ANESTHESIA FOR ENDOCRINE DISEASE Flashcards
1
Q
what are the 4 endocrine glands?
A
- thyroid
- parathyroids
- adrenal gland
- pancreas
2
Q
what hormones does the posterior pituitary secrete?
A
- vasopressin (ADH)
* oxytocin
3
Q
what hormones does the anterior pituitary secrete?
A
(HA – FLAT PG)
- FSH – follicle-stimulating hormone
- LH – luteinizing hormone
- ACTH – adrenocorticotrophic hormone
- TSH – thyroid stimulating hormon
- Prolactin
- GH – growth hormone
4
Q
the anterior pituitary produces hormones and releases them into the circulation under control of what?
A
hypothalamus
5
Q
where are the hormones secreted by the posterior pituitary produced?
A
hypothalamus
* secretion is dependent upon neural stimulation
6
Q
what part of the body does prolactin stimulate? what is the response to stimulation?
A
prolactin –> milk producing cells in breast –> lactation
7
Q
what part of the body does ACTH stimulate? what is the response to stimulation?
A
ACTH –> adrenal cortex –> release adrenaline
8
Q
what part of the body does GH stimulate? what is the response to stimulation?
A
GH –> body cells –> growth
9
Q
what part of the body does TSH stimulate? what is the response to stimulation?
A
TSH –> thyroid –> thyroxin –> stimulation of growth and metabolism
10
Q
what part of the body does FSH/LH stimulate? what is the response to stimulation?
A
- FSH/LH –> testes –> androgen, sperm production
* FSH/LH –> ovaries –> egg production
11
Q
what part of the body does vasopressin (ADH) stimulate? what is the response to stimulation?
A
ADH –> kidney –> regulation of water retention
12
Q
what part of the body does oxytocin stimulate? what is the response to stimulation?
A
oxytocin –> uterus –> labour contractions
13
Q
what are the two hormones produced by the thyroid?
A
- triiodothyronine (T3)
* thyroxine (T4)
14
Q
where else is T3 produced and how?
A
T3 is also formed in the peripheral tissues by deiodination of T4
15
Q
how are T3 and T4 formed?
A
- dependent on dietary iodine
* dietary iodine absorbed by GI tract, converted to iodide, actively transported to thyroid for T3/T4 formation
16
Q
which thyroid hormone is released in greater quantity and which is more potent?
A
- glandular release T4 > T3 (10:1)
* T3 is more potent and less protein bound
17
Q
graves disease is an autoimmune disease causing what?
A
hyperthyroidism
18
Q
describe the pathophysiology of hyperthyroidism
A
- hyper function of the thyroid gland w/ excessive secretion of T3, T4 or both
19
Q
what is the mechanism of action of thyroid hormones?
A
- T3 and T4 act on adenylate cyclase to affect speed of reactions, body oxygen use, and energy output (heat production)
- increased levels will increase metabolism resulting in increased animate ventilation, HR and contractility
20
Q
what are the common causes of hyperthyroidism?
A
- graves disease (most common – women 20-40yo)
- TSH-secreting pituitary tumors
- iatrogenic
- thyroiditis
21
Q
describe the symptoms of hyperthyroidism
A
hypermetabolic state
- weight loss despite increased caloric intake
- muscle weakness
- heat intolerance
- fatigue
- arrhythmias – a-fib, SVTs
- anxiety
- exopthalmos (graves)
22
Q
describe graves disease
A
- autoimmune disease
* thyroid stimulating antibodies bind to TSH receptors on thyroid
23
Q
what are the pharmacologic treatment options for hyperthyroidism?
A
- antithyroids – propylthiouracil, methimazole, carbimazole to prevent conversion of T4 to T3
- beta antagonists –propranolol, atenolol, nadolol to treat tachycardia
- radioiodine – destroys thyroid cell function
24
Q
what are the surgical treatment options for hyperthyroidism?
A
total, subtotal, or lobar thyroidectomy
* subtotal for pts with large multi nodular goiters or solitary toxic adenomas, ineffective antithyroid drugs
25
how is graves disease currently treated?
thyroid drugs or radioiodine
26
what are the preoperative concerns with hyperthyroidism?
* optimize pt to euthyroid – HR
27
what are maintenance concerns for hyperthyroidism?
* esmolol (50-300mcg/kg/min)
* avoid SNS stimulants – ketamine, pancuronium, atropine, meperidine
* hypovolemia – exaggerated hypotensive response upon induction
* hyperthyroidism does not increase anesthetic requirements
28
what are the post-operative concerns for hyperthyroidism?
* unilateral RLN injury – hoarseness
* bilateral RLN injury – aphonia, stridor, AW obstruction w/ inspiration (reintubation)
* AW obstruction due to tracheomalacia/hematoma
* hypocalcemia due to hypoparathyroidism (accidental removal of parathyroid) 24-72hr post-op
29
describe thyrotoxic crisis (thyroid storm)
* life-threatening exacerbation of hyperthyroidism that may be caused by trauma, infection, surgery of medical illness
* abrupt tachycardia, hyperthermia, agitation, skeletal muscle weakness, congestive heart failure, dehydration, shock – due to abrupt release of T3/T4 into circulation
* 6-18hr post-op
30
what does thyroid storm mimic?
malignant hyperthermia (look at CO2 for differential)
31
how is thyroid storm treated?
* IV cooled crystalloids
* continuous infusion of esmolol
* dexamethasone or cortisol to decrease hormone release/conversionof T4 to T3
* propylthiouracil PO to inhibit T4 –> T3 conversion
32
describe primary hypothyroidism
* dysfunction/destruction of thyroid tissue
* high TSH, low T3/T4
* hashimoto's thyroiditis (autoimmune)
33
describe secondary hypothyroidism
* hypothalamic-pituitary (CNS) dysfunction
* normal or low TSH, low T3/T4
* (iatrogenic) thyroidectomy, antithyroid meds
34
describe myxedema coma
* rare, extreme case of hypothyroidism
* more common in elderly women with long history of hypothyroidism
* characterized by loss of deep tendon reflexes, severe hypothermia, hypoventilation, hyponatremia, hypoxia, hypotension, delirium
35
what is the treatment for myxedema coma?
* T3/T4 given
* ECG monitored for MI or arrhythmias
* steroid replacement in case of coexisting adrenal gland suppression
36
what is the treatment for hypothyroidism?
* L-thyroxine (PO T4; synthyroid) – physiologic effect several days; clinical improvement several weeks
* IV T3 – effect seen within 6hr
37
what are the symptoms of hypothyroidism?
* lethargy
* weight gain
* cold intolerance
* hypoactive reflexes
38
preop concerns for hypothyroidism
* minimal premed – sensitive to drugs and prone to resp depression
* decreased gastric emptying times
* synthyroid
* warming
39
intraoperative concerns for hypothyroidism
* hypotension
* increased sensitivity to agents – decreased CO = faster onset
* blunted baroreceptors
* regional anesthesia if surgery permits – if GA, use ketamine
40
postoperative concerns for hypothyroidism
* resedation
* hypothermia
* hypoglycemic, hyponatremic, anemia
* hypoventilation – impaired pulmonary function due to decreased surfactant production
41
parathyroid hormone (PTH) increases serum levels of what?
calcium – increased bone reabsorption, decreased renal excretion of calcium
42
parathyroid hormone (PTH) decreases serum levels of what?
phosphate – increased renal excretion
43
describe primary hyperparathyroidism
* increased PTH due to increased gland size
* adenoma, carcinoma, hyperplasia of parathyroid glands
* stimulate increased calcium circulation
44
describe secondary hyperparathyroidism
* compensatory increase in PTH secretion due to hypocalcemia (renal disease or GI malabsorption)
* seldom see elevated calcium
45
symptoms of hyperparathyroidism
(usually due to hypercalcemia – may be asymptomatic)
* renal stones
* hypertension
* constipation
* fatigue
46
medical treatment for hyperparathyroidism
* saline
| * loop diuretics
47
surgical treatment for hyperparathyroidism
* (primary) parathyroidectomy for symptomatic hypercalcemia
| * (secondary) treat underlying condition – VitD deficiency [rickets], chronic renal failure after renal transplant
48
perioperative considerations for hyperparathyroidism
* hydration/maintenance of UOP
* possible hypotension on induction
* monitor NMB carefully – hypercalcemia can either decrease or increase NMB requirements
49
describe hypoparathyroidism
* decreased PTH or resistance to PTH
* hypocalcemia
* * almost always iatrogenic
50
describe psuedohypoparathyroidism
* congenital
| * normal PTH, but kidneys don't respond
51
symptoms of hypoparathyroidism
result from hypocalcemia – muscle/abdominal cramps, neuromuscular irritability
52
symptoms of acute (postoperative) hypoparathyroidism
* perioral paresthesia
* restlessness
* neuromuscular irritability
* positive chvostek sign – facial muscle twitching with tapping angle of mandible
* positive trousseau sign – carpopedal spasm after 3min tourniquet ischemia
53
symptoms of chronic hypoparathyroidism
* ECG changes – long T-wave interval
* lethargy
* cataracts
54
treatment for hypoparathyroidism
* calcium infusion
| * PO calcium + vitD
55
perioperative concerns for hypoparathyroidism
(common after thyroidectomy)
* optimize Ca levels
* avoid alkalosis/hyperventilation
* monitor pH
* be aware of citrate in PRBCs
* hypotension w/ GA may be exaggerated
56
the thymus is a specialized gland of what system?
immune system
57
describe the function of the thymus
differentiates developing lymphocytes into mature T-cells, which are critical cells of the adaptive immune system
58
pathophysiology of digeorge syndrome (congenital thymic hypoplasia)
* hypoplasia/aplasia of parathyroid and thymus
* causes hypocalcemia and increased incidence of infections (b/c of defects in cell-mediated immunity)
* often also have congenital cardiac defects (right aortic arch, tetrology of fallot, persistent truncus arteriosus)
59
perioperative considerations for digeorge syndrome (congenital thymic hypoplasia)
* micrognathia may make DL difficult
* hyperventilation intraop could exacerbate hypocalcemia
* unpredictable NMB
60
cushing's disease is an excess of which hormone?
cortisol
61
describe stimulation of cortisol release
* ant pit secretes corticotropin (ACTH) in response to CRH from hypothalamus
* ACTH stimulates adrenal cortex to release cortisol
62
three substances secreted from the adrenal cortex?
* glucocorticoids (cortisol) (anti-insulin)
* minerocorticoids (aldosterone
* androgens
63
describe the function of glucocorticoids (cortisol)
* gluconeogenesis
* inhibition of peripheral glucose utilization (anti-insulin – hyperglycemia occurs with high circulating volume
* anti-inflammatory effects (shared also by other glucocorticoids like cortisone, prednisone, methylprednisone, dexamethasone)
64
describe the function of aldosterone
* RAAS regulated fluid and electrolyte balance
* increased Na reabsorption in distal tubules in exchange for K+ and H+
* net effect: increased extracellular fluid volume, decreased plasma K+, metabolic alkalosis
65
what is the only important disease associated with adrenal medulla?
pheochromocytoma
66
substances secreted by adrenal medulla
catecholamines
* norepinephrine
* epinephrine
* dopamine
67
three structures/responses to angiotensin II
* brain – thirst
* blood vessels – vasoconstriction
* adrenal cortex – aldosterone
68
describe cushing's syndrome
excessive cortisol (glucocorticoid)
* abnormal adrenocortical tissue
* microadenoma – ACTH-secreting pituitary adenoma = hyper secretion of cortisol and androgens
* small-cell lung carcinoma
69
symptoms of cushing's syndrome
* systemic HTN
* muscle wasting/skeletal muscle weakness
* osteoporosis (reduced bone formation)
* central obesity
* poor wound healing
* susceptibility to infections
* glucose intolerance – insulin resistance
* gonadal dysfunction
* 'moon face'
70
treatment for cushing's syndrome
* transsphenoidal resection can remove microadenoma (pituitary ACTH-secreting tumor)
* radiotherapy
71
preoperative considerations for cushing's syndrome
* consideration of BP, electrolyte balance, blood sugar
* tend to ve volume overloaded, HTN, hypokalemic
* preop muscle weakness may indicate sensitivity to NMBs
72
intraop considerations for cushing's syndrome
* choice of drugs probably won't change
| * careful positioning (osteoporosis, obesity)
73
postop considerations for cushing's syndrome
* panhypopituitarism due to disruption of hypothalamic-pituitary axis
* poor wound healing
* infection
* steroids (glucocorticoids) may be given
74
if conn syndrome involves over secretion of aldosterone, pt would be expected to have what?
hypokalemic metabolic alkalosis (increased Na reabsorption in exchange for increased K+/H+ elimination)
75
describe primary hyperaldosteronism (conn syndrome)
* excessive secretion of aldosterone, usually by tumor (independent of physiologic stimulus)
* bilateral hyperplasia or carcinoma of adrenal gland
* sometimes associated with pheochromocytoma or acromegaly
76
aldosteromas occur more often in
women
77
symptoms of hyperaldosteronism/conn syndrome
often asymptomatic; symptoms often nonspecific:
* headache (due to HTN)
* muscle cramp (due to hypokalemia)
* metabolic alkalosis
* hypokalemia
78
treatment for hyperaldosteronism/conn syndrome
* supplemental potassium
* competitive aldosterone antagonist (spironolactone – K+ sparing diuretic with antihypertensive properties)
* anti-HTN drugs
* excision of aldosterone secreting tumor
79
perioperative considerations for hyperaldosteronism/conn syndrome
* correction of hypokalemia
* treatment of systemic HTN
* careful not to hyperventilate – decreases K+ more
80
pathophysiology of primary adrenocorticoid insufficiency (addison's disease)
* autoimmune
* decreased release of glucocorticoids and minerocorticoids
* absence of cortisol and aldosterone
81
pathophysiology of secondary adrenocorticoid insufficiency
* decreased ACTH from pituitary
* cortisol deficiency with normal aldosterone
* can be iatrogenic from use of synthetic steroids
82
symptoms of adrenocorticoid deficiency
absence of cortisol
* weakness/fatigue
* hypoglycemia
* hypotension
* weight loss
absence of aldosterone
* hyponatremia
* hypovolemia
* hyperkalemia
* metabolic alkalosis
83
describe addisonian crisis
* steroid dependent pt under stress
* can be triggered when steroid doses are not increased during periods of stress (trauma, infection, surgery)
* severe hypotension leading to coma
84
treatment for adrenocorticoid deficiency
* replace minero-/gluco-corticoids with hydrocortisone (100mg q6hr)
* fludrocortisone when withdrawing steroids
85
perioperative considerations for adrenocorticoid deficiency
* keep stress free
* be aware of steroid withdrawal (redose steroids)
* AVOID ETOMIDATE (may decrease synthesis/release of cortisol by adrenal cortex)
* prone to infections
* replace Na/H2O deficits
86
if adrenocorticoid deficient pt (periop) hypotensive and can revive with fluids and vasopressors, what should be considered?
pt might have addison's disease – need steroids (addisonian crisis)
87
pathophysiology of hypoaldosteronism
* congenital deficiency of aldosterone synthase
* hyporeninemia due to deficient juxtaglomerular apparatus
* unilateral adrenalectomy
88
symptoms of hypoaldosteronism
* hyperkalemia without renal insufficiency (may result in heart block, orthostatic hypotension)
* hyperchloremic
* metabolic acidosis
89
treatment for hypoaldosteronism
fludrocortisone
90
pathophysiology pheochromocytoma
* catecholamine-secreting tumor of adrenal medula (right gland > left)
* NE:Epi = 85:15
* avg-size adult pheochromocytoma contains 100-800mg NE
91
symptoms of pheochromocytoma
* sudden onset malignant hypertension – tachycardia
* cardiac dysrhythmias
* headache
* perspiration
* * can mimic MH
* * triggered by compression of tumor, increased abdominal pressure (coughing, straining)
92
treatment for pheochromocytoma
* excision of tumor
| * management of BP with alpha-antagonists (phenoxybenzamine 10mg POq12hr), beta blockers (propranolol preop)
93
periop considerations pheochromocytoma
* hemodynamic instability – HTN crisis before removal, hypotensive after removal
* HTN can result in sudden blindness, CVA
* premed to reduce periop anxiety
* A-line
* may be volume depleted (ARBs)
94
acromegaly is associated with an oversecretion of which hormone?
growth hormone
95
pathophysiology of acromegaly
excessive GH secretion, usually due to adenoma in pituitary gland
96
symptoms of acromegaly
* skeletal, connective and soft tissue overgrowth
* headache
* papilledema (increased ICP from expansion of ant pit adenoma)
* visual disturbances
* excessive soft tissue in airway
* overgrowth of cartilage (in airway can cause hoarseness and abnormal movement/paralysis of vocal cords due to RLN stretching)
* peripheral neuropathy
* glucose intolerance
97
treatment for acromegaly
surgical
* transsphenoidal resection of pituitary adenoma (best)
* radiation
medical
* suppressant drugs (bromocriptine)
98
periop considerations with acromegaly
* caution with AW – difficulty masking, enlarged tongue/epiglottis make obstruction more likely, narrowed glottic opening – difficult DL
* hx of dyspnea or stridor = smaller OETT due to increased incidence of subglottic stenosis
* awake FFOB intubation may be necessary
* allen's test if placing A-line (1/2 pts have inadequate ulnar artery flow)
* unpredictable NMB w/ skeletal muscle weakness
99
pathophysiology of diabetes insipidus
deficiency or resistance to vasopressin – poor absorption of water from kidney
100
symptoms of diabetes insipidus
* extreme thirst (polydipsia)
| * excretion of large amounts of dilute urine (2-20L/d)
101
causes of diabetes insipidus
* neurogenic – lack of vasopressin secretion (idiopathic, familial, tumors)
* nephrogenic – decreased response to vasopressin (kidney damage, protein starvation, acute tubular necrosis)
102
treatment for diabetes insipidus
* neurogenic – desmopressin (synthetic vasopressin)
| * nephrogenic – keep Na low (diuretics) since vasopressin levels are normal
103
periop considerations for diabetes insipidus
watch for electrolyte imbalances
* high Na
* low K
* low Mg
104
pathophysiology of diabetes mellitus
chronic disease caused by abnormal glucose metabolism that results in predictable long-term morbidity
105
describe normal glucose physiology
* balance between glucose utilization and endogenous production or dietary delivery
* liver is primary source of endogenous glucose
* insulin release promotes glucose utilization
106
long-term morbidities from DM
* peripheral vascular disease
* ischemic heart disease
* renal disease
* blindness
* peripheral neuropathy
107
what is normal hemoglobin A1C?
6%
108
describe anatomy of pancreas
islets of langerhans
* beta cells – 75% of islets and form core – secrete insulin (~50u/d) when blood glucose is high
* alpha cells – 20%; surround beta cells – secrete glucagon when blood glucose is low (glucagon –> liver increases glycogen breakdown, increases gluconeogenesis)
109
describe innervation of pancreas
* sympathetic – T5-T10 (insulin inhibition, glucagon stimulation)
* parasympathetic – vagus (insulin release)
110
other hormones that stimulate insulin secretion
GH, cortisol, progesterone, estrogen
| * prolonged secretion may exhaust beta cells and cause DM
111
describe insulin function
triggers glucose transport into cells, usage of glucose by cells
* stimulates protein synthesis and limits protein lysis
* stimulates lipid synthesis and limit lypolysis
* brain cells are permeable to glucose – don't need insulin for uptake
112
pathophysiology of DM
* decreased secretion of insulin from beta cells
* increased resistance of receptors to circulating insulin
* * hereditary
113
how does obesity relate to DM
* chronic high levels of glucose cause increased insulin secretion & downregulation of receptors
* beta cells become less responsive to high levels of glucose
114
effects of lack of insulin
* decreased utilization of glucose by cells
* use fat as energy source = increased lipase activity = increased cholesterol = increased incidence of atherosclerosis
* depletion of tissue proteins = muscle wasting
115
define type I DM
* idiopathic or immune related destruction of beta cells by autoimmune mechanism (5-10% of all cases)
* require insulin – no insulin production
* more inclined to hypoglycemia
* rapid progression to complications
* ketones in urine, DKA
* unexplained weight loss in children
116
define type II DM
* insulin resistance
* plasma insulin normal or high, but inappropriate for blood sugar
* high serum glucose, hyperosmolar state
* managed with diet
117
define gestational DM
* glucose intolerance that first develops during pregnancy like NIDDM
* maternal hyperglycemia predisposes fetus to defects and stillbirth
* glucose intolerance resolves post-partum, but 50% develop NIDDM within 10yr
118
symptoms of DM
* classic triad – polyurea, polydipsia, polyphagia
* weight loss – muscle/fat breakdown for energy
* asthenia – no strength/energy
* sweet breath from acetone/ketone breakdown
* genital pruritis
* vision impairment from osmotic changes to lens
119
complications of DM
* vascular disease – both peripheral and cerebral
* neuropathy – peripheral and autonomic
* cellular dehydration due to increased osmotic pressure on ECF
* glucose in urine – osmotic diuresis
120
heart end-organ pathology of DM
* CHF
* CAD
* get an EKG
* silent MI
* 20x greater risk of MI periop
121
vascular end-organ pathology of DM
circulation damage cause by hyperglycemia
* HTN – accelerates changes, esp in coronaries
* atherosclerosis
122
first sign of DM-related autonomic neuropathy
postural hypotension
123
describe stiff joint syndrome as DM-related end-organ pathology
* result of chronic hyperglycemia = glycosylation (stiffening) of tissue proteins
* C1, C2 vertebrae stiffining of cartilaginous discs
* TMJ stiffening = decreased mouth opening
* "prayer sign" – inability to approximate palms = stiffness of digital joints
124
cause of diabetic ketoacidosis (DKA)
* decrease insulin activity –> metabolism of free fatty acids –> accumulation of organic acid byproducts
125
what type DM does DKA occur in?
primarily type I (IDDM) when exogenous insulin source is interrupted
* NIDDM are ketosis-resistant – circulating insulin sufficient enough to prevent ketogenesis
126
clinical signs of DKA
* infection is often the first manifestation of IDDM in adolescents
* tachypnea/kussmal
* dehydration
* altered sensorium
* ketones in urine
127
treatment for DKA
* correct hypovolemia with NS
* correct hyperglycemia with insulin
* correct electrolyte deficiencies
128
describe hyperosmolar nonketotic coma (HONK)
* hyperglycemic diuresis resulting in dehydration and hyperosmolality
129
symptoms of hyperosmolar nonketotic coma
* high BG (>600mg/dl)
* no acidosis, no ketones
* ketoacidosis not a feature due to enough insulin available to prevent ketone body formation
* thirst
* lethargy and confusion
130
treatment of HONK coma
* hypotonic saline to correct hypovolemia and hyperosmolarity
* low-dose insulin infusion to lower BS to
131
describe hypoglycemia
decreased glucose resulting from excessive insulin relative to carbohydrate intake
* commonly in IDDM
* counter regulatory mechanisms fail in brittle diabetics due to autonomic neuropathy
132
what organ is at greatest risk with hypoglycemia?
brain – can only utilize blood glucose as its energy source
133
symptoms of hypoglycemia
* SNS/catecholamine discharge (agitation, diaphoresis, tachycardia, nervousness)
* mental status change (neuroglycopenia)
* may be completely masked by general anesthesia
134
treatment for hypoglycemia
* IV 50% glucose
| * each ml of 50% glucose raises BG by 2mg/dl
135
management of type I IDDM
regular insulin therapy (IV)
| * novalin R, humalin R, NPH/reg (SC)
136
management of type II NIDDM
* 1st line – diet and exercise
* avoid high cholesterol diet
* weight loss is key
* 2nd line – oral hypoglycemics if BS can't be controlled with diet alone
137
preoperative DM drug administration
* morning does of insulin often withheld or only half given
| * metformin discontinued 24hrs prior to surgery
138
function of secretagogues/sulfonylureas
(tolazamide, tolbutamide) increase insulin availability
139
function of biguanidines
(glipizide, glyburide) inhibition of gluconeogenesis/ enhance glucose uptake to skeletal muscle
140
function metformin (glucophage)
works to overcome insulin resistance
| * decrease insulin requirements when used in combination with insulin in type II diabetics
