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Assessment w/ Mordecai > T4 - Endocrine Assessment > Flashcards

T4 - Endocrine Assessment Flashcards

1
Q

Which organ is the primary source of endogenous glucose production?

A

The liver, via glycogenolysis and gluconeogenesis.

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2
Q

What percentage of the glucose released by the liver is metabolized by insulin-insensitive tissues?

A

70-80%.

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3
Q

When does a transition from exogenous glucose usage to endogenous production occur after eating?

A

2-4 hours after eating, when glucose usage exceeds production.

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4
Q

What is fundamental for maintaining normal blood glucose during the transition from exogenous usage to endogenous production?

A

Diminished insulin production.

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5
Q

What hormones make up the glucose counterregulatory system?

A

Glucagon, epinephrine, growth hormone, and cortisol.

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6
Q

What is the primary role of glucagon in glucose regulation?

A

Glucagon stimulates glycogenolysis and gluconeogenesis, while inhibiting glycolysis.

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7
Q

What are the primary causes of diabetes mellitus?

A

It results from either an inadequate supply of insulin or an inadequate tissue response to insulin.

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8
Q

What are the consequences of untreated diabetes mellitus?

A

Increased circulating glucose levels leading to eventual microvascular and macrovascular complications.

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9
Q

What causes Type 1a diabetes?

A

Type 1a diabetes is caused by T-cell–mediated autoimmune destruction of β cells within pancreatic islets, resulting in minimal or absent circulating insulin levels.

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10
Q

How does Type 2 diabetes develop?

A

Type 2 diabetes results from defects in insulin receptors and post-receptor intracellular signaling pathways, and it is not immune mediated.

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11
Q

What percentage of all diabetes mellitus cases does Type 1 diabetes account for?

A

Type 1 diabetes accounts for 5-10% of all diabetes mellitus cases.

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12
Q

At what age is Type 1 diabetes usually diagnosed?

A

Type 1 diabetes is usually diagnosed before age 40.

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13
Q

What precedes the onset of symptoms in Type 1 diabetes?

A

A long pre-clinical period (9-13 years) of B-cell antigen production precedes the onset of symptoms.

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14
Q

How much B-cell function is typically lost before hyperglycemia occurs in Type 1 diabetes?

A

At least 80-90% of B-cell function is lost before hyperglycemia ensues.

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15
Q

What percentage of all diabetes mellitus cases does Type 2 diabetes account for?

A

Type 2 diabetes accounts for over 90% of all diabetes mellitus cases.

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16
Q

How long before diagnosis is Type 2 diabetes typically present but underrecognized?

A

Type 2 diabetes is normally present 4-7 years before it is diagnosed.

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17
Q

What occurs in the initial stages of Type 2 diabetes?

A

Insensitivity to insulin on peripheral tissues leads to increased pancreatic insulin secretion.

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18
Q

What are the three main abnormalities seen in Type 2 diabetes?

A

Increased hepatic glucose release due to a reduction in insulin’s inhibitory effect on the liver, impaired insulin secretion, and insufficient glucose uptake in peripheral tissues.

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19
Q

What are some causes of insulin resistance in DM2?

A

Causes include abnormal insulin molecules, circulating insulin antagonists, and insulin receptor defects.

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20
Q

What acquired and contributing factors are associated with insulin resistance in DM2?

A

Obesity and sedentary lifestyle.

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21
Q

What are some dietary adjustments recommended for managing diabetes?

A

Dietary adjustments involve controlling carbohydrate intake, managing portion sizes, and maintaining a balanced diet.

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22
Q

How does exercise and weight loss benefit individuals with diabetes?

A

Exercise and weight loss can improve hepatic and peripheral insulin sensitivity, leading to better blood glucose control.

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23
Q

What is the primary mechanism of action of Metformin in diabetes management?

A

Metformin, a biguanide, enhances glucose transport into tissues.

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24
Q

What are the effects of Metformin on triglyceride (TGL) and low-density lipoprotein (LDL) levels?

A

Metformin decreases triglyceride (TGL) and low-density lipoprotein (LDL) levels.

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25
Q

What is the mechanism of action of Sulfonylureas in diabetes management?

A

Sulfonylureas stimulate insulin secretion and enhance glucose transport into tissues.

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26
Q

Why are Sulfonylureas not effective in the long term for some diabetic patient

A

Due to diabetic progressive loss of B cell function, Sulfonylureas are not effective in the long term.

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27
Q

What are some common side effects of Sulfonylureas?

A

Common side effects include hypoglycemia, weight gain, and potential cardiac effects.

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28
Q

In what cases is insulin necessary for diabetes management?

A

Insulin is necessary in all cases of Type 1 diabetes (DM1) and in approximately 30% of cases of Type 2 diabetes (DM2).

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29
Q

What are the categories of insulin based on duration of action?

A

Insulin is categorized into rapid-acting (e.g., Lispro, Aspart),
short-acting (regular),
basal/intermediate-acting (e.g., NPH, Lente), and
long-acting (e.g., Ultralente, Glargine).

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30
Q

What is the most dangerous complication associated with insulin therapy?

A

Hypoglycemia is the most dangerous complication.

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31
Q

What factors can exacerbate hypoglycemia?

A

Exacerbating factors include alcohol (ETOH), metformin, sulfonylureas, ACE inhibitors (ACE-I’s), monoamine oxidase inhibitors (MAOI’s), and non-selective beta-blockers (BB’s).

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32
Q

What can repetitive hypoglycemic episodes lead to?

A

Repetitive hypoglycemic episodes can lead to “hypoglycemia unawareness,” where the patient becomes desensitized to hypoglycemia and doesn’t show autonomic symptoms. Neuroglycopenia may ensue, leading to symptoms such as fatigue, confusion, headache, seizures, coma

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33
Q

What is the treatment for hypoglycemia?

A

PO or IV glucose (may give SQ or IM if unconscious)

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34
Q

In which type of diabetes is Diabetic Ketoacidosis (DKA) more common, and what often triggers it?

A

DKA is more prevalent in DM1 and is frequently triggered by infection or illness.

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35
Q

What happens when glucose levels exceed the renal reabsorption threshold in diabetes?

A

Elevated glucose levels surpass the renal reabsorption threshold, leading to osmotic diuresis and subsequent hypovolemia.

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36
Q

What metabolic coupling in the liver can result in excessive production of ketoacids during DKA?

A

The tight metabolic coupling of gluconeogenesis and ketogenesis in the liver can lead to overproduction of ketoacids during DKA.

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37
Q

Typical labs in DKA:
glucose
pH
Bicarb
serum osmolality
serum/urine ketones

A
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38
Q

What is the recommended method for IV volume replacement in diabetic emergencies?

A

IV volume replacement is recommended.

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39
Q

What is the loading dose and infusion rate for insulin in diabetic emergencies?

A

The loading dose is 0.1 units/kg of Regular insulin, followed by a low-dose infusion at 0.1 units/kg/hr.

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40
Q

What electrolytes should be supplemented in diabetic emergencies?

A

Electrolyte supplements should include potassium (K+), phosphorus, magnesium (Mg), and sodium.

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41
Q

What caution should be exercised when correcting glucose levels in diabetic emergencies?

A

Correction of glucose without simultaneous correction of sodium may result in cerebral edema.

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42
Q

What are the key characteristics of Hyperosmolar Hyperglycemic State (HHS)?

A

HHS is characterized by severe hyperglycemia, hyperosmolarity, and dehydration. It typically occurs in individuals with DM2 over 60 years old. It evolves over days to weeks with persistent glucosuric diuresis.

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43
Q

What symptoms are associated with Hyperosmolar Hyperglycemic State (HHS)?

A

Symptoms include polyuria, polydipsia, hypovolemia, hypotension, tachycardia, and organ hypoperfusion. Hyperosmolarity can lead to coma. Patients may exhibit some degree of acidosis but not to the extent seen in DKA.

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44
Q

How is Hyperosmolar Hyperglycemic State (HHS) treated?

A

Treatment involves fluid resuscitation, insulin bolus and infusion, and electrolyte supplementation. The mortality rate ranges from 10-20%.

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45
Q

What characterizes microvascular complications in diabetes?

A

Microvascular complications involve nonocclusive microcirculatory disease with impaired blood flow autoregulation.

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46
Q

What are the key features of diabetic nephropathy?

A

Diabetic nephropathy affects 30-40% of DM1 and 5-10% of DM2 patients, leading to end-stage renal disease (ESRD). Kidneys develop glomerulosclerosis, arteriosclerosis, and tubulointerstitial disease. Symptoms include hypertension, proteinuria, peripheral edema, and decreased glomerular filtration rate (GFR).

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47
Q

How does the progression of diabetic nephropathy affect electrolyte balance?

A

When GFR falls below 15-20, kidneys no longer effectively clear potassium, leading to hyperkalemia and acidosis. ACE inhibitors can slow the progression of proteinuria and the rate of GFR decline.

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48
Q

What treatment options are available for end-stage renal disease (ESRD) in diabetic patients?

A

Treatment options for ESRD include hemodialysis (HD), peritoneal dialysis (PD), and kidney transplant. Combined kidney-pancreas transplant may prevent recurrent nephropathy.

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49
Q

What characterizes Peripheral Neuropathy in diabetes?

A

Peripheral Neuropathy typically presents as a distal symmetric diffuse sensorimotor polyneuropathy.

  • Starts in the toes and feet and progressing proximally. It involves the loss of large sensory and motor fibers, reducing light touch and proprioception
  • Loss of small nerve fibers, decreasing pain and temperature perception, leading to neuropathic pain
  • Ulcers can develop from unnoticed mechanical and traumatic injuries, resulting in significant morbidity from recurrent infections and amputation wounds.
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50
Q

What are the features and treatment options for Peripheral Neuropathy?

A

Treatment involves optimal glucose control, NSAIDs, antidepressants, and anticonvulsants.

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51
Q

What are the characteristics and management strategies for Retinopathy in diabetes?

A

Retinopathy is characterized by microvascular changes, including vessel occlusion, dilation, increased permeability, and microaneurysms.

Visual impairment can range from color loss to blindness.

Glycemic control and blood pressure control can reduce the progression of retinopathy.

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52
Q

What characterizes Autonomic Neuropathy in diabetes?

A

Autonomic Neuropathy can affect any part of the Autonomic Nervous System (ANS) and is caused by damaged vasoconstrictor fibers, impaired baroreceptors, and ineffective cardiovascular activity.

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53
Q

What cardiovascular symptoms are associated with Autonomic Neuropathy?

A

Cardiovascular symptoms include abnormal heart rate control and vascular dynamics, resting tachycardia, loss of heart rate variability, and progression to orthostatic hypotension and dysrhythmias.

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54
Q

What gastrointestinal symptoms and treatments are associated with Autonomic Neuropathy?

A

Gastrointestinal symptoms include decreased gastric secretions and motility, eventually leading to gastroparesis. Symptoms include nausea, vomiting, early satiety, bloating, and epigastric pain. Treatment involves glucose control, consuming small meals, and using prokinetics.

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55
Q

What cardiovascular considerations are important in autonomic neuropathy?

A

Autonomic neuropathy can lead to silent ischemia. Stress tests may be necessary for patients with multiple cardiac risk factors and poor exercise tolerance.

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56
Q

Why is meticulous attention to hydration and renal function crucial in autonomic neuropathy?

A

Hydration status should be carefully monitored, nephrotoxins should be avoided, and renal blood flow should be preserved to prevent complications in the renal system.

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57
Q

How does autonomic neuropathy impact perioperative care?

A

Autonomic neuropathy predisposes patients to perioperative dysrhythmias and hypotension, requiring careful management during surgical procedures.

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58
Q

What considerations should be made regarding gastrointestinal symptoms and autonomic neuropathy?

A

Gastroparesis may increase the risk of aspiration regardless of NPO (nothing by mouth) status. Patients with autonomic neuropathy should avoid hypoglycemic medications and noninsulin injectables.

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59
Q

What characterizes Insulinoma?

A

Insulinoma is a rare, benign pancreatic islet tumor that secretes insulin. It occurs more frequently in women than men, typically in the 50s-60s age range.

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60
Q

How is Insulinoma diagnosed?

A

Diagnosis is based on Whipple triad: hypoglycemia with fasting, glucose levels below 50 with symptoms, and symptom relief with glucose intake.

Diagnosis is confirmed by inappropriately high insulin levels during a 48-72 hour fast.

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61
Q

What are the treatment options for Insulinoma?

A

Preoperatively, diazoxide may be used to inhibit insulin release from beta cells.

Other treatment options include verapamil, phenytoin, propranolol, glucocorticoids, and octreotide.

Surgery is curative.

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62
Q

What precautions should be taken during surgery for Insulinoma?

A

Intraoperative hypoglycemia can occur, followed by hyperglycemia once the tumor is removed. Tight glycemic control is essential during and after surgery.

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63
Q

What are the anatomical features of the thyroid gland?

A

The thyroid gland weighs approximately 20g and consists of two lobes joined by an isthmus.

It is located anteriorly and laterally to the trachea, with the upper border just below the cricoid cartilage.

The parathyroid glands are situated on the posterior aspect of each lobe.

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64
Q

What important structures are in close proximity to the thyroid gland?

A

The recurrent laryngeal nerve and the external motor branch of the superior laryngeal nerve are in close proximity to the thyroid gland.

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65
Q

How is the availability of thyroid hormones affected by iodine?

A

Production of normal quantities of thyroid hormones depends on the availability of exogenous iodine, primarily obtained from the diet.

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66
Q

What is the process of thyroid hormone synthesis?

A

Iodine is reduced to iodide in the gastrointestinal tract, rapidly absorbed into the blood, and transported into thyroid follicular cells.

The binding of iodide to thyroglobulin is catalyzed by an iodinase enzyme, yielding inactive monoiodotyrosine and diiodotyrosine.

About 25% of monoiodotyrosine and diiodotyrosine undergo coupling with thyroid peroxidase to form active triiodothyronine (T3) and thyroxine (T4).

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67
Q

What factors contribute to the stability of thyroid hormone levels?

A

The thyroid gland contains a large store of hormones and has a low turnover rate, which protects against depletion if hormone synthesis is impaired.

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68
Q

How is thyroid function regulated in the body?

A

Thyroid function is regulated by a classic feedback control system involving the hypothalamus, pituitary, and thyroid glands.

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69
Q

What is the role of thyrotropin-releasing hormone (TRH) and thyrotropin-stimulating hormone (TSH) in thyroid regulation?

A

TRH, secreted from the hypothalamus, stimulates the release of TSH from the anterior pituitary. TSH binds to receptors on the thyroid cell membrane, enhancing the synthesis and secretion of T3 and T4.

70
Q

How does TSH secretion affect thyroid hormone synthesis and gland characteristics?

A

Decreased TSH leads to reduced T3 and T4 synthesis, decreased follicular cell size, and decreased vascularity, while increased TSH results in increased hormone production, gland cellularity, and vascularity.

71
Q

How are plasma levels of T3 and T4 involved in regulating TSH secretion?

A

TSH secretion is also influenced by plasma levels of T3 and T4 via a negative feedback loop, ensuring proper regulation of thyroid hormone levels.

72
Q

What is the primary test for evaluating thyroid hormone action at the cellular level?

A

The TSH assay is the best test for assessing thyroid hormone action at the cellular level. Small changes in thyroid function can lead to significant alterations in TSH secretion.

73
Q

What are the normal levels of TSH?

A

The normal range for TSH levels is 0.4-5.0 milliunits/L.

74
Q

What other diagnostic tests are used for thyroid disorders?

A

Other diagnostic tests include serum anti-microsomal antibodies, antithyroglobulin antibodies, and thyroid-stimulating immunoglobulins.

Thermal thyroid scans assess thyroid nodules as “warm” (normally functioning), “hot” (hyperfunctioning), or “cold” (hypofunctioning).

75
Q

How accurate is ultrasound (US) in evaluating thyroid lesions?

A

Ultrasound is 90-95% accurate in determining whether a thyroid lesion is cystic, solid, or mixed, aiding in the diagnosis and characterization of thyroid nodules.

76
Q

What characterizes hyperfunctioning thyroid gland?

A

Hyperfunctioning thyroid gland involves excessive secretion of active hormones, leading to a hypermetabolic state. The majority of cases are caused by one of three pathologies: Graves disease, toxic multinodular goiter, or toxic adenoma.

77
Q

What symptoms are associated with hyperfunctioning thyroid gland?

A

Symptoms are related to the hypermetabolic state and include sweating, heat intolerance, fatigue with inability to sleep. Osteoporosis and weight loss may also occur.

78
Q

How does T3 affect cardiovascular function?

A

T3 acts directly on the myocardium and peripheral vasculature to cause cardiovascular responses, contributing to the cardiovascular manifestations of hyperthyroidism.

79
Q

What is Graves disease, and what is its prevalence?

A

Graves disease is the leading cause of hyperthyroidism, affecting approximately 0.4% of the population. It typically occurs in females (7:1 ratio) aged 20-40 years.

80
Q

What is the suspected etiology of Graves disease, and what are its characteristic features?

A

Graves disease appears to be autoimmune, characterized by thyroid-stimulating antibodies that bind to TSH receptors, stimulating growth, vascularity, and hypersecretion. The thyroid is usually diffusely enlarged, and ophthalmopathy occurs in 30% of cases.

81
Q

How is Graves disease diagnosed, and what are its clinical manifestations?

A

Diagnosis is confirmed with TSH antibodies in the context of low TSH and high T3 and T4 levels. Graves disease may present with extreme enlargement causing dysphagia, globus sensation, and inspiratory stridor from tracheal compression.

82
Q

What is the first-line treatment for Graves disease, and what are the alternatives?

A

The first-line treatment for Graves disease is antithyroid drugs, such as methimazole or propylthiouracil (PTU). High concentrations of iodine reduce release of thryroid hormone and can also be used, but are typically reserved for pre-operative preparation or thyroid storm.

83
Q

How do beta-blockers contribute to the management of Graves disease?

A

Beta-blockers, such as propranolol, may relieve symptoms by blocking the effects of excess thyroid hormones. However, they do not address the underlying abnormality.

84
Q

What are the options for ablative therapy or surgery in Graves disease?

A

Ablative therapy or surgery is recommended when medical treatment has failed. Surgery, specifically subtotal thyroidectomy, is effective and associated with a lower incidence of hypothyroidism compared to radioactive iodine therapy.

85
Q

What is the recommended preoperative thyroid level status for elective cases of Graves’ disease surgery?

A

Thyroid levels should be normalized preoperatively.

86
Q

How long do antithyroid drugs take to reach therapeutic levels?

A

about 6-8 weeks for antithyroid drugs to take effect.

87
Q

What are the necessary emergency interventions for emergent cases of Graves’ disease prior to surgery?

A

In emergent cases, intravenous beta-blockers, glucocorticoids, and propylthiouracil (PTU) are usually necessary. Additionally, evaluating the upper airway for evidence of tracheal compression or deviation caused by a goiter is important.

88
Q

What can precipitate a life-threatening thyroid storm?

A

A thyroid storm can be precipitated by trauma, infection, medical illness, or surgery.

89
Q

How can thyroid storm and malignant hyperthermia be differentiated, considering their similar presentations?

A

Surprisingly, thyroid hormone levels in a thyroid storm may not be much higher than in basic hyperthyroidism. A thyroid storm most often occurs postoperatively in untreated or inadequately treated hyperthyroid patients after emergency surgery.

90
Q

What is the mortality rate associated with thyroid storm, and what does treatment include?

A

The mortality rate for thyroid storm is 20%, and treatment includes rapid alleviation of thyrotoxicosis and supportive care.

91
Q

What percentage of adults are affected by hypothyroidism or myxedema, and what is the primary result of primary hypothyroidism?

A

Hypothyroidism or myxedema affects 0.5-0.8% of adults. Primary hypothyroidism, which accounts for 95% of cases, results in decreased T3 & T4 production despite adequate TSH levels.

92
Q

What are the first and second most common causes of primary hypothyroidism?

A

The first most common cause is ablation of the gland by radioactive iodine or surgery, and the second most common cause is idiopathic, probably autoimmune, with antibodies blocking TSH receptors.

93
Q

What are the symptoms of hypothyroidism in adults, and what other conditions are commonly associated with it?

A

Symptoms of hypothyroidism in adults include cold intolerance, weight gain, and nonpitting edema. Associated conditions include SIADH, fluid overload, pleural effusions, dyspnea, slow GI function, and the potential for an adynamic ileus to occur.

94
Q

How is secondary hypothyroidism diagnosed and what does a TRH stimulation test indicate in primary vs pituitary dysfunction?

A

Secondary hypothyroidism is diagnosed by reduced levels of T3, T4, and TSH.

A TRH stimulation test confirms pituitary cause by measuring pituitary responsiveness to intravenous TRH.

In primary hypothyroidism, TRH further elevates TSH, while with pituitary dysfunction, there is no response to TRH.

95
Q

What is euthyroid sick syndrome, and what are its characteristics in critically ill patients?

A
  • abnormal thyroid function tests in critically ill patients, with low T3 and T4 but a normal TSH level
  • likely a response to stress and can be induced by surgery.
96
Q

What is the drug of choice for treating hypothyroidism, and when should thyroid treatment be initiated before elective surgery?

A

L-thyroxine is the drug of choice for treating hypothyroidism. For elective surgery, thyroid treatment should be initiated at least 10 days prior.

97
Q

What are the pre-operative implications and assessments for a patient with hypothyroidism?

A
  • Pre-operatively, assess for airway compromise due to swelling, edematous vocal cords, or goitrous enlargement.
  • Expect slower gastric emptying and an increased risk of aspiration.
  • The cardiovascular system may be hypodynamic
  • Respiratory function may be compromised, and
  • More prone to hypothermia and electrolyte imbalances.
98
Q

How should emergent surgery be managed in a patient with hypothyroidism?

A

If emergent surgery is required, intravenous thyroid replacement along with steroids should be administered as soon as possible.

99
Q

What is myxedema coma, and what are its characteristics?

A

Myxedema coma is a rare, severe form of hypothyroidism characterized by delirium, hypoventilation, hypothermia, bradycardia, hypotension, and severe dilutional hyponatremia.

100
Q

Who is most commonly affected by myxedema coma, what triggers it, and what is a cardinal feature?

A
  • Myxedema coma occurs most commonly in elderly women with a long history of hypothyroidism
  • can be triggered by infection, trauma, cold, and CNS depressants
  • Hypothermia is a cardinal feature due to impaired thermoregulation.
101
Q

What is the treatment for myxedema coma, and what is the usual time frame for improvement of heart rate, blood pressure, and temperature?

A

Treatment for myxedema coma includes:
* IV L-thyroxine or L-triiodothyronine,
* IV hydration with glucose-saline solutions,
* temperature regulation,
* correction of electrolyte imbalances, and
* stabilization of cardiac and pulmonary systems.

Mechanical ventilation is frequently required. Heart rate, blood pressure, and temperature usually improve within 24 hours. The mortality rate is greater than 50%.

102
Q

What is a goiter, and what are the common causes?

A

A goiter is the swelling of the thyroid gland due to hypertrophy and hyperplasia of the follicular epithelium.

It can be caused by a lack of iodine, ingestion of goitrogens like cassava, phenylbutazone, lithium, or a defect in the hormonal biosynthetic pathway.

103
Q

When is surgery indicated for a goiter?

A

Surgery is indicated only if medical therapy is ineffective, and the goiter compromises the airway or is cosmetically unacceptable.

104
Q

What preoperative history is predictive of possible airway obstruction during general anesthesia?

A

A history of dyspnea in both upright or supine positions is predictive of possible airway obstruction during general anesthesia.

105
Q

What diagnostic tests should be examined to assess the extent of a thyroid tumor and the site and degree of obstruction?

A

A CT scan should be examined to assess the extent of the tumor, and flow-volume loops in the upright and supine positions will demonstrate the site and degree of obstruction.

106
Q

How do limitations in flow-volume loops indicate the location of obstruction, and what can an echocardiogram reveal?

A

Limitations in the inspiratory limb of the flow-volume loop indicate extra-thoracic obstruction, while delayed flow in the expiratory limb indicates intra-thoracic obstruction.

An echocardiogram in the upright and supine positions can indicate the degree of cardiac compression.

107
Q

What is the overall morbidity rate from thyroid surgery, and what are the possible outcomes of recurrent laryngeal nerve (RLN) injury?

A

The morbidity from thyroid surgery approaches 13%. RLN injury may be unilateral or bilateral, and temporary or permanent.

Unilateral trauma can cause hoarseness but typically not airway obstruction, and function usually returns in 3-6 months.

108
Q

What are the consequences of bilateral RLN injury, and how might it be managed?

A

Bilateral RLN injury is more serious, potentially causing airway obstruction and difficulty coughing, which may warrant a tracheostomy.

109
Q

What complications may arise from damage to the parathyroid glands during thyroid surgery, and what should be kept at the bedside during the immediate postoperative period?

A

Hypoparathyroidism may result from inadvertent parathyroid damage, with symptoms of hypocalcemia occurring in the first 24-48 hours postoperatively.

A hematoma may lead to tracheal compression, hence a tracheostomy set should be kept at the bedside during the immediate postoperative period.

110
Q

What hormones are synthesized by the adrenal cortex, and what is the pathway of hormonal stimulation that leads to cortisol production?

A

The adrenal cortex synthesizes glucocorticoids, mineralocorticoids (such as aldosterone), and androgens.

The hypothalamus releases corticotropin-releasing hormone (CRH) to the anterior pituitary, which in turn stimulates the release of corticotropin (ACTH).

ACTH stimulates the adrenal cortex to produce cortisol.

111
Q

What role does cortisol play in the adrenal medulla and in glucose metabolism?

A

Cortisol facilitates the conversion of norepinephrine (NE) to epinephrine (EPI) in the adrenal medulla. It also induces hyperglycemia by promoting gluconeogenesis and inhibiting glucose uptake by cells.

112
Q

What is the combined effect of cortisol and aldosterone on electrolyte balance?

A

Together, cortisol and aldosterone cause sodium retention and potassium excretion.

113
Q

What is a pheochromocytoma and what serious conditions can uncontrolled catecholamine release from these tumors cause?

A

A pheochromocytoma is a catecholamine-secreting tumor that arises from chromaffin cells of the sympathoadrenal system.

Uncontrolled catecholamine release can result in malignant hypertension, cerebrovascular accidents (CVA), and myocardial infarction (MI).

114
Q

Where are pheochromocytomas most commonly located and what is their usual secretion ratio of norepinephrine to epinephrine?

A

80% of pheochromocytomas occur in the adrenal medulla, 18% in the organ of Zuckerkandl, and 2% in the neck or thorax.

Most pheochromocytomas secrete a norepinephrine to epinephrine ratio of 85:15, which is the inverse of normal adrenal secretion.

115
Q

What is the duration of pheochromocytoma attacks and what can trigger them?

A

Attacks can range from occasional to frequent, lasting between 1 minute to several hours, and may occur spontaneously or be triggered by injury, stress, or medications.

116
Q

What are the symptoms of a pheochromocytoma attack and what cardiac complications can arise?

A

Symptoms include headaches, pallor, sweating, palpitations, and orthostatic hypotension. Cardiac complications can include coronary vasoconstriction, cardiomyopathy, congestive heart failure, and EKG changes.

117
Q

How is pheochromocytoma diagnosed and what imaging techniques help localize the tumor?

A

Diagnosis of pheochromocytoma is made through a 24-hour urine collection for metanephrines and catecholamines. CT & MRI, along with I-metaiodobenzylguanidine (MIBG) scintigraphy, are used to help localize the tumor.

118
Q

What is the purpose of preoperative α-blockade in pheochromocytoma patients, and which drug is most frequently used for this?

A

Preoperative α-blockade aims to lower blood pressure, decrease intravascular volume, allow sensitization of adrenergic receptors, and decrease myocardial dysfunction.

Phenoxybenzamine is the most frequently used preoperative α-blocker.

119
Q

How are tachycardia and hypertension managed preoperatively in pheochromocytoma patients?

A

Tachycardia after α-blockade should be treated with beta-blockers (BB), but nonselective BB should never be given before α-blockade due to the risk of unopposed α agonism, leading to vasoconstriction and hypertensive crises.

120
Q

What is the role of calcium channel blockers (CCBs) in the preoperative management of pheochromocytoma, and why are they used?

A

CCBs are used to control hypertension. Calcium triggers catecholamine release from the tumor, and excess calcium entry into myocardial cells contributes to catecholamine-mediated cardiomyopathy.

121
Q

What are the two forms of Cushing syndrome and how is ACTH related to each?

A

The two forms of Cushing syndrome are ACTH-dependent and ACTH-independent.

In ACTH-dependent Cushing’s, high plasma ACTH stimulates the adrenal cortex to produce excessive cortisol.

In ACTH-independent Cushing’s, excessive cortisol production is by abnormal adrenocortical tissue not regulated by CRH and ACTH, with CRH and ACTH levels actually suppressed.

122
Q

What is the acute ectopic ACTH syndrome, and with which condition is it most often associated?

A

Acute ectopic ACTH syndrome is a form of ACTH-dependent Cushing’s syndrome most often associated with small cell lung carcinoma.

123
Q

What is the most common cause of ACTH-independent Cushing syndrome?

A

Benign or malignant adrenocortical tumors are the most common cause of ACTH-independent Cushing syndrome.

124
Q

What is the treatment of choice for a resectable microadenoma in Cushing syndrome?

A

The treatment of choice for a resectable microadenoma in Cushing syndrome is transsphenoidal microadenomectomy.

125
Q

What surgical treatments are available for patients with Cushing syndrome when a microadenoma is not resectable?

A

If a microadenoma is not resectable, patients may undergo 85-90% resection of the anterior pituitary, pituitary irradiation, or bilateral total adrenalectomy.

126
Q

What are the preoperative considerations for a patient undergoing surgery for Cushing syndrome?

A

Preoperative considerations include evaluation and treatment of blood pressure, electrolyte imbalance, and blood glucose levels. Additionally, consider the risk of osteoporosis when positioning the patient for surgery.

127
Q

Cushing’s appearance:

A
128
Q

What is primary hyperaldosteronism and how does it differ from secondary hyperaldosteronism?

A

Primary hyperaldosteronism, also known as Conn syndrome, is the excess secretion of aldosterone from a functional tumor (aldosteronoma) that acts independently of a physiological stimulus.

Secondary hyperaldosteronism presents when serum renin is increased, stimulating the release of aldosterone.

129
Q

In whom is primary hyperaldosteronism more common, and with which conditions can it be occasionally associated?

A

Primary hyperaldosteronism is more common in women than in men and can occasionally be associated with conditions such as pheochromocytoma, hyperparathyroidism, or acromegaly.

130
Q

What are the symptoms and signs of hyperaldosteronism?

A

Symptoms of hyperaldosteronism can be nonspecific and some individuals are asymptomatic. However, common signs include hypertension, hypokalemia, and hypokalemic metabolic alkalosis.

131
Q

What clinical presentation is highly suggestive of hyperaldosteronism and how do plasma renin levels differ between primary and secondary hyperaldosteronism?

A

Spontaneous hypokalemia in the presence of systemic hypertension is highly suggestive of hyperaldosteronism.

In primary hyperaldosteronism, plasma renin activity is suppressed, whereas in secondary hyperaldosteronism, plasma renin activity is high.

132
Q

What can cause a syndrome that mimics the features of hyperaldosteronism and what are its manifestations?

A

Long-term ingestion of licorice can cause a syndrome that mimics the features of hyperaldosteronism, which includes hypertension, hypokalemia, and suppression of the renin-angiotensin-aldosterone system (RAAS).

133
Q

What are the treatment options for hyperaldosteronism?

A

Treatment options for hyperaldosteronism include the use of competitive aldosterone antagonists (such as Spironolactone), potassium replacement, antihypertensives, diuretics, tumor removal, and possibly adrenalectomy.

134
Q

What clinical indicator suggests hypoaldosteronism and what may enhance hyperkalemia in these patients?

A

Hyperkalemia in the absence of renal insufficiency suggests hypoaldosteronism. This condition may be enhanced by hyperglycemia.

135
Q

What are common manifestations of hypoaldosteronism and what can cause a lack of aldosterone?

A

Common manifestations of hypoaldosteronism include hyperchloremic metabolic acidosis, heart block due to hyperkalemia, orthostatic hypotension, and hyponatremia.

Lack of aldosterone may be caused by a congenital deficiency of aldosterone synthetase or hyporeninemia due to defects in the juxtaglomerular apparatus or ACE inhibitors.

136
Q

Who typically experiences hyporeninemic hypoaldosteronism, what is a reversible cause of this syndrome, and how is it treated?

A

Hyporeninemic hypoaldosteronism typically occurs in patients over 45 with chronic renal failure or diabetes mellitus.

Indomethacin-induced prostaglandin deficiency is a reversible cause of this syndrome. Treatment includes liberal sodium intake and daily administration of fludrocortisone.

137
Q

What distinguishes primary adrenal insufficiency (Addison’s disease) from secondary adrenal insufficiency?

A

In primary adrenal insufficiency (Addison’s disease), the adrenal glands are unable to produce sufficient amounts of glucocorticoid, mineralocorticoid, and androgen hormones, often due to autoimmune adrenal destruction.

Secondary adrenal insufficiency results from hypothalamic-pituitary disease or suppression, leading to a lack of CRH or ACTH production and causing a deficiency only in glucocorticoids.

138
Q

What is the most common cause of primary adrenal insufficiency, and how much of the adrenal glands must be involved before signs appear?

A

The most common cause of primary adrenal insufficiency is autoimmune destruction of the adrenal glands, and more than 90% of the glands must be affected before clinical signs become apparent.

139
Q

How are secondary adrenal insufficiency patients different from those with Addison’s disease in terms of clinical presentation?

A

Patients with secondary adrenal insufficiency typically lack hyperpigmentation and may only show mild electrolyte abnormalities.

This is because, unlike Addison’s disease, there is a glucocorticoid deficiency but not a mineralocorticoid deficiency.

Most cases are iatrogenic, due to factors such as the use of synthetic glucocorticoids, pituitary surgery, or radiation.

140
Q

How is adrenal insufficiency diagnosed using baseline cortisol levels and ACTH stimulation?

A

Adrenal insufficiency is diagnosed when the baseline cortisol is less than 20 μg/dL and remains below 20 μg/dL after ACTH stimulation. A poor response to ACTH indicates impairment of the adrenal cortex.

141
Q

What distinguishes absolute adrenal insufficiency from relative adrenal insufficiency in terms of diagnostic testing?

A

Absolute adrenal insufficiency is characterized by a low baseline cortisol level and a positive ACTH stimulation test. Relative adrenal insufficiency is indicated when the baseline cortisol level is higher but there is still a positive response to the ACTH stimulation test.

142
Q

What is the treatment for adrenal insufficiency?

A

The treatment for adrenal insufficiency is the administration of steroids.

143
Q

Where are the parathyroid glands located and what hormone do they produce?

A

The four parathyroid glands are located behind the upper and lower poles of the thyroid gland, and they produce parathyroid hormone (PTH).

144
Q

How is the release of PTH regulated in the body?

A

The release of parathyroid hormone (PTH) is regulated by a negative feedback mechanism that depends on plasma calcium levels; hypocalcemia stimulates PTH release, whereas hypercalcemia suppresses hormonal synthesis and release.

145
Q

What role does PTH play in maintaining normal plasma calcium levels?

A

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

146
Q

What are the causes of primary hyperparathyroidism?

A
  • benign parathyroid adenoma (90%)
  • parathyroid carcinoma (<5%),
  • parathyroid hyperplasia.
147
Q

What are the symptoms of hyperparathyroidism and how is it diagnosed and treated?

A

Symptoms of hyperparathyroidism can include sedation, nausea/vomiting, decreased strength and sensation, polyuria, renal stones, peptic ulcer disease, and cardiac disturbances.

It is diagnosed by measuring plasma calcium and 24-hour urinary calcium. Treatment typically involves surgical removal of the abnormal portions of the gland.

148
Q

What is secondary hyperparathyroidism and what condition commonly leads to it?

A

Secondary hyperparathyroidism is a compensatory response of the parathyroid glands to chronic hypocalcemia, such as that seen with chronic renal failure (CRF).

149
Q

Why does secondary hyperparathyroidism rarely produce hypercalcemia?

A

Because secondary hyperparathyroidism is an adaptive response to a separate disease process producing hypocalcemia, it does not typically result in hypercalcemia.

150
Q

How is secondary hyperparathyroidism treated?

A

Treatment of secondary hyperparathyroidism involves controlling the underlying disease and normalizing phosphate levels in patients with renal disease by administering a phosphate binder.

151
Q

What causes hypoparathyroidism and what is pseudohypoparathyroidism?

A

Hypoparathyroidism is typically present when there is a deficiency of PTH or resistance to its effects in peripheral tissues.

It is most often iatrogenic, due to inadvertent removal of parathyroid glands during thyroidectomy.

Pseudohypoparathyroidism is a congenital disorder where PTH levels are adequate, but the kidneys are resistant to its effects.

152
Q

How is hypoparathyroidism diagnosed?

A

Hypoparathyroidism is diagnosed by the presence of hypocalcemia with total calcium less than 4.5 mEq/L and ionized calcium less than 2.0 mg/dL, accompanied by decreased PTH and increased phosphate levels.

153
Q

What are the symptoms of acute and chronic hypoparathyroidism, and how is the condition treated?

A

Acute hypoparathyroidism, such as after thyroidectomy, may cause inspiratory stridor due to irritability of the laryngeal musculature.

Chronic hypoparathyroidism is associated with fatigue, cramps, prolonged QT interval, lethargy, cataracts, subcutaneous calcifications, thickening of the skull, and neurologic deficits.

Chronic renal failure is the most common cause of chronic hypocalcemia.

Treatment includes calcium replacement and vitamin D.

154
Q

Where is the pituitary gland located and what are its two main parts?

A

The pituitary gland is located in the sella turcica at the base of the brain and consists of two main parts: the anterior pituitary and the posterior pituitary.

155
Q

What hormones are secreted by the anterior pituitary and how is their secretion controlled?

A

The anterior pituitary secretes six hormones: growth hormone (GH), adrenocorticotropic hormone (ACTH), thyroid-stimulating hormone (TSH), follicle-stimulating hormone (FSH), luteinizing hormone (LH), and prolactin. The secretion of these hormones is under the control of the hypothalamus.

156
Q

How are vasopressin and oxytocin related to the pituitary gland and what triggers their release?

A

Vasopressin and oxytocin are synthesized in the hypothalamus, then transported and stored in the posterior pituitary.

The release of these hormones from the posterior pituitary is triggered by osmoreceptors in the hypothalamus that sense plasma osmolarity.

Overproduction of anterior pituitary hormones is often associated with hypersecretion of ACTH, leading to conditions like Cushing syndrome, caused by anterior pituitary adenomas.

157
Q

What is the primary cause of acromegaly, and how is it typically diagnosed?

A

Acromegaly is primarily caused by excessive secretion of growth hormone (GH) in adults, often due to an adenoma in the anterior pituitary gland.

Diagnosis is typically confirmed by elevated levels of serum insulin-like growth factor 1 (IGF-1).

158
Q

Describe how an oral glucose tolerance test can aid in the diagnosis of acromegaly.

A

An oral glucose tolerance test involves measuring plasma growth hormone levels before and after ingestion of 75 grams of glucose. In patients with acromegaly, plasma growth hormone remains elevated (>1 ng/mL) even 2 hours after glucose ingestion.

159
Q

What are some clinical manifestations and complications of acromegaly, and what are the treatment options?

A

Acromegaly can lead to overgrowth of soft tissues, causing susceptibility to upper airway obstruction, hoarseness, abnormal movement of vocal cords, and paralysis of the recurrent laryngeal nerve.

Peripheral neuropathy may also occur due to nerve trapping by connective tissues.

Treatment typically involves transsphenoidal surgical excision of the pituitary adenoma. If surgery is not feasible, long-acting somatostatin analogues are used.

160
Q

How might distorted facial anatomy in patients with acromegaly affect airway management during anesthesia induction?

A

Distorted facial anatomy in patients with acromegaly may interfere with the placement of a face mask, making it challenging to achieve a proper seal for ventilation.

161
Q

What are the challenges related to upper airway obstruction during intubation in patients with acromegaly?

A

Enlarged tongue and epiglottis in patients with acromegaly predispose them to upper airway obstruction and interfere with the visualization of vocal cords during direct laryngoscopy. Mandible overgrowth also increases the distance between the lips and vocal cords, and vocal cord enlargement may narrow the glottic opening.

162
Q

What specific considerations should be taken into account when selecting airway management techniques for patients with acromegaly?

A

Patients with acromegaly may require smaller endotracheal tubes (ETT), video laryngoscopy (VL), or awake fiberoptic intubation to navigate the challenges posed by their enlarged upper airway anatomy.

163
Q

What characterizes diabetes insipidus (DI), and what are its two main types?

A

Diabetes insipidus (DI) results from the absence of vasopressin (antidiuretic hormone, ADH) due to either the destruction of the posterior pituitary (neurogenic DI) or the failure of renal tubules to respond to ADH (nephrogenic DI).

164
Q

How can neurogenic and nephrogenic DI be differentiated, and what is the characteristic response to desmopressin?

A

Neurogenic and nephrogenic DI can be differentiated based on their response to desmopressin. Desmopressin causes urine concentration in neurogenic DI but not in nephrogenic DI.

165
Q

What are the typical symptoms of DI, and what is the initial treatment approach?

A

Symptoms of DI include polydipsia (excessive thirst) and high output of poorly concentrated urine despite increased serum osmolarity.

The initial treatment approach involves intravenous electrolytes to offset polyuria. For neurogenic DI, desmopressin (DDAVP) is used, while nephrogenic DI is managed with a low-salt, low-protein diet, diuretics, and NSAIDs.

166
Q

What anesthesia considerations are important for patients with DI?

A

Anesthesia management for patients with DI involves monitoring urine output (UOP) and serum electrolyte concentrations closely to ensure proper fluid balance and electrolyte levels during the perioperative period.

167
Q

What are some pathologies associated with the development of syndrome of inappropriate antidiuretic hormone secretion (SIADH)?

A

SIADH can occur in the presence of diverse pathologies, including intracranial tumors, hypothyroidism, porphyria, and lung carcinoma.

168
Q

How can SIADH be diagnosed based on laboratory findings, and what are the potential complications of abrupt decreases in serum sodium concentration?

A

In SIADH, there is inappropriately increased urinary sodium and osmolarity despite hyponatremia and decreased serum osmolarity. Abrupt decreases in serum sodium concentration can lead to cerebral edema and seizures.

169
Q

What are the treatment options for SIADH, and how is hyponatremia managed?

A

Treatment for SIADH includes fluid restriction, salt tablets, loop diuretics, and ADH antagonists such as demeclocycline. Hyponatremia may be treated with hypertonic saline infusion at a rate of less than 8 mEq/L over 24 hours to prevent complications.

170
Q

What hormonal response occurs during DKA, and what is its effect on lipolysis and ketogenesis?

A

DKA results in an excessive release of glucose-counterregulatory hormones, including glucagon, which activates lipolysis, releasing free fatty acids that serve as substrates for ketogenesis.v

171
Q

What are the common diagnostic tests for DM2?

A

Fasting blood glucose and HbA1c levels are used for diagnosis.

172
Q

What characterizes Type 2 diabetes mellitus (DM2) in terms of insulin resistance?

A

DM2 is characterized by insulin resistance in skeletal muscle, adipose tissue, and the liver.

Assessment w/ Mordecai (6 decks)

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