Endocrine

Question 1

common EKG finding in patients with hypocalcemia:

Do you see a lot of T wave issues with hypocalcemia?

Answer 1

Prolonged QT
No
It prolongs phase 3 of the cardiac cylce (repolarization of the myocyte)

Question 2

What are causes of a widened QRS?

Answer 2

hyperkalemia, RBBB, WPW

Question 3

Do you see pleural effusions in people with hyperthyroidism? Can you have CHF d/t hyperthyroidism? What about anemia and thrombocytopenia? Fatigue?

Answer 3

No
Yes, you can have CHF
Yes, you can have anemia and thrombocytopenia in Hyperthyroidism
Yes even fatigue

Question 4

Intraoperative management of acute hypertension for patients undergoing removal of pheochromocytoma includes

Answer 4

avoiding medications that are histamine-releasing and utilization of direct-acting vasodilators (e.g., nicardipine (A), nitroprusside (D), and nitroglycerin) or α-blockers (e.g., phentolamine (B)).

Question 5

Which drug inhibits the rate limiting step in catecholamine synthesis?

Answer 5

AMPT aka metryrosine. It can help with inoperable pheochromocytomas

Question 6

How do alpha 2 agonists work?

Answer 6

Alpha2-agonists (e.g. dexmedetomidine) generally produce bradycardia, sedation, and lower blood pressure. This is via inhibition of norepinephrine (NE) release from presynaptic nerve terminals when alpha-2 receptors are stimulated.

Question 7

How does phenoxybenzamine work? Half life of it?

Answer 7

it’s a non-specific (irreversible) alpha blocker, so it can acutally block alpha 2 which casues bradycardia, sedation, and lower BP. It has a 24 hour half life which means that you can experience hypotension after the pheo is out.

Question 8

What is Conn’s syndrome? How do they present? Which electrolytes are low? Metabolic state?

Answer 8

Conn’s syndrome is primary hyperaldosteronism from secretion from a tumor. It results in elevated serum Na+, reduced serum K+, and reduced renin activity. Patients typically present with increased blood pressure, fatigue, and a hypokalemic metabolic alkalosis-due to loss of H+ ions

Question 9

How do you manage patient’s with Conn’s syndrome (anesthetic wise)

Answer 9

You can give them K+ preoperatively, avoid hyperventilation, and just know you may need to give cortisol if both glands are being excised for the surgery.

Question 10

What does aldosterone do? where does it work?

Answer 10

It functions in the distal renal tubules by absorbing Na+ ions in exchange for urinary loss of K+ and H+ ions. The effect of aldosterone is volume expansion as H2O follows Na+ ions.

Question 11

Plans for patient’s with Conn’s syndrome prior to surgery:

Answer 11

The standard preoperative management of Conn’s syndrome should include the institution of spironolactone, an aldosterone antagonist, and potassium supplementation. Potassium repletion may take some time as whole body levels may be very low. Spironolactone may also take several weeks to correct hypertension and metabolic changes. There is no ideal management strategy, but some attempt at restoration of homeostasis should be implemented prior to general anesthesia. Where possible, a serum K+ level < 3 mEq/L should be treated due to increased arrhythmogenicity. Potassium-sparing diuresis may be implemented by the administration of triamterene.

Question 12

what does hyperventilation due to potassium?

Answer 12

It decreases serum potassium (hyperventilation causes acidosis and H+ will move out of cell, while K+ moves in.

Question 13

what is a common cause of stridor s/p parathyroidectomY?

Answer 13

Laryngeal edema.

Question 14

When does hypocalcemia cause stridor s/p parathyroidectomy?

Answer 14

24-48 hours

Question 15

PTH and bicarbonate: what does PTH due to bicarb? In presence of hyperPTH, what do you see with pH, paCO2?

Answer 15

PTH can increase renal bicarbonate loss=acidosis
PTH also inhibits the sodium chloride transporter in DCT, leading to hyperchloremia
Although not particularly common, patients with hyperparathyroidism may have a lower than normal pH, slightly decreased PaCO2 due to respiratory compensation, a decreased bicarbonate level, and a normal anion gap.

Question 16

when grater than 24 hours post-op, what is the most common cause of stridor?

Answer 16

Hypocalcemia

Question 17

When recurrent laryngeal nerve is damaged in thyroidectomies, what will you see? What about unilateral nerve damage?

Answer 17

Airway obstruction can also occur secondary to bilateral recurrent laryngeal nerve injury, but this would be apparent immediately after extubation and would likely require re-intubation. Unilateral nerve damage would generally only result in hoarseness.

Question 18

First step in DKA:

Answer 18

Hydration!

Question 19

Explain primary hyperaldosteronism: aka ____
Why does it happen?
Most common symptoms? why?

Answer 19

Primary hyperaldosteronism (Conn Syndrome) occurs from excess secretion of aldosterone, usually from an adrenal adenoma. The most common symptoms include fatigue, muscle cramps/weakness, polyuria, and headache. These are the result of hypertension and hypokalemia caused by excess aldosterone. When caused by a functional tumor(s), definitive treatment is surgical excision of the tumor(s).

Question 20

Where does aldosterone primarily work?

Answer 20

ldosterone primarily acts in the renal distal tubules and collecting ducts to upregulate Na+/K+ pumps.

Question 21

What does hydrocortisone do?

Answer 21

Hydrocortisone (cortisol) promotes sodium retention and renal potassium secretion due to weak mineralocorticoide activity.

Question 22

What is midodrine?

Answer 22

Midodrine is a α1 receptor agonist. Since it is a vasopressor, its use would be contraindicated in patients with hypertension.

Question 23

octreotide and primary hyperaldosteronism?

Answer 23

Octreotide is a synthetic somatostatin analogue. It will not and does not play a role in management of patients with primary hyperaldosteronism.

Question 24

How to treat hyperaldosteronism?

Answer 24

Spironolactone, a competitive aldosterone receptor antagonist, is used to treat the hypertension and hypokalemia associated with primary hyperaldosteronism. Potassium supplementation and additional antihypertensives are usually required when first initiating treatment.

Question 25

What is octreotide used for?

Answer 25

Octreotide is the primary pharmacologic treatment of acromegaly as it suppresses growth hormone production.

Question 26

What is thyroid storm? What can precipitate it? Treatment?

Answer 26

Thyroid storm is a life-threatening exacerbation of hyperthyroidism that presents with hyperthermia, tachycardia, arrhythmias, agitation, and confusion.

Two conditions for its development are untreated hyperthyroidism and precipitating factor such as emergency surgery.

Treatment for Thyroid storm: Treatment includes hydration, beta blockers and more specific therapies (steroids, antithyroid medications, iodine).

Question 27

Are labs necessary prior to treating thyroid storm?

Answer 27

No. Elevated blood levels of T3 and free T4 levels can be used, but are not required before starting treatment in suspected thyroid storm.

Question 28

malignant hyperthermia vs thyroid storm

Answer 28

Malignant hyperthermia should be considered in hyperthermic patients and although most cases present intraoperatively or soon after, 2 hours after surgery is still possible. However, the absence of hypercarbia, rigidity, and lactic acidosis make this diagnosis less likely

Question 29

What is Addison’s disease? What are the most common lab abnormalities?

Answer 29

They’re the people without aldosterone. They will have hypotension, nausea, vomiting, and darkening of the skin due to increased ACTH.The most common lab abnormalities with Addison disease are hyponatremia, hyperkalemia, hypoglycemia, hyperchloremic metabolic acidosis, and hypercalcemia.

Question 30

How do patients with Addison’s disease get hypercalcemia?

Answer 30

Hypercalcemia occurs through a reduction in glomerular filtration brought on by the hypovolemia of adrenal insufficiency along with a concomitant increased release of calcium from bone.

Question 31

How do you diagnose Addison’s disease? How can you differentiate between Addison’s disease and someone with primary hypothalamus or pituitary disorders?

Answer 31

Addison disease is diagnosed by noting low blood and urine cortisol levels, even after administration of synthetic ACTH. Patients with primary adrenal insufficiency should have minimal or no response to ACTH, whereas patients with primary hypothalamus or pituitary disorders will have increased cortisol levels in response to ACTH.

Question 32

Addisonian crisis: What is it? When could it happen?

Answer 32

ne: Addison disease is primary adrenal insufficiency and causes hyponatremia, hyperkalemia, hypoglycemia, hyperchloremia, and hypercalcemia. Skin hyperpigmentation is a classic finding secondary to increased ACTH stimulation.

TrueLearn Insight : Patients with Addison disease on chronic steroids can present in Addisonian crisis if they have abrupt discontinuation of their steroids or in times of stress (e.g. surgery) if not treated with stress dose steroids. The same lab abnormalities as above can be seen, just more pronounced, and patients can also have severe abdominal cramping, nausea, vomiting, hypotension, and even cardiovascular collapse.

Question 33

Why do people with carcinoid tumors not always have carcinoid syndrome?

Answer 33

Many of these tumors arise in the gut, and their secretory products are broken down in the liver via first pass metabolism before reaching the systemic circulation. For this reason, patients generally do not become symptomatic unless they have liver metastases, cirrhosis, or tumor location outside of the gut.

Question 34

What is carcinoid syndrome? Why is the right side of the heart involved more than the left? How is it diagnosed? Treatment?

Answer 34

When a patient does present with carcinoid syndrome, the most common manifestations are cutaneous flushing, diarrhea, cardiac abnormalities (generally right-sided fibrous deposits on the valves or myocardium), and bronchospasm. Right-sided cardiac involvement is more common due to lung metabolism of serotonin. They can also develop wide swings in blood pressure as well as cardiac arrhythmias.

The diagnosis of a carcinoid tumor is generally made by detecting high levels of 5-hydroxyindoleacetic acid, which is a breakdown product of serotonin, in the urine. Treatment then varies based on location and metastases and can include surgical resection and/or medical treatment with octreotide or other drugs.

Question 35

The three main causes of primary hyperparathyroidism, in order of occurrence,

Answer 35

The three main causes of primary hyperparathyroidism, in order of occurrence, are a singular adenoma, hyperplasia of all four parathyroid glands, and malignancy

Question 36

What does PTH do?

Answer 36

Parathyroid hormone (PTH) is secreted from the four parathyroid glands in response to low serum calcium (see image below). It stimulates osteoclast activity, thereby releasing calcium stored in bones into the bloodstream. In addition, PTH increases renal tubular calcium reabsorption and activation of vitamin D to improve gastrointestinal calcium absorption.

Question 37

Look at PTH photo

Answer 37

Okay

Question 38

Active form of vitamin D, and explain how PTH brings that out:

Answer 38

Parathyroid hormone triggers the enzyme Vitamin D 1-hydroxylase to catalyze the conversion of vitamin D to its active form (1,25-dihydroxy-Vitamin D) within the kidneys. The active form of Vitamin D promotes intestinal absorption of calcium and phosphate.

Question 39

What does PTH do to phosphorus? When is PTH stimulated?

Answer 39

PTH also decreases renal phosphorus reabsorption, decreases renal bicarbonate reclamation, and increases synthesis of 1-alpha-hydroxylase in the kidney. Normally, PTH secretion is stimulated by low calcium or high phosphorus. Secretion is typically suppressed by high calcium or low phosphorus

Question 40

Elevated serum calcium with a normal or minimally elevated intact PTH may be either :
How to distinguish between the two?

Answer 40

primary hyperparathyroidism with concomitant vitamin D deficiency or familial hypocalciuric hypercalcemian this scenario, a 24-hour urinary calcium and serum 25-hydroxyvitamin D levels may be needed to distinguish between the two conditions. Patients with familial hypocalciuric hypercalcemia have low urinary calcium excretion which does not increase if vitamin D replacement if given.

Question 41

Look at these conditions associated with hypercalcemia:

Answer 41

Table 1: Conditions Associated With Hypercalcemia:
PARATHYROID MEDIATED 
- Primary hyperparathyroidism 
- Familial hypocalciuric hypercalcemia
NON-PARATHYROID MEDIATED
- Hypercalcemia of malignancy (multiple myeloma, PTHrp, osteolytic bone metastases)
- Vitamin D intoxication
- Chronic granulomatous disorders (sarcoidosis)
MEDICATIONS
- Thiazide diuretics 
- Lithium
- Theophylline
- Vitamin A
MISCELLANEOUS
- Hyperthyroidism
- Acromegaly
- Pheochromocytoma
- Addison's disease
- Immobilization
- Parenteral nutrition 
(PTHrp = parathyroid related protein)

Table 2: Causes of Secondary Hyperparathyroidism

• Decreased calcium intake
• Calcium malabsorption (Vit D deficiency, celiac’s, bariatric surgery)
• Calcium loss (idiopathic hypercalciuria, loop diuretics)
• Renal failure (increased phosphorus, decreased calcium, decreased calcitriol)
• Bisphosphonates

Question 42

Metabolic acidosis in people with primary hyperparathyroidism:

Answer 42

hypophosphatemia, non gap metabolic acidosis, and normal to high 24-hour urinary calcium.

Question 43

DKA and HHS chart

Answer 43

Okay

Question 44

Type 2 diabetics and really high sugar levels:

Answer 44

Significant hyperglycemia in patients with type II diabetes mellitus can lead to increased serum osmolality. Neurologic symptoms, including seizure, may occur as a result of the extracellular shift of cerebral fluid

Question 45

HHS parameters:

Answer 45

Diagnostic features of hyperglycemic hyperosmolar syndrome also include pH >7.3, bicarbonate >18 mEq/L, and serum osmolality >320 mOsm/L.

Question 46

How to differentiate between thyroid storm and MH:

Answer 46

alignant hyperthermia can be distinguished from TS by the presence of muscle rigidity (present with MH, not a sign of TS), rate of EtCO2 rise (MH&raquo_space; TS), the temperature increase (MH usually greater and faster than TS), and the degree of hypertension (TS > MH). On laboratory testing, hyperkalemia, elevated CK, and lactic acidosis are found with MH but usually not TS. Hypokalemia and elevated thyroid hormones are commonly seen with TS but not MH.

Question 47

What is the most commonly injured nerve during parathyroid and thyroid surgery?

Answer 47

Superior laryngeal nerve

Question 48

Symptoms of SLN damage: ____. Who is this detrimental to? What does the SLN innervate?

Answer 48

When injury occurs to the superior laryngeal nerve, the symptoms are often subtle. The voice may become slightly weak or hoarse. The most prevalent symptom is that the patient’s voice often tires easily, which could be detrimental to some professions (e.g. radio host)

The superior laryngeal nerve innervates that cricothyroid muscle. The cricothyroid is the only tensor of the vocal cords and is associated with a voice that tires more easily.

Question 49

SLN damage: unilateral vs bilateral:

Answer 49

Unilateral: minimal effects
Bilateral: Hoarseness and tiring of voice

Question 50

RLN damage: unilateral vs bilateral:

Answer 50

Unilateral: Hoarseness
Bilateral-acute-stridor/respiratory distress
b/l chronic: aphonia

Question 51

Vagus nerve damage: unilateral vs bilateral:

Answer 51

unilateral: hoarseness
bilateral: aphonia

Question 52

Diagnosis of carcinoid syndrome:

Answer 52

The diagnosis of carcinoid syndrome can be made by measuring 24-hour urinary levels of 5-HIAA.

Question 53

Signs and symptoms of diabetic autonomic neuropathy include ____.

Answer 53

Signs and symptoms of diabetic autonomic neuropathy include loss of heart rate variability, resting tachycardia, dysrhythmias, impaired ventilatory responses, gastroparesis with increased risk of aspiration on induction, and unawareness of hypoglycemia. NOT increased sweating, they usually have decreased sweating.

Question 54

Primary hyperthyroidism is characterized by:

Answer 54

Primary hyperthyroidism is characterized by elevated T3, T4 (free and total), and thyroid hormone binding ratio, and a low or normal TSH.

Question 55

Sodium levels and urine sodium in SIADH

Answer 55

Hyponatremia with a urine sodium greater than 20 mmol/L (A) are classic findings associated with the syndrome of inappropriate antidiuretic hormone (SIADH).

Question 56

Treatment for CSW:

Answer 56

reatment for CSW includes volume expansion and sodium administration.

Question 57

SIADH/CSW/DI chart

Answer 57

Okay

Question 58

What is one contributor to less urine being made during surgery?

Answer 58

An increase in antidiuretic hormone secretion from surgical stress can lead to conservation of plasma volume and decreased urine output in the postoperative period.

Question 59

The most common cause of sudden stridor 24 to 96 hours post thyroidectomy is
How do you treat this?

Answer 59

Hypocalcemia

IV calcium is the treatment

Question 60

Trousseau and Chvostek sign:

Answer 60

Physical exam signs of hypocalcemia include Trousseau and Chvostek signs. Trousseau sign is elicited by inflating a blood pressure cuff and watching for carpal spasm. Chvostek sign is elicited by tapping over the zygoma and watching for facial spasms.