FU(6): Metabolism, Obesity, Malnutrition, & Endocrine Flashcards

1
Q

A 32-year-old female with a known history of acute intermittent porphyria is scheduled for elective surgery. She reports a history of mild abdominal pain and neurological symptoms that have been well controlled. Which of the following anesthetic plans is MOST appropriate for this patient?

A

Use of benzos for predmedication and propofol for induction, avoid barbiturates and sulfonamide antibiotics

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2
Q

A patient with hereditary coproporphyria presents with acute abdominal pain and neurological symptoms suggestive of an acute porphyric crisis. Which of the following treatment strategies is MOST appropriate?

A

Immediate administration of IV glucose followed by heme therapy if no improvement is seen

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3
Q

A 40-year-old female with a history of acute intermittent porphyria (AIP) presents for an emergency laparotomy due to suspected intestinal obstruction. She is currently symptomatic, reporting severe abdominal pain, and her medical record indicates a history of psychiatric disturbances during acute porphyric attacks. Laboratory tests reveal hyponatremia and elevated urinary porphobilinogen. Given her condition and the emergent nature of the surgery, which of the following anesthesia management plans is MOST appropriate to mitigate the risk of exacerbating her porphyria and managing her symptoms effectively?

A

Preop carb loading with glucose infusion, use of propofol for induction, and maintenance with a non-triggering volatile anesthetic like sevo, ensuring avoidance of barbiturates sulfonamide abx, and any drugs known to induce ALA synthase. Post op pain management with opioids and careful correction of hyponatremia.

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4
Q

A 52-year-old male with a long-standing history of primary hemochromatosis, managed with routine phlebotomy, presents for elective abdominal surgery. His preoperative workup reveals a serum ferritin level of 1500 μg/L and a fasting transferrin saturation of 55%. He has a history of diabetes and is on oral hypoglycemics, with recent echocardiography showing mild left ventricular hypertrophy but preserved ejection fraction. Given his condition, which of the following anesthesia management strategies is MOST appropriate?

A

Utilization of low dose prop and avoidance of volatile anesthetics d/t potential for worsening liver damage, monitor for cardiac arrhythmias given the left ventricle hypertrophy, and careful glucose monitoring

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5
Q

A 27-year-old female with Wilson disease, presenting with acute neurologic deterioration including dysarthria and tremors, requires emergency decompressive neurosurgery. Her current medications include zinc and trientine. Preoperative evaluation reveals elevated liver enzymes, indicative of ongoing liver involvement, and Kayser-Fleischer rings are noted. In planning her anesthetic care, which of the following considerations is MOST critical?

A

Preference for TIVA with agents such as prop and remifentanil to minimize hepatic metabolism burden, along with careful monitoring for neuro changes postop

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6
Q

A 58-year-old male with metabolic syndrome (MetS) is scheduled for elective abdominal aortic aneurysm repair. He has a BMI of 34 kg/m^2, blood pressure of 150/95 mmHg, fasting blood glucose of 110 mg/dL, and dyslipidemia. Given the increased risk of cardiovascular events associated with MetS, which of the following anesthetic management strategies would be MOST appropriate for this patient?

A

Utilize a balance anesthesia technique with careful titration of volatile anesthetics and vasopressors to maintain hemodynamic stability, intraoperative glucose monitoring and consideration of post-op pain management to reduce stress response

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7
Q

A rare case involves a 35-year-old male diagnosed with both hemochromatosis and Wilson disease, scheduled for elective laparoscopic cholecystectomy due to symptomatic gallstones. His hemochromatosis is managed with phlebotomy, maintaining serum ferritin levels below 1000 μg/L, while Wilson disease is controlled with trientine and dietary modifications. He has mild hepatomegaly but no signs of cirrhosis or acute liver failure. His cardiac function is normal, but he has a history of mild neuropsychiatric symptoms including anxiety and depression. In planning his anesthetic management, which of the following strategies is MOST appropriate?

A

Implement balanced anesthesia technique with careful use of low-dose volatile and TIVA avoiding narcotics that may exacerbate neuropsych symptoms, and close monitoring of liver function tests pre and post op

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8
Q

A 60-year-old patient with metabolic syndrome, nonalcoholic steatohepatitis (NASH), and compensated cirrhosis is scheduled for partial hepatic resection due to a hepatic adenoma. The patient’s preoperative evaluation indicates well-controlled hypertension and diabetes, mild portal hypertension, and preserved liver function with a Child-Pugh score of A. In the context of this patient’s complex condition, which of the following perioperative management strategies aligns best with optimizing surgical outcomes and maintaining hemodynamic stability?

A

Tailor anesthetic management to ensure minimal changes in portal venous pressure, utilizing a combo of low-dose vasopressors and careful fluid administration to maintain normovolemia and avoid exacerbating portal HTN

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9
Q

A 55-year-old patient with metabolic syndrome, nonalcoholic steatohepatitis (NASH), and poorly controlled diabetes (HbA1c 8.5%) is undergoing major colorectal surgery. Considering the intricate pathophysiological interactions between insulin resistance inherent in metabolic syndrome, hepatic dysfunction due to NASH, and the surgical stress response, which of the following strategies most effectively aligns anesthetic management with optimal glycemic control?

A

Implement comprehensive intraop management that integrates continuous insulin infusion based on real time glucose monitoring with anesthetic technique adjusted for hepatic function. This approach should be supported by rigorous hemodynamic monitoring

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10
Q

In managing anesthesia for a patient with clinically severe obesity, understanding the impact of obesity on the pharmacokinetics of anesthetic drugs is crucial. Which of the following statements BEST explains the pathophysiological alterations in drug metabolism in obese patients?

A

Increased adipose tissue leads to altered drug distribution, requiring adjustments in dosing based on lean body weight.

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11
Q

During laparoscopic surgery in obese patients, the creation of pneumoperitoneum and patient positioning have significant effects on physiological parameters. Which of the following BEST describes a pathophysiological effect of pneumoperitoneum on cardiovascular function in these patients?

A

Pneumoperitoneum decreases venous return, increasing the risk of thromboembolic events due to decreased cardiac output

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12
Q

Considering the pathophysiological changes in obese patients, which of the following is a PRIMARY concern for airway management during anesthesia?

A

Decreased FRC in obese patients leads to rapid desaturation during apnea, necessitating preoxygenation and careful airway management.

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13
Q

Which of the following best describes the primary pathophysiological mechanism by which malnutrition increases the risk of perioperative infection?

A

Malnutrition induced mitochondrial malfunction and proinflammatory cytokine release impair leukocyte mobilization and function

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13
Q

What is the primary pathophysiological defect that characterizes the early stage of type 2 diabetes mellitus?

A

Insulin resistance in skeletal muscle, adipose tissue, and the liver with relative B-cell insufficiency

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14
Q

How does the coexistence of obesity and malnutrition (malnourished obesity) uniquely affect perioperative risk management?

A

Hypoalbuminemia in obese patients signifies a compounded risk for complications, necessitating targeting nutritional interventions.

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15
Q

Which mechanism is primarily responsible for insulin resistance in type 2 diabetes, particularly affecting skeletal muscle glucose uptake?

A

Impaired insulin receptor substrate phosphorylation leading to dysfunctional insulin signaling pathways

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16
Q

Which counter-regulatory hormone exacerbates hyperglycemia by increasing glucose production during insulin deficiency?

A

Glucagon through its actions on gluconeogenesis and glycogenolysis in the liver

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17
Q

What differentiates the pathophysiological mechanism of hyperglycemic hyperosmolar syndrome (HHS) from diabetic ketoacidosis (DKA)?

A

Severe dehydration and hyperosmolarity due to sustained hyperglycemia without significant ketoacidosis

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17
Q

Which of the following best explains the primary pathophysiological process leading to the development of diabetic ketoacidosis (DKA)?

A

Increased counter-regulatory hormones promote gluconeogenesis and ketogenesis exacerbating hyperglycemia and acidosis

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18
Q

Which treatment strategy is essential in managing Hyperglycemic Hyperosmolar Syndrome (HHS) due to the risk of severe dehydration and hyperosmolarity?

A

Aggressive fluid resuscitation with hypotonic saline

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19
Q

Which counter-regulatory hormone exacerbation primarily contributes to the onset of diabetic ketoacidosis (DKA) by enhancing lipolysis and providing substrates for ketone body production?

A

Glucagon

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20
Q

In the management of DKA, what is the primary mechanism through which insulin administration resolves metabolic acidosis?

A

Insulin inhibits ketogenesis and promotes the shift of potassium into cells

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21
Q

In diabetic nephropathy, why are ACE inhibitors particularly beneficial for slowing disease progression?

A

They directly reduce glomerular hypertension, slowing the decline in renal function

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21
Q

Which factor is primarily responsible for the onset and progression of microvascular complications in diabetic patients?

A

Hyperglycemia induced changes in micro-circulation leading to impaired blood flow and vascular tone

22
Q

Which mechanism contributes most to the initial stages of diabetic retinopathy and its progression to proliferative retinopathy?

A

Decrease in renal blood flow and oxygenations, leading to neovascularization

22
Q

What is the primary pathophysiological process underlying the development of distal symmetric polyneuropathy in diabetic patients?

A

Chronic hyperglycemia leading to structural nerve damage and impaired nerve conduction

22
Q

What aspect of autonomic neuropathy in diabetic patients most critically affects anesthetic management due to altered hemodynamic responses?

A

Loss of compensatory sympathetic responses leading to intraoperative hypotension and dysrhythmias

23
Q

Why is aggressive intraoperative glycemic control crucial in diabetic patients undergoing surgery to optimize wound healing?

A

Hyperglycemia impairs phagocyte function and inhibits effective wound healing by promoting a pro-inflammatory state

24
Q

Which component of Whipple’s triad is crucial for diagnosing insulinoma by confirming the inappropriate insulin secretion in response to hypoglycemia?

A

An inappropriately high insulin level (.5–10 microunits/mL) during a 48- to 72-hour fast

25
Q

In the surgical management of insulinoma, why is the potential for marked hyperglycemia following tumor removal a critical consideration?

A

Because the removal of the insulin secreting tumor abruptly ceases, the source of excess insulin, leading to a rapid reversal of hypoglycemia

26
Q

What is the essential role of iodine in thyroid hormone synthesis, highlighting its importance in the management of thyroid disease?

A

Iodine is actively transported into the thyroid follicular cells where it is essential for the synthesis of T3 and T4 by organification and coupling process

27
Q

How do thyroid hormones, particularly T3, directly affect cardiac function, underscoring the critical consideration in hyperthyroidism management?

A

T3 enters cardiac myocytes, binds to nuclear receptors, and influences the expression of genes important for myocardial contractility and relaxation

27
Q

Why is establishing adequate anesthetic depth particularly crucial in hyperthyroid patients to prevent exaggerated sympathetic nervous system responses?

A

Hyperthyroid patients are at increased risk of sympathetic nervous system overactivity during surgery, which can precipitate thyroid storm or exacerbate cardiovascular instability

28
Q

How does primary hypothyroidism affect the cardiovascular system, specifically in terms of systolic and diastolic function?

A

Primary Hypothyroidism leads to decreased myocardial contractility & impaired diastolic relaxation, contributing to systolic and diastolic dysfunction

28
Q

In the regulation of thyroid function, what is the critical role of Thyroid-Stimulating Hormone (TSH) within the hypothalamic-pituitary-thyroid axis?

A

TSH binds to specific receptors on thyroid cell membranes, enhancing the synthesis and secretion of T4 and T3, and modulating the gland’s cellular its and vascularity

28
Q

Why are patients with hypothyroidism particularly sensitive to the effects of anesthetic drugs during surgery?

A

Hypothyroid patients also appear to have an increased sensitivity to anesthetic drugs, although the effect of thyroid activity on the minimum alveolar concentration of volatile anesthetics is negligible. Increased sensitivity is probably secondary to reduced cardiac output, decreased blood volume, abnormal baroreceptor function, decreased hepatic metabolism, and decreased renal excretion of drugs

29
Q

What makes differentiating thyroid storm from malignant hyperthermia particularly challenging in the perioperative setting?

A

Thyroid storm and malignant hyperthermia can present with similar intraoperative and postoperative signs and symptoms (i.e. hyperpyrexia, tachycardia, hypermetabolism); therefore, differentiation between the two may be extremely difficult.

30
Q

In the management of myxedema coma, why is the correction of hypothermia with external warming measures approached with caution?

A

External warming may precipitate vasodilation and vascular collapse due to the compromised thermoregulatory responses in severely hypothyroid patients

31
Q

What is the primary compensatory mechanism leading to goiter formation in response to thyroid hormone insufficiency?

A

Compensatory hypertrophy and hyperplasia of follicular epithelium due to reduced thyroid hormone output

32
Q

How does cortisol contribute to the maintenance of systemic blood pressure during the stress of surgery, highlighting its critical role in the hypothalamic-pituitary-adrenal (HPA) axis activation?

A

Cortisol facilitates the conversion of norpei to epi in the adrenal medulla, enhancing the body’s ability to maintain systemic BP thru increased catecholamine availability

33
Q

Why do cortisol levels remain elevated for several days postoperatively, and what implications does this have for patient recovery and management?

A

The sustained elevation of cortisol postop reflects the continued activation of the HPA axis in response to the physiological stress of surgery, supporting the body’s metabolic needs during recovery by enhancing gluconeogenesis and providing anti-inflammatory effects

33
Q

How does the electrolyte imbalance associated with hypercortisolism present a challenge in anesthetic management?

A

The presence of hypokalemia may influence responses to nondepolarizing muscle relaxants. Mechanical ventilation of the patient’s lungs during surgery is recommended because skeletal muscle weakness, with or without coexisting hypokalemia, may decrease the strength of the muscles of breathing.

33
Q

What is the rationale for using α-blockade as the cornerstone of preoperative management in patients with pheochromocytoma, and how does it influence the surgical outcome?

A

Since most pheochromocytomas secrete predominately norepinephrine, medical therapy has depended on α-blockade to lower blood pressure, increase intravascular volume, prevent paroxysmal hypertensive episodes, allow sensitization of adrenergic receptors, and decrease myocardial dysfunction.

33
Q

What underlies the potential reversibility of catecholamine-induced cardiomyopathy following the successful resection of a pheochromocytoma?

A

Cardiomyopathy appears reversible if catecholamine stimulation is removed early before fibrosis has occurred

34
Q

How do catecholamines secreted by pheochromocytomas induce cardiomyopathy, and what are the implications for management?

A

Catecholamines induce cardiomyopathy through permeability changes in sarcolemma membranes leading to excess calcium influx, oxidative stress from metabolized catecholamines, and myocardial damage by free radicals, necessitating early intervention to prevent irreversible cardiac damage

34
Q

What pathophysiological mechanisms contribute to the development of cardiomyopathy in patients with pheochromocytoma, and why is early detection and removal of the tumor pivotal for cardiac outcomes?

A

Catecholamine-induced cardiomyopathy in pheochromocytoma patients involves increased intracellular calcium, oxidative stress from catecholamine metabolites, and direct myocardial damage from free radicals. Early tumor removal can reverse cardiomyopathy by halting excessive catecholamine exposure, preventing irreversible myocardial fibrosis and improving cardiac function.

35
Q

In the context of pheochromocytoma resection, how does the pharmacological blockade of α-adrenergic receptors and the nuanced application of vasopressors modulate intracellular calcium handling and adrenergic receptor signaling, and what are the implications for mitigating perioperative catecholamine surges?

A

Alpha blockade preop inhibits excessive a1 receptor mediated intracellular calcium increase, attenuating vasoconstriction and myocardial excitability

35
Q

Why is orthostatic hypotension a common clinical finding in patients with pheochromocytoma, despite the elevated catecholamine levels typically associated with hypertension?

A

Orthostatic hypotension in pheochromocytoma patients results from hypovolemia and impaired vasoconstrictor reflex due to chronic catecholamine-induced vasodilation and reduced effective blood volume, challenging management of fluid and hemodynamic stability.

36
Q

A patient with primary adrenal insufficiency presents with severe hyperkalemia and hyponatremia. The pathophysiological mechanism most directly responsible for these electrolyte abnormalities is:

A

Loss of aldosterone leading to decreased sodium reabsorption and decreased potassium secretion in the renal tubules

37
Q

In a patient with secondary adrenal insufficiency due to long-term exogenous glucocorticoid therapy, which of the following pathophysiological responses is primarily responsible for the adrenal glands’ reduced ability to produce cortisol during stress?

A

Suppression of HPA axis leading to diminished ACTH release from the pituitary gland

38
Q

A 62-year-old patient presents with profound weakness, particularly in the proximal muscles of the lower extremities, and has a history of recurrent renal stones. Laboratory findings reveal hypercalcemia with a serum calcium concentration of 6.2 mEq/L and elevated parathyroid hormone (PTH) levels. The patient also exhibits polyuria and polydipsia. Based on the patient’s presentation, which of the following is the most likely diagnosis?

A

Primary Hyperparathyroidism due to parathyroid adenoma

38
Q

A 43-year-old patient presents with fatigue, weight loss, and hypotension. Laboratory tests reveal hyponatremia and hyperkalemia. The patient has no history of glucocorticoid therapy. An ACTH stimulation test shows no significant increase in cortisol levels. Another patient, a 38-year-old with a significant history of chronic systemic glucocorticoid use for severe asthma, presents with similar symptoms of fatigue and weight loss but demonstrates normal potassium levels and mild hyponatremia. An ACTH stimulation test in this patient also shows a blunted cortisol response. Based on these presentations, which of the following statements most accurately distinguishes the underlying condition in these patients?

A

The first patient likely has primary adrenal insufficiency, and the second patients likely has secondary adrenal insufficiency

39
Q

A patient diagnosed with primary hyperparathyroidism is undergoing parathyroidectomy. During the perioperative period, the anesthetic management should specifically focus on:

A

Ensuring adequate hydration and urine output to manage the pre-existing hypercalcemia, while being cautious with the use of muscle relaxant due to potential muscle weakness and the unpredictable response to nondepolarizing muscle relaxant.

40
Q

A patient with a known diagnosis of acromegaly is scheduled for elective surgery. The preoperative assessment reveals a significantly enlarged tongue, prognathism, and hoarseness. These findings are most likely related to which of the following pathophysiological processes?

A

Overproduction of growth hormone by an anterior pituitary adenoma, causing overgrowth of soft tissues including the upper airway structures

41
Q

During the management of anesthesia for a patient with acromegaly, which of the following considerations is of utmost importance due to the pathophysiological effects of excess growth hormone?

A

Preparation for potential difficult airway management, including the possibility for awake fiberoptic intubation.

42
Q

In the management of diabetes insipidus (DI), the differential response to desmopressin (DDAVP) is pivotal for distinguishing between neurogenic and nephrogenic DI. Which of the following best describes the underlying pathophysiological mechanism for this differential response?

A

Neurogenic DI responds to DDAVP due to intact renal tubule sensitivity to vasopressin, while nephrogenic DI does not respond due to a failure of renal tubules to respond to ADH or its analogues.

43
Q

During the perioperative management of a patient with inappropriate secretion of antidiuretic hormone (SIADH), careful monitoring and treatment aim to prevent acute complications from hyponatremia. What is the primary rationale for the recommended rate of correction for chronic hyponatremia?

A

To prevent the development of central pontine myelinolysis, a condition resulting from overly rapid correction of hyponatremia that damages the myelin sheath of neurons in the brainstem

44
Q

A patient presenting with polydipsia, polyuria, and a high output of poorly concentrated urine despite increased serum osmolarity is suspected to have diabetes insipidus (DI). In addition to these classic manifestations, which laboratory finding is crucial for diagnosing DI and initiating appropriate treatment?

A

Increased serum osmolarity coupled with a low urine osmolarity, indicating an inability of the kidneys to concentrate urine in response to ADH or a lack of ADH itself