The Endocrine System Flashcards
1
Q
What type of communication is used in the endocrine system?
A
Amplitude modulated signals
2
Q
What determines the strength of the signal in endocrine communication?
A
The amount of the hormone determines the strength of the signal
3
Q
What type of communication is used in the nervous system?
A
Frequency modulated signals
4
Q
What determines the strength of the signal in the nervous system?
A
The frequency of action potentials produced by neurons
5
Q
Why is it that endocrine and nervous systems are thought to be inseparable?
A
Neurohormones secreted by the nervous system act on endocrine tissues
6
Q
What is the scope of action for the endocrine system?
A
Broad
7
Q
What is the scope of action for the nervous system?
A
Precise
8
Q
What is the speed of the endocrine response?
A
Slow
9
Q
What is the speed of the nervous system response?
A
Fast
10
Q
Where do autocrine signals act?
A
On the same cells that secrete them
11
Q
Where do paracrine signals act?
A
Diffuse locally and act on neighboring cells
12
Q
What types of chemical messengers never enter the blood and only communicate from the interstitial fluid?
A
Autocrine and Paracrine
13
Q
How do endocrine signals function?
A
Hormones carried between cells by the blood or other body fluids, bind to specialized receptors on the plasma membrane and induce a response with or without entering the target cell
14
Q
How do neural signals function?
A
Diffuse a short distance between neurons
15
Q
How do neuroendocrine signals function?
A
They are released from neurons but act on distant cells
16
Q
What are pheromones?
A
Hormones released into the environment and act on different individuals
17
Q
What three feedback mechanisms regulate the synthesis and secretion of hormones of the endocrine system?
A
Neural control
Genetically encoded or acquired biorhythms
Feedback mechanisms
18
Q
What is the most common feedback system used in the body to maintain homeostasis?
A
Negative Feedback System
19
Q
What is the goal of the negative feedback system?
A
To have a plasma level of the hormone that feeds back to the hypothalamus to ensure proper levels are maintained
20
Q
What is the mechanism behind a positive feedback system?
A
The rate of the process increases as the concentration product increases
21
Q
How do protein/peptide hormone receptors function?
A
The receptor is located on the cell surface of the target cell which triggers a response by activating an intracellular enzyme system generating a second messenger
22
Q
What is the process of signal pathway?
A
Signal molecule binds to Receptor protein that activates Intraceullular signal molecules altering Target proteins which creates RESPONSE
23
Q
What is an important aspect of endocrine signaling?
A
Amplification, the end result is large
24
Q
What are the two most common second messengers?
A
cAMP & Ca
25
What is the predominant effect of second messengers?
Activate protein kinases
26
What is the general rule of thumb for hormones considered to be peptides or proteins?
All hormones are protein based except those that are secured from the adrenal cortex (steroid hormones)
27
What are considered amine derived hormones?
Tyrosine
| Tryptophan
28
What hormones are tyrosine based?
Thyroid hormone
Dopamine
Epinephrine
Norepinephrine
29
What is the tryptophan derived hormone?
Serotonin
30
What is unique about the thyroid hormone storage?
There is no storage in the cell, when ready for release, the molecules move to the edge of the cell for exocytosis into the circulation
31
How do thyroid hormones act like steroids?
Thyroid hormones must be bound to protein in the thyroid follicles
32
What are characteristics of steroid hormones?
All are lipid soluble and derived from cholesterol or have a chemical structure similar to cholesterol
33
What are the steroid hormones?
Cortisol, aldosterone, estrogen, progesterone and testosterone
34
How are steroid hormones stored?
Not stored in discrete secretory granules but are compartmentalized within the endocrine cell and released into the ECF by simple diffusion through the cell membrane
35
Why is the half life of steroid hormone greater than other hormones?
Al steroid hormones (and thyroid) are bound to transport proteins which increase the half life significantly
36
What do steroid hormones take so much more time compared to other hormones?
They travel bound to a protein, once reach the correct cell membrane, diffuse across cytoplasm where is binds with the DNA, induces start of transcription. Many mRNA are produced amplifying the signal
37
What two factors determine hormone clearance?
Rate of secretion into the blood
| Rate of removal from the blood
38
How are hormones cleared?
Metabolic destruction by tissues/target cells
Binding with tissues
Excretion into the bile
Excretion by kidneys into the urine
39
How are water soluble hormones broken down?
Degraded by enzymes in the blood
40
What are the two components of receptor modulation?
Up and Down Regulation
41
What occurs during up regulation of receptors?
Due to a lack of stimulation, neural receptors increase in number
42
What occurs during down regulation of receptors?
Due to continuous stimulation of a receptor, neural receptors decrease in number
43
What does the pituitary gland regulate?
Energy and water balance
Growth
Response to stress
Reproduction
44
How many hormones does the pituitary gland secrete?
Eight
Six anterior
Two posterior
45
What does the term trophic indicate?
Act to modulate other endocrine glands, control the function of other tissues
46
Where is the hypothalamus located?
Floor and lateral walls of the third ventricle
47
What is the significance of the hypothalamus?
Area of the brain where the endocrine and ANS work together
48
How is the hypothalamus connected to the pituitary gland?
Pituitary stalk
49
What surrounds the pituitary gland?
Encased in the sella tunica bounded above by the optic chasm and laterally by the cavernous sinuses
50
What regulates the anterior pituitary gland?
Negative feedback via hormones from the target organs in the periphery
51
Where are the four major feedback loops?
GH
TSH
ACTH
LH & FSH ( count as one)
52
What term is used to describe all of the hypothalamic neuropeptides?
Trophic, releasing hormones that go to the anterior pituitary to release hormones
53
What part of the pituitary gland has neural connection?
Posterior pituitary gland has direct neural connection
54
How does the posterior pituitary form?
Downward growth of neural tissues that begins at the diencephalon
55
How does the anterior pituitary gland form?
Up growth of ectodermal tissue that begins as an evagination of an area of the roof of the mouth
56
How do the two glands eventually combine?
As the upgrowth expands, it begins to meet the down growth
57
How does the anterior pituitary gland communicate with the hypothalamus?
Two capillary beds
58
What is the only hormone of the pituitary gland that is not a trophic hormone?
Growth hormone
59
What are tropes?
Cell of the pituitary gland, specifically the anterior, which manufacture and secrete anterior pituitary hormones
60
What is the function of growth hormone?
Skeletal development and body growth, regulates protein and CHO metabolism
61
What is the function of ACTH?
Regulates growth of the adrenal cortex and the release of cortisol and androgenic hormones from the adrenal gland
62
What is the function of TSH?
Controls growth and metabolism of the thyroid gland and the secretion of thyroid hormones
63
What is the function of FSH?
Stimulates ovarian follicle, development/spermatogenesis
64
What is the function of LH?
Induces ovulation and corpus luteum development, stimulates testes to produce testosterone
65
What is the function of prolactin?
Promotes lactogenesis, inhibits synthesis and secretion of LH and FSH
66
How does the thyroid gland get stimulates to release T3 and T4?
Thyrotropin releasing hormone stimulates thyrotroph cells of AP gland --> Thyroid stimulating hormone produces and acts on target tissues at the thyroid gland
67
Where is growth hormones target site?
All tissues
68
What is the most common cause of pituitary pathology?
Adenoma
69
What are the functions of growth hormone?
```
Sodium retention
Decreased insulin sensitivity
Lipolysis
Protein synthesis
Epiphyseal Growth
```
70
What is the effect of growth hormone on the liver?
Insulin like growth factor I released
71
What are the functions of insulin like growth factor I?
Insulin like activity
Anti lipolytic activity
Protein synthesis
Epiphyseal growth
72
What is another name for growth hormone inhibiting hormone?
Somatostatin
73
How is growth hormone secreted?
Pulsatile with circadian rhythms
74
What pathophysiology occurs with excess of growth hormone before puberty?
Giantism, response at epiphyseal plates
75
What pathophysiology occurs with excess of growth hormone after puberty?
Acromegaly, the diameter increases
76
What are symptoms typically seen in acromegaly?
Coarsening of facial features, widened fingers, toes, hands and feet, prominent eyebrow ridge and jaws, all organs increase in size
77
What pathology is present when there is a normal amount of GH but there is low or absent ICF1
Pygmies
78
How are GH abnormalities diagnosed?
Random GH elevations (know what point of circadian cycle) High normal GH that fails to suppress with glucose administration
Elevated IGF 1 (this does not undergo daily variation)
79
What airway abnormalities are seen with acromegaly?
Facial deformities, large nose, macroglossia, enlarged thyroid, prognathism, obstructive teeth, hypertrophy of epiglottis, general soft tissue overgrowth and MP 3,4
80
What cardiac abnormalities are seen in acromegaly?
Arrhythmias, CAD and HTN
81
What can be done to a patient with Acromegaly to assess from entrapment neuropathies?
Allen test
82
How can Octreotide be used in the treatment of Acromegaly?
It is a somastatin analog, inhibits GH secretion by binding to somatostatin 2 and 5 receptors
83
What drug is a GH receptor antagonist used for treating Acromegaly?
Pegvisomant
84
What is typically the cause of giantism?
Noncancerous pituitary tumor
85
What symptoms are typically seen in giantism?
Large tongue, coarse body hair, skin thickness, heart failure, weakness and visual problems
86
What is considered dwarfism?
An adult hight of 4'10
87
What are the two main categories of Dwarfism?
Disproportionate and Proportionate
88
What are common characteristics of Achondroplasia?
Average torso, shorter arms and legs, OR short trunk with longer limbs
Large head, protruding jaw, crowded and misaligned teeth, double jointed, spine curves forward
89
How is dwarfism acquired?
Autosomal dominant genetic syndrome
90
What are the characteristics of proportionate dwarfism?
The body parts are in proportion but shortened (GH deficiency after birth)
91
What is the function of ACTH?
Regulates the growth of the adrenal cortex and the release of cortisol and androgenic hormones from the adrenal gland
92
What is one of the most potent activators of the HPA axis?
Surgery
93
When does the largest release of ACTH occur during surgical stimulation?
Reversal of anesthesia, extubation and the immediate post operative period
94
What hormone is released from the adrenal cortex?
Cortisol
95
Based on circadian rhythms, when is the most amount of cortisol released?
In the morning and during stress
96
How can ACTH cause hyper pigmentation?
Possesses mild melanocyte stimulating hormone
97
What is precursor protein that is cleaved to create ACTH?
Pro Opiomelanocortin (POMC)
98
what controls the release of aldosterone?
Renin --> Angiotensin I --> Angiotensin II
99
Where does ACTH act in the body?
Acts on the adrenal cortex to release glucocorticoids (cortisol)
100
What is the process for ACTH to be released?
Hypothalamus --> CRH --> AP --> ACTH
101
What pathology occurs with hyper secretion of ACTH?
Cushing's Syndrome
102
What is typically the cause of Cushing's Syndrome?
Pituitary gland adenoma or over secretion of corticotropin from the hypothalamus
103
Why might ACTH be increased without the presence of Cushing's syndrome?
Adrenal cortex atrophy, cortisol secretion is reduced and does not close the negative feedback loop
104
What can occur when there is hypo secretion of ACTH as a primary pituitary disorder?
Results in decreased cortisol secretion from the adrenal cortex (fatal)
105
What are typically the causes of hypo secretion of ACTH?
Pituitary hyopfunction or failure due to intrapituitary bleed or autoimmune adrenal dysfunction
106
How could an adrenal adenoma causes hypo secretion of ACTH?
Over secretion of cortisol in the negative feedback loop response
107
What two hormones are released from the posterior pituitary gland?
Vasopressin and Oxytocin
108
Where is vasopressin synthesized?
Optic nucleus
109
What are the functions of the two vasopressin receptors?
V1 in blood vessels (high concentration in splenic areas) causes vasoconstriction and increased arterial pressure
V2 in kidneys that cause renal fluid reabsorption and increase blood volume
110
What are additional factors that can cause the release of vasopressin?
At the level of the hypothalamus pain, trauma, nausea, vomiting and increased temperature
111
What pathology can occur when there is an overproduction of ADH?
Syndrome of Inappropriate ADH (SIADH)
112
What are symptoms of SIADH?
Water retention, increased urine osmolality, headache, nausea, vomiting altered LOC and death
113
What is a very serious complication of SIADH?
Water intoxication causing dilutional hyponatremia leading to brain edema
114
What is the treatment for SIADH?
Correct hyponatremia with caution and restrict fluids
115
If profound hyponatremia occurs with SIADH what can be given to prevent deterioration?
Hypertonic 3% saline and IV lasix to correct sodium levels slowly
116
What pathology can occur with underproduction of ADH?
Diabetes Insipidous
117
What are common causes of DI?
Trauma, pituitary tumor, surgery or autoimmune
118
What are symptoms of DI?
Large volumes of dilute urine, dehydration, thirst increased plasma osmolality
119
What is the treatment of DI?
DDAVP a vasopressin analogue
120
What is the function of oxytocin?
Stimulates lactation and is thought to help with social affiliation, infant bonding, trust and love
121
What is the most common cause of hormone pathology?
Anterior pituitary adenoma
122
What are the three most common types of pituitary adenomas?
```
Prolactin secreting
Growth hormone (acromegaly)
ACTH secreting (cushings)
```
123
What is the presentation of hypopituitarism?
Decreased thyroid function, depressed glucocorticoid production and suppressed sexual development and reproductive function
124
What are the causes of depletion of pituitary function?
Primary pituitary destruction or destruction of the hypothalamus
125
What can occur if a pituitary adenoma grows upward?
Compresses the optic chasm which leads to visual changes
126
What type of visual changes are seen with compression of optic chasm?
Outer peripheral visual loss (bi temporal hemianopsia)
| When severe the patient can only see what is in front of them
127
What is the stalk effect?
Compression of the pituitary stalk may cause elevated prolactin levels and irregular menses
128
What is Sheehan syndrome?
Postpartum pituitary necrosis (enlarged pituitary gland from pregnancy becomes compressed and necrosis occurs)
129
What is pituitary apoplexy?
Occurs when pituitary adenomas suddenly bleed internally leasing to an abrupt in size
The tumor can also outgrow its blood supply leading to swelling and dead tissue
130
What is the treatment of pituitary apoplexy?
Rapid Transphenoidal decompression with consideration of replacement of glucocorticoids and ICP resolution
131
What symptoms are typically seen in Sheehan Syndrome?
Failure to start post part lactation, increased fatigue, cold intolerance and HoTN unresponsive to volume and pressers
132
What are the three layers of the adrenal cortex?
Zona glomerulosa
Zona fasciculata
Zona Reticularis
133
What portion forms the bulk of the adrenal gland?
The adrenal cortex
134
What hormones are secreted from the adrenal cortex?
Secretes Minerocorticoids, Glucocorticoids and Sex hormones
135
What is the function of the adrenal medulla?
SNS mediation, secretes epi and norepi
136
What does the Zona Glomerulosa secrete and what controls its release?
Aldosterone which is controlled by Angiotensin II
137
What is a consequence to the adrenal cortex if there are elevated levels of aldosterone for a prolonged period of time?
Hypertrophy of zona glomerulosa
138
Why are mineralcorticoids the only hormones released from the zona glomerulosa?
They lack an enzyme required from cortisol synthesis
139
What is the largest zone of the adrenal cortex and what does it secrete?
Zona Fasciculata which secretes glucocorticoids (cortisol) and a small amount of sex hormones
140
What is the major controller of cortisol?
ACTH which is released from the anterior pituitary gland
141
What is secreted from the zona reticularis?
Sex hormones and some glucocorticoids which are stimulated by ACTH
142
How is cortisol transported in the blood?
Highly bound to corticosterone binding globulin (CBG)
143
What factors increase CBG production?
Estrogen and pregnancy
144
What factors decrease circulating CBG?
Liver disease and nephrotic syndrome
145
What is the most accurate measure of cortisol activity?
Urinary cortisol
146
What is the plasma half life of cortisol?
80-100 minutes
147
Why is cortisol essential for life?
```
CHO and protein metabolism
Fatty acid metabolism
Electrolyte and water balance
Anti inflammatory and immunosuppressive actions
Catecholamine synthesis
Normal vascular peremeability
```
148
How is cortisol released by the adrenal cortex?
Hypothalamus --> CTRH --> Anterior Pituitary --> ACTH --> adrenal cortex --> cortisol
149
What are the target cells for aldosterone?
Epithelial cells in the distal convoluted tubule in the kidney to regulate absorption and potassium secretion
150
What can alter the amount of Aldosterone secreted?
Angiotensin II
ACTH
K
Na
151
Why isn't ACTH the primary stimulus for aldosterone secretion?
ACTH does not appear to be able to stimulate the enzymes unique to the aldosterone pathway very well
152
How does sodium intake affect the activity of aldosterone?
Activity of RAAS inversely related to the dietary Na intake and K stimulates aldosterone secretion
153
What additional factors can cause the release of aldosterone?
ACTH, Na, Dopamine, Beta adrenergic agents
154
What is the function of Aldosterone?
Reabsorption of sodium and secretion of potassium and hydrogen ions contributing to electrolyte and volume homeostasis
155
How is the RAAS activated?
Macula densa cells sense low sodium and chloride concentration
Communicate with the Juxtaglomerular cells which sense low volume and secrete renin
Renin splits angiotensinogen to angiotensin I
ACE found in lungs and kidneys converts angiotensin I to angiotensin II
Angiotensin II binds to receptors that cause mineralocorticoid release
156
What is the rate limiting step in mineralocorticoid and glucocorticoid synthesis?
Cholesterol to pregnenolone
157
How does etomidate affect glucocorticoid production?
It inhibits Beta 17-hydroxyprogesterone conversion to cortisol
158
Why is cortisol a vital mediator of the stress response?
It facilitates catecholamine action and secretion thus helping to maintain CV stability
159
What are the causes of cushing's syndrome?
Endogenous adrenal cortical over secretion OR chronic treatment with glucocorticoids at higher than physiologic doses
160
What is the typical presentation of Cushing;s syndrome?
Moon-faced, tranquil obesity, skinny extremities, thin skin, easy bruising, osteopenia, fluid retention, HTN, hyperglycemia and DM
161
What is the most common cause of Cushing's syndrome?
Administration of glucocorticoids for such conditions as arthritis, asthma and allergies
162
What causes the buffalo hump often seen in Cushing's syndrome?
Redistribution of fat to the back and abdomen
163
What is the goal of treatment in patients with Cushing's syndrome?
Regulating diabetes and hypertension, ensuring intravascular fluid volume and electrolyte concentrations are normal
164
What medication can be given to stop potassium loss and mobilize fluids?
Spironolactone
165
What is a major risk of an open adrenalectomy?
Pneumothorax 20%
166
What drug can be given to patients with Cushing's syndrome if the effects of carcinoma are not cured by surgery?
Mitotaine, an inhibitor of steroid synthesis
167
What is the pathology of primary adrenal insufficiency?
Adrenals are unable to produce sufficient amounts of glucocorticoids, mineralocorticoids and androgen hormones
168
What typically causes Addison's disease?
Autoimmune bilateral adrenal destruction
169
What are symptoms typically seen in Addison's disease?
Fatigue, weakness, anorexia, nausea, vomiting, hyperpigmentation and hypovolemia
170
What electrolyte abnormalities are seen in Addison's disease?
Hyponatremia and Hyperkalemia
171
What causes secondary adrenal insufficiency?
Failure to produce CRH or ACTH caused by HPA disease or suppression
172
What are the causes of secondary adrenal insufficiency?
Most are iatrogenic:
Exogenous glucocorticoid administration
Pituitary surgery or radiation
173
What is the only deficit in secondary AI?
Cortisol is the only deficit, aldosterone is not affected therefore there is no hyper pigmentation and only mild electrolyte imbalances are present
174
What communicable disease is known to cause adrenal insufficiency?
TB
175
What causes adrenal atrophy?
Chronic administration of steroids
176
What does a positive ACTH stimulating test indicate?
Demonstrates a poor response to ACTH and indicates an impairment of the adrenal cortex
177
What is considered absolute adrenal insufficiency?
Low baseline cortisol level and a positive result on the ACTH stimulation test
178
What is considered relative adrenal insufficiency?
Higher baseline cortisol but positive ACTH test
179
What dosage of oral prednisone puts a patient a risk for adrenal insufficiency?
Greater than 20mg/day
180
What dosage of topical or inhaled prednisone puts a patient a risk for adrenal insufficiency?
Greater than 2g/day topical
| Greater than 0.8mg/day inhaled
181
What drug has more mineralocorticoid activity?
Hydrocortisone, methylprednisone has less
182
How is glucocorticoid supplementation determined for surgery?
Supplementation is individualized based on the surgery
183
Why is it better to give hydrocortisone compared to methylprednisolone when high doses are required?
Hydrocortisone is less likely to produce fluid retention, edema and hypokalemia
184
What is the glucocorticoid potency and equivalent dose of cortisol?
Potency: 1
| Equivalent dose: 20mg
185
What is the glucocorticoid potency and equivalent dose of cortisone?
Potency: 0.8
| Equivalent dose: 25mg
186
What is the glucocorticoid potency and equivalent dose of prednisone?
Potency: 4
| Equivalent dose: 5mg
187
What is the glucocorticoid potency and equivalent dose of Methylprednisolone?
Potency: 5
| Equivalent dose: 4mg
188
What is the glucocorticoid potency and equivalent dose of Triamcinolone?
Potency: 5
| Equivalent dose: 4mg
189
What is the glucocorticoid potency and equivalent dose of Betamethasone?
Potency: 25
| Equivalent dose: 0.6mg
190
What is the glucocorticoid potency and equivalent dose of Dexamethasone?
Potency: 30
| Equivalent dose: 0.75
191
What type of patients are at risk for adrenal insufficiency?
Systematic inflammation: TB, HIV, DIC
Sepsis
Etomidate for sedation
Hemodynamic instability
192
How does Conn's syndrome occur?
Functional tumor that acts independently of a physiologic stimulus
193
What conditions can Conn's syndrome be associated with?
Pheochromocytoma
Primary hyperparathyroisism
Acromegaly
194
What is the cause of secondary hyperaldosteronism?
Increased circulating renin which stimulates aldosterone release (renovascular hypertension)
195
What is the primary difference in diagnosing primary versus secondary hyperaldosteronism?
In primary there is suppressed plasma renin activity and in secondary there is elevated plasma renin activity
196
What are symptoms associated with both primary and secondary hyperaldosteronism?
Spontaneous hypokalemia, systemic hypertension, polyuria, metabolic alkalosis and muscle weakness
197
What syndrome can mimic hyperaldosteronism?
Licorice syndrome, due to long term licorice ingestion
198
What is the immediate treatment for primary hyperalsosteronism?
Potassium replacement, administer spironolactone to block aldosterone effect
Potassium sparing and antihypertensive
199
What are some anesthetic considerations for primary hyperaldosteronsim?
Avoid Sevo if hypokalemic neuropathy and polyuria are present
Hypokalemia may modify response to NDNMBA
Avoid hypoventilation and worsening hypokalemia
Be cautious to over correct volume status, HoTN effects of CV drugs may be magnified
200
What is another metabolic disturbance seen in hyperaldosteronism?
Hyperglycemia
201
What does isolated hypoaldosteronism describe?
Lowered aldosterone without corresponding changes in cortisol
202
What is typically the cause of isolated hypoaldosteronism?
Due to renin or angiotensin II regulation issues (hyporeninemia)
Can be congenital
NSAID induced
203
What are the symptoms of hypoaldosteronism?
Hyperkalemia, acidosis, sodium loss, cardiac conduction defects, volume depletion and HoTN
204
What is the treatment for hypoaldosteronism?
Mineralocorticoids and glucocorticoids if cortisol deficiency is present
205
What are the hormones of the adrenal medulla?
Epinephrine, Norepinephrine and Dopamine
206
What are the physiologic effects of Epinephrine?
Promotes energy mobilization, glycogen converted to glucose, fat to fatty acids
CV changes
Shunts blood from gut/skin to muscles and bronchodilation
207
What are the physiologic effects of Norepinephrine?
Neurotransmitter of the sympathetic division of the ANS
208
What is the breakdown of epi to norepi release from the adrenal medulla?
Epi 80%
| Norepi 20%
209
What type of cells produce the adrenal medulla hormones?
Chromaffin cells principle site where tyrosine is converted to catecholamines
210
Where do pheochromocytomas arise?
In the chromaffin cells of the adrenal medulla
211
What is the typical breakdown of catecholamines released when a pheochromocytoma is present?
Norepi: 85%
Epi: 15%
212
Where is the most common extra-adrenal location for a pheochromocytoma?
Organ of Zuckerkandl, near the aortic bifurcation
213
What are the rules of 10s when speaking about pheochromocytomas?
10% Found in children
10% are bilateral
10% are malignant
10% are extra-adrenal
214
What are the three most common symptoms of pheochromocytoma?
Palpitations
Headaches
Episodic sweating
215
What are the hyperadrenergic symptoms of a pheochromocytoma?
```
Pressure (elevated BP)
Pain
Perspiation
Palpitations
Pallor
```
216
What are patients hyperglycemic with a pheochromocytoma?
Secondary to catecholamine glycohenolysis and insuline release inhibition
217
What are additional symptoms seen with pheochromocytoma?
Cardiomyopathy
Anxiety
Weight loss
218
What is the most sensitive test for high risk patients if a pheochromocytoma is suspected?
Measurement of plasma free metanephrines
219
If there is a low probability of pheochromocytoma, what test is done?
Urinary vanillylmandelic acid (VMA) which is a breakdown byproduct of norepinephrine and plasma catecholamines
220
What are byproducts of catecholamines?
Metanephrines
221
What test is used to determine if a pheochromocytoma is present if the VMA and Metanephrine tests are inconclusive?
Clonidine suppression test
222
What is the best indicator for a pheochromocytoma?
CT scan
223
What is the result if a pheo is present in a clonidine suppression test?
There will be no change in catecholamine levels after Clonidine is given, if no pheo catecholamine level is lower
224
What is the first line treatment for pheochromocytoma?
Alpha blockade
225
What medication is used most frequently in preoperative pheochromocytoma?
Phenoxybenzamine, a long acting non competitive alpha 1 antagonist
226
Which alpha antagonist is easier to titrate in the treatment of a pheo?
Prazosin, pure alpha 1 competitive blocker
227
What drug is used in the treatment of a pheo to decrease catecholamine production?
Metyrosine
228
What are the treatment goals for a pheo?
Normotensive, resolution of symptoms and elimination of any EKG changes
229
What can occur if you over treat a pheo?
Severe orthostatic hypotension
230
What is the rule of thumb for giving both alpha and beta antagonists in treating a pheo?
ALWAYS give alpha before beta, if you give beta first the patient will have to eject against massive SVR sending patient into heart failure
231
What drugs should be avoided in pheo surgery?
Histamine releasing drugs and Vasolytics
232
What actions can induce the release of catecholamines that should be avoided for surgical removal of a pheo?
Fear, pain, shivering, hypercarbia and hypoxia
233
What is the antihypertensive drug of choice when removing a pheo?
Nitroprusside because it does not act on alpha at all it is a direct smooth muscle relaxant
234
What drug is preferred for intraoperative HTN in a epi secreting tumor?
Labetalol has beta blocking properties
235
How can a patient become hypoglycemia intraperatively while removing a pheo?
Decreased catecholamine levels leave insulin unopposed, dextrose containing fluids should be given after tumor removal
236
What can cause hypertensive episodes when removing a pheo?
Tumor manipulation
237
What can cause hypotensive episodes when removing a pheo?
Removal, alpha blockade is unmasked
238
What is Diabetes Mellitus?
A heterogeneous group of disorders that have the common feature of a relative or absolute lack of insulin
239
What is the pathology of Type I DM?
Associated with T cell mediated autoimmune diseases
| There is an insulin deficiency that makes the patient susceptable to ketoacidosis
240
What is the pathology of Type II DM?
Not immune mediated, susceptible to hyperosmotic non ketotic coma if insulin is deficient
241
What is the number one cause of blindness, chronic kidney disease and non-traumatic limb amputation in the US?
Diabetes
242
Where is insulin produced?
Pancreatic beta cells
243
What is the metabolic affect of insulin?
Inhibits gluconeogenesis
244
Where does insulin not influence glucose uptake?
The brain
245
What stimulates the secretion of insulin?
Plasma glucose
246
What should occur after a meal in regards to glucose and insulin?
Glucose utilization exceeds glucose production and a transition from exogenous glucose delivery to endogenous glucose production occurs
247
What are counter regulatory hormones?
Support glucose production and oppose insulins functions
248
What are examples of counter regulatory hormones?
Glucagon, epinephrine, growth hormone and cortisol
249
What causes diabetes?
Either an inadequate supply (Type I) or a inadequate tissue response (Type II) to insulin
250
Where is glucagon produced?
Pancreatic alpha cells and processed in the gut
251
Where is glucagon receptor location?
In the liver
252
What causes glucagon production to halt?
Glucose
253
What is the function of Glucagon?
Increases breakdown of hepatic glycogen stores and hepatic glucose synthesis
Stimulates fatty acid oxidation and ketogenesis
Stimulates hepatic uptake of amino acids
254
What type of response can occur when there is multiple hormonal inputs?
Additive or Synergistic
255
What is a protective mechanism to prevent rapid fluctuations in glucose production?
Push-pull mechanism on the alpha and beta cells of the pancreas
256
What are the rapid effects of insulin on the body?
Increased transport of glucose, amino acids and K into the insulin sensitive cells
257
What are the intermediate effects of insulin on the body?
Stimulation of protein synthesis
Inhibition of protein degradation
Activation of glycolytic enzymes and glycogen synthase
Inhibition of phosphorylase and gluconeogenic enzymes
258
What are the delayed effects of insulin on the body?
Increase in mRNA for lipogenic and other enzymes
259
What what glucose level does the body inhibit insulin secretion?
90mg/dL
260
At what glucose level does the body secrete glucagon, epinephrine and growth hormone
75mg/dL
261
At what blood glucose level does cortisol secretion occur and the patient experiences cognitive dysfunction?
60mg/dL
262
At what blood glucose level does lethargy occur?
45mg/dL
263
At what blood glucose level does coma and convulsions occur?
30mg/dL
264
At what blood glucose level does permanent brain damage and death occur?
15mg/dL
265
What is the incidence of type I diabetes out of all of the current diabetics?
5-10%
266
What is thought to cause type I DM?
Autoimmune pathology, unknown trigger although environmental triggers such as viruses, dietary proteins, drugs or chemicals may initiate the autoimmune process
267
When does the preclinical period of type I DM occur?
Lasts from 9-13 years and is characterized by production of antibodies to beta cell antigens with loss of beta cell function
268
When do clinical symptoms begin to manifest in type I DM?
After 80-90% of lost beta cell function
269
What are the manifestation of type I DM?
```
Sudden sever onset of hyperglycemia
Fatigue
Weight loss
Polyuria, polydypsia
Blurred vision
Intravascular volume depletion
```
270
How is diabetes diagnosed?
Fasting glucose greater than 126mg/dL
Random glucose greater than 200mg/dL
HA1C greater than 7
271
What is the incidence of type II DM out of all diabetics?
85-95%
272
What are common themes associated with type II diabetes?
Overweight, resistant to ketoacidosis, susceptible to hyperglycemia, hyperosmolar non-ketotic state
273
What lifestyle choices are associated with type II diabetes?
Poor food choices
Inactivity
Aging
Genetic influences
274
What is the pathophysiology behind type II DM?
A relative beta cell insufficiency and insulin resistance
275
What is unique regarding the diagnosis of type II DM?
Most people are not diagnosed for approximately 4-7years after the disorder appears
276
Why dont type II DM patients experience ketoacidosis?
They are making insulin but have a peripheral resistance to it
277
What are the three important defects in type II DM?
An increase rate of hepatic glucose release
Impaired basal and stimulates insulin secretion
Inefficient use of glucose by peripheral tissues
278
What causes the increase in hepatic glucose release in type I DM?
The reduction of insulin's normal inhibitory effects on the liver and abnormalities in regulation of glucagon secretion
279
What is metabolic syndrome?
A constellation of clinical biochemical characteristics frequently seen in patient who have or at risk of developing type II DM
280
What are characteristics of metabolic syndrome?
Fasting plasma glucose greater than 100mg/dL
Abdominal obesity
Serum triglyceride levels greater than 150
Low serum HDL cholesterol
Blood pressure greater than 130/85
281
What does the HA1C measure?
Long term glucose control
282
What is the normal range for HA1C?
4-6%
283
At what HA1C puts a patient at risk of microvasculature and microvascular disease?
Greater than 6.5%
284
What is the first line treatment for DM?
Dietary control and exercise, reduces adiposity and improves hepatic /peripheral tissues insulin sensitiveit, enhances post receptor insulin action and may increase insulin secretion
285
What pharmacologic treatments can be given for diabetics?
Oral antidiabetics
| IV or IM insulin preparations
286
What adverse effects are associated with Sulfonylureas and meglitinides oral anti diabetics?
Delays contractile recovery after myocardial ischemia and expand ischemic zone
287
What are adverse effects of Metformin?
Lactic acidosis especially with renal insufficiency
288
How would you calculate a daily dose of insulin for your patient?
kg x 0.3 (divide by 24 if you want an hourly dose)
289
Why is it essential to have tight control over blood glucose levels?
To prevent continues progression of microvascular complications
290
What is the pathology of DKA?
A profound loss of insulin production and activity that stimulate lipolysis and fatty acid breakdown which leads to ketosis
291
What are the primary ketones produced during DKA?
Acetoacetate and beta-hydroxybutyrate
292
What clinical manifestation occur during DKA episode?
Profound hyperglycemia, polydypsia, polyuria, dehydration, decreased renal blood flow, coma and kussmaul breathing
293
Why is rehydrating the patient essential in treating DKA?
If insulin is administered in the absence of electrolyte replacement, water will move from the extracellular space back into the cells causing vascular collapse
294
What are characteristics of hyperglycemic hyperosmolar coma?
Severe hyperglycemia
| Hyperosmolarity and dehydration
295
How does Hyperglycemic hyperosmolar coma occur?
Precipitated by decreased fluid intake
296
Why does HHNS cause a higher incidence of coma?
Osmolality may exceed 340mOsm/L
297
If the plasma osmolality is greater than 320 what can be given for fluid replacement?
Large volumes of hypotonic saline
298
What type of microvascular complications are associated with diabetes?
Non-occlusive microcirculatory disease and impaired auto regulation of blood flow and vascular tone
299
What is the most common neuropathy experienced by diabetics?
A distal polyneuropathy
300
What are symptoms of distal polyneuropathy?
Large sensory and motor fibers
Small fibers areas affect proprioception
Sensitivity to touch pain and temperature is impaired
301
What is the result of damage to the vasoconstrictor fibers and impaired baroreceptor function in patients with DM?
Autonomic neuropathy
302
What are CV symptoms associated with autonomic neuropathy?
Abnormalities in heart rate control (does not respond to exercise)
Systolic and diastolic dysfunction with reduced EF
Orthostatic HoTN
Silent ischemia
303
What GI effects associated with autonomic neuropathy?
Impaired gastric secretion and motility
Gastroparesis diabeticorum
Diarrhea/Constipation
304
What is the treatment for gastroparesis?
Small meals, reduced fat content and a prokinetic (reglan)
305
When should an insulin infusion be initiated for intraoperative use?
Ideally a continuous insulin infusion should be started at least two hours before surgery
306
What is an appropriate range for glucose intraoperatively?
Between 120-180mg/dL
307
At what glucose level does glycosuria and dehydration begin to occur?
Greater than 200mg/dL
308
What is the typical rule of thumb when giving one unit of insulin?
Decreases glucose by 25-30mg/dL
309
What is the typical dose for an insulin infusion pump?
0.02u/kg/hr
310
When does the onset of gestational diabetes typically occur?
During the second half of gestation and resolves at parturition
311
What is thought to cause gestational diabetes?
Increasing levels of progesterone, cortisol, prolactin and somatotrophin (counter regulatory hormones)
312
How can gestational diabetes affect the pregnancy?
Associated with an increased rate of C-sections as well as perinatal morbidity and mortality
313
Who are at risk for gestational diabetes?
```
Those who have family history of diabetes, especially on the maternal side
Older than 25
Baby more than 9 lbs/ birth defect
Too much amniotic fluid
Overweight before pregnancy
Unexplained stillbirth or miscarriage
```
314
Where are thyroidglobulins located?
In the colloid portion of the follicle
315
What is unique about the action of thyroid hormone?
Although an amine, it enters the affected cell and changes the mRNA like a steroid hormone
316
If a thyroid deficiency occur, how long might it take to see changes in thyroid levels?
2-3 months
317
How is T3 and T4 synthesized?
Iodide converted to iodine
iodine attaches to tyrosine on TGP
T3 and T4 formed and TGH is removed in lysosomes
318
What is the active form of thyroid hormone?
T3
319
What is the breakdown of thyroid hormone released?
T4 93%
| T3 7%
320
How is thyroid hormone absorbed?
Via ion trapping
321
How does TSH function to increase the amount of thyroid hormone?
Increases the amount of iodide into the cell for synthesis
| Enzyme synthesis via increased DNA transcription of RNA
322
What protein is T4 bound to?
Thyroid binding globulin
323
What protein is T3 bound to?
Mainly to albumin
324
When is thyroid hormone active?
The unbound form
325
What pathology is associated with an elevated TSH?
Hypothyroidism
326
What diseases are associated with hypothyroidism?
Goiter
| Hashimotos
327
What pathology occurs when there is a decrease in circulating TSH?
Hyperthyroidism
328
What disease is associated with hyperthyroidism?
Graves disease
329
How does thyroid hormone exert its affects?
By binding to specific receptors in the nuclei of cells in target tissues
330
What effects does thyroid hormone have on the body?
Metabolism
Thermoregulation
Growth/Development
Myelination in childhood
331
What metabolic processes does T3 and T4 stimulate?
Oxidative metabolism
Basal metabolic rate
Heat production
332
What are the main causes of hyperthyroidism?
```
Graves disease
Pregnancy
Thyroiditis
Adenoma
TSH secreting pituitary adenoma
```
333
What treatment is given to patients with hyperthyroidism?
Propylthiouracil (PTU)
| Propranolol
334
What is the goal in treating hyperthyroidism?
Euthyroid
335
What are clinical manifestation of hyperthyroidism?
Weight loss, diarrhea, warm moist skin, weakness of large muscles, osteopenia, jittery, heat intolerance, tachycardia, HTN and heart failure
336
What are the two most common differential diagnoses associated with thyroid storm?
MH and Neuroleptic malignant syndrome
337
Why should the provider use caution in patients with a history of long term use of amiodarone?
Can cause thyroid storm because it increases plasma thyroid hormone
338
What are clinical manifestation of thyroid storm?
```
Hyperpyrexia >40 degrees
Sweating
Tachycardia
Afib
N/V/D
Tremors, delirium, apathy
```
339
What are triggers for thyroid storm or crisis?
Surgery, infection or trauma
340
How should thyroid storm be managed?
```
Hydration
O2
Cooling
Pentothal
Inotropes
Beta blockade
```
341
What drugs should be avoided in thyroid storm?
Aspirin
| Ketamine
342
How does Propylthiouracil treat hyperthyroidism?
It prevents the production of more T3 and T4 in the thyroid and blocks the conversion of T4 to T3 outside of the thyroid
343
How does Iodides (Lugol's solutionl treat hyperthyroidism?
Blocks release of stored thyroid hormone from thyroid gland
344
How do glucocorticoids treat hyperthyroidism?
Blocks conversion of T4 to T3
345
How are beta blockers used in the treatment of hyperthyroidism?
Reduces symptoms caused by heightened response to catecholamine, blocks conversion of T4 to T3
346
How is Lugol's solution administered?
Via NG tube
347
What is the mechanism of action of methimazole in treating hyperthyroidism?
Prevents production (synthesis) of more thyroid hormone
348
What term is used to describe fetal hypothyroidism?
Cretinism
349
What are clinical presentations of hypothyroidism?
```
Slow mental function
Dry skin
Arthralgias
CV depression
intolerance to cold
slow gastric emptying
```
350
If hypothyroidism is left untreated what is the end result?
Myxedema Coma
351
What are clinical manifestations of Myxedema Coma?
Typically seen in elderly obese females
Become increasingly withdrawn, lethargic, sleepy and confused
Slip into coma
352
What findings in a patients history may cause concern for Myxedema coma?
Previous thyroid surgery
Radioiodine
Default hormone therapy
353
What is the most common reason for hypothyroidism to occur?
Previous thyroid surgery thyroid adenoma
354
What diagnostic test is typically used in determining thyroid pathology?
TSH
355
What are some anesthetic implication for patients undergoing a thyroidectomy?
Must be euthyroid preoperatively
Thorough airway assessment
Avoid drugs that stimulate the SNS
356
What are the main airways concerns in patients with goiters?
Positional dyspnea
Dysphagia
Vena Caval obstruction if tumor extends into the chest
357
What are some intraoperative considerations for patients having a thyroidectomy?
Avoid premedication/use regional when possible
CV monitoring
Protect against hypothermia
358
Where are the parathyroid glands located?
Four glands on the posterior aspect of the thyroid gland
359
What lab value is often drawn when removal the of thyroid gland has occurred?
Ionized Calcium due to removal of the thyroid gland
360
What stimulates the release of parathyroid hormone?
Hypocalcemia
361
How does hypercalemia affect PTH?
Suppresses both hormonal synthesis and release of calcium
362
How does PTH maintain normal plasma concentration of calcium?
Promotes the movement of calcium across three interfaces
GI tract
Renal tubules
Bone
363
What is required in order for the parathyroid gland to function?
Vitamin D
364
What is the active form of vitamin D?
Calcitrol
365
What hormones promotes the storage of calcium?
Calcitonin
366
Why is calcitonin said to be counter regulatory to PTH?
It inhibits bine mobilization and lowers blood calcium
367
What is typically the cause of primary hyperparathyroidism?
Adenoma
368
What is typically the cause of secondary hyperparathyroidism?
Inadequate D3 produced, hypocalcemia stimulates hight PTH levels
369
What are clinical manifestations of hyperparathyroidism?
Dehydration, bone pain, confusion, anorexia, constipation, muscle weakness, HoTN, shortened QT
370
What is the most common cause of primary hypoparathyoidism?
Surgical parathyroid resection
371
What arecommon causes of secondary hypoparathyroidism?
```
Acute hypomagnesiumesmia
Reduced vitamin D
Chronic renal insuffiency
Acute systemic illness
Blood transfusion
Resistent tissues
```
372
What drugs have been known to cause hypoparathyroidism?
Ketoconazole
| Doxorubicin
373
What are clinical presentations of hypocalcemia?
```
Tetany
Perioral numbness
Paresthesias
Muscle cramping Seizures
Hyper reflexia
HoTN
Bradycardia
Prolonged QT
```
374
What two signs are used to determine if hypocalcemia is present?
Ckvostek sign
| Trousseau sign
375
What is the most common post op complication associated with removal of the parathyroid glands?
Tetany, be aware if the patient develops stridor can be cord tetany
376
What may cause refractory hypocalcemia after removal of the parathyroid glands?
Hypomagnesaemia
377
How might hypocalcemia affect neuromuscular blockade?
Hypocalcemia causes muscle weakness and sensitivity to muscle relaxants
