KLE-Endocrine modules 1-9 Flashcards

(157 cards)

1
Q

What are the messengers of the endocrine system

A

hormones

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2
Q

Define endocrine

A

a cell releases a substance that travels through the bloodstream before acting on different cells

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3
Q

Define paracrine

A

Cell releases a substance that acts on adjacent cells

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4
Q

Define autocrine

A

Cell releases a substance that acts on the surface of the same cell

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5
Q

Define negative feedback

A

Response is negative (opposite) the initiating stimulus

Returns the parameter to a set point to maintain stability

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6
Q

Define positive feedback

A

Provides an unstable cycle which the system responds in a way that increases the magnitude of the response

Results is amplification of the original signal

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7
Q

What is the function of the hypothalamus

A

Links the CNS to the endocrine system by monitoring hormone concentrations in circulation then influencing output from pituitary gland

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8
Q

How is the hypothalamus able to monitor hormone concentration in circulation

A

It resides outside the BBB

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9
Q

How does the hypothalamus communicate with the anterior pituitary

A

Releasing and inhibiting hormones are released from the hypothalamus into the hypophyseal portal vessels, traveling along the pituitary stalk

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10
Q

Where is ADH produce

A

Primarily in supraoptic nuclei of hypothalamus

secondary = paraventricular nuclei

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11
Q

Where is oxytocin produced

A

primarily in paraventricular nuclei of the hypothalamus

Secondary = supraoptic nuclei

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12
Q

How are posterior pituitary hormones transported from the hypothalamus

A

Via axonal transport along the pituitary stalk

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13
Q

What are 7 hypothalamic hormones

A
  1. Luteinizing hormone-releasing hormone
  2. Corticotropin-releasing hormone
  3. Thyrotropin-releasing hormone
  4. Prolactin-releasing factor
  5. Prolactin-inhibiting factor
  6. Growth hormone-releasing hormone
  7. Growth hormone-inhibiting hormone
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14
Q

What is the target hormone for luteinizing hormone-releasing hormone
Where

A

In anterior pituitary

  1. Inc follicle-stimulating hormone (FSH)
  2. Inc luteinizing hormone
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15
Q

What is the target hormone for corticotropin-releasing hormone
Where

A

In anterior pituitary

Inc adrenocorticotropic hormone (ACTH)

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16
Q

What is the target hormone for thyrotropin-releasing hormone

Where

A

In anterior pituitary

Inc TSH

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17
Q

What are the target hormones for prolactin-releasing/inhibiting factors
Where

A

In anterior pituitary
Prolactin releasing = INC prolactin
Prolactin inhibiting = DEC prolactin

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18
Q

What are the target hormones for growth hormone-releasing/inhibiting hormone
Where

A

In anterior pituitary
Growth hormone-releasing = INC GH
Growth hormone-inhibiting = DEC GH

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19
Q

What are 6 hormones released from the anterior pituitary

A

FLAT PiG

  1. Follicle-stimulating hormone
  2. Luteinizing hormone
  3. Adrenocorticotropic hormone
  4. Thyroid stimulating hormone
  5. Prolactin
  6. Growth hormone
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20
Q

Where is the pituitary gland located

A

In the sella turcica

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21
Q

What are other names for the anterior and posterior pituitary

A
Anterior = adenohypophysis
posterior = neurohypophysis
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22
Q
Follicle-stimulating hormone:
Released from=
Action=
Hyposecretion=
Hypersecretion=
A

Released from= anterior pituitary
Action= germ cell maturation, ovarian follicle growth (fem)
Hypersecretion= early puberty
Hyposecretion= infertility

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23
Q
Luteinizing hormone:
Released from=
Action=
Hypersecretion=
Hyposecretion=
A

Released from= anterior pituitary
Action= testosterone production (male), ovulation (fem)
Hypersecretion= early puberty
Hyposecretion= infertility

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24
Q
Adrenocorticotropic hormone:
Released from=
Action=
Hypersecretion=
Hyposecretion=
A

Released from= anterior pituitary
Action= adrenal hormone release
Hypersecretion= Cushing’s disease
Hyposecretion= Addison’s disease

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25
``` Thyroid stimulating hormone: Released from= Action= Hypersecretion= Hyposecretion= ```
Released from= anterior pituitary Action= thyroid hormone release Hypersecretion= hyperthyroidism Hyposecretion= hypothyroidism, cretinism
26
``` Prolactin: Released from= Action= Hypersecretion= Hyposecretion= ```
Released from= anterior pituitary Action= lactation Hypersecretion= infertility Hyposecretion= menstrual dysfunction
27
``` Growth hormone: Released from= Action= Hypersecretion= Hyposecretion= ```
Released from= anterior pituitary Action= cell growth Hypersecretion= acromegaly, gigantism Hyposecretion= dwarfism
28
``` Antidiuretic hormone: Released from= Action= Hypersecretion= Hyposecretion= ```
Released from= posterior pituitary Action= water retention Hypersecretion= SIADH Hyposecretion= Diabetes insipidus
29
``` Oxytocin: Released from= Action= Hypersecretion= Hyposecretion= ```
Released from= posterior pituitary Action= uterine contraction, breast feeding Hypersecretion= nada Hyposecretion= Uterine atony
30
What are the negative feedback hormones that regulate the following hormones: Thyrotropin-releasing hormone= Luteinizing hormone-releasing hormone= Corticotropin-releasing hormone= Growth hormone-releasing/inhibiting hormone=
Thyrotropin-releasing hormone= Triiodothyronine (T3) Luteinizing hormone-releasing hormone= Testosterone, estrogen, progesterone Corticotropin-releasing hormone= cortisol Growth hormone-releasing/inhibiting hormone= Growth hormone, insulin growth factor-1
31
Which hormones are not affected by negative feedback regulation
Oxytocin | Prolactin
32
How is oxytocin release regulated
Via positive feedback loop | More oxytocin = more uterine contractions = more oxytocin...
33
How is prolactin regulated
Output is under neural control | Increased dopamine decreases prolactin release
34
What are 4 associated conditions causing SIADH
1. TBI 2. Cancer (small-cell lung ca) 3. Noncancerous lung dz 4. Carbamazepine
35
What are 3 associated conditions causing DI
1. Pituitary surgery (most common) 2. TBI 3. SAH
36
Presentation of: SIADH DI
``` SIADH = hyponatremia DI = polyuria ```
37
What is the plasma content of the following in SIADH: Volume= Osmolarity= Sodium=
``` Volume= euvolemic or hyper Osmolarity= hypotonic (<275) Sodium= Low (<135) ```
38
What is the plasma content of the following in DI: Volume= Osmolarity= Sodium=
``` Volume= Euvolemic or hypo Osmolarity= hypertonic (>290) Sodium= High (>145) ```
39
What is the urine content of the following in SIADH: Volume= Osmolarity= Sodium=
``` Volume= Low Osmolarity= Higher than plasma osmo Sodium= High ```
40
What is the urine content of the following in DI: Volume= Osmolarity= Sodium=
``` Volume= high Osmolarity= lower than plasma osmo Sodium= normal ```
41
What are 4 treatments for SIADH
1. Fluid restriction 2. Demeclocycline (decreases responsiveness to ADH) 3. Hypertonic NaCl if symptomatic
42
When is hypertonic NaCl indicated in SIADH | How is it corrected
Symptomatic Na <120 | Don't exceed correction of Na >1 mEq/L/Hr
43
What are treatments for DI
1. DDAVP or vasopressin | 2. Supportive
44
What can cause over secretion of growth hormone
pituitary adenoma
45
What are 4 ventilation and intubation considerations for pts with acromegaly
1. Distorted facial features = difficult mask ventilation 2. Large mouth structures = difficult DL 3. Subglottic narrowing and VC enlargement = difficult ETT placement, smaller ETT 4. Enlarge turbinates = Risk of epistaxis with nasal intubation
46
7 Common comorbid conditions with acromegaly
1. OSA 2. HTN 3. CAD 4. Rhythm disturbances 5. glucose intolerance 6. Skeletal muscle weakness 7. Entrapment neuropathies
47
Where is the thyroid gland located
1. anterior to trachea 2. inferior to cricoid cartilage 3. superior to suprasternal notch
48
RLN location with respect to thyroid gland
Courses along the lateral border of each thyroid lobe
49
Why is RLN injury increased with thyroid and parathyroid surgery
D/t its location running along side of the thyroid gland lateral borders
50
Thyroxine (T4): Source= Highest concentration= half-life=
Source= direct release from thyroid Highest concentration= in blood half-life= 7
51
Triiodothyronine (T3): Source= Highest concentration= half-life=
Source= Extrathyroid conversion of T4 to T3 Highest concentration= converted from T4 in target cell half-life= 1 day
52
Thyroxin (T4) vs Triiodothyronine (T3): Protein binding = Potency =
Protein binding = more | Potency = less
53
Triiodothyronine (T3) vs thyroxine (T4): Protein binding = Potency =
Protein binding = less | Potency = more
54
What is TSH action on the thyroid gland
1. stimulates iodide pump so thyroid produces T3 and T4 | 2. Stimulates follicular tissue to produce thyroglobulin colloid
55
How is TSH level regulated
Negative feedback via T3 and T4 suppressing TSH release
56
Why is TSH elevated in hypothyroidism
There isn't enough thyroid hormone for T3/T4 production so TSH release isn't suppressed by the negative feedback loop
57
How does a goiter form
When thyroid hormone is deficient there is too much TSH to stimulate the follicles and make thyroglobulin colloid (which doesn't require iodine for production)
58
How does increased thyroid hormone affect metabolism (simple)
INC thyroid hormone => INC BMR => INC O2 consumption + INC CO2 production
59
What are 4 ways increased thyroid hormone affects myocardial performance
1. INC chronotropy 2. INC contractility 3. INC Lusitropy 4. dec SVR (vasodilation)
60
What are 2 ways increased thyroid hormone affects ANS which is passed to the heart
1. INC number/sensitivity of beta receptors | 2. dec number of cardiac muscarinic receptors
61
How does increased thyroid hormone affect respiratory pattern
INC BMR => INC CO2 production => Vm (inc Vt and RR)
62
How does increased thyroid hormone affect volatile MAC
No effect on MAC b/c CNS isn't affect by INC O2 consumption
63
How does increased thyroid hormone affect inhaled induction
INC CO => INC anesthetic uptake into blood => dec rate of rise of FA/FI => slower induction
64
How does increased thyroid hormone affect GI tract
hypermotility = diarrhea
65
What effect does increased thyroid hormone have on cellular metabolism of nutrients Fat Protein CHO
Fat: inc utilization of fat stores = weight loss Protein: inc catabolism = skeletal muscle weakness CHO: inc gluconeogenesis, inc insulin release, inc glucose intake
66
Why are pts with hyperthyroidism heat intolerant
inc O2 consumption => inc CO2 production => vasodilation => heat loss
67
Why do pts with hyperthyroidism experience tremors
Inc sensitivity of neuronal synapses in spinal cord
68
What are 7 causes of hyperthyroidism
1. Grave's disease (autoimmune) 2. Myasthenia gravis (autoimmune) 3. Multinodular goiter 4. Carcinoma 5. Pregnancy 6. Pituitary adenoma 7. Amiodarone
69
What are the most common causes of hyper/hypothyroidism
hyper = Grave's disease hypo = hashimoto's thyroiditis Both autoimmune
70
What are 6 causes of hypothyroidism
1. Hashimoto's thyroiditis 2. Iodine deficiency 3. Hypothalamic-pituitary dysfunction 4. Neck radiation 5. thyroidectomy 6. amiodarone
71
How is hypothyroidism diagnosed
High TSH | Low T3/T4
72
How is hyperthyroidism diagnosed
Low TSH | High T3/T4
73
What are 3 cardiac manifestations of hyperthyroidism
1. HTN 2. Tachycardia 3. A-Fib
74
What are 5 cardiac manifestations of hypothyroidism
1. peripheral vasoconstriction 2. decreased HR 3. decreased contractility 4. heart failure 5. pericardial effusion
75
What are 4 respiratory manifestations of hypothyroidism
1. decreased Vm 2. Reduced response to hypoxia 3. Reduced response to hypercarbia 4. Pleural effusion
76
What are 8 physical manifestations of hyperthyroidism
1. Goiter 2. Weight loss 3. muscle weakness 4. moist, warm skin 5. heat intolerance 6. Fine hair 7. tremors 8. exopthalmos
77
What are 8 physical manifestations of hypothyroidism
1. Goiter 2. Weight gain 3. muscle fatigue 4. lethargy 5. Dry, thick skin 6. cold intolerance 7. dry brittle hair 8. constipation
78
What is thyroid storm
Increased thyroid hormone output in response to a stressful event
79
When is thyroid storm most likely to happen in the perioperative period
6-18 hours after surgery
80
What is a complication of hypothyroidism
Myxedema coma d/t severley impaired thyroid function
81
What is the result of neonatal hypothyroidism
Cretinism = limited physical and mental development
82
What medications are used to inhibit thyroid synthesis in hyperthyroidism
Thionamides - propylthiouracil - methimazole - carbimazole
83
What is the MOA of thionamides
Inhibition of thyroid synthesis by blocking iodine addition to tyrosine on thyroglobulin PTU inhibits T4 to T3 conversion peripherally
84
How long before euthyroid is achieved once thionamides are initiated for hyperthyroidism
6-7 weeks
85
What medications are used to reduce SNS stimulation in hyperthyroidism
beta blockers
86
What is unique about the use of propranolol in hyperthyroidism
It also inhibits peripheral conversion of T4 to T3
87
What medication reduces thyroid hormone synthesis
potassium iodide
88
When should potassium iodide be initiated in perioperative hyperthyroid pt
10 days before surgery
89
What medication destroys thyroid tissue
radioactive iodine
90
Guidelines for surgery of the hyperthyroid pt
Do not proceed to elective surgery until pt is euthyroid
91
What 3 medications should be available to give in hyperthyroid pts that require emergency surgery
1. beta blockers 2. Potassium iodide 3. glucocorticoids
92
How does a goiter affect airway manipulation
Can cause tracheal deviation and tracheomalacia
93
What type of intubation should be performed in goiter pts
Awake intubation | Any method that maintains spontaneous ventilation
94
What 4 medications or classes should be avoided in the hyperthyroid pt
1. sympathomimetics 2. anticholinergics 3. ketamine 4. pancuronium
95
Why is there increased risk for corneal abrasion in hyperthyroid pts
Pts may have exopthalmos which increases risk
96
Signs of unilateral RLN injury w/ thyroid surgery
ipsilateral VC positioned midline | Hoarseness
97
Signs of bilateral RLN injury w/ thyroid surgery
Both VC positioned midline on inspiration | Airway obstruction
98
How can nerve injury be assessed following extubation
Have pt say E or moon
99
How is RLN function assessed intraoperatively
NIM tube with electrodes positioned between the VC
100
When does hypocalcemia occur with thyroidectomy including parathyroid glands
24-48 hrs post surgery
101
8 s/sx of hypocalcemia
1. muscle spasm-tetany 2. laryngospasm 3. mental status change 4 HoTN 5. prolonged QT 6. Paresthesias 7. Chvostek's sign 8. trousseau's sign
102
What are 7 s/sx of thyroid storm
1. Fever >38.5*C 2. Tachycardia or dysrhythmias 3. HTN 4. CHF 5. Shock 6. Confusion and agitation 7. N/V
103
What conditions can thyroid storm mimic while under anesthesia
1. MH 2. pheochromocytoma 3. neuroleptic malignant syndrome 4. light anesthesia
104
What are the 4 main managements for thyroid storm
1. Block synthesis (methimazole, PTU) 2. Block release (radioactive I) 3. Block T4/T3 conversion (propranolol, glucocorticoids) 4. Block beta receptors (beta blockers)
105
Why are glucocorticoids used in hyperthyroidism
They block conversion of T4/T3 | Support stress response-hypermetabolism consumption of endogenous steroids
106
What are anesthetic management considerations for thyroid storm
1. Cardiopulm support 2. glucocorticoids 3. active cooling 4. Acetaminophen for fever
107
How is hypothyroidism medically managed
Levothyroxine | Thyroid hormone is replaced with synthetic T4
108
What are 2 initial responses to initiation of levothyroxine
1. Natriuresis | 2. Decreased TSH
109
How is airway manipulation affected in the hypothyroid pt
Airway obstruction can be d/t large tongue, swollen VS, and/or goiter
110
Why is there an increased risk of aspiration in hypothyroid pt
They have delayed gastric emptying
111
Describe the CV effects of hypothyroidism
1. dec HR 2. dec SV 3. dec contractility 4. dec CO 5. dec baroreceptor responsiveness - inc risk of HoTN
112
Why is inhalation induction faster in hypothyroidism
b/c dec CO
113
What vasoactive drugs are best in hypothyroidism
sympathomimetics | avoid phenylephrine
114
How is adrenal function affected by hypothyroidism | Anesthetic implications
Decreased adrenal function is common | Hotn unresponsive to catecholamines can be treated with corticosteroids
115
How is metabolism and excretion affected by hypothyroidism
Hepatic metabolism and renal excretion are slowed | This can prolong drug effects
116
Which fluid may be best in hypothyroid pt and why
D5NS | Provides glucose and combats hyponatremia d/t impaired H2O clearance
117
What response can hypothyroid pts have to nondepolarizing NMB
They can have increased sensitivity
118
How do osteoblasts affect serum Ca++
They reduce iCa++ by promoting Ca++ bone deposition
119
How do osteoclasts affect serum Ca++
They increase iCa++ by promoting bone resorption
120
What is the relationship between PTH and calcitonin
PTH works to increase Ca++ levels | Calcitonin works to decrease Ca++ levels
121
How do PTH and calcitonin affect serum Ca++ and phosphate levels
PTH= inc Ca++, dec phosphate Calcitonin= dec Ca++, inc phosphate
122
PTH: site of production= site of release= stimulator for release=
site of production= chief cells in parathyroid gland site of release= parathyroid gland stimulator for release= dec iCa++, inc phosphate
123
PTH: physiologic effect= mechanism=
physiologic effect= Inc iCa++, dec phosphate mechanism= - inc Ca++ bone resorption - inc intestinal Ca++ absorption by upregulating kidney enzymes for calcitrol - kidney Ca++ reabsorption inc - kidney phosphate elimination inc
124
Calcitonin: site of production= site of release= stimulator for release=
site of production= C cells in thyroid gland site of release= thyroid gland stimulator for release= inc iCa++
125
Calcitonin: physiologic effect= mechanism=
physiologic effect= dec iCa++, inc phosphate mechanism= -inc Ca++ deposition in bone
126
What is the most common cause of hypercalcemia
hyperparathyroidism
127
What is the most common cause of primary hyperparathyroidism
Parathyroid adenoma
128
What lab abnormalities are present in the hyperparathyroid pt
incr PTH levels hypercalcemia hypophosphatemia
129
What is the best treatment for primary hyperparathyroidism
resection of PT glands
130
What is the most common cause of secondary hyperparathyroidism
kidney disease
131
What is the term for PTH induced bone disease in renal pts
renal osteodystrophy
132
What is the treatment for primary hypoparathyroidism
1. Ca++ supplement 2. Vitamin D 3. Mg++ supplement
133
What are CV effects of hyperparathyroidism
1. HTN | 2. Shortened QT interval
134
What are musculoskeletal effects of hyperparathyroidism
1. bone pain 2. osteopenia 3. pathologic fractures 4. muscle weakness
135
What are GI effects of hyperparathyroidism
1. Anorexia 2. N/V 3. abd pain 4. PUD 5. Pancreatitis
136
What are GU effects of hyperparathyroidism
1. polyuria 2. polydipsia 3. kidney stones
137
What are CV effects of hypoparathyroidism
1. HoTN 2. myocardial depression 3. long QT interval
138
What are musculoskeletal effects of hypoparathyroidism
muscle spasms | paresthesia
139
4 ways the body responds to hypocalcemia
1. parathyroid gland releases PTH 2. osteoclasts in bone release Ca++ 3. Ca++ is reabsorbed in the kidneys 4. Ca++ absorption in gut increases in presence of vitamin D
140
What are the zones of the adrenal cortex
1. Zona glomerulosa 2. Zona fasciculata 3. Zona reticularis
141
Which hormones are released from each adrenal cortical zone
(G) Glomerulosa = mineralocorticoids (salts) (F) Fasciculata = glucocorticoids (sugar) (R) Reticularis = androgens (sex)
142
What is released from the adrenal medulla
Catecholamines: Epinephrine (80%) Norepinephrine (20%)
143
Example of a mineralocorticoid
aldosterone
144
What ions are excreted with aldosterone action on kidneys
K+ | H+
145
3 reasons aldosterone release is increased
1. RAAS activation 2. hyperkalemia 3. Hyponatremia
146
Example of a glucocorticoid
cortisol
147
Where is the site of action of cortisol
It diffuses through the lipid bilayer and binds with intracellular steroid receptors
148
What is the mechanism of cortisol action
Activation or inhibition of DNA transcription, it influences protein synthesis inside the target cell
149
What effect does cortisol have on the hypothalamus and anterior pituitary
Inhibition via negative feedback loop
150
What is normal daily cortisol production
15-30 mg/day
151
What can increase serum cortisol
stress
152
What are the 3 main jobs of cortisol
1. Energy mobilization 2. Anti-inflammatory effects 3. Hemodynamics
153
3 ways cortisol affects energy mobilization
1. Gluconeogenesis = converts AA to glucose and increased glucose 2. Protein catabolism = muscle breakdown to inc AA availability 3. Fatty acid mobilization = inc FFA oxidation and ability to use fat for energy
154
How does cortisol mitigate anti-inflammatory effects
Mitigates the inflammatory cascade by stabilizing lysosomal membranes and reducing cytokine release
155
What 2 types of blood cells are decreased as a result of cortisol
Eosinophils | Lymphocytes
156
What effect does cortisol have on myocardial performance
Myocardial performance improves by increased number and sensitivity of beta receptors on myocardium
157
Why is exogenous cortisol required for BP management
It is required for vasculature to respond to vasoconstrictive effects of catecholamines