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Endocrine (4) Flashcards

1
Q

The _________ is the primary source of glucose production via glycogenolysis & gluconeogenesis

A

Liver

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2
Q

_____% of the glucose released by the liver is freely metabolized by brain, GI tract, and RBCs

A

75%

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3
Q

What hormones help regulate blood glucose level?

A
  • Glucagon
  • Epinephrine
  • Growth Hormone
  • Cortisol
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4
Q

What happens to T3, T4 and TSH in hypothyroidism?

A

↓T3 & T4 despite adequate TSH

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5
Q

What is the most common cause of hypothyroidism?

A

Ablation of the gland by radioactive iodine or surgery

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6
Q

What is the 2nd most common cause of hypothyroidism?

A

Idiopathic and probably autoimmune

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7
Q

Hashimoto thyroiditis is an ____ hypothyroidism, often involving a ____ and usually affects ____:

A

autoimmune hypothyroidism; goiter; middle-aged women

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8
Q

In adults, hypothyroidism has a ___, _____ course

A

Slow, progressive

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9
Q

What are the roles of glucagon?

A
  • Stimulate glycogenolysis
  • Stimulate gluconeogenesis
  • Inhibit glycolysis
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10
Q

Symptoms of hypothyroidism:

A
  • Cold intolerance
  • Weight gain
  • Nonpitting edema
  • SIADH
  • Fluid overload
  • Pleural effusions
  • Dyspnea
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11
Q

_________ is the most common endocrine disease

A

Diabetes

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12
Q

How is GI function affected in hypothyroidism?

A

It is slow, and an ileus may occur

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13
Q

Diabetes affect 1 in ___ adults

A

10

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14
Q

What causes diabete?

A

Inadequate supply of insulin and/or tissue resistance to insulin

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15
Q

Hypothyroidism s/s graph:

A
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16
Q

What happens to the body when blood sugar is high?

A

Microvascular and macrovascular damage

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17
Q

Treatment for hypothyroidism:

A

L-thyroxine is DOC

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18
Q

Airway considerations for hypothyroidism:

A
  • Airway compromise
  • Swelling
  • Edematous vocal cords
  • Goiter
  • Aspiration risk d/t slower gastric emptying
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19
Q

What is the disease process of Type 1a DM?

A

Autoimmune destruction of pancreatic beta cells→ causes minimal/no insulin production

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20
Q

CV system considerations in hypothyroidism:

A

May be hypodynamic

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21
Q

What is type 1b DM?

A

Non-immune disease of absolute insulin deficiency

RARE

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22
Q

Other pre-op implications for hypothyroidism:

A
  • Respiratory function may be compromised
  • More prone to hypothermia
  • Electrolyte imbalances possible
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23
Q

What type of diabetes is non-immune and results from defects in insulin receptors and signaling pathways?

A

Type 2 DM

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24
Q

If elective case in a pt with hypothyroid, thyroid tx should be initiated at least __ days prior:

A

10

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25
Q

If emergent surgery, what do you give for hypothyroidism?

A

IV thyroid replacement along with steroids ASAP

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26
Q

What percent of total DM cases account for type 1?

A

5-10%

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27
Q

What is myxedema coma?

A

Rare, severe form of hypothyroidism characterized by delirium, hypoventilation, hypothermia, bradycardia, HoTN, and dilutional hyponatremia

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28
Q

What is the cause of autoimmune destruction of beta cells in T1D?

A
  • Exact cause is unknown
  • A long period (9-13yrs) of B-cell antigen production occurs before onset symptoms
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29
Q

What is the cardinal feature of myxedema coma?

A

Hypothermia d/t impaired thermoregulation

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30
Q

T1D is usually diagnosed before what age?

A

40

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31
Q

What population does myxedema coma most commonly occur?

A

Elderly women with long history of hypothyroidism

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32
Q

What percent of beta cell dysfunction before hyperglycemia is sustained?

A

80-90%

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33
Q

What can trigger myxedema coma?

A
  • Infection
  • Trauma
  • Cold
  • CNS depressants
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34
Q

What is the mortality of myxedema coma?

A

> 50%

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35
Q

Treatment for myxedema coma:

A
  • IV L-thyroxine or L-triiodothyronine
  • IV hydration w/ glucose solutions
  • Temp regulation
  • Electrolyte correction
  • Supportive care
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36
Q

What are common S/S of T1D related to prolonged hyperglycemia?

A
  • Fatigue
  • Weight loss
  • Polyuria
  • Polydipsia
  • Blurry vision
  • Hypovolemia
  • Ketoacidosis
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37
Q

What is goiter?

A

Swelling of thyroid gland d/t hypertrophy and hyperplasia of follicular epithelium

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38
Q

T2D accounts for ____% of DM cases

A

> 90%
Increasingly seen in younger patients and kids over last decade

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39
Q

What can cause goiter?

A
  • Lack of iodine
  • Ingestion of goitrogen
  • Hormonal defect
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40
Q

What are the initial stages of T2D? What happens over time?

A
  • Tissues desensitized to insulin→ causes increase secretion
  • Over time pancreatic function decreases and insulin levels are inadequate
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41
Q
A
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42
Q

In most cases, a goiter is associated with what?

A

A compensated euthyroid state

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43
Q

How are most goiter cases treated?

A

L-thyroxine

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44
Q

When is surgery indicated for goiter?

A

If medical treatment is ineffective, and goiter compromises airway or is cosmetically unacceptable

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45
Q

How are thyroid tumors examined?

A

CT scan

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46
Q

What symptoms are predictive of airway obstruction during general anesthesia in patients with thyroid tumors?

A

Dyspnea in upright or supine position

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47
Q

What are the 3 main abnormalities seen with DM2?

A
  • Impaired insulin secretion
  • increase hepatic glucose release (reduced in insulin inhibitory effect on liver)
  • Insufficient glucose uptake in peripheral tissues
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48
Q

For patients with thyroid tumors, what can indicate location/degree of obstruction?

A

Flow-volume loops in upright and supine positions

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49
Q

Limitations in the inspiratory limb of the loop indicates ____ obstruction:

A

extra-thoracic

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50
Q

DM2 is characterized by insulin resistance in which tissues?

A
  • Skeletal muscle
  • Adipose
  • Liver
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51
Q

Delayed flow in the expiratory limb indicates an _____ obstruction:

A

intra-thoracic

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52
Q

What is the cause of insulin resistance in T2D?

A
  • Abnormal insulin molecules
  • Circulating insulin antagonists
  • Insulin receptor defects
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53
Q

How do you assess the degree of cardiac compression with a thyroid tumor?

A

Echocardiogram

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54
Q

How is T2D diagnosed?

A
  • Fasting BG
  • HbA1C

Obesity and sedentary lifestyle are acquired and contributing factors

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55
Q

In thyroid surgery, if unilateral vocal hoarseness occurs without obstruction, how long does it take to resolve?

A

3-6 months

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56
Q

Normal A1C:
Prediabetic A1C:
Diabetes:

A

Norm: <5.7%
Prediabetes: 5.7-6.4%
Diabetes: >6.5%

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57
Q

Bilateral thyroid involvement can cause what?

A

Airway obstruction and warrant tracheostomy

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58
Q

Hypoparathyroidism may result from what?
Symptoms?

A

Inadvertent parathyroid damage with thyroid surgery

Sx of hypocalcemia occur within 48 hours postop

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59
Q

What are ADA criteria for Dx of diabetes?

A
  • A1C >6.5
  • Fasting glucose >126
  • 2hr glucose >200 during oral glucose tolerance test
  • Random glucose >200
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60
Q

What can lead to tracheal compression in thyroid surgery?

A

Hematoma

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61
Q

What should be kept at bedside during immediate postop period after thyroid surgery?

A

Trach set

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62
Q

Each adrenal gland consists of what?

A

A cortex and medulla

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63
Q

What does the cortex of the adrenal gland synthesize?

A
  • Glucocorticoids
  • Mineralcorticoids (aldosterone)
  • Androgens
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64
Q

What is the treatment DM2?

A
  • Dietary adjustment
  • Exercise and weight loss (improve hepatic and peripheral insulin sensitivity)
  • PO antidiabetic drugs
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65
Q

How is corticotropin (ACTH) released?

A

Hypothalamus sends corticotropin-releasing hormone (CRH) to the anterior pituitary, which stimulates release of corticotropin

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66
Q

ACTH stimulates the adrenal cortex to produce ____:

A

Cortisol

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67
Q

What is the function of cortisol?

A

Helps convert NE to epi and induces hyperglycemia

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68
Q

Together, cortisol and aldosterone cause what two things?

A

Sodium retention and K+ excretion

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69
Q

What is a pheochromocytoma?

A

Catecholamine-secreting tumor that originates from chromaffin cells

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70
Q

Excess catecholamines can lead to what??

A

Malignant HTN, CVA and MI

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71
Q

80% of pheo occur where?

A

Adrenal medulla

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72
Q

18% of pheos occur where?

A

In organ of Zuckerkandle

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73
Q

2% of pheos occur where?

A

Neck/thorax

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74
Q

Where do malignant pheos spread through?

A

Venous and lymph systems

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75
Q

What is the preferred initial drug tx for DM2?

A
  • Metformin (biguanide)
  • Enhances glucose transport into tissues
  • Decrease TG and LDL levels
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76
Q

What is the ratio of NE:epi secreted in pheos?

A

85:15 - the inverse of normal adrenal secretion
*some secrete higher levels of epi, and more rarely dopamine

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77
Q

When can pheo attacks occur?

A
  • Attacks range from occasional to frequent and may last minutes or hours
  • May occur spontaneously or triggered by injury, stress or meds
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78
Q

What is the MOA of sulfonylurea PO antidiabetic drugs?

A
  • Stimulate insulin secretion
  • Enhance glucose transport into tissues
  • Not effective long term (progressive loss of beta cell fx)
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79
Q

Symptoms of pheochromocytoma:

A
  • Headache
  • Pallor
  • Sweating
  • Palpitations
  • HTN
  • Orthostatic HoTn
  • Coronary vasoconstriction, cardiomyopathy, CHF and EKG changes may occur
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80
Q

How do you diagnose a pheo?

A
  • 24 hours urine collection for metanephrines and catecholamines
  • CT and MRI
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81
Q

What are side effects of sulfonylureas?

A
  • Hypoglycemia
  • Weight gain
  • Cardiac effects
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82
Q

PO antidiabetics:

A
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83
Q

What do you give preop to patients with a pheo?

A

α blocker to lower BP, decrease intravascular volume

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84
Q

Which diabetics need insulin?

A

All DM1 and 30% DM2

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85
Q

What is the most frequently used preop α-blocker?
How does it work?

A

Phenoxybenzamine;
Noncompetitive α1 antagonist with some α2 blocking properties

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86
Q

What are the different types of insulin?

A
  • Rapid acting (lispro, aspart= meal time)
  • Short acting (regular)
  • Basal/intermediate (NPH, Lente)
  • Long acting (Ultralente, glargine)
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87
Q

What are two other pure α1 blockers?

A

Prazosin and Doxazosin - shorter acting with less tachycardia

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88
Q

What is the most dangerous complication of DM?

A

Hypoglycemia

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89
Q

How do you treat tachycardia after giving an α1 blocker?

A

Beta blocker

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90
Q

What can increase incidence of hypoglycemia in DM?

A
  • ETOH
  • Metformin
  • Sulfonylureas
  • ACE-Is
  • MAOIs
  • Non-selective beta blockers
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91
Q

Why do you not give nonselective beta-blockers before an α blocker?

A

blocking vasodilatory β2 receptors results in unopposed α agonism, leading to vasoconstriction and hypertensive crises

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92
Q

What is the issue with repeated episodes of hypoglycemia?

A
  • Hypoglycemia unawareness
  • Densensitization to hypoglycemia= no autonomic symptoms
  • Neuroglycopenia
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93
Q

What defines ACTH dependent Cushings syndrome?

A

High plasma ACTH stimulates adrenal cortex to produce excess cortisol

94
Q

What defines ACTH-independent Cushings syndrome?

A

Excessive cortisol production by abnormal adrenocortical tissue that is not regulated by CRH and ACTH
- CRH and ACTH levels are actually suppressed
- adrenocortical tumors are the most common cause of ACTH-independent cushings

95
Q

Symptoms of hypercortisolism (cushings)

A
  • Sudden weight gain
  • Usually central w/ moon face
  • ecchymoses
  • HTN
  • glucose intolerance
  • Muscle wasting
  • Depression
  • Insomnia
96
Q

How do you diagnose cushings?

A

24 hour urine cortisol

97
Q

What is required to determine if cushings is ACTH dependent or independent?

A

ACTH level

98
Q

What are signs of neuroglycopenia?

A
  • Fatigue
  • Confusion
  • Headache
  • Seizures
  • Coma
99
Q

For Cushings, is CT/MRI/US useful?

A

Useful for determining tumor location, but not helpful in gauging adrenal function

100
Q

What is treatment for neuroglycopenia?

A

PO or IV glucose (SQ of IM if unconscious)

101
Q

Treatment of choice for cushings:

A

Transsphenoidal microadenomectomy if resectable

102
Q

Alternate treatment for cushings:

A
  • Subtotal resection of the anterior pituitary
  • Pituitary irradiation and adrenalectomy maybe necessary
103
Q

What is the treatment for adrenal adenoma or carcinoma?

A

Surgical adrenalectomy

104
Q

Preop considerations for cushings:

A
  • Evaluate/treat BP
  • Correct electrolyte imbalance
  • Correct blood glucose
  • Consider osteoporosis
105
Q

Hottie with cushings:

106
Q

What causes primary hyperaldosteronism (conn syndrome)?

A

Excess secretion of aldosterone caused by tumor (aldosteronoma)

107
Q

Is conns syndrome more common in men or women?

108
Q

Conn syndrome is occasionally associated with what?

A

Pheochromocytoma, hyperparathyroidism or acromegaly

109
Q

What causes secondary hyperaldosteronism?

A

Elevated renin levels

110
Q

Symptoms of hyperaldosteronism:

A

*Non-specific, some are asymptomatic
- HTN
- Hypokalemia
- hypokalemic metabolic alkalosis

111
Q

Hallmark symptom of hyperaldosteronism:

A

Spontaneous HTN with hypokalemia

112
Q

Renin activity in primary vs secondary hyperaldosteronism:

A

Primary = renin activity is suppressed
Secondary = renin activity is elevated

113
Q

What can cause a syndrome that mimics hyperaldosteronism?

A

Long term ingestion of licorice
(sx = HTN, hypokalemia, suppression of RAAS)

114
Q

Treatment for hyperaldosteronism:

A
  • Aldosterone antagonist (spironolactone)
  • K+ replacement
  • Antihypertensives
  • Diuretics
  • Tumor removal
  • Possible adrenalectomy
115
Q

Hallmark sign of hypoaldosteronism:

A

Hyperkalemia in the absence of renal insufficiency

116
Q

What else is common in hypoaldosteronism?

A

Hyperchloremic metabolic acidosis

117
Q

What are some symptoms of hypoaldosteronism?

A

May experience heart block, orthostatic HoTN, hyponatremia

118
Q

What are some things that can cause hypoaldosteronism?

A
  • Congenital deficiency of aldosterone
  • Low renin
  • ACE inhibitors
119
Q

What is a reversible cause of hypoaldosteronism?

A

Indomethacin-induced prostaglandin deficiency

120
Q

Treatment for hypoaldosteronism:

A

Increased sodium intake and daily fludrocortisone

121
Q

What is primary adrenal insufficiency?

A

Autoimmune adrenal gland suppression
*Addison’s disease

122
Q

What is secondary adrenal insufficiency?

A

Hypothalamic-pituitary suppression leading to a lack of CRH or ACTH production

123
Q

Unlike Addison’s, there is only a ____ deficiency in secondary AI

A

glucocorticoid

124
Q

What are some causes of iatrogenic cases of secondary adrenal insufficiency?

A
  • Synthetic glucocorticoids
  • Pituitary surgery
  • Radiation
125
Q

Patients with secondary AI lack ____

A

hyperpigmentation

126
Q

Diagnosis for adrenal insufficiency:

A

Baseline cortisol <20 Mcg/dL and remains <20 after ACTH stimulation

A positive test demonstrates a poor response to ACTH

127
Q

What is absolute AI characterized by?

A

Low baseline cortisol level and a positive ACTH stimulation test

127
Q

What indicates relative adrenal insufficiency?

A

When the baseline cortisol level is higher, but the ACTH stimulation test is positive

128
Q

What is the treatment for adrenal insufficiency?

129
Q

How many parathyroid glands are there and where are they?

What do they do?

A

4 glands located behind the upper and lower poles of the thyroid

Produce PTH because of a negative feedback that depends on plasma calcium level

130
Q

Hypocalcemia ____ the release of PTH, where hypercalcemia ____ PTH synthesis and release

A

stimulates; suppresses

131
Q

How does PTH maintain normal plasma calcium levels?

A

Promotes the movement of calcium across GI tract, renal tubules, and bone

132
Q

Primary hyperparathyroidism is caused by:

A
  • benign parathyroid adenoma
  • Carcinoma (<5%)
  • Parathyroid hyperplasia
133
Q

Symptoms of hyperparathyroidism:

A
  • Lethargy
  • Weakness
  • N/V
  • Polyuria
  • Renal stones
  • PUD
  • Cardiac disturbances
134
Q

Diagnosis for hyperparathyroidism:

A
  • Plasma calcium
  • 24 hour urinary calcium
135
Q

Treatment for primary hyperparathyroidism:

A

Surgical removal of abnormal portions of the gland

136
Q

What is secondary hyperparathyroidism?

A

Compensatory response of the parathyroid glands to counteract a separate disease process involving hypocalcemia (ex. CRF)

137
Q

Treatment for secondary hyperparathyroidism:

A

Controlling the underlying disease, normalizing phosphate levels with a phosphate binder

138
Q

Why is deficient PTH almost always iatrogenic?

A

Caused by inadvertent removal of parathyroid glands - may occur during thyroidectomy

139
Q

What is pseudohypoparathyroidism?

A

Disorder where PTH is adequate, but the kidneys are unable to respond to it

140
Q

Diagnostic labs for hypoparathyroidism:

A
  • ↓PTH,
  • ↓Ca++,
  • ↑phos
141
Q

What are symptoms of hypoparathyroidism dependent on?

A

Speed of onset

142
Q

Acute hypocalcemia such as after accidental parathyroid removal may cause what?

A

Inspiratory stridor or laryngospasm

143
Q

What is chronic hypocalcemia associated with?

A
  • Fatigue
  • Cramps
  • Prolonged QT
  • Cataracts
  • SQ calcifications
  • Neurologic deficits
144
Q

Treatment for hypoparathyroidism:

A
  • Calcium replacement
  • Vitamin D
145
Q

What are the 6 hormones secreted by the anterior pituitary under the control of the hypothalamus?

A
  • GH
  • ACTH
  • TSH
  • FSH
  • LH
  • Prolactin
146
Q

What is stored in the posterior pituitary after being synthesized in the hypothalamus?

A

Vasopressin and oxytocin

147
Q

What causes acromegaly?

A

Excessive growth hormone, most often seen with anterior pituitary adenomas

148
Q

Diagnostic labs for acromegaly:

A

insulin-like growth factor 1 (IGF 1) is elevated

149
Q

In acromegaly, overgrowth of soft tissues make the patients susceptible to what?

A

Upper airway obstruction

150
Q

With acromegaly, what causes hoarseness and abnormal movement of vocal cords or RLN paralysis?

A

Overgrowth of surrounding cartilage

151
Q

What is common in acromegaly due to nerve trapping by connective tissues?

A

Peripheral neuropathy

152
Q

Treatment for acromegaly:

A
  • Removal of pituitary adenoma (usually transsphenoidal approach)
  • If surgery is not feasible, LA somatostatin analogues are the medical treatment
153
Q

Anesthesia implications for acromegaly:

A
  • Distorted facial anatomy may interfere with mask placement
  • Enlarged tongue and epiglottis
  • Increased distance between lips and vocal cords due to mandible overgrowth
  • Glottic opening may be narrowed due to vocal cord enlargement
  • May require smaller ETT, VL, awake fiberoptic intubation
154
Q

What are the two main causes of Diabetes insipidus (vasopressin deficiency)?

A
  • Central/neurogenic DI: destruction/dysfunction of the posterior pituitary
  • Nephrogenic DI: failure of kidneys to respond to ADH
155
Q

Which form of DI causes urine-concentration?

A

Neurogenic, not nephrogenic - d/t response to DDAVP

156
Q

Symptoms of DI:

A
  • polydipsia
  • excessive, dilute UOP despite increased serum osmolarity
157
Q

Initial treatment for DI:

A
  • IV electrolytes to offset polyuria
158
Q

Treatment for neurogenic DI:

159
Q

Treatment for nephrogenic DI:

A
  • low salt and low protein diet
  • thiazide diuretics
  • NSAIDs
160
Q

Anesthesia considerations for DI:

A

Monitor UOP and serum electrolyte concentrations

161
Q

What can cause SIADH?

A
  • intracranial tumors
  • hypothyroidism
  • porphyria
  • lung cancer
162
Q

Diagnosis for SIADH:

A
  • hyponatremia
  • decreased serum osmolarity
  • increased urine sodium and osmolarity
163
Q

Abrupt drop in serum sodium can cause what??

A

Cerebral edema and seizures

165
Q

Treatment for SIADH:

A
  • Fluid restriction
  • Na+ tablets
  • loop diuretics
  • ADH antagonists (demeclocycline)
166
Q

How can severe hyponatremia be treated?

A

Hypertonic saline

167
Q

What is the onset/peak/duration of short, intermediate, and long acting insulin?

168
Q

Which insulin peaks first vs last?

169
Q

What is ketoacidosis a complication from?

A

Decompensated T1D (mortality 1-2%)

170
Q

What usually triggers DKA?

A

Infection/illness

171
Q

What is the MOA of DKA?

A
  • High glucose exceeds threshold for renal absorption (hypovolemia and diuresis)
  • Liver over produces ketoacids
172
Q

What is the diagnostic criteria for DKA?

A
  • Glucose ≥ 300
  • pH ≤ 7.3
  • HCO3 ≤ 18
  • Serum Osmolarity < 320
  • Serum/urine ketone moderate to high
173
Q

What is the treatment for DKA?

A
  • IV volume replacement
  • Regular insulin
  • Correct acidosis (Bicarb)
  • Electrolyte supplement (K,Mg,Na,Phos)
    Correction of glucose without correction of sodium might cause cerebral edema
174
Q

What is the dose of regular insulin (IV) for DKA correction?

A
  • Loading dose 0.1u/kg
  • Low dose infusion 0.1u/kg/hr
175
Q

What are characteristics of HHNKS? Which disease process does this occur in?

A
  • Severe hyperglycemia
  • Hyperosmolarity
  • Dehydration

Normally occur in DM2 >60y/o

176
Q

What are S/S of HHNKS?

A
  • polyuria
  • polydipsia
  • hypovolemia
  • hypotension
  • tachycardia
  • coma (from hyperosmolarity)
  • Some degree of acidosis

when blood glucose exceeds renal glucose absorption→ causes massive glucosuria

177
Q

What is the treatment for hyperglycemia hyperosmolar syndrome?

A
  • Fluid restriction
  • Insulin bolus and infusion
  • electrolytes
178
Q

What is the mortality of DKA vs HHNKS?

A

DKA: 1-2%
HHNKS: 10-20%

179
Q

Primary complications of DM:

A
  • Microvascular: nonocclusive microcirculatory with impaired blood flow
  • Nephropathy
  • Peripheral neuropathy
  • Retinopathy
  • Autonomic Neuropathy
180
Q

How common is nephropathy in DM1 vs DM2? What are the symptoms of nephropathy?

A
  • DM1: 30-40%
  • DM2: 5-10%
  • S/S: HTN, proteinuria, peripheral edema, low GFR
181
Q

Why is hyperkalemia associated with nephropathy?

A

GRF <15-20= kidneys no longer clear K+ → hyperkalemic acidosis

182
Q

What medication is used to slow the progression of proteinuria and decreased GFR in diabetics?

A

Ace-inhibitors

183
Q

What are treatment options for ESRD?

A
  • HD
  • PD
  • Kidney transplant

Combined kidney-pancreas transplant may prevent recurrent nephropathy

184
Q

How does diabetic peripheral neuropathy present/impact patients?

A
  • Distal symmetric diffuse sensorimotor neuropathy
  • Starts in toes and progresses proximally
  • Loss of large sensory and motor fibers (reduces touch and proprioception)
  • Loss of small nerve fibers (decrease pain/temp perception)
  • Neuropathic pain
  • Ulcers develop (unnoticed injury)
  • Recurrent infection/ amputation wounds
185
Q

What causes DM retinopathy? How can retinopathy progression be reduced?

A
  • Microvascular damage
  • Visual impairment (range: color loss to blindness)
  • Glycemic control and BP control reduce progression
186
Q

What happens to CV and GI systems from DM autonomic neuropathy ?

A
  • CV: abnormal cardiovascular dynamics, loss of HR variability, orthohypotension, dysrhythmias (potential for silent MI)
  • GI: decrease secretion and motility→ gastroparesis
187
Q

What are S/S and treatments for DM autonomic neuropathy?

A

S/S: N/V, early satiety, bloating, epigastric pain
Tx: glucose control, small meals, prokinetics

188
Q

What are important factors in preop eval for DM patients?

A
  • CV/Renal/Neurologic/Musculoskeletal systems
  • Consider stress test
  • Assess hydration status
  • Avoid nephrotoxins/ preserve RBF
  • Periop dysrhythmias/hypotension for autonomic neuropathy
  • Gastroparesis increases aspiration risk
  • Hold PO diabetic drugs to avoid low BG
189
Q

What is insulinoma?

A

Rare benign insulin-secreting pancreatic tumor

190
Q

Which population is more at risk for Insulinoma?

A

2X more in women age 50-60

191
Q

How is Insulinoma diagnosed?

A

Whipple Triad:
- Hypoglycemia with fasting
- Blood glucose <50 with symptoms
- Symptoms relief with glucose

192
Q

Patients that have insulinoma have high blood ________ level during 48-72h fast

A

insulin (causes hypoglycemia)

193
Q

What med can be given in preop for patient with an insulinoma? What are other treatments?

A

Diazoxide Preop: Inhibits insulin release from beta cells

TX: verapamil, phenytoin, propranolol, glucocorticoids, octreotide
Surgery= curative

194
Q

What is a concern for patient with insulinomas intra op and post op?

A
  • Hypoglycemia intra-op
  • Hyperglycemia post op (when tumor removed)

tight glycemic monitoring and treatment

195
Q

The thyroid gland is composed of 2 lobes joined by an _______

A

Isthmus (small narrow band of tissue)

196
Q

The thyroid is attached to anterior and lateral _________ with the upper border below ________ cartilage

A

Trachea
Cricoid

197
Q

What nervous systems innervate the capillary network of the thyroid?

A

Adrenergic and Cholinergic nervous systems

198
Q

Which nerves are in close proximity to the thyroid?

A
  • Recurrent laryngeal nerve
  • Superior laryngeal nerve (idk what SLN abbreviation means in her PPT so this is my best guess 🥸)
199
Q

_________ hormones stimulate virtually all metabolic processes

200
Q

What exogenous substance is needed for production of thyroid hormones?

A

Exogenous idodine

201
Q

How is iodine transformed into thyroid hormones?

A
  • Iodine in GI tract reduced to iodide→absorbed and sent to thyroid follicular cells
  • Iodide binds to thyroglobulin= inactive monoiodotyrosine and diiodotyrosine (form T3/T4)
202
Q

25% Monoiodotyrosine and diiodotyrosine undergo coupling with _______ _________ to form T4 and T3.

A

Thyroid peroxidase

203
Q

What is another name for T4?

204
Q

What is another name for T3?

A

Triiodothyronine

205
Q

What is the ratio of T4:T3?

206
Q

What 3 structures regulate thyroid function?

A
  • Hypothalamus (TRH)
  • Anterior pituitary (TSH)
  • Thyroid glands
207
Q

What is the function of TSH binding to thyroid receptors?

A

Synthesis and release of T3 and T4

208
Q

How is TSH release triggered?

A
  • Hypothalamus releases TRH which signals ant pituitary to release TSH
  • TSH also influenced by plasma T3/T4 levels (negative feedback)
209
Q

The thyroid has an __________ mechanism to maintain consistent levels.

A

Autoregulatory

210
Q

What is the best test of thyroid action at the cellular level?

A

TSH assay (sensitive to small changes)

Norm TSH level: 0.4-5.0 miliunits/L

211
Q

What is TRH stimulation test used to test?

A

Pituitary function and TSH secretion

212
Q

What is the disease process that causes hyper-functioning thyroid gland with excessive hormone secretion?

A

Hyperthyroidism

213
Q

Most cases of hyperthyroidism are caused by 1 of 3 pathologies. What are the 3 pathologies?

A
  • Graves disease
  • Toxic goiter
  • Toxic adenoma
214
Q

What are symptoms of hyperthyroidism?

A
  • Sweating
  • Heat intolerance
  • Fatigue
  • Insomnia
  • Osteoporosis/ weight loss
  • CV compromise (T3 effect on myocardium and peripheral vaculature)
215
Q

List of hyperthyroid S/S 😑

216
Q

What is the leading cause of hyperthyroidism?

A

Graves disease (0.4% of population)

more common in females 20-40y/o

217
Q

What is the MOA of graves?

A

Autoimmune→ thyroid stimulating antibodies that cause growth, vascularity, and hypersecretion

(thyroid gets bigger= common to have goiter)

218
Q

How is graves diagnosed?

A
  • Positive TSH antibodies
  • Low TSH
  • High T3/T4
219
Q

What is an anesthesia concern for patients with graves?

A

Extreme thyroid enlargement may cause:
- Dysphagia
- Inspiratory stridor
- Tracheal compression

220
Q

What is the 1st line treatment for Graves?

A

Antithyroid drugs→ Methimazole or Propylthiouracil (PTU)

221
Q

Why is iodine therapy not the best long term treatment option for patients with Graves?

A

It can inhibit the release of thyroid hormone BUT effect is temporary

Good to use Preop correction or in thyroid storm

222
Q

How can propranolol impact Graves disease?

A

Impairs the peripheral conversion to T4/T3

223
Q

If medical management for Graves fails what surgery is recommended? What are complications of the surgery?

A
  • Subtotal Thyroidectomy
  • Complications: Hypothyroid, hemorrhage, hematoma, tracheal compression, RLN damage, parathyroid damage
224
Q

What should be assessed in patient with Graves preop?

A
  • Thyroid levels
  • Upper airways for evidence of tracheal compression or deviation d/t goiter
225
Q

A women with graves started taking methimazole last week. How long does she need to wait before elective surgery?

A

6-8 weeks after starting antithyroid drugs (so drugs can take effect)

226
Q

If a patient with Graves requires emergent surgery what meds should be given?

A
  • IV beta blockers
  • glucocorticoids
  • PTU
227
Q

What are S/S or Graves?

228
Q

Life threatening hyperthyroid exacerbation:

A

Thyroid storm

229
Q

What triggers thyroid storm?

A
  • Stress
  • Trauma
  • Infection
  • Medical illness
  • Surgery
230
Q

When is postop thyroid storm most common? What is the treatment?

A

Inadequately treated hyperthyroid patients after emergency surgery

TX: antithyroid dugs and supportive care (20% mortality)

231
Q

Are thyroid levels crazy high with thyroid storm?

A

Nope→ Thyroid levels may not be much higher than basic hyperthyroid

Health Assessment (22 decks)

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