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ANESTHESIA PRACTICE 3 > ANESTHESIA FOR ENDOCRINE DISEASE > Flashcards

ANESTHESIA FOR ENDOCRINE DISEASE Flashcards

1
Q

what are the 4 endocrine glands?

A
  • thyroid
  • parathyroids
  • adrenal gland
  • pancreas
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2
Q

what hormones does the posterior pituitary secrete?

A
  • vasopressin (ADH)

* oxytocin

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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
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4
Q

the anterior pituitary produces hormones and releases them into the circulation under control of what?

A

hypothalamus

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5
Q

where are the hormones secreted by the posterior pituitary produced?

A

hypothalamus

* secretion is dependent upon neural stimulation

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6
Q

what part of the body does prolactin stimulate? what is the response to stimulation?

A

prolactin –> milk producing cells in breast –> lactation

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7
Q

what part of the body does ACTH stimulate? what is the response to stimulation?

A

ACTH –> adrenal cortex –> release adrenaline

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8
Q

what part of the body does GH stimulate? what is the response to stimulation?

A

GH –> body cells –> growth

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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

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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

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11
Q

what part of the body does vasopressin (ADH) stimulate? what is the response to stimulation?

A

ADH –> kidney –> regulation of water retention

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12
Q

what part of the body does oxytocin stimulate? what is the response to stimulation?

A

oxytocin –> uterus –> labour contractions

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13
Q

what are the two hormones produced by the thyroid?

A
  • triiodothyronine (T3)

* thyroxine (T4)

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14
Q

where else is T3 produced and how?

A

T3 is also formed in the peripheral tissues by deiodination of T4

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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

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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

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17
Q

graves disease is an autoimmune disease causing what?

A

hyperthyroidism

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18
Q

describe the pathophysiology of hyperthyroidism

A
  • hyper function of the thyroid gland w/ excessive secretion of T3, T4 or both
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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
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20
Q

what are the common causes of hyperthyroidism?

A
  • graves disease (most common – women 20-40yo)
  • TSH-secreting pituitary tumors
  • iatrogenic
  • thyroiditis
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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)
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22
Q

describe graves disease

A
  • autoimmune disease

* thyroid stimulating antibodies bind to TSH receptors on thyroid

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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
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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

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25
Q

how is graves disease currently treated?

A

thyroid drugs or radioiodine

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26
Q

what are the preoperative concerns with hyperthyroidism?

A
  • optimize pt to euthyroid – HR
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27
Q

what are maintenance concerns for hyperthyroidism?

A
  • esmolol (50-300mcg/kg/min)
  • avoid SNS stimulants – ketamine, pancuronium, atropine, meperidine
  • hypovolemia – exaggerated hypotensive response upon induction
  • hyperthyroidism does not increase anesthetic requirements
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28
Q

what are the post-operative concerns for hyperthyroidism?

A
  • 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
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29
Q

describe thyrotoxic crisis (thyroid storm)

A
  • 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
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30
Q

what does thyroid storm mimic?

A

malignant hyperthermia (look at CO2 for differential)

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31
Q

how is thyroid storm treated?

A
  • 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
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32
Q

describe primary hypothyroidism

A
  • dysfunction/destruction of thyroid tissue
  • high TSH, low T3/T4
  • hashimoto’s thyroiditis (autoimmune)
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33
Q

describe secondary hypothyroidism

A
  • hypothalamic-pituitary (CNS) dysfunction
  • normal or low TSH, low T3/T4
  • (iatrogenic) thyroidectomy, antithyroid meds
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34
Q

describe myxedema coma

A
  • 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
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35
Q

what is the treatment for myxedema coma?

A
  • T3/T4 given
  • ECG monitored for MI or arrhythmias
  • steroid replacement in case of coexisting adrenal gland suppression
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36
Q

what is the treatment for hypothyroidism?

A
  • L-thyroxine (PO T4; synthyroid) –physiologic effect several days; clinical improvement several weeks
  • IV T3 – effect seen within 6hr
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37
Q

what are the symptoms of hypothyroidism?

A
  • lethargy
  • weight gain
  • cold intolerance
  • hypoactive reflexes
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38
Q

preop concerns for hypothyroidism

A
  • minimal premed – sensitive to drugs and prone to resp depression
  • decreased gastric emptying times
  • synthyroid
  • warming
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39
Q

intraoperative concerns for hypothyroidism

A
  • hypotension
  • increased sensitivity to agents – decreased CO = faster onset
  • blunted baroreceptors
  • regional anesthesia if surgery permits – if GA, use ketamine
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40
Q

postoperative concerns for hypothyroidism

A
  • resedation
  • hypothermia
  • hypoglycemic, hyponatremic, anemia
  • hypoventilation – impaired pulmonary function due to decreased surfactant production
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41
Q

parathyroid hormone (PTH) increases serum levels of what?

A

calcium – increased bone reabsorption, decreased renal excretion of calcium

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42
Q

parathyroid hormone (PTH) decreases serum levels of what?

A

phosphate – increased renal excretion

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43
Q

describe primary hyperparathyroidism

A
  • increased PTH due to increased gland size
  • adenoma, carcinoma, hyperplasia of parathyroid glands
  • stimulate increased calcium circulation
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44
Q

describe secondary hyperparathyroidism

A
  • compensatory increase in PTH secretion due to hypocalcemia (renal disease or GI malabsorption)
  • seldom see elevated calcium
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45
Q

symptoms of hyperparathyroidism

A

(usually due to hypercalcemia – may be asymptomatic)

  • renal stones
  • hypertension
  • constipation
  • fatigue
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46
Q

medical treatment for hyperparathyroidism

A
  • saline

* loop diuretics

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47
Q

surgical treatment for hyperparathyroidism

A
  • (primary) parathyroidectomy for symptomatic hypercalcemia

* (secondary) treat underlying condition – VitD deficiency [rickets], chronic renal failure after renal transplant

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48
Q

perioperative considerations for hyperparathyroidism

A
  • hydration/maintenance of UOP
  • possible hypotension on induction
  • monitor NMB carefully – hypercalcemia can either decrease or increase NMB requirements
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49
Q

describe hypoparathyroidism

A
  • decreased PTH or resistance to PTH
  • hypocalcemia
    • almost always iatrogenic
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50
Q

describe psuedohypoparathyroidism

A
  • congenital

* normal PTH, but kidneys don’t respond

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51
Q

symptoms of hypoparathyroidism

A

result from hypocalcemia – muscle/abdominal cramps, neuromuscular irritability

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52
Q

symptoms of acute (postoperative) hypoparathyroidism

A
  • 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
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53
Q

symptoms of chronic hypoparathyroidism

A
  • ECG changes – long T-wave interval
  • lethargy
  • cataracts
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54
Q

treatment for hypoparathyroidism

A
  • calcium infusion

* PO calcium + vitD

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55
Q

perioperative concerns for hypoparathyroidism

A

(common after thyroidectomy)

  • optimize Ca levels
  • avoid alkalosis/hyperventilation
  • monitor pH
  • be aware of citrate in PRBCs
  • hypotension w/ GA may be exaggerated
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56
Q

the thymus is a specialized gland of what system?

A

immune system

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57
Q

describe the function of the thymus

A

differentiates developing lymphocytes into mature T-cells, which are critical cells of the adaptive immune system

58
Q

pathophysiology of digeorge syndrome (congenital thymic hypoplasia)

A
  • 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
Q

perioperative considerations for digeorge syndrome (congenital thymic hypoplasia)

A
  • micrognathia may make DL difficult
  • hyperventilation intraop could exacerbate hypocalcemia
  • unpredictable NMB
60
Q

cushing’s disease is an excess of which hormone?

A

cortisol

61
Q

describe stimulation of cortisol release

A
  • ant pit secretes corticotropin (ACTH) in response to CRH from hypothalamus
  • ACTH stimulates adrenal cortex to release cortisol
62
Q

three substances secreted from the adrenal cortex?

A
  • glucocorticoids (cortisol) (anti-insulin)
  • minerocorticoids (aldosterone
  • androgens
63
Q

describe the function of glucocorticoids (cortisol)

A
  • 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
Q

describe the function of aldosterone

A
  • 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
Q

what is the only important disease associated with adrenal medulla?

A

pheochromocytoma

66
Q

substances secreted by adrenal medulla

A

catecholamines

  • norepinephrine
  • epinephrine
  • dopamine
67
Q

three structures/responses to angiotensin II

A
  • brain – thirst
  • blood vessels – vasoconstriction
  • adrenal cortex – aldosterone
68
Q

describe cushing’s syndrome

A

excessive cortisol (glucocorticoid)

  • abnormal adrenocortical tissue
  • microadenoma – ACTH-secreting pituitary adenoma = hyper secretion of cortisol and androgens
  • small-cell lung carcinoma
69
Q

symptoms of cushing’s syndrome

A
  • 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
Q

treatment for cushing’s syndrome

A
  • transsphenoidal resection can remove microadenoma (pituitary ACTH-secreting tumor)
  • radiotherapy
71
Q

preoperative considerations for cushing’s syndrome

A
  • consideration of BP, electrolyte balance, blood sugar
  • tend to ve volume overloaded, HTN, hypokalemic
  • preop muscle weakness may indicate sensitivity to NMBs
72
Q

intraop considerations for cushing’s syndrome

A
  • choice of drugs probably won’t change

* careful positioning (osteoporosis, obesity)

73
Q

postop considerations for cushing’s syndrome

A
  • panhypopituitarism due to disruption of hypothalamic-pituitary axis
  • poor wound healing
  • infection
  • steroids (glucocorticoids) may be given
74
Q

if conn syndrome involves over secretion of aldosterone, pt would be expected to have what?

A

hypokalemic metabolic alkalosis (increased Na reabsorption in exchange for increased K+/H+ elimination)

75
Q

describe primary hyperaldosteronism (conn syndrome)

A
  • 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
Q

aldosteromas occur more often in

A

women

77
Q

symptoms of hyperaldosteronism/conn syndrome

A

often asymptomatic; symptoms often nonspecific:

  • headache (due to HTN)
  • muscle cramp (due to hypokalemia)
  • metabolic alkalosis
  • hypokalemia
78
Q

treatment for hyperaldosteronism/conn syndrome

A
  • supplemental potassium
  • competitive aldosterone antagonist (spironolactone – K+ sparing diuretic with antihypertensive properties)
  • anti-HTN drugs
  • excision of aldosterone secreting tumor
79
Q

perioperative considerations for hyperaldosteronism/conn syndrome

A
  • correction of hypokalemia
  • treatment of systemic HTN
  • careful not to hyperventilate – decreases K+ more
80
Q

pathophysiology of primary adrenocorticoid insufficiency (addison’s disease)

A
  • autoimmune
  • decreased release of glucocorticoids and minerocorticoids
  • absence of cortisol and aldosterone
81
Q

pathophysiology of secondary adrenocorticoid insufficiency

A
  • decreased ACTH from pituitary
  • cortisol deficiency with normal aldosterone
  • can be iatrogenic from use of synthetic steroids
82
Q

symptoms of adrenocorticoid deficiency

A

absence of cortisol

  • weakness/fatigue
  • hypoglycemia
  • hypotension
  • weight loss

absence of aldosterone

  • hyponatremia
  • hypovolemia
  • hyperkalemia
  • metabolic alkalosis
83
Q

describe addisonian crisis

A
  • 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
Q

treatment for adrenocorticoid deficiency

A
  • replace minero-/gluco-corticoids with hydrocortisone (100mg q6hr)
  • fludrocortisone when withdrawing steroids
85
Q

perioperative considerations for adrenocorticoid deficiency

A
  • 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
Q

if adrenocorticoid deficient pt (periop) hypotensive and can revive with fluids and vasopressors, what should be considered?

A

pt might have addison’s disease – need steroids (addisonian crisis)

87
Q

pathophysiology of hypoaldosteronism

A
  • congenital deficiency of aldosterone synthase
  • hyporeninemia due to deficient juxtaglomerular apparatus
  • unilateral adrenalectomy
88
Q

symptoms of hypoaldosteronism

A
  • hyperkalemia without renal insufficiency (may result in heart block, orthostatic hypotension)
  • hyperchloremic
  • metabolic acidosis
89
Q

treatment for hypoaldosteronism

A

fludrocortisone

90
Q

pathophysiology pheochromocytoma

A
  • catecholamine-secreting tumor of adrenal medula (right gland > left)
  • NE:Epi = 85:15
  • avg-size adult pheochromocytoma contains 100-800mg NE
91
Q

symptoms of pheochromocytoma

A
  • sudden onset malignant hypertension – tachycardia
  • cardiac dysrhythmias
  • headache
  • perspiration
    • can mimic MH
    • triggered by compression of tumor, increased abdominal pressure (coughing, straining)
92
Q

treatment for pheochromocytoma

A
  • excision of tumor

* management of BP with alpha-antagonists (phenoxybenzamine 10mg POq12hr), beta blockers (propranolol preop)

93
Q

periop considerations pheochromocytoma

A
  • 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
Q

acromegaly is associated with an oversecretion of which hormone?

A

growth hormone

95
Q

pathophysiology of acromegaly

A

excessive GH secretion, usually due to adenoma in pituitary gland

96
Q

symptoms of acromegaly

A
  • 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
Q

treatment for acromegaly

A

surgical

  • transsphenoidal resection of pituitary adenoma (best)
  • radiation

medical
* suppressant drugs (bromocriptine)

98
Q

periop considerations with acromegaly

A
  • 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
Q

pathophysiology of diabetes insipidus

A

deficiency or resistance to vasopressin – poor absorption of water from kidney

100
Q

symptoms of diabetes insipidus

A
  • extreme thirst (polydipsia)

* excretion of large amounts of dilute urine (2-20L/d)

101
Q

causes of diabetes insipidus

A
  • neurogenic – lack of vasopressin secretion (idiopathic, familial, tumors)
  • nephrogenic – decreased response to vasopressin (kidney damage, protein starvation, acute tubular necrosis)
102
Q

treatment for diabetes insipidus

A
  • neurogenic – desmopressin (synthetic vasopressin)

* nephrogenic – keep Na low (diuretics) since vasopressin levels are normal

103
Q

periop considerations for diabetes insipidus

A

watch for electrolyte imbalances

  • high Na
  • low K
  • low Mg
104
Q

pathophysiology of diabetes mellitus

A

chronic disease caused by abnormal glucose metabolism that results in predictable long-term morbidity

105
Q

describe normal glucose physiology

A
  • balance between glucose utilization and endogenous production or dietary delivery
  • liver is primary source of endogenous glucose
  • insulin release promotes glucose utilization
106
Q

long-term morbidities from DM

A
  • peripheral vascular disease
  • ischemic heart disease
  • renal disease
  • blindness
  • peripheral neuropathy
107
Q

what is normal hemoglobin A1C?

A

6%

108
Q

describe anatomy of pancreas

A

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
Q

describe innervation of pancreas

A
  • sympathetic – T5-T10 (insulin inhibition, glucagon stimulation)
  • parasympathetic – vagus (insulin release)
110
Q

other hormones that stimulate insulin secretion

A

GH, cortisol, progesterone, estrogen

* prolonged secretion may exhaust beta cells and cause DM

111
Q

describe insulin function

A

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
Q

pathophysiology of DM

A
  • decreased secretion of insulin from beta cells
  • increased resistance of receptors to circulating insulin
    • hereditary
113
Q

how does obesity relate to DM

A
  • chronic high levels of glucose cause increased insulin secretion & downregulation of receptors
  • beta cells become less responsive to high levels of glucose
114
Q

effects of lack of insulin

A
  • 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
Q

define type I DM

A
  • 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
Q

define type II DM

A
  • insulin resistance
  • plasma insulin normal or high, but inappropriate for blood sugar
  • high serum glucose, hyperosmolar state
  • managed with diet
117
Q

define gestational DM

A
  • 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
Q

symptoms of DM

A
  • 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
Q

complications of DM

A
  • 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
Q

heart end-organ pathology of DM

A
  • CHF
  • CAD
  • get an EKG
  • silent MI
  • 20x greater risk of MI periop
121
Q

vascular end-organ pathology of DM

A

circulation damage cause by hyperglycemia

  • HTN – accelerates changes, esp in coronaries
  • atherosclerosis
122
Q

first sign of DM-related autonomic neuropathy

A

postural hypotension

123
Q

describe stiff joint syndrome as DM-related end-organ pathology

A
  • 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
Q

cause of diabetic ketoacidosis (DKA)

A
  • decrease insulin activity –> metabolism of free fatty acids –> accumulation of organic acid byproducts
125
Q

what type DM does DKA occur in?

A

primarily type I (IDDM) when exogenous insulin source is interrupted
* NIDDM are ketosis-resistant – circulating insulin sufficient enough to prevent ketogenesis

126
Q

clinical signs of DKA

A
  • infection is often the first manifestation of IDDM in adolescents
  • tachypnea/kussmal
  • dehydration
  • altered sensorium
  • ketones in urine
127
Q

treatment for DKA

A
  • correct hypovolemia with NS
  • correct hyperglycemia with insulin
  • correct electrolyte deficiencies
128
Q

describe hyperosmolar nonketotic coma (HONK)

A
  • hyperglycemic diuresis resulting in dehydration and hyperosmolality
129
Q

symptoms of hyperosmolar nonketotic coma

A
  • 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
Q

treatment of HONK coma

A
  • hypotonic saline to correct hypovolemia and hyperosmolarity
  • low-dose insulin infusion to lower BS to
131
Q

describe hypoglycemia

A

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
Q

what organ is at greatest risk with hypoglycemia?

A

brain – can only utilize blood glucose as its energy source

133
Q

symptoms of hypoglycemia

A
  • SNS/catecholamine discharge (agitation, diaphoresis, tachycardia, nervousness)
  • mental status change (neuroglycopenia)
  • may be completely masked by general anesthesia
134
Q

treatment for hypoglycemia

A
  • IV 50% glucose

* each ml of 50% glucose raises BG by 2mg/dl

135
Q

management of type I IDDM

A

regular insulin therapy (IV)

* novalin R, humalin R, NPH/reg (SC)

136
Q

management of type II NIDDM

A
  • 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
Q

preoperative DM drug administration

A
  • morning does of insulin often withheld or only half given

* metformin discontinued 24hrs prior to surgery

138
Q

function of secretagogues/sulfonylureas

A

(tolazamide, tolbutamide) increase insulin availability

139
Q

function of biguanidines

A

(glipizide, glyburide) inhibition of gluconeogenesis/ enhance glucose uptake to skeletal muscle

140
Q

function metformin (glucophage)

A

works to overcome insulin resistance

* decrease insulin requirements when used in combination with insulin in type II diabetics

ANESTHESIA PRACTICE 3 (5 decks)

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