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Board Exam > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Systemic hormones involved in hypothalamic negative feedback systems

A

T3 regulates TRH release
Cortisol regulates CRH
Testosterone, progesterone, and estrogen regulate LHRH
GH and Insulin GF-1 regulate GHRH and GHIH release

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2
Q

Causes of DI

A 
Pituitary surgery (Most common)
TBI or SAH
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3
Q

Causes of SIADH

A

TBI or SAH (most common)
Non-small cell lung CA
Noncancerous lung disease
Carbamazepine (anticonvulsant)

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4
Q

Treatment for SIADH

A

Fluid restriction

Hypertonic saline if Na

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5
Q

Treatment for DI

A

DDAVP / Vasopressin

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6
Q

Thyroid gland releases these three hormones

A

1) T4 (thyroxine) (pro-hormone)
2) T3 (Triiodothyronine) (ACTIVE hormone)
3) Calcitonin

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7
Q

Release of thyroid stimulating hormone from the pituitary tells the thyroid gland to do what two things?

A

1) Make T4 and T3 (requires iodine)

2) Tells the follicular tissue to make thyroglobulin colloid (does NOT require iodine)

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8
Q

CV effects of hyperthyroidism

A

Will see an increase in the number and sensitivity of B receptors

  • Increased everything heart (HR, inotropy, CO, etc)
  • Decreased SVR (B2)
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9
Q

GI effects of hyperthyroidism

A

DIARRHEA

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10
Q

Metabolic effects of hyperthyroidism

A

Increased BMR
Utilization of fat stores –> weight loss
Protein breakdown for energy (muscle wasting and weakness)
Release of glucose for energy (increased gluconeogenesis, insulin release, and glucose uptake)

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11
Q

Cause of tremors in hyperthyroidism

A

Increased sensitivity of neuronal synapses in the spinal cord

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12
Q

Most common cause of hypothyroidism

A

Hashimoto’s thyroiditis

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13
Q

Diagnosis of hyperthyroidism

A

High T3 and T4

Low TSH

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14
Q

Diagnosis of hypothyroidism

A

Low T3 and T4

High TSH

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15
Q

Timing of thyroid storm

A

Usually 6-18 hours post-op

Can happen in both hyperthyroid AND euthyroid patients

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16
Q

This medication can induce hyperthyroidism OR hypothyroidism

A

Amiodarone (contains a lot of iodine)

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17
Q

Why is esmolol a good choice for hyperthyroid patients?

A

They have increased Beta receptors
Short acting
Inhibits the conversion of T4 to T3

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18
Q

MOA and examples of thioamides and what are their SEs?

A

Examples:

  • PTU
  • Mathimazole
  • Carbimazole

MOA:

  • Inhibits TH synthesis by blocking the addition of iodine to the tyrosine residues on thyroglobulin
  • Also prevents peripheral conversion of T4 to T3 (like BBs)
  • Takes 6-7 weeks to work
  • PO form only

Serious SE:

  • Hepatitis
  • Agranulocytosis
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19
Q

These medications should be avoided in the pt with hyperthyroidism

A

Anything that activates the SNS!
- Anticholinergics, ketamine, pancuronium, etc

Also avoid hypoxia and hypercarbia because these can stimulate the SNS as well

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20
Q

S/S of thyroid storm

A 
Fever > 38.5C
Tachycardia and tachyarrhythmias 
HTN
CHF
Shock
Confusion and agitation
N/V
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21
Q

Under anesthesia, thyroid storm may mimic

A

MH
Pheochromocytoma
Neuroleptic malignant syndrome
Light anesthesia

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22
Q

Management of thyroid storm

A 
Manage hemodynamics (BBs)
Treat fever (active cooling and tylenol)
PTU or methimazole (crushed via NGT)
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23
Q

Anesthetic considerations for hypothyroidism

A
  • Risk of airway obstruction (large tongue, swollen cords, possible goiter)
  • Delayed gastric emptying
  • Hypodynamic circulation (opposite of hyperthyroid)
  • Hemodynamic support is best with drugs that improve myocardial performance (i.e- NOT phenylephrine)
  • Muscle weakness = sensitivity to NMBs)
  • D5NS for glucose and to combat hyponatremia
24
Q

Aldosterone release is increased by

A

RAAS Activation
Hyponatremia
Hyperkalemia

25
Q

Effects of aldosterone in the kidney

A

Reabsorption of Na
Excretion of K+ and H+

Net effect is increasing intravascular volume
NO effect on osmolarity (this is controlled by ADH)

26
Q

Physiologic effects of cortisol

A

Remember, this binds to steroid receptors within the cell to alter DNA transcription and protein synthesis. Takes a while to start working.

THREE BIG THINGS

1) Energy mobilization
- Gluconeogenesis (in liver from amino acids)
- Protein catabolism (to make glucose)
- FFA mobilization (to make glucose)

2) Anti-inflammatory effects
- Stabilizes the membranes of lysosomes, which reduces cytokine release
- Decreased amount of eosinophils and lymphocytes in the blood

3) Increased response to catecholamines
- Improves cardiac performance by increasing the number and sensitivity of Beta receptors on the myocardium
- Cortisol is also needed to BVs to respond well to catecholamines

Also has androgenic effects

27
Q

Normal cortisol production per day

A

15-30mg per day

May increase to 100mg per day after major surgery

28
Q

Cortisol’s mineral/glucocorticoid effects

A

Has EQUAL glucocorticoid and mineralcorticoid effects

29
Q

These steroids have the strongest glucocorticoid effects

A

Dexamethasone and betamethasone

30
Q

This is the strongest mineralcorticoid

A

Aldosterone

Also has NO glucocorticoid effect

31
Q

Cortisol vs. cortisone

A

Cortisol and cortisone BOTH have equal gluc/min properties.

Cortisone is 0.8x as potent

32
Q

These glucocorticoids have NO mineralocorticoid effects

A

Dexamethasone, betamethasone, and triamcinolone

33
Q

Treatment of Conn’s Syndrome

A
  • Aldosterone antagonist (Spironolactone or elperenone)
  • K+ supplementation
  • Na+ restriction
34
Q

S/S of Cushing’s Syndrome

A

Break it down by cortisol’s clinical effects

1) Glucocorticoid effects
- Hyperglycemia
- Increased risk of infection
- Weight gain
- Osteoporosis
- Muscle weakness (catabolism to make glucose)
- Mood disorder

2) Mineralocorticoid effects
- Think of effects of too much aldosterone, Na reabsorption, and K+ and H+ excretion:
- HTN
- Hypokalemia
- Metabolic alkalosis

3) Androgenic effects
- Women become masculinized
- Men become feminized

35
Q

Anesthetic implications for Cushin’s disease

A
  • Infection risk
  • Position with osteoporosis
  • Consider supplemental steroids
  • DI may develop after removal of anterior pituitary
36
Q

Most common cause of Addison’s disease

A

Chronic steroid administration

37
Q

S/S of Addison’s disease

A

Opposite of Cushing’s

  • Hypoglycemia
  • Anorexia and weight loss
  • Fatigue and muscle weakness
  • HypoTN
  • N/V
  • Hyperpigmentation of the knees, elbows, knuckles, lips, and buccal mucosa

Acute adrenal crisis

  • Hemodynamic instability and collapse
  • Hypoglycemia
  • Fever
  • Impaired mental status
38
Q

Treatment of acute adrenal crisis

A
  • Exogenous steroids (Hydrocortisone)
  • ECF expansion (D5LR)
  • Hemodynamic support
39
Q

This steroid is given for those who need supplemental steroid peri-op

A

Hydrocortisone

40
Q

What does insulin tell the body to do?

A

Time to store energy!

Released when we eat. So it tells the body we have a surplus, and it’s time to store it for the future.

  • Increases uptake into skeletal muscle, liver, and fat
  • Glycogen formation
  • Fat formation
  • Encouraging protein synthesis
41
Q

Diagnosis of DM

A

Fasting glucose > 125
Randome glucose level > 200
Two hour plasma glucose > 200 during glucose tolerance test
HbA1C > 6.5

42
Q

Metabolic syndrome diagnosis

A

At least 3 of the following:

  • Fasting glucose > 110
  • Abdominal obesity (>40 inches for men and 35 for women)
  • TG > 150
  • HDL 130/85
43
Q

ANS dysfunction in DM

A
  • Painless MI
  • Reduced vagal tone –> tachycardia
  • Risk of dysrhythmias
  • Orthostatic hypoTN
  • Impaired compensation to hypoxia and hypercarbia
  • Delayed gastric emptying
  • Impaired thermoregulation (risk of hypothermia)
  • Constipation and diarrhea
44
Q

Give an example of a biguanide and how do they work? Give some key facts about this class of drugs

A

Metformin

MOA:

  • Inhibits gluconeogenesis
  • Inhibits glycogenolysis
  • Decreases peripheral insulin resistance

Key facts:

  • NO risk of hypoglycemia***
  • Discontinue 48 hours prior to surgery
  • Risk of acidosis 2/2 increased anaerobic metabolism
  • Increased risk of lactic acidosis with drug accumulation (so avoid if liver or renal dz, acute MI, contrast being given, etc)
  • May cause vitamin B12 deficiency
  • Used for PCOS
45
Q

Give an example of a sulfonylurea and how do they work? Give some key facts about this class of drugs

A

Examples:

  • Glipizide
  • Glyburide
  • Glimepiride

MOA:
- Stimulates release of insulin from beta cells

Facts:

  • Risk of hypoglycemia!
  • Avoid in sulfa allergies
  • D/C 48 hours prior to surgery
46
Q

These classes of oral hypoglycemics do NOT carry a risk of hypoglycemia

A
  • Biguanides
  • Alpha-glucosidase inhibitors
  • Thiazolidinediones
47
Q

These are VERY RAPID acting insulins

A

Lispro
Aspart
Glulisine

All have onset of 5-15 minutes
All peak 45-75 minutes
All have duration of 2-4 hours

48
Q

Insulin resistance occurs once daily insulin requirement excess ____ units/day

A

100

49
Q

These drugs make insulin induced hypoglycemia even worse

A

MAOIs
ASA
Tetrycycline

50
Q

Common S/S of carcinoid syndrome

A

If carcinoid hormones are NOT cleared by the liver, then they cause:
- Flushing and diarrhea (Most common!!)

From histamine:

  • Bronchoconstriction
  • Vasodilation (flushing)
  • HypoTN

From kinins and kallikrein:

  • Bronchoconstriction
  • Vasodilation and flushing
  • HypoTN
  • Exacerbates histamine release

From serotonin:

  • Bronchoconstriction
  • Vasoconstriction
  • HTN
  • SVT
  • Increased GI motility
51
Q

S/S of carcinoid crisis

A

Tachy
HTN or HypoTN
Intense flushing
Abd pain and diarrhea

52
Q

Drugs to give and avoid in carcinoid patients

A

GIVE:

  • Somatostatin (Octreotide)
  • Antihistamines
  • Serotonin antagonists
  • Steroids
  • Pressors for hypoTN (phenylephrine and vasopressin)

AVOID:

  • Histamine releasing drugs
  • Sux (fasciculations can cause hormone release from tumor)
  • Exogenous catecholamines may worsen hormone release
  • Anything that stimulates the SNS (ephedrine and ketamine)
53
Q

When is GH released?

A
  • Fasting
  • Hypoglycemia
  • Decreased FFAs
  • Increased amino acids
  • Sleep
  • Stress and anxiety
  • GHRH from pituitary
  • Dopamine
  • Estrogen
  • Alpha agonists
54
Q

Most common cause of cushing’s syndrome

A

Chronic glucocorticoid therapy

55
Q

Effects of GH (somatotropin)

A
  • Facilitates growth everywhere in the body
  • Increases protein synthesis
  • Enhances use of FFAs for energy

Board Exam (21 decks)

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