Exam 2 Tables From Endocrine To Know Flashcards
(84 cards)
1
Q
What is the plasma glucose range for Diabetic Ketoacidosis (DKA)?
A
250-600 mg/dL
2
Q
What is the plasma glucose range for Hyperglycemic Hyperosmolar Syndrome (HHS)?
A
600-1200 mg/dL
3
Q
What is the pH level range for Diabetic Ketoacidosis (DKA)?
A
6.8-7.3
4
Q
What is the pH level for Hyperglycemic Hyperosmolar Syndrome (HHS)?
A
> 7.3
5
Q
What is the serum bicarbonate level in Diabetic Ketoacidosis (DKA)?
A
<15 mEq/L
6
Q
What is the serum bicarbonate level in Hyperglycemic Hyperosmolar Syndrome (HHS)?
A
Normal or slightly decreased
7
Q
What is the serum osmolarity range for Diabetic Ketoacidosis (DKA)?
A
300-320 mOsm/L
8
Q
What is the serum osmolarity range for Hyperglycemic Hyperosmolar Syndrome (HHS)?
A
350-380 mOsm/L
9
Q
What is the level of ketonemia in Diabetic Ketoacidosis (DKA)?
A
++++
10
Q
What is the level of ketonemia in Hyperglycemic Hyperosmolar Syndrome (HHS)?
A
+/-
11
Q
Is mental obtundation present in Diabetic Ketoacidosis (DKA)?
A
Variable
12
Q
Is mental obtundation present in Hyperglycemic Hyperosmolar Syndrome (HHS)?
A
Present
13
Q
Is hypovolemia present in Diabetic Ketoacidosis (DKA)?
A
Present
14
Q
Is hypovolemia present in Hyperglycemic Hyperosmolar Syndrome (HHS)?
A
Present
15
Q
What is the serum potassium level in Diabetic Ketoacidosis (DKA)?
A
Normal or slight increase
16
Q
What is the serum potassium level in Hyperglycemic Hyperosmolar Syndrome (HHS)?
A
Normal
17
Q
What is the arterial Pco2 range in Diabetic Ketoacidosis (DKA)?
A
20-30 mm Hg
18
Q
What is the arterial Pco2 in Hyperglycemic Hyperosmolar Syndrome (HHS)?
A
Normal
19
Q
In Diabetic Ketoacidosis (DKA), plasma potassium levels may be _______ but total body stores are usually depleted.
A
normal or high
20
Q
Q: What is the initiating factor in the metabolic pathway of diabetic ketoacidosis (DKA)?
A
A: Insulin lack combined with “stress” (e.g., infection, trauma).
21
Q
Q: How does insulin deficiency affect glucose utilization?
A: It decreases glucose uptake by cells and increases glucose production, leading to hyperglycemia.
A
A: It decreases glucose uptake by cells and increases glucose production, leading to hyperglycemia.
22
Q
Q: What are the effects of hyperglycemia in DKA?
A
A: Causes glucosuria and osmotic diuresis.
23
Q
Q: What are the consequences of glucosuria and osmotic diuresis?
A
A: Electrolyte loss, volume depletion, and cell dehydration.
24
Q
Q: How does insulin deficiency affect fat metabolism?
A
A: Increases lipolysis and triglyceride breakdown → raises circulating free fatty acids (FFA).
25
Q: What do increased free fatty acids (FFAs) lead to in DKA?
A: Increased hepatic ketogenesis → metabolic acidosis.
26
Q: How does insulin deficiency affect protein metabolism?
A: Increases protein catabolism → raises plasma amino acids.
27
Q: What do increased plasma amino acids contribute to?
A: Enhanced gluconeogenesis → worsens hyperglycemia.
28
Flashcard 9
Q: What is the result of increased gluconeogenesis in the liver during DKA?
A: Further elevation of blood glucose levels.
29
Q: What is the final acid-base disturbance resulting from increased ketogenesis in DKA?
A: Metabolic acidosis.
30
Q: What causes increased lipolysis in diabetic ketoacidosis?
A: Lack of insulin removes inhibition on hormone-sensitive lipase, promoting triglyceride breakdown.
31
Q: What is the role of FFAs (free fatty acids) in the development of acidosis during DKA?
A: FFAs are converted to ketone bodies in the liver, leading to acidosis.
32
Q: Why does volume depletion occur in DKA?
A: Osmotic diuresis from hyperglycemia causes excessive urination, leading to fluid and electrolyte loss.
33
Q: How does protein catabolism contribute to worsening hyperglycemia?
A: It increases circulating amino acids, which are substrates for gluconeogenesis in the liver.
34
Q: What is the link between stress and hyperglycemia in DKA?
A: Stress hormones (like cortisol and catecholamines) increase gluconeogenesis and worsen insulin resistance.
35
Q: What is the major source of ketone production in DKA?
A: The liver, via conversion of free fatty acids to ketone bodies.
36
Q: What is a consequence of cellular dehydration in DKA?
A: Impaired cellular function and risk of mental status changes or coma.
37
Q: What does gluconeogenesis rely on during DKA?
A: Increased plasma amino acids from protein catabolism.
38
Q: How does glucosuria perpetuate the metabolic imbalance in DKA?
A: It leads to osmotic diuresis, worsening volume loss and concentrating blood glucose further.
39
Q: What feedback loop failure contributes to the DKA spiral?
A: Lack of insulin prevents negative feedback on glucose, lipolysis, and ketogenesis.
40
What are the properties of short-acting insulin?
Onset: 30 min, Peak: 2-4 hr, Duration: 5-8 hr
## Footnote
Examples: Human regular, Lispro (Humalog), Aspart (NovoLog)
41
What are the properties of intermediate-acting insulin?
Onset: 1-2 hr, Peak: 6-10 hr, Duration: 10-20 hr
## Footnote
Examples: Human NPH, Lente
42
What are the properties of long-acting insulin?
Onset: 4-6 hr, Peak: 8-20 hr, Duration: 24-48 hr
## Footnote
Examples: Ultralente, Glargine (Lantus)
43
Which insulin can be administered via IV route?
Short acting insulin is the only insulin able to be administered via IV route.
44
What are the types of insulin?
Rapid Acting: Insulin aspart, insulin lispro; Short acting: Regular insulin; Intermediate acting: NPH; Long acting: Insulin detemir (Levemir) or Insulin glargine (Lantus).
45
What are the signs and symptoms of hyperglycemia?
Fatigue, Weight loss, Polyuria, Polydipsia, Blurred vision
46
What are the signs and symptoms of hypoglycemia?
Sweating, Tachycardia, Palpitations, Restlessness, Pallor, Fatigue, Confusion, Headache, Convulsions, Coma
47
What is Diabetes Insipidus (DI)?
DI is a condition characterized by water wasting.
48
What is Neurogenic DI?
Neurogenic DI, also known as central DI, occurs when the pituitary fails to secrete antidiuretic hormone (ADH) due to pituitary damage.
49
What is Nephrogenic DI?
Nephrogenic DI occurs when the kidneys fail to respond to ADH, often due to kidney damage, which is frequently drug-induced.
50
What is the hallmark symptom of Diabetes Insipidus?
The hallmark symptom of Diabetes Insipidus is polyuria.
## Footnote
This is why it is called 'diabetes'.
51
What is the syndrome associated with inappropriate ADH?
Syndrome of Inappropriate ADH (SIADH)
## Footnote
Also known as water intoxication.
52
What is the osmolarity level in SIADH?
Less than 270 mOsm/L
## Footnote
Indicates low serum osmolarity.
53
What is the osmolarity level in Diabetes Insipidus (DI)?
Greater than 290 mOsm/L
## Footnote
Indicates high serum osmolarity.
54
What is the serum sodium level in SIADH?
Less than 130 mEq/L
## Footnote
Indicates hyponatremia.
55
What is the serum sodium level in Diabetes Insipidus (DI)?
Greater than 145 mEq/L
## Footnote
Indicates hypernatremia.
56
What is the urine volume in SIADH?
Low
## Footnote
Urine volume is less than 2 mL/kg/hour.
57
What is the urine osmolarity in SIADH?
Hypertonic urine relative to plasma
## Footnote
Indicates concentrated urine.
58
What is the urine osmolarity in Diabetes Insipidus (DI)?
Hypotonic urine relative to plasma
## Footnote
Indicates dilute urine.
59
What is the treatment for SIADH?
Fluid restriction
## Footnote
Consider hypertonic saline if symptomatic or serum Na+ less than 115-120 mEq/L.
60
What medication is used for Diabetes Insipidus?
DDAVP or vasopressin
## Footnote
Helps to manage DI.
61
BOX 33-9 Clinical Manifestation of Thyroid Storm
• Fever greater than 38.5° C
• Tachycardia
• Confusion and agitation
• Dysrhythmias
• Nausea and vomiting
• Hypertension
• Congestive heart failure
• Abnormal liver function tests
62
What is the mortality rate even with quick intervention with thyroid storm?
Mortality is 20-30%.
63
What condition is caused by hypermetabolism?
Severe metabolic acidosis.
64
What is the treatment approach for thyroid storm?
Treatment is symptomatic with glucose containing fluids for hydration while correcting underlying pathology.
65
BOX 37.13 Anesthesia Implications for the Hypothyroidism
● Preoperatively, aim for euthyroid state for all patients.
● Evaluate the airway closely (macroglossia, goiter).
● Continue thyroid medication on the day of surgery.
● Monitor for exaggerated central nervous system depression with anes
thetic agents.
● Consider decreased hepatic metabolism and renal elimination when dosing
medications.
● Monitor core temperature; utilize patient warming devices.
● Titrate muscle relaxants carefully, considering possible coexisting muscle
weakness.
● Monitor patient respiratory status closely, considering blunted ventilatory
response to hypercarbia and hypoxia,
● Consider possible depressed myocardial function with anesthesia selection
and dosing.
● Consider possible reduction in plasma volume when calculating fluid
replacement-
66
BOX 37.8 Clinical Features of Glucocorticoid Excess (Cushing Syndrome)
* Hyperglycemia
* Systemic hypertension
* Weight gain; central obesity: fat pad on back of neck (buffalo hump); moon
facies
* Increased susceptibility to infection
* Poor wound healing
* Hypokalemia
* Alkalosis
* Hirsutism: acne; loss of libido; menstrual disturbances
* Osteopenia; osteoporosis
* Skeletal muscle weakness (especially proximal muscle weakness)
* Cataracts
* Skin striae; spontaneous ecchymoses; facial plethora
* Depression: cognitive dysfunction; emotional lability
67
BOX 37.9 Clinical and Laboratory Features of Adrenal (Addisonian) Crisis
* Dehydration; hypotension or shock
* Nausea and vomiting; weight loss; anorexia
* Severe fatigue and weakness
* Abdominal pain (acute abdomen}
* Hypoglycemia
* Fever
* Hyponatremia, hyperkalemia (in primary adrenal disease), hypercalcemia
* Prerenal azotemia
* Hyperpigmentation (in primary adrenal disease)
* Delirium, obtundation, coma
68
69
CUSHING SYNDROME S&S
- Sudden weight gain
- Facial fat (Moon face), Buffalo Hump
- HTN
- Glucose intolerance
- Oligomenorrhea or amenorrhea
- Decreased libido
- Skeletal muscle wasting
- Depression or insomnia
- Poor wound healing
- Prone to infection
- Osteoporosis
70
TABLE 22.20 Perioperative Steroid (Hydrocortisone) Supplementation
Superficial surgery (e.g., dental surgery,
biopsy)
= None
71
TABLE 22.20 Perioperative Steroid (Hydrocortisone) Supplementation
Minor surgery (e.g., inguinal hernia repair)
25 mg IV
72
TABLE 22.20 Perioperative Steroid (Hydrocortisone) Supplementation
Moderate surgery (e.g., cholecystectomy,
colon resection)
50-75 mg IV, taper 1-2 days
73
TABLE 22.20 Perioperative Steroid (Hydrocortisone) Supplementation
Major surgery (e.g., cardiovascular surgery,
Whipple procedure)
100-150 mg IV, taper 1-2 days
74
TABLE 22.20 Perioperative Steroid (Hydrocortisone) Supplementation
Intensive care unit (e.g., sepsis, shock)
50-100 mg q6-8h for 2 days to 1 wk,
followed by slow taper
75
Q: What triggers the release of renin from the juxtaglomerular apparatus?
A: Decreased renal perfusion.
76
Q: What is the substrate released by the liver that initiates the RAAS cascade?
A: Angiotensinogen.
77
Q: What enzyme converts angiotensinogen to angiotensin I?
A: Renin.
78
Q: Where is angiotensin-converting enzyme (ACE) primarily located?
A: On the surface of pulmonary and renal endothelium.
79
Q: What does ACE convert angiotensin I into?
A: Angiotensin II.
80
Q: What are the main effects of angiotensin II?
A:
• Stimulates aldosterone secretion from the adrenal cortex
• Causes arteriolar vasoconstriction
• Increases ADH secretion from the posterior pituitary
81
Q: What effect does aldosterone have on the kidneys?
A: Increases Na⁺ and Cl⁻ reabsorption and K⁺ excretion in the distal tubule, promoting water retention.
82
Q: What hormone is released by the posterior pituitary in response to angiotensin II?
A: Antidiuretic hormone (ADH).
83
Q: How does ADH affect the kidneys?
A: Increases water absorption in the collecting ducts
84
Q: What is the overall goal of the RAAS system?
A: To increase water and salt retention, restore circulating volume, and improve renal perfusion.
