Endocrine - Exam IV 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 Diabetes Mellitus?

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
If emergent surgery, what do you give for hypothyroidism?
IV thyroid replacement along with steroids ASAP
26
What percent of total DM cases account for type 1?
5-10%
27
What is myxedema coma?
Rare, severe form of hypothyroidism characterized by delirium, hypoventilation, hypothermia, bradycardia, HoTN, and dilutional hyponatremia
28
What is the cause of autoimmune destruction of beta cells in T1D?
- Exact cause is unknown - A long period (9-13yrs) of B-cell antigen production occurs before onset symptoms
29
What is the cardinal feature of myxedema coma?
Hypothermia d/t impaired thermoregulation
30
T1D is usually diagnosed before what age?
40
31
What population does myxedema coma most commonly occur?
Elderly women with long history of hypothyroidism
32
What percent of beta cell dysfunction before hyperglycemia is sustained?
80-90%
33
What can trigger myxedema coma?
- Infection - Trauma - Cold - CNS depressants
34
What is the mortality of myxedema coma?
>50%
35
Treatment for myxedema coma:
- IV L-thyroxine or L-triiodothyronine - IV hydration w/ glucose solutions - Temp regulation - Electrolyte correction - Supportive care
36
What are common S/S of T1D related to prolonged hyperglycemia?
- Fatigue - Weight loss - Polyuria - Polydipsia - Blurry vision - Hypovolemia - Ketoacidosis
37
What is goiter?
Swelling of thyroid gland d/t hypertrophy and hyperplasia of follicular epithelium
38
T2D accounts for ____% of DM cases
>90% Increasingly seen in younger patients and kids over last decade
39
What can cause goiter?
- Lack of iodine - Ingestion of goitrogen - Hormonal defect
40
What are the initial stages of T2D? What happens over time?
- Tissues desensitized to insulin→ causes increase secretion - Over time pancreatic function decreases and insulin levels are inadequate
41
42
In most cases, a goiter is associated with what?
A compensated euthyroid state
43
How are most goiter cases treated?
L-thyroxine
44
When is surgery indicated for goiter?
If medical treatment is ineffective, and goiter compromises airway or is cosmetically unacceptable
45
How are thyroid tumors examined?
CT scan
46
What symptoms are predictive of airway obstruction during general anesthesia in patients with thyroid tumors?
Dyspnea in upright or supine position
47
What are the 3 main abnormalities seen with DM2?
- Impaired insulin secretion - increase hepatic glucose release (reduced in insulin inhibitory effect on liver) - Insufficient glucose uptake in peripheral tissues
48
For patients with thyroid tumors, what can indicate location/degree of obstruction?
Flow-volume loops in upright and supine positions
49
Limitations in the inspiratory limb of the loop indicates ____ obstruction:
extra-thoracic
50
DM2 is characterized by insulin resistance in with tissues?
- Skeletal muscle - Adipose - Liver
51
Delayed flow in the expiratory limb indicates an _____ obstruction:
intra-thoracic
52
What is the cause of insulin resistance in T2D?
- Abnormal insulin molecules - Circulating insulin antagonists - Insulin receptor defects
53
How do you assess the degree of cardiac compression with a thyroid tumor?
Echocardiogram
54
How is T2D diagnosed?
- Fasting BG - HbA1C *Obesity and sedentary lifestyle are acquired and contributing factors*
55
In thyroid surgery, if unilateral vocal hoarseness occurs without obstruction, how long does it take to resolve?
3-6 months
56
Normal A1C: Prediabetic A1C: Diabetes:
Norm: <5.7% Prediabetes: 5.7-6.4% Diabetes: >6.5%
57
Bilateral thyroid involvement can cause what?
Airway obstruction and warrant tracheostomy
58
Hypoparathyroidism may result from what? Symptoms?
Inadvertent parathyroid damage with thyroid surgery Sx of hypocalcemia occur within 48 hours postop
59
What are ADA criteria for Dx of diabetes?
- A1C >6.5 - Fasting glucose >126 - 2hr glucose >200 during oral glucose tolerance test - Random glucose >200
60
What can lead to tracheal compression in thyroid surgery?
Hematoma
61
What should be kept at bedside during immediate postop period after thyroid surgery?
Trach set
62
Each adrenal gland consists of what?
A cortex and medulla
63
What does the cortex of the adrenal gland synthesize?
- Glucocorticoids - Mineralcorticoids (aldosterone) - Androgens
64
What is the treatment DM2?
- Dietary adjustment - Exercise and weight loss (improve hepatic and peripheral insulin sensitivity) - PO antidiabetic drugs
65
How is corticotropin (ACTH) released?
Hypothalamus sends corticotropin-releasing hormone (CRH) to the anterior pituitary, which stimulates release of corticotropin
66
ACTH stimulates the adrenal cortex to produce ____:
Cortisol
67
What is the function of cortisol?
Helps convert NE to epi and induces hyperglycemia
68
Together, cortisol and aldosterone cause what two things?
Sodium retention and K+ excretion
69
What is a pheochromocytoma?
Catecholamine-secreting tumor that originates from chromaffin cells
70
Excess catecholamines can lead to what??
Malignant HTN, CVA and MI
71
80% of pheo occur where?
Adrenal medulla
72
18% of pheos occur where?
In organ of Zuckerkandle
73
2% of pheos occur where?
Neck/thorax
74
Where do malignant pheos spread through?
Venous and lymph systems
75
What is the preferred initial drug tx for DM2?
- Metformin (biguanide) - Enhances glucose transport into tissues - Decrease TG and LDL levels
76
What is the ratio of NE:epi secreted in pheos?
85:15 - the inverse of normal adrenal secretion *some secrete higher levels of epi, and more rarely dopamine
77
When can pheo attacks occur?
- Attacks range from occasional to frequent and may last minutes or hours - May occur spontaneously or triggered by injury, stress or meds
78
What is the MOA of sulfonylurea PO antidiabetic drugs?
- Stimulate insulin secretion - Enhance glucose transport into tissues - Not effective long term (progressive loss of beta cell fx)
79
Symptoms of pheochromocytoma:
- Headache - Pallor - Sweating - Palpitations - HTN - Orthostatic HoTn - Coronary vasoconstriction, cardiomyopathy, CHF and EKG changes may occur
80
How do you diagnose a pheo?
- 24 hours urine collection for metanephrines and catecholamines - CT and MRI
81
What are side effects of sulfonylureas?
- Hypoglycemia - Weight gain - Cardiac effects
82
PO antidiabetics:
83
What do you give preop to patients with a pheo?
α blocker to lower BP, decrease intravascular volume
84
Which diabetics need insulin?
All DM1 and 30% DM2
85
What is the most frequently used preop α-blocker? How does it work?
Phenoxybenzamine; Noncompetitive α1 antagonist with some α2 blocking properties
86
What are the different types of insulin?
- Rapid acting (lispro, aspart= meal time) - Short acting (regular) - Basal/intermediate (NPH, Lente) - Long acting (Ultralente, glargine)
87
What are two other pure α1 blockers?
Prazosin and Doxazosin - shorter acting with less tachycardia
88
What is the most dangerous complication of DM?
Hypoglycemia
89
How do you treat tachycardia after giving an α1 blocker?
Beta blocker
90
What can increase incidence of hypoglycemia in DM?
- ETOH - Metformin - Sulfonylureas - ACE-Is - MAOIs - Non-selective beta blockers
91
Why do you not give nonselective beta-blockers before an α blocker?
blocking vasodilatory β2 receptors results in unopposed α agonism, leading to vasoconstriction and hypertensive crises
92
What is the issue with repeated episodes of hypoglycemia?
- Hypoglycemia unawareness - Densensitization to hypoglycemia= no autonomic symptoms - Neuroglycopenia
93
What defines ACTH dependent Cushings syndrome?
High plasma ACTH stimulates adrenal cortex to produce excess cortisol
94
What defines ACTH-independent Cushings syndrome?
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
Symptoms of hypercortisolism (cushings)
- Sudden weight gain - Usually central w/ moon face - ecchymoses - HTN - glucose intolerance - Muscle wasting - Depression - Insomnia
96
How do you diagnose cushings?
24 hour urine cortisol
97
What is required to determine if cushings is ACTH dependent or independent?
ACTH level
98
What are signs of neuroglycopenia?
- Fatigue - Confusion - Headache - Seizures - Coma
99
For Cushings, is CT/MRI/US useful?
Useful for determining tumor location, but not helpful in gauging adrenal function
100
What is treatment for neuroglycopenia?
PO or IV glucose (SQ of IM if unconscious)
101
Treatment of choice for cushings:
Transsphenoidal microadenomectomy is resectable
102
Alternate treatment for cushings:
- Subtotal resection of the anterior pituitary - Pituitary irradiation and adrenalectomy maybe necessary
103
What is the treatment for adrenal adenoma or carcinoma?
Surgical adrenalectomy
104
Preop considerations for cushings:
- Evaluate/treat BP - Correct electrolyte imbalance - Correct blood glucose - Consider osteoporosis
105
Hottie with cushings:
106
What causes primary hyperaldosteronism (conn syndrome)?
Excess secretion of aldosterone caused by tumor (aldosteronoma)
107
Is conns syndrome more common in men or women?
Women
108
Conn syndrome is occasionally associated with what?
Pheochromocytoma, hyperparathyroidism or acromegaly
109
What causes secondary hyperaldosteronism?
Elevated renin levels
110
Symptoms of hyperaldosteronism:
*Non-specific, some are asymptomatic - HTN - Hypokalemia - hypokalemic metabolic alkalosis
111
Hallmark symptom of hyperaldosteronism:
Spontaneous HTN with hypokalemia
112
Renin activity in primary vs secondary hyperaldosteronism:
Primary = renin activity is suppressed Secondary = renin activity is elevated
113
What can cause a syndrome that mimics hyperaldosteronism?
Long term ingestion of licorice (sx = HTN, hypokalemia, suppression of RAAS)
114
Treatment for hyperaldosteronism:
- Aldosterone antagonist (spironolactone) - K+ replacement - Antihypertensives - Diuretics - Tumor removal - Possible adrenalectomy
115
Hallmark sign of hypoaldosteronism:
Hyperkalemia in the absence of renal insufficiency
116
What else is common in hypoaldosteronism?
Hyperchloremic metabolic acidosis
117
What are some symptoms of hypoaldosteronism?
May experience heart block, orthostatic HoTN, hyponatremia
118
What are some things that can cause hypoaldosteronism?
- Congenital deficiency of aldosterone - Low renin - ACE inhibitors
119
What is a reversible cause of hypoaldosteronism?
Indomethacin-induced prostaglandin deficiency
120
Treatment for hypoaldosteronism:
Increased sodium intake and daily fludrocortisone
121
What is primary adrenal insufficiency?
Autoimmune adrenal gland suppression *Addison's disease
122
What is secondary adrenal insufficiency?
Hypothalamic-pituitary suppression leading to a lack of CRH or ACTH production
123
Unlike Addison's, there is only a ____ deficiency in secondary AI
glucocorticoid
124
What are some causes of iatrogenic cases of secondary adrenal insufficiency?
- Synthetic glucocorticoids - Pituitary surgery - Radiation
125
Patients with secondary AI lack ____
hyperpigmentation
126
Diagnosis for adrenal insufficiency:
Baseline cortisol <20 Mcg/dL and remains <20 after ACTH stimulation A positive test demonstrates a poor response to ACTH
127
What indicates relative adrenal insufficiency?
When the baseline cortisol level is higher, but the ACTH stimulation test is positive
128
What is the treatment for adrenal insufficiency?
Steroids
129
How many parathyroid glands are there and where are they? What do they do?
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
Hypocalcemia ____ the release of PTH, where hypercalcemia ____ PTH synthesis and release
stimulates; suppresses
131
How does PTH maintain normal plasma calcium levels?
Promotes the movement of calcium across GI tract, renal tubules, and bone
132
Primary hyperparathyroidism is caused by:
- benign parathyroid adenoma - Carcinoma (<5%) - Parathyroid hyperplasia
133
Symptoms of hyperparathyroidism:
- Lethargy - Weakness - N/V - Polyuria - Renal stones - PUD - Cardiac disturbances
134
Diagnosis for hyperparathyroidism:
- Plasma calcium - 24 hour urinary calcium
135
Treatment for primary hyperparathyroidism:
Surgical removal of abnormal portions of the gland
136
What is secondary hyperparathyroidism?
Compensatory response of the parathyroid glands to counteract a separate disease process involving hypocalcemia (ex. CRF)
137
Treatment for secondary hyperparathyroidism:
Controlling the underlying disease, normalizing phosphate levels with a phosphate binder
138
Why is deficient PTH almost always iatrogenic?
Caused by inadvertent removal of parathyroid glands - may occur during thyroidectomy
139
What is pseudohypoparathyroidism?
Disorder where PTH is adequate, but the kidneys are unable to respond to it
140
Diagnostic labs for hypoparathyroidism:
- ↓PTH, - ↓Ca++, - ↑phos
141
What are symptoms of hypoparathyroidism dependent on?
Speed of onset
142
Acute hypocalcemia such as after accidental parathyroid removal may cause what?
Inspiratory stridor or laryngospasm
143
What is chronic hypocalcemia associated with?
- Fatigue - Cramps - Prolonged QT - Cataracts - SQ calcifications - Neurologic deficits
144
Treatment for hypoparathyroidism:
- Calcium replacement - Vitamin D
145
What are the 6 hormones secreted by the anterior pituitary under the control of the hypothalamus?
- GH - ACTH - TSH - FSH - LH - Prolactin
146
What is stored in the posterior pituitary after being synthesized in the hypothalamus?
Vasopressin and oxytocin
147
What causes acromegaly?
Excessive growth hormone, most often seen with anterior pituitary adenomas
148
Diagnostic labs for acromegaly:
insulin-like growth factor 1 (IGF 1) is elevated
149
In acromegaly, overgrowth of soft tissues make the patients susceptible to what?
Upper airway obstruction
150
With acromegaly, what causes hoarseness and abnormal movement of vocal cords or RLN paralysis?
Overgrowth of surrounding cartilage
151
What is common in acromegaly due to nerve trapping by connective tissues?
Peripheral neuropathy
152
Treatment for acromegaly:
- Removal of pituitary adenoma (usually transsphenoidal approach) - If surgery is not feasible, LA somatostatin analogues are the medical treatment
153
Anesthesia implications for acromegaly:
- 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
What are the two main causes of Diabetes insipidus (vasopressin deficiency)?
- Central/neurogenic DI: destruction/dysfunction of the posterior pituitary - Nephrogenic DI: failure of kidneys to respond to ADH
155
Which form of DI causes urine-concentration?
Neurogenic, not nephrogenic - d/t response to DDAVP
156
Symptoms of DI:
- polydipsia - excessive, dilute UOP despite increased serum osmolarity
157
Initial treatment for DI:
- IV electrolytes to offset polyuria
158
Treatment for neurogenic DI:
DDAVP
159
Treatment for nephrogenic DI:
- low salt and low protein diet - thiazide diuretics - NSAIDs
160
Anesthesia considerations for DI:
Monitor UOP and serum electrolyte concentrations
161
What can cause SIADH?
- intracranial tumors - hypothyroidism - porphyria - lung cancer
162
Diagnosis for SIADH:
- hyponatremia - decreased serum osmolarity - increased urine sodium and osmolarity
163
Abrupt drop in serum sodium can cause what??
Cerebral edema and seizures
164
165
Treatment for SIADH:
- Fluid restriction - Na+ tablets - loop diuretics - ADH antagonists (demeclocycline)
166
How can severe hyponatremia be treated?
Hypertonic saline
167
What is the onset/peak/duration of short, intermediate, and long acting insulin?
168
Which insulin peaks first vs last?
169
What is ketoacidosis a complication from?
Decompensated T1D (mortality 1-2%)
170
What usually triggers DKA?
Infection/illness
171
What is the MOA of DKA?
- High glucose exceeds threshold for renal absorption (hypovolemia and diuresis) - Liver over produces ketoacids
172
What is the diagnostic criteria for DKA?
- Glucose ≥ 300 - pH ≤ 7.3 - HCO3 ≤ 18 - Serum Osmolarity < 320 - Serum/urine ketone moderate to high
173
What is the treatment for DKA?
- 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
What is the dose of regular insulin (IV) for DKA correction?
- Loading dose 0.1u/kg - Low dose infusion 0.1u/kg/hr
175
What are characteristics of HHNKS? Which disease process does this occur in?
- Severe hyperglycemia - Hyperosmolarity - Dehydration *Normally occur in DM2 >60y/o*
176
What are S/S of HHNKS?
- polyuria - polydipsia - hypovolemia - hypotension - tachycardia - coma (from hyperosmolarity) - Some degree of acidosis *when blood glucose exceeds renal glucose absorption→ causes massive glucosuria*
177
What is the treatment for hyperglycemia hyperosmolar syndrome?
- Fluid restriction - Insulin bolus and infusion - electrolytes
178
What is the mortality of DKA vs HHNKS?
DKA: 1-2% HHNKS: 10-20%
179
Primary complications of DM:
- Microvascular: nonocclusive microcirculatory with impaired blood flow - Nephropathy - Peripheral neuropathy - Retinopathy - Autonomic Neuropathy
180
How common is nephropathy in DM1 vs DM2? What are the symptoms of nephropathy?
- DM1: 30-40% - DM2: 5-10% - S/S: HTN, proteinuria, peripheral edema, low GFR
181
Why is hyperkalemia associated with nephropathy?
GRF <15-20= kidneys no longer clear K+ → hyperkalemic acidosis
182
What medication is used to slow the progression of proteinuria and decreased GFR in diabetics?
Ace-inhibitors
183
What are treatment options for ESRD?
- HD - PD - Kidney transplant *Combined kidney-pancreas transplant may prevent recurrent nephropathy*
184
How does diabetic peripheral neuropathy present/impact patients?
- Distal symmetric diffuse sensorimotor neuropathy - Starts in toes and progresses proximally - Loss of large sensory and motor fibers (reduces tough and proprioception) - Loss of small nerve fibers (decrease pain/temp perception) - Neuropathic pain - Ulcers develop (unnoticed injury) - Recurrent infection/ amputation wounds
185
What causes DM retinopathy? How can retinopathy progression be reduced?
- Microvascular damage - Visual impairment (range: color loss to blindness) - Glycemic control and BP control reduce progression
186
What happens to CV and GI systems from DM autonomic neuropathy ?
- CV: abnormal cardiovascular dynamics, loss of HR variability, orthohypotension, dysrhythmias (potential for silent MI) - GI: decrease secretion and motility→ gastroparesis
187
What are S/S and treatments for DM autonomic neuropathy?
S/S: N/V, early satiety, bloating, epigastric pain Tx: glucose control, small meals, prokinetics
188
What are important factors in preop eval for DM patients?
- 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
What is insulinoma?
Rare benign insulin-secreting pancreatic tumor
190
Which population is more at risk for Insulinoma?
2X more in women age 50-60
191
How is Insulinoma diagnosed?
Whipple Triad: - Hypoglycemia with fasting - Blood glucose <50 with symptoms - Symptoms relief with glucose
192
Patients that have insulinoma have high blood ________ level during 48-72 fast
insulin (causes hypoglycemia)
193
What med can be given in preop for patient with an insulinoma? What are other treatments?
Diazoxide Preop: Inhibits insulin release from beta cells TX: verapamil, phenytoin, propranolol, glucocorticoids, octreotide Surgery= curative
194
What is a concern for patient with insulinomas intra op and post op?
- Hypoglycemia intra-op - Hyperglycemia post op (when tumor removed) *tight glycemic monitoring and treatment*
195
The thyroid gland is composed of 2 lobes joined by an _______
Isthmus (small narrow band of tissue)
196
The thyroid is attached to anterior and lateral _________ with the upper border below ________ cartilage
Trachea Cricoid
197
What nervous systems innervate the capillary network of the thyroid?
Adrenergic and Cholinergic nervous systems
198
Which nerves are in close proximity to the thyroid?
- Recurrent laryngeal nerve - Superior laryngeal nerve (idk what SLN abbreviation means in her PPT so this is my best guess 🥸)
199
_________ hormones stimulate virtually all metabolic processes
Thyroid
200
What exogenous substance is needed for production of thyroid hormones?
Exogenous idodine
201
How is iodine transformed into thyroid hormones?
- Iodine in GI tract reduced to iodide→absorbed and sent to thyroid follicular cells - Iodide binds to thyroglobulin= inactive monoiodotyrosine and diiodotyrosine (from T3/T4)
202
25% Monoiodotyrosine and diiodotyrosine undergo coupling with _______ _________ to form T4 and T3.
Thyroid peroxidase
203
What is another name for T4?
Throxine
204
What is another name for T3?
Triiodothyronine
205
What is the ratio of T4:T3?
10:1
206
What 3 structures regulate thyroid function?
- Hypothalamus (TRH) - Anterior pituitary (TSH) - Thyroid glands
207
What is the function of TSH binding to thyroid receptors?
Synthesis and release of T3 and T4
208
How is TSH release triggered?
- Hypothalamus releases TRH which signals ant pituitary to release TSH - TSH also influenced by plasma T3/T4 levels (negative feedback)
209
The thyroid has an __________ mechanism to maintain consistent levels.
Autoregulatory
210
What is the best test of thyroid action at the cellular level?
TSH assay (sensitive to small changes) Norm TSH level: 0.4-0.5 miliunits/L
211
What is THR stimulation test used to test?
Pituitary function and TSH secretion
212
What is the disease process that causes hyper-functioning thyroid gland with excessive hormone secretion?
Hyperthyroidism
213
Most cases of hyperthyroidism are caused by 1 or 3 pathologies. What are the 3 pathologies?
- Graves disease - Toxic goiter - Toxic adenoma
214
What are symptoms of hyperthyroidism?
- Sweating - Heat intolerance - Fatigue - Insomnia - Osteoporosis/ weight loss - CV compromise (T3 effect on myocardium and peripheral vaculature)
215
List of hyperthyroid S/S 😑
216
What is the leading cause of hyperthyroidism?
Graves disease (0.4% of population) *more common in females 20-40y/o*
217
What is the MOA of graves?
Autoimmune→ thyroid stimulating antibodies that cause growth, vascularity, and hypersecretion (thyroid gets bigger= common to have goiter)
218
How is graves diagnosed?
- Positive TSH antibodies - Low TSH - High T3/T4
219
What is an anesthesia concern for patients with graves?
Extreme thyroid enlargement may cause: - Dysphagia - Inspiratory stridor - Tracheal compression
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What is the 1st line treatment for Graves?
Antithyroid drugs→ Methimazole or Propylthiouracil (PTU)
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Why is iodine therapy not the best long term treatment option for patients with Graves?
It can inhibit the release of thyroid hormone BUT effect is temporary *Good to use Preop correction or in thyroid storm*
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How can propranolol impact Graves disease?
Impairs the peripheral conversion to T4/T3
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If medical management for Graves fails what surgery is recommended? What are complications of the surgery?
- Subtotal Thyroidectomy - Complications: Hypothyroid, hemorrhage, hematoma, tracheal compression, RLN damage, parathyroid damage
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What should be assessed in patient with Graves preop?
- Thyroid levels - Upper airways for evidence of tracheal compression or deviation d/t goiter
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A women with graves started taking methimazole last week for Graves. How long does she need to wait before elective surgery?
6-8 weeks after starting antithyroid drugs (so drugs can take effect)
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If a patient with Graves requires emergent surgery what meds should be given?
- IV beta blockers - glucocorticoids - PTU
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What are S/S or Graves?
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Life threatening hyperthyroid exacerbation:
Thyroid storm
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What triggers thyroid storm?
- Stress - Trauma - Infection - Medical illness - Surgery
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When is postop thyroid storm most common? What is the treatment?
Inadequately treated hyperthyroid patients after emergency surgery TX: antithyroid dugs and supportive care (20% mortality)
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Are thyroid levels crazy high with thyroid storm?
Nope→ Thyroid levels may not be much higher than basic hyperthyroid
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What is absolute Adrenal Insuff characterized by?
Low baseline cortisol level and a positive ACTH stimulation test