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Physical & Health Assessment (Updated Spring 2025) > Endrocine-(Exam IV, Mordecai) > Flashcards

Endrocine-(Exam IV, Mordecai) Flashcards

1
Q

What are the 3 sources of glucose in the body?

A

Dietary intake, liver glycogenolysis, and gluconeogenesis.

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2
Q

What hormones raise blood glucose?

A

Glucagon
epinephrine
growth hormone
cortisol

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3
Q

Stimulates what two processes? And inhibits what?

Primary action of glucagon?

A

Stimulates glycogenolysis, gluconeogenesis, and inhibits glycolysis.

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4
Q

What causes Type 1a diabetes?

A

Autoimmune destruction of pancreatic beta cells minimal or no insulin production.

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5
Q

Key signs of Type 1 diabetes onset?

A

Fatigue, weight loss, polyuria, polydipsia, blurry vision, ketoacidosis.

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6
Q

What are the 3 main defects in Type 2 DM?

A

Impaired insulin secretion
↑ hepatic glucose output,
↓ glucose uptake in tissues

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7
Q

4 listed

Causes of insulin resistance in Type 2 DM?

A

Abnormal insulin molecules, receptor defects, obesity, sedentary lifestyle.

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8
Q

First-line treatment for Type 2 DM?

A

Metformin (a biguanide).

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9
Q

Side effects of sulfonylureas?

A

Hypoglycemia, weight gain, cardiac effects. Not effective long-term.

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10
Q

What is hypoglycemia unawareness?

A

Repetitive hypoglycemia dulls autonomic warning symptoms → neuroglycopenia.

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11
Q

How is diabetic ketoacidosis (DKA) treated?

A

Fluids, insulin infusion, correct acidosis & electrolytes (esp. K+).

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12
Q

What is HHS and who gets it?

A
  • Hyperglycemic hyperosmolar syndrome glucose
  • seen in older Type 2 DM patients
  • Severe dehydration + high glucose
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13
Q

3

Main microvascular complications of diabetes?

A

Nephropathy, neuropathy, retinopathy.

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14
Q

What is autonomic neuropathy?

A

Diabetic nerve damage to ANS:

  • CV dysrhythmia
  • gastroparesis
  • orthostatic hypotension
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15
Q

Concerned for silent….?

Preop concerns in diabetics?

A

Silent ischemia, renal function, gastroparesis, autonomic instability.

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16
Q

What is insulinoma and how is it diagnosed?

A

Insulin-secreting tumor.
Dx by Whipple’s triad:
symptoms + BG <50 + relief w/ glucose.

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17
Q

What hormones does the thyroid produce and what are their effects?

A

T3 and T4; stimulate almost all metabolic processes.

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18
Q

What regulates thyroid hormone production?

A

TRH from the hypothalamus → TSH from anterior pituitary → stimulates thyroid.

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19
Q

What is the T4:T3 ratio?

A

10:1

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20
Q

What is the best test for thyroid function?

A

TSH assay (most sensitive to small changes).

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21
Q

What are the 3 common causes of hyperthyroidism?

A

Graves disease, toxic goiter, toxic adenoma.

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22
Q

Key symptoms of hyperthyroidism?

A

Heat intolerance, sweating, insomnia, weight loss, fatigue.

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23
Q

What is Graves Disease?

A

Autoimmune hyperthyroidism caused by thyroid-stimulating antibodies → gland growth and hormone release.

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24
Q

5 Findings listed

Key Graves Disease findings?

A

Goiter, ophthalmopathy, low TSH, high T3/T4, positive TSH antibodies.

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25
First-line treatment for Graves disease?
Methimazole or PTU (antithyroid drugs).
26
What is thyroid storm and how is it treated?
Life-threatening hyperthyroid crisis. Treat with: * antithyroid meds * steroids * beta-blockers * supportive care
27
# What is an airway concern? What are pre-op concerns for hyperthyroid patients?
Ensure euthyroid state, assess for tracheal compression, prepare for possible thyroid storm.
28
What are the 2 most common causes of hypothyroidism?
Autoimmune destruction (Hashimoto's) or post-surgical/radioiodine ablation.
29
Symptoms of hypothyroidism?
Cold intolerance, weight gain, non-pitting edema, dyspnea, bradycardia, pleural effusion.
30
# S/S we will see? Mortality? What is myxedema coma?
Severe hypothyroidism with: * hypothermia * hypoventilation * bradycardia * delirium Emergency with >50% mortality.
31
Treatment for hypothyroidism?
L-thyroxine. In emergencies, give IV thyroid hormone + steroids.
32
# Injury of what nerve? Complications of thyroid surgery?
RLN injury, hypoparathyroidism, hematoma, airway compression.
33
What hormones are produced by the adrenal cortex?
* Glucocorticoids (cortisol) * mineralocorticoids (aldosterone) * androgens
34
What stimulates cortisol release?
CRH (hypothalamus) → ACTH (pituitary) → cortisol (adrenal cortex).
35
# Increases what? Converts what catecholamine? Retains? Excretes? What are the effects of cortisol?
* Increases blood glucose * helps convert NE to EPI * retains sodium * excretes potassium
36
What is a pheochromocytoma?
Catecholamine-secreting tumor from chromaffin cells (usually adrenal medulla).
37
Classic symptoms of pheochromocytoma?
* Headache * pallor * palpitations * sweating * hypertension
38
What is the diagnostic test for pheochromocytoma?
24h urine for metanephrines and catecholamines; CT/MRI.
39
# What med should be given first? Pre-op management of pheochromocytoma?
Alpha-blocker first (phenoxybenzamine or prazosin), then beta-blocker if needed.
40
What’s the difference between ACTH-dependent and ACTH-independent Cushing’s?
ACTH-dependent: Pituitary adenoma → ↑ACTH → ↑cortisol ACTH-independent: Adrenal tumor → ↑cortisol, ↓ACTH
41
Symptoms of Cushing Syndrome?
Central obesity, moon face, hypertension, glucose intolerance, ecchymosis, muscle wasting.
42
Best diagnostic test for Cushing’s?
24h urine cortisol, plus ACTH levels to determine dependency.
43
Treatment for Cushing’s syndrome?
Transsphenoidal pituitary surgery or adrenalectomy. Pre-op control of BP, glucose, electrolytes.
44
What causes primary hyperaldosteronism?
Aldosterone-secreting tumor (aldosteronoma).
45
Hallmark signs of hyperaldosteronism?
Spontaneous hypertension + hypokalemia.
46
How is secondary hyperaldosteronism different?
Due to high renin levels (vs. low renin in primary).
47
Treatment for hyperaldosteronism?
Spironolactone, K+ replacement, antihypertensives, adrenalectomy if needed.
48
What is the hallmark of hypoaldosteronism?
Hyperkalemia with normal renal function.
49
Treatment for hypoaldosteronism?
Sodium intake and daily fludrocortisone.
50
Difference between primary and secondary adrenal insufficiency?
Primary (Addison's): Adrenal failure → ↓cortisol & ↓aldosterone Secondary: Pituitary/hypothalamic failure → ↓ACTH → ↓cortisol only
51
Diagnostic test for adrenal insufficiency?
Baseline cortisol <20 that doesn't increase after ACTH stimulation.
52
Treatment for adrenal insufficiency?
Steroid replacement (hydrocortisone or equivalent).
53
What does parathyroid hormone (PTH) do?
Maintains plasma calcium by increasing absorption in gut, reabsorption in kidneys, and mobilization from bone.
54
What triggers PTH release?
Hypocalcemia. ## Footnote High calcium suppresses PTH.
55
What causes primary hyperparathyroidism?
Usually a benign parathyroid adenoma (90%).
56
Symptoms of hyperparathyroidism?
"Bones, stones, groans, and psychiatric overtones" ## Footnote Lethargy, weakness, polyuria, kidney stones, PUD, cardiac arrhythmias.
57
What causes secondary hyperparathyroidism?
Chronic renal failure → hypocalcemia → compensatory PTH increase.
58
Treatment for hyperparathyroidism?
Surgical removal of abnormal glands (primary) or treating the underlying disease (secondary).
59
What is the most common cause of hypoparathyroidism?
Iatrogenic — accidental removal during thyroid surgery.
60
What is pseudohypoparathyroidism?
Normal PTH levels, but kidneys are unresponsive to it.
61
# Acute vs Chronic Symptoms of hypocalcemia from hypoparathyroidism?
Acute: stridor, laryngospasm. Chronic: fatigue, cramps, long QT, cataracts, neurologic deficits.
62
Treatment for hypoparathyroidism?
Calcium and Vitamin D replacement.
63
# 6 Listed What hormones does the anterior pituitary secrete?
* GH * ACTH * TSH * FSH (Follicle Stimulating Hormone) * LH (Luteinizing Hormone) * prolactin
64
What hormones are released from the posterior pituitary?
Vasopressin (ADH) and oxytocin — made in hypothalamus, stored in posterior pituitary.
65
What causes acromegaly?
Excess growth hormone, usually from a pituitary adenoma.
66
Key features of acromegaly?
* Enlarged hands/face/tongue * airway obstruction * peripheral neuropathy * soft tissue overgrowth
67
Anesthetic implications of acromegaly?
Difficult airway (large tongue, distorted anatomy), consider small ETT, VL or awake fiberoptic.
68
What are the 2 types of DI?
* Neurogenic (central): ↓ADH secretion. * Nephrogenic: kidneys don’t respond to ADH.
69
How is DI diagnosed?
Polyuria with dilute urine, high serum osmolality. ## Footnote DDAVP test differentiates type (responds in neurogenic, not in nephrogenic).
70
Treatment for DI?
Neurogenic: DDAVP. Nephrogenic: low-salt/protein diet, thiazide diuretics, NSAIDs. Anesthesia: monitor fluids and electrolytes closely.
71
What is SIADH?
Excess ADH secretion → water retention → hyponatremia.
72
Causes of SIADH?
* Intracranial tumors * hypothyroidism * porphyria (group of rare disorders caused by problems in the production of heme) * lung cancer
73
Symptoms and treatment of SIADH?
Sx: Hyponatremia, low serum osmolality, high urine Na/osmolality. ## Footnote Tx: Fluid restriction, Na+ tabs, loop diuretics, ADH antagonists, hypertonic saline if severe.

Physical & Health Assessment (Updated Spring 2025) (27 decks)

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