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Endo exam 4 Flashcards

Hormones baby!!!! (103 cards)

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1
Q

Name the organs of the Endocrine system?

A

Hypothalamus
pineal gland
pituitary
Thyroid
parathyroid
thymus
pancreas
ovaries
testes
adrenals

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2
Q

this organ is our primary source for glucose?

A

The liver

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3
Q

What is the percent range for the endogenous glucose metabolized ? by what cells/tissues?

A

70-80% Brain, Fat, muscles, RBCs

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4
Q

Roughly how long does it take to switch from exogenous to endogenous glucose production post eating?

A

2-4 hours

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5
Q

Formerly known as juvenile diabetes, an autoimmune destruction of Beta cells of the pancreas

A

Type 1a
Can occur up to 40 years of age, usually diagnosed in children, near their teens.

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6
Q

Type 1a vs Type 1b

A

Type 1a is an autoimmune destruction (causation undetermined)

Type 1b is an idiosyncratic lack of insulin production (rare).

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7
Q

Describe type 2 DM.

A

Tissues become resistant to insulin, nothing is technically wrong with the pancreas. This leads to a hyperglycemic state, and a global inflammatory response, which results in the multi organ dysfunction associated with the disease process.

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8
Q

What is the frequency in adults and is DM the most common endocrine disorder?

A

1 in 10 adults and yes.

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9
Q

Name a rapid, short, intermediate, and long acting insulin.

A

rapid= lispro
short= regular
intermediate= NPH
long= lantus

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10
Q

Phenomenon in which people are unaware their glucose levels are low?

A

hypoglycemia unawareness

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11
Q

How do you diagnose DM, what is your HgbA1C if your diabetic?

A

Fasting glucose or HgbA1C
>6.5%

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12
Q

This drug opposes the action of glucagon?

A

Metformin

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13
Q

These drugs stimulate the pancreas to release insulin?

A

Sulfonylureas

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14
Q

Why are Sulfonylureas not a good choice long term?

A

over time the pancreas either manufactures an abnormal insulin peptide or stops releasing all together.

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15
Q

What is DKA?

A

Usually precipitated by illness or stress. High levels of glucose cause an excessive release of glucagon. Fatty acid oxidation occurs, and we are left with an excess of ketones. Hyperglycemia leads to dehydration and electrolyte imbalance due to osmotic diuresis.

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16
Q

Prototypical DKA treatment?

A

IV volume replacement
Insulin: Loading dose 0.1u/kg Regular + low dose infusion @ 0.1u/kg/hr
Correct acidosis: sodium bicarb
Electrolyte supplement: k+, phos, mag, sodium
*Correction of glucose w/o simultaneous correction of sodium may result in cerebral edema

Pretty much isolated to type 1 for the most part.

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17
Q

DKA’s evil twin?

A

Hyperosmotic Hyperosmolar Nonketotic syndrome.

Presents very similar to DKA, just no ketones.

Tx: fluid resuscitation, insulin bolus + infusion, e-lytes

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18
Q

What are the long term consequences of DM?

A

Retinopathy, Nephropathy, microvascular, neuropathy, and ANS neuropathy.

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18
Q

This drug class prevents cardiac remodeling and can also attenuate the loss of GFR in DM?

A

ACE-Is

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19
Q

Treatment options for DM?

A

Diet, Lose weight, strength train, insulin, PO meds. Tight glycemic control in order to reduce HgBA1C and improve insulin resistance.

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20
Q

DM preop considerations?

A

Think multi system involvement. CNS, CV, Renal.

Hydration & Lytes

Gastroparesis

Holding or reduced medication dosing

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21
Q

Rare tumor found in the pancreas?

A

insulinoma

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22
Q

Insulinomas present with what features?

A

Hypoglycemia w/fasting
Glucose <50 w/sx
Sx relief w/glucose

aka Whipples triad

Preop- Diazoxide, which inhibits insulin release from B cells
Other tx: verapamil, phenytoin, propranolol, glucorticoids, octreotide
Surgery is curative

watchout for hypoglycemia

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23
Q

These two nerves run right next to the thyroid.

A

recurrent and superior laryngeal nerve (motor branch)

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24
Why are thyroid procedures such a risk?
Highly vascular and nerve proximity.
25
What exogenous element do we need in low amounts to maintain our T3/T4 levels
iodine
26
Typical T3/T4 ratio?
10:1
27
Why is the thyroid so vital?
Thyroid hormones stimulate virtually all metabolic processes. They influence growth and maturation of tissues, enhance tissue function, and stimulate protein synthesis and carbohydrate and fat metabolism
28
What are the major players anatomically when it comes to the thyroid?
hypothalamus, pituitary, and thyroid
29
The hormonal pathway for thyroxine synthesis?
TRH (Hypothalamus) TSH (Anterior pituitary) T3/T4 ( Thyroid) T3/T4 turn off hypothalamus via negative feedback loop in the normal system
30
Common diagnostic testing for the thyroid?
TSH assay TRH stimulation test assesses the functional state of the TSH-secreting mechanism serum anti-microsomal antibodies, antithyroglobulin antibodies, and thyroid-stimulating immunoglobulins
31
Normal TSH level?
normal TSH level is 0.4-5.0 milliunits/L
32
Hyperthyroidism manifestations?
sweating, heat intolerance & fatigue w/inability to sleep (Hypermetabolic state)
33
What hormone presentation of Grave's disease is typical and whom does it typically effect?
low TSH + high T3 & T4 Women
34
What might occur in/around the airway with graves?
dysphagia, globus sensation, and inspiratory stridor from tracheal compression
35
Firstline treatment for graves?
PTU or methimazole Typical goal is to shrink the gland before operation is performed.
36
Complications of thyroidectomy?
Complications from surgery include hypothyroidism, hemorrhage with tracheal compression, RLN damage, and damage to or inadvertent removal of the parathyroid glands
37
Medication for symptom management in the context of Grave's?
β-blockers Propranolol (non selective) impairs the peripheral conversion of T4 to T3
38
Pre op concerns with graves?
Thyroid levels should be established preoperatively Elective cases may need to wait 6-8 weeks for antithyroid drugs to take effect  In emergent cases, IV BBs,  glucocorticoids, and PTU usually necessary Evaluate upper airway for evidence of tracheal compression or deviation caused by a goiter
39
Condition is similar to MH, what is it and how do we manage?
Thyroid storm. Get them through with symptom management. Try and shut down the thyrotoxicosis. 20% mortality rate.
40
Hormone presentation in hypothyroidism or hashimotos?
↓T3 & T4 production despite adequate TSH
41
Textbook presentation with hypothyroidism?
cold intolerance, weight gain, nonpitting edema. Their body is in slow motion.
42
How to differentiate primary vs secondary hypothyroidism?
test to determine if its the pituitary or the thyroid. TRH test is performed. If there is an appropiate TSH response, the pituitary is fine. No TSH= Bad pituitary gland.
43
Patients can experience a psuedohypothyroidism , True or False?
True. Low T3 & T4 w/normal TSH level Likely a response to stress, and it can be induced by surgery
44
TSH >10 milliunits/L puts you at risk for what?
CAD.
45
What is the DOC for hypothyroidism.
L-thyroxine
46
Hypothyroidism preop concerns?
Assess for airway compromise d/t swelling, edematous vocal cords, goitrous enlargement Expect slower gastric emptying, aspiration rx Cardiovascular system may be hypodynamic Respiratory function may be compromised More prone to hypothermia Electrolyte imbalances possible If elective case, Thyroid tx should be initiated at least 10 days prior If emergent surgery: IV Thyroid replacement along with steroids ASAP
47
This is rare in hypothyroidism but can be deadly?
myxedema coma 50% mortality rate
48
Treatment for myxedema coma?
IV T4 & T3 IV hydration w/glucose-saline solutions, temp regulation, correction of e-lyte imbalances, and stabilization of cardiac & pulmonary systems are necessary 
49
When is a surgery indicative for goiter?
Surgery indicated only if medical therapy is ineffective, and goiter is compromises AW or is cosmetically unacceptable Most goiters go away if Iodine is adequate, and T4 is given.
50
Pre op airway concerns for goiter?
Evaluate airway, especially if dyspnea is present. CT for tumor eval. Limitations in the inspiratory limb of the loop indicate extra-thoracic obstruction Delayed flow in the expiratory limb indicates an intra-thoracic obstruction
51
Why does thyroid surgery result in hoarseness?
RLN injury may be unilateral or bilateral and temporary or permanent If there is bilateral involvement. We have paralyzed the vocal cords, person will most likely need a trach
52
A useful emergency measure to keep around for thyroid surgery?
A trach kit. Mark that membrane!!!!
53
Why would your patient be hypocalcemic post thyroidectomy?
Damage or removal of the parathyroids.
54
What function do the adrenals perform?
glucocorticoids, mineralocorticoids (aldosterone), and androgens Catecholamine production
55
Hormonal pathway of the HPA
CRH --> ACTH --> Coritcoids
56
Why does cortisol raise our blood sugar, cause weight gain, and can lead to hypokalemia?
causes gluconeogenesis, reduces uptake into tissues. Tells kidneys to hold onto to sodium. (water follows sodium, leading to retention) Aldosterone and high enough levels of corticoids act on the eNAC. Absorbing Na+ in the collecting duct and secreting K+
57
This tumor reveals itself through impressive hypertension and thunderclap headaches?
Pheochromocytoma
58
How is Pheochromocytoma confirmed?
24h urine collection for metanephrines and catecholamines CT & MRI, I-metaiodobenzylguanidine (MIBG) scintigraphy help localize the tumor
59
What paradoxical finding might you find with pheos?
orthostatic hypotension. Thier carotid receptors have been desensitized.
60
why do we worry about Calcium when it comes to pheos?
Calcium triggers catecholamine release from the tumor, and excess calcium entry into myocardial cells contributes to a catecholamine-mediated cardiomyopathy
61
How do we medically treat pheos?
Phenoxybenzamine Prazosin & Doxazosin
62
why do we need to be careful when it comes to betablockers in the setting of pheos?
BB before α blocker b/c blocking vasodilatory β2 receptors results in unopposed α agonism, leading to vasoconstriction and hypertensive crises
63
What are the two forms of cushings?
ACTH dependent and ACTH independent
64
Clinical presentation of dependent cushings?
high plasma ACTH stimulates the adrenal cortex to produce excessive cortisol 
65
Presentation of independent cushings?
excessive cortisol production by abnormal adrenocortical tissue that is not regulated by CRH and ACTH Typically the result of a tumor. CRH and ACTH levels are actually suppressed 
66
Clinical presentation of cushings?
sudden weight gain, usually central w/↑facial fat(moon face), ecchymoses, HTN, glucose intolerance, muscle wasting, depression, insomnia  Diagnosed via cortisol level
67
Cushing treatment options?
Surgery of pituitary, or removal of tumor present on the adrenal gland.
68
conn syndrome is also known as?
Primary hyperaldosteronism
69
Symptoms of Primary hyperaldosteronism?
HTN, hypokalemia, hypokalemic metabolic alkalosis
70
What should make you suspicious of conn's or someone who likes licorice a bit too much?
Spontaneous hypokalemia in presence of systemic HTN is highly suggestive of hyper-aldosteronism
71
Why should one be careful with spirinolactone?
Hyperkalemia!!!
72
In which case of excessive aldosteronism is renin in excess?
secondary hyper-aldosteronism
73
hyper-aldosteronism in which renin is suppressed?
primary
74
Treatment for hypoaldosteronism?
liberal sodium intake and daily administration of fludrocortisone
75
What are you likely to see in hypoaldosteronism?
Hyperkalemia in the absence of renal insufficiency suggests hypoaldosteronism Hyperkalemia may be enhanced by hyperglycemia Hyperchloremic metabolic acidosis is common Pts may experience heart block d/t hyperkalemia, orthostatic HoTN, and hyponatremia 
76
Cause of hypoaldosteronism?
Lack of aldosterone may be c/b congenital deficiency of aldosterone synthetase or hyporeninemia d/t defects in the juxtaglomerular apparatus or ACE inhibitors
77
JFK was known to have this disease process?
Addison's
78
Addison or primary is defined by what?
Adrenal glands unable to produce enough glucocorticoid, mineralocorticoid, and androgen hormones The most common cause autoimmune adrenal destruction 
79
Secondary adrenal insufficiency is a malfunction or lack of what?
CRH or ACTH, something is wrong upstairs either at the hypothalamus or pituitary.
80
Adrenal insufficiency is confirmed by what levels?
baseline cortisol < 20 μg/dL and remains <20 μg/dL after ACTH stimulation
81
How does one treat adrenal insufficiency?
steroids
82
What stimulates the release of PTH?
Hypocalcemia PTH maintains normal plasma calcium levels by promoting the movement of calcium across GI tract, renal tubules, and the bone
83
Causes of hyperparathyroidism and what too watch out for?
Hypercalcemia benign parathyroid adenoma (90%) carcinoma (<5%) parathyroid hyperplasia
84
Management of hyperparathyroidism?
Sx: sedation, n/v,↓strength,↓sensation, polyuria, renal stones, PUD, cardiac disturbances Dx: Plasma calcium, 24 hr urinary calcium Tx: surgical removal of abnormal portions of the gland
85
What is secondary hyperparathyroidism a function of ?
Another disease process, think chronic renal failure.
86
What is almost always iatrogenic?
Hypoparathyroidism
87
Levels to confirm the diagnosis of hypoparathyroidism?
hypocalcemia < 4.5 mEq/L and iCa² < 2.0 mg/dL, along w/↓PTH & ↑phosphate
88
How do we treat low calcium levels
with calcium and vitamin D duh
89
congenital disorder in which the kidneys dont respond to PTH?
Pseudohypoparathyroidism
90
chronic Hypocalcemia symptoms?
assoc w/fatigue, cramps, prolonged QT interval, lethargy, cataracts, SQ calcifications, thickening of the skull, neurologic deficits
91
What to watch out for with acute hypocalcemia post parathyroid removal?
stridor, reflects irritation of the laryngeal nerves.
92
Most common cause of hypocalcemia?
chronic renal failure
93
Name the six hormones released by the anterior pituitary gland, the two released by the posterior?
anterior= GH, ACTH, TSH, FSH, LH, prolactin posterior= oxytocin, ADH
94
Why is acromegaly a concern for anesthesia?
Overgrowth of soft tissues make pts susceptible to upper AW obstruction Hoarseness & abnormal mvmt of vocal cords or RLN paralysis may result from overgrowth of the surrounding cartilaginous structures Peripheral neuropathy is common d/t nerve trapping by connective tissues
95
Treatment for acromegaly?
surgical excision of pituitary adenoma or long acting somatostatin
96
Airway management for acromegaly?
smaller ETT, VL, awake fiberoptic intubation
97
Hallmarks of DI, nephro and neuro?
Nephro- no longer responding to ADH, causing water wasting. neuro- damage to pituitary causing lack of available ADH.
98
How to treat neuro DI?
ADH or DDVAP
99
How to manage neprho DI?
low salt, low protein, thiazide diuretics, NSAIDs
100
Anesthesia concerns for DI?
: monitor UOP & serum electrolyte concentrations
101
What should you look for if you suspect SIADH?
High urine sodium low serum sodium. treatment- fluid restriction, salt tablets, loop diuretics & ADH antagonists-Demeclocycline Hyponatremia may be treated w/hypertonic saline @ <8 mEq/L over 24-hrs
102

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