands located?

Back 44

above the kidneys

Front 45

What are the three zones of the adrenal cortex? what hormones are secreted by each?

Back 45

Zona glomerulosa(outer)-mineralocorticoid
Zona Fascibulata (middle)-cortisol (ACTH)
Zona Reticularis (inner)-adrenal androgenic hormones
All are corticosteroids

Front 46

ACTH from the _________ gland stimulates the adrenal gland to make_________.

Back 46

Pituitary
Cortisol

Front 47

As the level of cortisol________, the amount of ___________ made by the pituitary is turned ________.

Back 47

rises
ACTH
down

Front 48

What are 4 specific actions of cortisol?

Back 48

Guconeogenesis
Stimulates protein metabolism
Oxidizes fatty acids
decreases inflammatory process

Front 49

What are the stimulants of aldosterone release?

Back 49

a)Hypokalemia
b)AngiotensinII
c) Hyponatremia
d)ACTH

Front 50

what is the primary mineralocorticoid?

Back 50

Aldosterone

Front 51

What is the major role of mineralocorticoids?

Back 51

Regulation of extracellular Na and K and total body fluid balance

Front 52

What is primary aldosteronism?

Back 52

Adrenal adenoma->increased aldosterone secretrion->renal excretion of K (hypokalemia)in wxchange for Na (hypernatremia)->HTN

Front 53

What are the anesthetic implications in management of hyperaldosteronism?

Back 53

1)Correct electrolyte, glucose imbalance
2)Hypokalemia ->prolonged NDMR
3) Hypertension controlled with K sparing diuretics (spironolactone)

Front 54

What syndrome does excess glucocorticoid cause?

Back 54

Cushings

Front 55

Cushings syndrome is an excess of ________.

Back 55

Glucocorticoid (cortisol)

Front 56

What causes Cushings syndrome?

Back 56

1)therapeutic administratin of glucocorticoids
2)endogenous:
a-pituitary tumor (Cushings disease)
b-adrenal tumor
c-hypothalamic tumor
d-ectopic hormone production

Front 57

What are clinical features of Cushings syndrome?

Back 57

Truncal obesity, HTN, glucose intolerance, striae, weakness(fat and muscle broken down), fluid retention, hypokalemic alkalosis, inhibition of immune system,increased incidence of DVT, hirsutism, trun

Front 58

What is the primary treatment for Cushings ?

Back 58

transphenoidal hypophysectomy

Front 59

What are anesthetic considerations for Cushings pt?

Back 59

Control HTN & glucose
Adm glucocorticoid steroids

Front 60

What is the pathophysiology of Pituitary Cushing's Syndrome?

Back 60

Pituitary hyperfunction(adenoma of microadenoma)->produce ACTH->adrenal cortial hyperplasia->cortisol release, acts on pituitary->suppression of normal pituitary

60-70% of Cushing's have elevated plasma cortisol and ACTH with loss of normal diurnal variation