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Health Assessment > Endo exam 4 > Flashcards

Endo exam 4 Flashcards

Hormones baby!!!!

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
Q

Why are thyroid procedures such a risk?

A

Highly vascular and nerve proximity.

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25
Q

What exogenous element do we need in low amounts to maintain our T3/T4 levels

A

iodine

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26
Q

Typical T3/T4 ratio?

A

10:1

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27
Q

Why is the thyroid so vital?

A

Thyroid hormones stimulate virtually all metabolic processes. They influence growth and maturation of tissues, enhance tissue function, and stimulate protein synthesis and carbohydrate and fatmetabolism

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28
Q

What are the major players anatomically when it comes to the thyroid?

A

hypothalamus, pituitary, and thyroid

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29
Q

The hormonal pathway for thyroxine synthesis?

A

TRH (Hypothalamus)
TSH (Anterior pituitary)
T3/T4 ( Thyroid)

T3/T4 turn off hypothalamus via negative feedback loop in the normal system

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30
Q

Common diagnostic testing for the thyroid?

A

TSH assay

TRH stimulation test assesses the functional state of the TSH-secreting mechanism

serum anti-microsomal antibodies, antithyroglobulin antibodies, and thyroid-stimulating immunoglobulins

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31
Q

Normal TSH level?

A

normal TSH level is 0.4-5.0 milliunits/L

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32
Q

Hyperthyroidism manifestations?

A

sweating, heat intolerance & fatigue w/inability to sleep
(Hypermetabolic state)

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33
Q

What hormone presentation of Grave’s disease is typical and whom does it typically effect?

A

low TSH + high T3 & T4

Women

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34
Q

What might occur in/around the airway with graves?

A

dysphagia, globus sensation, and inspiratory stridor from tracheal compression

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35
Q

Firstline treatment for graves?

A

PTU or methimazole

Typical goal is to shrink the gland before operation is performed.

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36
Q

Complications of thyroidectomy?

A

Complications from surgery include hypothyroidism, hemorrhage with tracheal compression, RLN damage, and damage to or inadvertent removal of the parathyroid glands

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37
Q

Medication for symptom management in the context of Grave’s?

A

β-blockers

Propranolol (non selective) impairs the peripheral conversion of T4 to T3

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38
Q

Pre op concerns with graves?

A

Thyroid levelsshould 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

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39
Q

Condition is similar to MH, what is it and how do we manage?

A

Thyroid storm.

Get them through with symptom management. Try and shut down the thyrotoxicosis.

20% mortality rate.

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40
Q

Hormone presentation in hypothyroidism or hashimotos?

A

↓T3 & T4 production despite adequate TSH

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41
Q

Textbook presentation with hypothyroidism?

A

cold intolerance, weight gain, nonpitting edema.

Their body is in slow motion.

42
Q

How to differentiate primary vs secondary hypothyroidism?

A

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
Q

Patients can experience a psuedohypothyroidism ,

True or False?

A

True.

Low T3 & T4 w/normal TSH level
Likely a response to stress, and it can be induced by surgery

44
Q

TSH >10 milliunits/L
puts you at risk for what?

A

CAD.

45
Q

What is the DOC for hypothyroidism.

A

L-thyroxine

46
Q

Hypothyroidism preop concerns?

A

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
Q

This is rare in hypothyroidism but can be deadly?

A

myxedema coma

50% mortality rate

48
Q

Treatment for myxedema coma?

A

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
Q

When is a surgery indicative for goiter?

A

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
Q

Pre op airway concerns for goiter?

A

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
Q

Why does thyroid surgery result in hoarseness?

A

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
Q

A useful emergency measure to keep around for thyroid surgery?

A

A trach kit. Mark that membrane!!!!

53
Q

Why would your patient be hypocalcemic post thyroidectomy?

A

Damage or removal of the parathyroids.

54
Q

What function do the adrenals perform?

A

glucocorticoids, mineralocorticoids (aldosterone), and androgens

Catecholamine production

55
Q

Hormonal pathway of the HPA

A

CRH –> ACTH –> Coritcoids

56
Q

Why does cortisol raise our blood sugar, cause weight gain, and can lead to hypokalemia?

A

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
Q

This tumor reveals itself through impressive hypertension and thunderclap headaches?

A

Pheochromocytoma

58
Q

How is Pheochromocytoma confirmed?

A

24h urine collection for metanephrines and catecholamines
CT & MRI, I-metaiodobenzylguanidine (MIBG) scintigraphy help localize the tumor

59
Q

What paradoxical finding might you find with pheos?

A

orthostatic hypotension. Thier carotid receptors have been desensitized.

60
Q

why do we worry about Calcium when it comes to pheos?

A

Calcium triggers catecholamine release from the tumor, and excess calcium entry into myocardial cells contributes to a catecholamine-mediated cardiomyopathy

61
Q

How do we medically treat pheos?

A

Phenoxybenzamine
Prazosin & Doxazosin

62
Q

why do we need to be careful when it comes to betablockers in the setting of pheos?

A

BB before α blocker b/c blocking vasodilatory β2 receptors results in unopposed α agonism, leading to vasoconstriction and hypertensive crises

63
Q

What are the two forms of cushings?

A

ACTH dependent and ACTH independent

64
Q

Clinical presentation of dependent cushings?

A

high plasma ACTH stimulates the adrenal cortex to produce excessive cortisol

65
Q

Presentation of independent cushings?

A

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
Q

Clinical presentation of cushings?

A

sudden weight gain, usually central w/↑facial fat(moon face), ecchymoses, HTN, glucose intolerance,muscle wasting, depression, insomnia

Diagnosed via cortisol level

67
Q

Cushing treatment options?

A

Surgery of pituitary, or removal of tumor present on the adrenal gland.

68
Q

conn syndrome is also known as?

A

Primary hyperaldosteronism

69
Q

Symptoms of Primary hyperaldosteronism?

A

HTN, hypokalemia, hypokalemic metabolic alkalosis

70
Q

What should make you suspicious of conn’s or someone who likes licorice a bit too much?

A

Spontaneous hypokalemia in presence of systemic HTN is highly suggestive of hyper-aldosteronism

71
Q

Why should one be careful with spirinolactone?

A

Hyperkalemia!!!

72
Q

In which case of excessive aldosteronism is renin in excess?

A

secondary hyper-aldosteronism

73
Q

hyper-aldosteronism in which renin is suppressed?

A

primary

74
Q

Treatment for hypoaldosteronism?

A

liberal sodium intake and daily administration of fludrocortisone

75
Q

What are you likely to see in hypoaldosteronism?

A

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
Q

Cause of hypoaldosteronism?

A

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
Q

JFK was known to have this disease process?

A

Addison’s

78
Q

Addison or primary is defined by what?

A

Adrenal glands unable to produce enough glucocorticoid, mineralocorticoid, and androgen hormones

The most common cause autoimmune adrenal destruction

79
Q

Secondary adrenal insufficiency is a malfunction or lack of what?

A

CRH or ACTH, something is wrong upstairs either at the hypothalamus or pituitary.

80
Q

Adrenal insufficiency is confirmed by what levels?

A

baseline cortisol < 20 μg/dL and remains <20 μg/dL after ACTH stimulation

81
Q

How does one treat adrenal insufficiency?

A

steroids

82
Q

What stimulates the release of PTH?

A

Hypocalcemia

PTH maintains normal plasma calcium levels by promoting the movement of calcium across GI tract, renal tubules, and the bone

83
Q

Causes of hyperparathyroidism and what too watch out for?

A

Hypercalcemia

benign parathyroid adenoma (90%)
carcinoma (<5%)
parathyroid hyperplasia

84
Q

Management of hyperparathyroidism?

A

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
Q

What is secondary hyperparathyroidism a function of ?

A

Another disease process, think chronic renal failure.

86
Q

What is almost always iatrogenic?

A

Hypoparathyroidism

87
Q

Levels to confirm the diagnosis of hypoparathyroidism?

A

hypocalcemia < 4.5 mEq/L and iCa² < 2.0 mg/dL, along w/↓PTH & ↑phosphate

88
Q

How do we treat low calcium levels

A

with calcium and vitamin D

duh

89
Q

congenital disorder in which the kidneys dont respond to PTH?

A

Pseudohypoparathyroidism

90
Q

chronic Hypocalcemia symptoms?

A

assoc w/fatigue, cramps, prolonged QT interval, lethargy,cataracts, SQcalcifications, thickening of theskull, neurologic deficits

91
Q

What to watch out for with acute hypocalcemia post parathyroid removal?

A

stridor, reflects irritation of the laryngeal nerves.

92
Q

Most common cause of hypocalcemia?

A

chronic renal failure

93
Q

Name the six hormones released by the anterior pituitary gland, the two released by the posterior?

A

anterior= GH, ACTH, TSH, FSH, LH, prolactin

posterior= oxytocin, ADH

94
Q

Why is acromegaly a concern for anesthesia?

A

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
Q

Treatment for acromegaly?

A

surgical excision of pituitary adenoma

or long acting somatostatin

96
Q

Airway management for acromegaly?

A

smaller ETT, VL, awake fiberoptic intubation

97
Q

Hallmarks of DI, nephro and neuro?

A

Nephro- no longer responding to ADH, causing water wasting.

neuro- damage to pituitary causing lack of available ADH.

98
Q

How to treat neuro DI?

A

ADH or DDVAP

99
Q

How to manage neprho DI?

A

low salt, low protein, thiazide diuretics, NSAIDs

100
Q

Anesthesia concerns for DI?

A

: monitor UOP & serum electrolyte concentrations

101
Q

What should you look for if you suspect SIADH?

A

High urine sodium
low serum sodium.

treatment- fluid restriction, salt tablets, loop diuretics & ADHantagonists-Demeclocycline
Hyponatremia may be treated w/hypertonic saline @ <8 mEq/L over 24-hrs

102
Q
A

Health Assessment (10 decks)

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