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andy 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 which 3 insulin-insensitive tissues?

A

70-80%
Brain, GI tract, RBCs

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4
Q

which 4 hormones SUPPORT glucose production

A

Glucagon, Growth hormone
Cortisol and Epinephrine

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5
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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6
Q

Which DM has a pre-clinical period (9-13 yrs) of B-cell antigen production?

A

Type 1a

At least 80-90% B cell function is lost before HYPERGLYCEMIA ONSET

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7
Q

Type 1a vs Type 1b

A

Type 1a is T cell mediated B cell destruction (causation undetermined)

Type 1b lack of insulin production; absolute insulin deficiency (rare).

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8
Q

Describe type 2 DM main abnormalities (3)

A
  • ↑hepatic glucose release (reduced insulin’s inhibitory effect)
  • Impaired insulin secretion
  • Insufficient glucose uptake in peripheral tissues
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9
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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10
Q

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

A

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

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11
Q

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

A

hypoglycemia unawareness

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12
Q

How do you diagnose DM, what is your HgbA1C if your diabetic?
Range for pre diabetes?

A

Fasting glucose or HgbA1C
>6.5%
Prediabetes: 5.7-6.4

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13
Q

This drug opposes the action of glucagon?

A

Metformin

↓TGL & LDL levels

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14
Q

These drugs stimulate the pancreas to release insulin?

A

Sulfonylureas

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15
Q

Why are Sulfonylureas not a good choice long term?

A

diabetic progressive loss of B cell function

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16
Q

Hypoglycemia EXACERBATED by
3 easy ones
2 BP meds
1 Psych

A

ETOH, metformin, sulfonylureas,
ACE-I’s, Non-selective BB’s
MAOIs,

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17
Q

What is DKA?

A

Cause: illness or stress.
- High glucose → excess glucagon.
- glucagon activating lipolysis & free fatty acids→ substrates for ketogenesis
- Fatty acid oxidation → excess ketones. Hyperglycemia leads to dehydration and electrolyte imbalance due to osmotic diuresis.

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18
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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19
Q

DKA’s evil twin?

Tx: (3)

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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20
Q

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

A

ACE-Is

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21
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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22
Q

DM preop considerations?

A

Think multi system involvement. CNS, CV, Renal.

Hydration & Lytes

Gastroparesis

Holding or reduced medication dosing

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23
Q

Rare tumor found in the pancreas?

A

insulinoma

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24
Q

Insulinomas present with what features?

Effect when f_____
___ w/ sx

PreOp drug (2)

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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25
Q

These two nerves run right next to the thyroid.

A

recurrent and superior laryngeal nerve (motor branch)

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26
Q

Why are thyroid procedures such a risk? (2)

A

Highly vascular and nerve proximity.

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27
Q

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

A

iodine

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28
Q

Typical T4/T3 ratio?

A

10:1

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29
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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30
Q

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

A

hypothalamus, pituitary, and thyroid

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31
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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32
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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33
Q

Normal TSH level?

A

normal TSH level is 0.4-5.0 milliunits/L

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34
Q

Hyperthyroidism manifestations? (3)

A

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

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35
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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36
Q

What might occur in/around the airway with graves? (3)

A

Dysphagia, globus sensation (lump in your throat)
Inspiratory stridor from tracheal compression

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37
Q

Firstline treatment for graves? (2)

A

PTU or methimazole

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

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38
Q

Complications of thyroidectomy? (4)

A
  • Hypothyroidism
  • Hemorrhage with tracheal compression
  • RLN damage
  • Inadvertent removal of the parathyroid glands
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39
Q

Medication for symptom management in the context of Grave’s? (2)

A

β-blockers

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

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40
Q

Pre op concerns with graves? (2)

Emergent cases meds (3)

Airway (2)

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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41
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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42
Q

Hormone presentation in hypothyroidism or hashimotos?

A

↓T3 & T4 production despite adequate TSH

43
Q

Textbook presentation with hypothyroidism?

A

cold intolerance, weight gain, nonpitting edema.

Their body is in slow motion.

44
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.

45
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

46
Q

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

A

CAD.

47
Q

What is the DOC for hypothyroidism.

A

L-thyroxine

48
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

49
Q

This is rare in hypothyroidism but can be deadly?

A

myxedema coma

50% mortality rate

50
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

51
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.

52
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

53
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

54
Q

A useful emergency measure to keep around for thyroid surgery?

A

A trach kit. Mark that membrane!!!!

55
Q

Why would your patient be hypocalcemic post thyroidectomy?

A

Damage or removal of the parathyroids.

56
Q

What function do the adrenals perform?

A

glucocorticoids, mineralocorticoids (aldosterone), and androgens

Catecholamine production

57
Q

Hormonal pathway of the HPA

A

CRH –> ACTH –> Coritcoids

58
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+

59
Q

This tumor reveals itself through impressive hypertension and thunderclap headaches?

A

Pheochromocytoma

60
Q

How is Pheochromocytoma confirmed?

A

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

61
Q

What paradoxical finding might you find with pheos?

A

orthostatic hypotension. Thier carotid receptors have been desensitized.

62
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

63
Q

How do we medically treat pheos? (3)

A

Phenoxybenzamine
Prazosin & Doxazosin

So all Alpha blockers

64
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

65
Q

What are the two forms of cushings?

A

ACTH dependent and ACTH independent

66
Q

Clinical presentation of dependent cushings?

A

high plasma ACTH stimulates the adrenal cortex to produce excessive cortisol

67
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

68
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

69
Q

Cushing treatment options?

A

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

70
Q

conn syndrome is also known as?

A

Primary hyperaldosteronism

71
Q

Symptoms of Primary hyperaldosteronism? (3)

A

HTN,
hypokalemia,
hypokalemic metabolic alkalosis

72
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

73
Q

Why should one be careful with spirinolactone?

A

Hyperkalemia!!!

74
Q

In which case of excessive aldosteronism is renin in excess?

A

secondary hyper-aldosteronism

75
Q

hyper-aldosteronism in which renin is suppressed?

A

primary

76
Q

Treatment for hypoaldosteronism? (2)

A
  • liberal (a lot) sodium intake
  • daily fludrocortisone
77
Q

What are you likely to see in hypoaldosteronism?

S/s (3)
_______ may be enhanced by ________

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

78
Q

Cause of hypoaldosteronism? (3)

A

Lack of aldosterone may be c/b
- congenital deficiency of aldosterone synthetase
- hyporeninemia d/t defects in the juxtaglomerular apparatus
- ACE inhibitors

79
Q

JFK was known to have this disease process?

A

Addison’s

80
Q

Addison or primary hypocortisolism is defined by what?

Most common cause

A

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

The most common cause autoimmune adrenal destruction

81
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.

82
Q

Adrenal insufficiency is confirmed by what levels?

A

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

83
Q

How does one treat adrenal insufficiency?

A

steroids

84
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

85
Q

Causes of hyperparathyroidism and what too watch out for? (4)

A

Hypercalcemia

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

86
Q

Management of hyperparathyroidism?
s/s (4)
dx (2)
tx

A

Sx: sedation,↓strength,↓sensation, n/v, polyuria, renal stones, PUD, cardiac disturbances

Dx: Plasma calcium, 24 hr urinary calcium

Tx: surgical removal of abnormal portions of the gland

87
Q

What is secondary hyperparathyroidism a function of ?

A

Another disease process, think chronic renal failure.

88
Q

What is almost always iatrogenic?

A

Hypoparathyroidism

89
Q

Levels to confirm the diagnosis of hypoparathyroidism? (4)

A

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

  • Remember: Calcium & Phosphate have an inverse relationship. *
90
Q

How do we treat low calcium levels

A

with calcium and vitamin D

duh

91
Q

congenital disorder in which the kidneys dont respond to PTH?

A

Pseudohypoparathyroidism

92
Q

Chronic Hypocalcemia symptoms?

heart
body (3)
head (3)

A

Prolonged QT interval
Fatigue, cramps
Soft tissuecalcifications
Cataracts, Neurologic deficits, Thick Skull

93
Q

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

A

stridor, reflects irritation of the laryngeal nerves.

94
Q

Most common cause of hypocalcemia?

A

chronic renal failure

95
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

96
Q

Why is acromegaly a concern for anesthesia?

airway
vocals
Nerves

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

97
Q

Treatment for acromegaly? (2)

A

surgical excision of pituitary adenoma

or long acting somatostatin

98
Q

Airway management for acromegaly? (2)

A

smaller ETT, VL, awake fiberoptic intubation

99
Q

Differences of DI:
Nephro and Neuro?

A

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

neuro- damage to pituitary causing lack of available ADH.

100
Q

How to treat neuro DI?

A

ADH or DDVAP

101
Q

How to manage neprho DI?

2 diet changes
2 meds

A

low salt, low protein, thiazide diuretics, NSAIDs

102
Q

Anesthesia concerns for DI? (2)

A

Monitor Urine Output
& Electrolyte concentrations

103
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

104
Q

What are the long term consequences of DM?

A

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

andy health assessment (9 decks)

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