Chapter 5 - Endocrine Disorders Flashcards
What is the pathophysiology of diabetes mellitus?
• A hormonal abnormality characterized by a deficiency of the hormone of fluid storage (insulin)
• Deficiency may be absolute (type 1) or relative (type 2)
• In patients with type 2 DM, relative deficiency can be due to:
o Developed insensitivity of insulin receptors (obese type 2)
o Decrease in insulin production (non-obese type 2)
What is the role of insulin?
- Catalyzes storage of all fuel types – carbs, fats, and proteins
- Fats are lipid-soluble and can pass through cell membranes without the help of insulin
- Carbs and protein are water-soluble and require insulin to transport them across cell membranes
Complete vs. Relative Insulin Deficiency
- Complete – type 1 DM – lipids/fats are the only source of intracellular fuel
- Relative – type 2 DM – may initially be a compensatory increase in insulin secretion but eventually the beta cell dysfunction and the relative insulin deficiency occurs
Diagnostic Criteria for DM
- HgbA1c (main): A1C ≥ 6.5% with repeat A1C recommended in asymptomatic adults with glucose ≤ 200; no repeat needed if glucose is > 200
- Plasma glucose: fasting glucose (no intake for ≥ 8 hours) ≥ 126 on 2 occasions or random glucose ≥ 200 with symptoms including polyphagia, polyuria, polydipsia, and unexplained weight loss or hyperglycemic crisis
- Oral glucose tolerance test: 2-h plasma glucose ≥ 200 after a 75-g glucose load
Comparing Type 1 and Type 2 DM: Pathophysiology
- Type 1: autoimmune activated by trigger → destroy beta cells
- Type 2: relative insufficiency d/t either distended/distorted peripheral receptors or beta cell dysfunction
Comparing Type 1 and Type 2 DM: Disease Trajectory
- Type 1: relatively short, weeks to months; beta cell destruction results in absolute insulin deficiency
- Type 2: years; approximately 10 years; beta cell dysfunction gradually decreases insulin production
Comparing Type 1 and Type 2 DM: Presenting s/s
- Type 1: weight loss, muscle mass loss, dehydration, paresthesias, acetone breath, ± mental status change (cells are having to use fats as energy source)
- Type 2: subtle; vascular changes d/t chronic hyperglycemia – non-healing rashes, skin insult, hair loss in extremities
Comparing Type 1 and Type 2 DM: Lab Findings
- Type 1: serum ketones, rising BUN/creatinine, hypokalemia, high anion gap (mostly seen with DKA)
- Type 2: chronic; BUN/creatinine can rise as a result of renal insult
Comparing Type 1 and Type 2 DM: Assessment
• Complete baseline assessment to include foot exam, eye exam, ECG, and diagnostic markers for both type 1 and 2
Comparing Type 1 and Type 2 DM: Treatment
- Type 1: insulin replacement mimicking physiologic insulin production and release – basal supplemented with pre-meal short- or ultra-short-acting
- Type 2: weight loss in obese patients, oral therapy to sensitize insulin receptors, insulin to help achieve initial glycemic control (help preserve function of working beta cells)
When to use insulin – type 1 treatment
- All patients need insulin
* Basal insulin with adjustments for meals via multiple injections or pump
When to use insulin – type 2 treatment
- At time of diagnosis to help achieve initial glycemic control and preserve function of working beta cells – OR –
- When ≥ 2 standard oral agents at optimized doses are inadequate to maintain glycemic control
- Acute illness – in critically ill surgical and non-surgical patients, blood glucose should be kept 140-180
Glycemic control targets
- HgbA1c: non-diabetic < 6%; diabetic < 7%
- Fasting glucose: non-diabetic: < 100; diabetic 80-130
- Obtain A1C at least 2x/year in patients with stable glycemic control; 4x/year in patients whose therapy has changed or who are not meeting glycemic goals
Pharmacologic interventions for type 2 DM: Biguanides
• Examples: Metformin (Glucophage)
• A1C reduction: 1-2%
• FIRST LINE MEDICATION UNLESS CONTRAINDICATED
• MOA: insulin sensitizer
• Hypoglycemia risk: no
• Side effects/comments:
o Renal function impairment – with conditions that alter hydration (surgery, contrast), hold for day of and 48 hours after, reinitiate once hydration status and renal function have been established
o Lactic acidosis (rare) – in those with hepatic impairment, hypovolemia, HF, advanced age
o Vitamin B12 deficiency – increased risk
Pharmacologic interventions for type 2 DM: Thiazolidinedione (TZD, glitazones)
• Examples: Pioglitazone (Actos)
• A1C reduction: 1-2%
• MOA: insulin sensitizer
• Hypoglycemia risk: none when used as solo product
• Side effects/comments:
o Edema – especially when used with insulin or SU. Do not start in HF patients
o MI – increased risk in patients taking insulin or nitrates
Pharmacologic interventions for type 2 DM: Sulfonylurea (SU)
• Examples: Glipizide (Glucotrol), Glyburide (DiaBeta)
• A1C reduction: 1-2%
• OFTEN CONSIDERED, IN ADDITION TO METFORMIN, WHEN A SECOND MEDICATION IS NEEDED
• MOA: increases insulin release
• Hypoglycemia risk: yes, especially in the elderly and those with renal impairment
• Side effects/comments:
o Hypoglycemia – elderly and those with renal impairment
Pharmacologic interventions for type 2 DM: Dipeptidyl peptidase-4 (DDP-4) inhibitor
• Example: Sitagliptin (Januvia) • A1C reduction: 0.6-1.4% • MOA: increases insulin release • Hypoglycemia risk: no • Side effects/comments: o Pancreatitis – FDA advisory o Unexplained joint aches
Pharmacologic interventions for type 2 DM: GLP-1 antagonist
• Example: Liraglutide (Victoza), Exenaide (Byetta)
• A1C reduction: 1-2%
• INJECTION ONLY
• MOA: increases insulin release
• Hypoglycemia risk: little
• Side effects/comments:
o Nausea/vomiting – improves with dose adjustment and continued use, contraindicated in gastroparesis
o Pancreatitis – rare, discontinue if develops
o Slows gastric emptying, often leads to appetite suppression and weight loss
Pharmacologic interventions for type 2 DM: Sodium glucose cotransporter-2 (SGLT-2) inhibitor
• Example: Canaglifozin (Invokana), dapaglifozin (Farxiga)
• A1C reduction: 0.7-1%
• MOA: lowers plasma glucose levels by increasing the amount of glucose excreted in urine
• Hypoglycemia risk: yes, risk increases when used with insulin
• Side effects/comments:
o Genital mycotic infection, UTI, increased urination
o Modest weight loss, greater with higher dose
o Renal impairment – adjust dose d/t risk of electrolyte imbalance
o DKA and urosepsis risk – FDA advisory
Insulin Types: Short-acting, rapid onset
- Examples: Lispro (Humalog), Aspart (NovoLog), regular (Humulin R)
- Onset of action: 15-30 minutes, give right around time of meals
- Peak: 1-3 hours
- Duration of action: 3-6 hours
Insulin Types: Intermediate-acting
- Example: NPH (Humulin N)
- Onset of action: 1-2 hours
- Peak: 6-14 hours
- Duration of action: 16-24 hours
Insulin Types: Long-acting – Glargine (Lantus)
- Onset of action: 1 hour
- Peak: none
- Duration of action: ≥ 24 hour
Insulin Types: Long-acting – Detemir (Levemir)
- Onset of action: 1-2 hours
- Peak: 6-8 (minimal)
- Duration of action: dose-dependent, 12 hours at 0.2 units/kg, 20 hours at 0.4 units/kg
Hyperglycemic control in the acute care setting: possible reversible causes
- Dietary changes
- Dextrose-containing IV fluids
- Glucocorticoids
- Post-op
Hyperglycemic control in the acute care setting: diagnostic studies to evaluate hyperglycemia
- FSBS (finger stick blood sugar) monitoring (AC and HS if eating; q6h if NPO)
- HgbA1C to rule out undiagnosed DM
Hyperglycemic control in the acute care setting: treatment goals
- Avoid hypoglycemia (sliding scale alone is not a good method of treatment)
- < 70 mg/dL is hypoglycemia; < 40 mg/dL is critical hypoglycemia
- Avoid extreme hyperglycemia (>180 mg/dL)
- Insulin therapy is preferred method of treatment in inpatient setting (basal, prandial, and supplemental). Orals are not recommended d/t risk of hypoglycemia, renal injury, and HF
- Non-ICU and ICU goals is 140-180 mg/dL (no less than 90-100; start drip if > 180 mg/dL)
- CV critical care goal is 110-140 mg/dL
- Perioperative goal is 80-180 mg/dL
Hyperglycemic control in the acute care setting: risk of oral medications
- Sulfonylureas – major cause of severe hypoglycemia (especially if patient is NPO)
- Metformin – contraindicated in decreased renal blood flow (i.e., acute HF, contrast dye)
- Thiazolidinediones – associated with the development of HF and edema
General Tips to insulin management in the acute care setting
- Don’t omit doses for good control or mild hypoglycemia
- Review glucose results daily and adjust insulin
- Review chart for unusual circumstances when glucose is not controlled
Total daily dose of insulin (TDD) – weight-based insulin
- Malnourished, elderly, CKD (on dialysis), severe liver disease = 0.3 units/kg
- Normal-weight patients, including type 1 DM = 0.4 units/kg
- Overweight based on BMOI – 0.5 units/kg
- Obese, high-dose steroids, or insulin resistance = 0.6 units/kg
General insulin dosing based on TDD
- Basal insulin = 50% of TDD (analogs preferred over NPH)
- Prandial insulin (nutritional) = 50% of TDD (divided in 3 daily doses a meal)
- Supplemental (correctional) = (current BG – target BG)/CF; CF = 1700/TDD
Adjusting insulin therapy
- If > 2 glucose levels are < 80 mg/dL in 24 hours, decrease TDD by 20%
- If > 2 glucose levels are > 180 and none are < 80 in 24 hours, increase TDD by 20%
General principles of converting IV to SubQ insulin
- Continue IV insulin until the patient is able to eat solid food
- Continue IV insulin for 2-4 hours after the first SC dose is given
- Do not switch to only oral agents from IV insulin in type 2 DM
Dosing subQ insulin from IV insulin drip
- Establish the 24-hour insulin requirement (TDD of IV insulin)
- Determine the SC TDD – 80% of IV TDD
- Determine basal SC TDD – 50% of SC TDD
- Determine prandial SC TDD - 50% of SC TDD divided into 3 doses with each meal
- Determine supplemental dose – (current BG – target BG)/CF; CF = 1700/SC TDD
Diabetic Crisis States: DKA – common causes
- Insulin deficiency
- Iatrogenesis (i.e., glucocorticoid use)
- Infection
- Inflammation
- Ischemia/infarction
- Intoxication
- *for exam purposes, DKA is only seen in Type 1 DM
Diabetic Crisis States: DKA – pathophysiology
• Hyperglycemia secondary to increased glucogenesis and decreased cellular glucose uptake → mobilization and oxidation of fatty acids leading to ketoacidosis
Diabetic Crisis States: DKA – symptoms
- Polyuria, polydipsia
- Dehydration
- Nausea/vomiting
- Abdominal pain, ileus
- Kussmaul’s respirations
- Changes in mental status
Diabetic Crisis States: DKA – treatment
- Isotonic fluid replacement (10-14 ml/kg/hr) after 1 L bolus
- Regular insulin 10 units followed by IV insulin drip (0.1 unit/kg/hr) until anion gap is normal (3-10)
- If anion gap is still open and glucose is ≤ 250, add dextrose to fluids
- Treat precipitating event
Hyperosmolar non-ketotic state (HNS) – common causes
- Same as DKA – insulin deficiency, iatrogenesis (i.e., glucocorticoid use), infection, inflammation, ischemia/infarction, intoxication
- Dehydration
- Renal failure
- *for exam purposes, HNS is only seen in type 2 DM
Hyperosmolar non-ketotic state (HNS) – pathophysiology
• Extreme hyperglycemia without ketoacidosis → OSMOTIC DIURESIS and volume depletion with electrolyte disturbances
Hyperosmolar non-ketotic state (HNS) – symptoms
- Dehydration
- Glucose > 600 mg/dL
- ↑ serum osmolality (thick serum, normal serum osmo 270-290)
Hyperosmolar non-ketotic state (HNS) – treatment
- Isotonic fluid replacement with NS initially followed by 0.45% NS (estimate at 8-10L deficit)
- As you correct the dehydration, the patient tends to correct their own electrolyte imbalances
- However, replace K only while fluid resuscitating because K will continue to drop as you continue giving insulin. Okay to correct if < 4.0. After resuscitation, can correct other electrolytes if needed
- Regular insulin 10 units followed by IV insulin drip (0.05-0.1 units/kg/hr
- Treat precipitating event
Hypothyroidism – general signs and symptoms
- Thick, dry skin
- Hyporeflexia
- Slowed mentation
- Small weight gain (5-10 lbs.), mainly fluid
- Constipation (↓ GI motility)
- Menorrhagia (or longer menstrual cycles)
- Easily cold (↓ metabolic rate)
Primary vs. Central Hypothyroidism
- Primary – problem with the thyroid gland itself
- Central – problem with the pituitary gland of hypothalamus (hypothalamus not releasing TRH or pituitary not releasing TSH
Common etiologies of hypothyroidism
- Primary hypothyroidism
- Autoimmune destruction of thyroid, occurs after a period of hyperthyroidism (i.e., thyroiditis, iodine deficiency, lithium use, amiodarone use)
- ↓ T4, ↑ TSH
Etiologies of hypothyroidism – post-radioactive iodine (RAI) treatment/surgical removal
- Primary hypothyroidism
- Typically s/p Graves’ disease treatment, thyroid cancer treatment
- ↓ T4, ↑ TSH
Etiologies of hypothyroidism – pituitary or hypothalamic dysfunction
- Central hypothyroidism
* ↓ T4, ↓/↑/normal TSH
Hypothyroidism crisis state – Myxedema Crisis
- Think s/s of hypothyroidism x10
- Hypothermia, hypotension, hypoventilation, changes in mental status (coma), hyponatremia, hypoglycemia
- Results typically from infection, major cardiopulmonary disease, major neurologic illness
Diagnostics of hypothyroidism
• ↓ T4, ↑ TSH
Treatment of hypothyroidism
• Levothyroxine (Synthroid)
o 1.5-1.7 mcg/kg/day (1.0 mcg/kg/day in elderly)
o Need to increase dose in pregnancy (by 33% initially and then titrate to 50% or greater)
o Follow up with TSH in 4-6 WEEKS and titrate to euthyroidism (normal TSH 0.5-5.0)
• Myxedema coma
o 5-8 mcg/kg T4 IV initially then 50-100 mcg IV daily until s/s resolve and underlying process fixed
Hyperthyroidism – general signs and symptoms
- Smooth, silky skin
- Hyperreflexia
- Mind racing
- Weight loss (~10 lbs.)
- Frequent, low volume, loose stools (↑ GI motility)
- Oligomenorrhea (↓ or no menstrual cycle)
- Heat intolerance
Hyperthyroidism – common etiologies
- Graves’ disease
- Thyroiditis
- Toxic adenoma
- TSH-secreting pituitary tumor
- Select medications
Hyperthyroidism etiologies – Graves’ disease
- Autoimmune
* Multisystem presentation including exophthalmos, tachycardia, proximal muscle weakness, goiter
Hyperthyroidism etiologies – thyroiditis
- Viral or autoimmune
- Post-partum
- Drug-induced
- Often transient
- Usually accompanied by thyroid tenderness
Hyperthyroidism etiologies –toxic adenoma
- Benign
* Metabolically active thyroid nodule(s)
Hyperthyroidism etiologies – TSH-secreting pituitary tumor
• A tumor of the pituitary gland secreting TSH (↑ TSH & T4)
Hyperthyroidism etiologies – select medications
• Amiodarone (also hypothyroidism), interferon (also hypothyroidism), others
Hyperthyroidism crisis state – thyroid storm
- Delirium
- Systolic HTN (with wide pulse pressure, normal SBP-SBP is 20-40) with ↓ MAP
- Hyperthermia
- 20-50% mortality
Diagnostics for hyperthyroidism
• ↑ T4 & ↓ TSH (unless there is a TSH-secreting tumor)
Treatment for hyperthyroidism
- Definitive treatment depends on etiology
- Beta blocker therapy (propranolol preferred – initial tx, symptom management)
- Graves’ disease – antithyroid drugs (i.e., methimazole) or radioactive iodine (RAI); surgical removal (not likely)
- Toxic adenoma – RAI or surgical removal
- Pituitary tumor – tumor removal
- Thyroid storm – beta blockade, PTU or methimazole, iopanoic or iodine, consider steroids
What are the primary adrenal cortex hormones?
- Cortisol
- Aldosterone
- Androgens
What are the functions of cortisol?
- Suppresses inflammation
- Maintains vascular tone
- Mobilizes glucose (and other fuel sources)
- Promotes free water clearance
- Released by ACTH
What are the functions of aldosterone?
- Increases renal absorption of sodium
* Subsequent water reabsorption
What is the function of androgens?
• Secondary sex characteristics
What are the two major adrenal cortex disorders?
- Cushing’s syndrome/disease – hypercortisolism
* Addison’s disease – adrenal insufficiency or hypocortisolism
Cushing’s – pathophysiology
- Cushing’s syndrome – excess cortisol (too much exogenous glucocorticoid)
- Cushing’s disease – typically caused by a pituitary adenoma (60-70%) causing a ↑ release of ACTH → a ↑ in cortisol production. Other causes include adrenal adenomas and ectopic ACTH secretion from certain cancers which both cause an increase in cortisol production
Cushing’s – signs and symptoms
- Central obesity (with extremity wasting)
- Dorsocervical fat pads (buffalo hump)
- Rounded face
- Spontaneous bruising
- Proximal myopathy
- Purple striae
- HTN
- Hirsutism
- Hyperpigmentation
- Poor wound healing/skin infections
Cushing’s – lab abnormalities
• Hypokalemia, hyperglycemia, leukocytosis, and hypernatremia
Cushing’s – diagnostic evaluation
• Dexamethasone suppression test
o Give 1 mg of dexamethasone at 11 PM, measure serum cortisol at 8 AM
o Positive result if cortisol is < 1.8 mcg/dL
Cushing’s – treatment
- Remove source of excess
* Management consequences (i.e., hypertension, hypokalemia, and hyperglycemia)
Addison’s disease – pathophysiology
- Primary – damage to adrenal cortex (autoimmune, TB, metastatic disease, drug-induced) → a ↓ in cortisol production
- Secondary – caused by pituitary failure to release ACTH → a ↓ in cortisol production. Or from a sudden withdrawal of systemic corticosteroids → a ↓ in cortisol production from induced corticosteroid suppression
Addison’s disease – signs and symptoms
• Weakness, fatigue, anorexia, orthostatic hypotension, nausea, and vomiting
Addison’s disease – lab abnormalities
- Hyponatremia, hyperkalemia, hypoglycemia
* Early AM serum cortisol < 3 mcg/dL is diagnostic
Addison’s disease – diagnostic evaluation
• Cosyntropin (ACTH) stimulation test
o Tests the ability of ACTH to ↑ cortisol production
o Administer 250 mcg of cosyntropin (ACTH) IM. If 60-minutes post-injection, the cortisol is ≥ 18, it means they can respond to ACTH
Addison’s disease – treatment
• Acute insufficiency
o Volume resuscitation with NS
o Dexamethasone 2-4 mg IV q6h + fludrocortisone (Florinef) 50 mcg IV daily prior to ACTH stimulation test, then hydrocortisone 50-100 mg IV q6-8 hours
• Chronic insufficiency
o Hydrocortisone 20-30 mg PO daily (2/3 in AM, 1/3 in early PM)
o Prednisone 15 mg AM, 10 mg PM
o Dexamethasone 4 mg IM prefilled syringes for emergencies
What are the hormones of the adrenal medulla?
- Epinephrine
- Norepinephrine
- Dopamine
What are the functions of epinephrine?
- Activation of the sympathetic nervous system
* Activation of all α and β receptors
What are the functions of norepinephrine?
- Synthesized from dopamine
- Activation of the sympathetic nervous system
- Activation of α1 and α2 receptors
What is the function of dopamine?
• Vasoconstriction secondary to the breakdown of norepinephrine
Pheochromocytoma – what is it?
• A condition characterized by a rare, benign hormone-producing tumor of the adrenal medulla causing excess release of catecholamines (10% are malignant)
Pheochromocytoma – signs and symptoms
- The 5 P’s
- Pressure (persistent/resistant HTN)
- Pain (headache)
- Palpitations (tachycardia and tremors)
- Perspiration (profuse with flushing)
- Pallor (secondary to vasoconstriction)
- The common triad – HTN, headache, and tachycardia
Pheochromocytoma – lab abnormalities
- Increased urinary metanephrines – 24-hour urine study, the excess catecholamines the body didn’t use get dumped into the urine
- Increased urinary vanillylmandelic acid (VMA) – breakdown of used catecholamines
- CT scan or MRI of the adrenals to confirm diagnosis (if metamephrine and VMA levels are > 2x normal limit)
Pheochromocytoma – treatment
- Control cardiovascular status with alpha blockers followed by beta blockers (initial tx; s/s control) until tumor removal (definitive tx)
- Pre-op volume expansion to prevent post-op hypotension
What is the role of ADH?
• ADH is synthesized in the hypothalamus and released by the pituitary gland causing an increase in the reabsorption of water by the renal tubule
Diabetes Insipidus – what is it?
- Insufficient ADH or decreased renal sensitivity to ADH
* Nephron cannot conserve water
Diabetes Insipidus – pathophysiology
- Central – commonly caused by damage to the pituitary gland or hypothalamus (i.e., surgery, tumor, meningitis, head injury)
- Nephrogenic – inability of the kidneys to respond to ADH
Diabetes Insipidus – lab abnormalities
- Plasma FREE WATER DEPLETION results in:
- Serum hypernatremia (normal Na 135-145)
- Serum hyperosmolality (normal serum osmo 270-290)
- Urine hyponatremia (normal urine Na 10-20)
- Urine hypoosmolality (normal urine osmo 30-900)
- Thick serum, thin urine
Diabetes Insipidus – signs and symptoms
• Findings consistent with hypernatremia and volume depletion
Diabetes Insipidus – treatment
- Supportive fluid replacement until underlying condition resolves
- May replaced ADH (DDAVP) in severe cases
Syndrome of Inappropriate ADH (SIADH) – what is it?
- Excess ADH production
* Nephron conserves excess water
Syndrome of Inappropriate ADH (SIADH) – pathophysiology
• Commonly caused by head injury or lung cancers
Syndrome of Inappropriate ADH (SIADH) – lab abnormalities
- Vascular WATER OVERLOAD results in:
- Serum hyponatremia (normal Na 135-145)
- Serum hypoosmolality (normal serum omos: 270-290)
- Urine hypernatremia (normal urine Na 10-20)
- Urine hyperosmolality (normal urine osmo 300-900)
- Thin serum, thick urine
Syndrome of Inappropriate ADH (SIADH) – signs and symptoms
• Findings consistent with hyponatremia and volume overload
Syndrome of Inappropriate ADH (SIADH) – treatment
- Treatment depends on degree of symptom presentation
- Free water restriction
- Loop diuretic with NS
- In extreme symptoms, 3% NS is given
Prolactinoma
- Pathophysiology – pituitary tumor that causes the release of prolactin
- Usually found in infertility workups
- Presentation – failure to conceive, irregular menses, chronic headaches
A 16-year-old male patient arrives in the ER with a 4-day history of nausea, vomiting, abdominal pain, and progressive confusion. While reviewing the patient’s labs, the AGACNP notes the following significant findings - serum glucose 800, serum ketones positive, pH 7.1, CO2 37, HCO3 17. The AGACNP orders NS at 10 ml/kg/hr. The next step in treatment is to:
a. Start an IV insulin drip at 0.1 unit/kg/hr
b. Start an IV insulin drip at 0.05 unit/kg/hr
c. Give D5W 1000 ml at 125 ml/hr
d. Give insulin on a sliding scale
a. Start an IV insulin drip at 0.1 unit/kg/hr
A is correct because: this is a picture of DKA
A 23-year-old female with type 1 DM who has been taking insulin for 4 years is hospitalized after a hernia repair. The patient was given her evening insulin dose but did not have a snack at bedtime. While monitoring her blood sugars the nurse reports the following results. These findings suggest which of the following abnormalities?
10: 00 PM - 125 mg/dL
2: 00 AM - 45 mg/dL
6: 00 AM - 350 mg/dL
a. Dawn phenomenon – this is a constant rise in sugar throughout the night and into the morning
b. Somyogi effect
c. Beta cell dysfunction
d. Insulin de-sensitivity
b. Somyogi effect
B is correct because: the Somyogi effect is acute hypoglycemia that causes a sudden rebound hyperglycemia
You are initiating treatment for a 17-year-old male patient with type 1 DM who is experiencing diabetic ketoacidosis. ABGs are as follows: pH 7.16, PaO2 80, PaCO2 19, HCO3 7. In addition to a 1 L bolus of isotonic solution, which of the following is the most appropriate intervention?
a. NS at 250 ml/hr, 20 units short-acting insulin IV push, and O2 at 2L
b. NS with 40 mEq HCO3 at 500 ml/hr and 10 units short-acting insulin IV push
c. NS at 700 ml/hr, 20 units short-acting insulin IV push, and O2 at 2L
d. NS at 800 m/hr, 10 units short-acting insulin IV push, and monitor urine output
d. NS at 800 m/hr, 10 units short-acting insulin IV push, and monitor urine output
D is correct because: Rate is best and insulin dose is good
A is incorrect because: Not enough fluid and too much insulin
B is incorrect because: Better NS rate but don’t want bicarb yet, need to fluid resuscitate first
C is incorrect because: Better NS rate but too much insulin
A 47-year-old female patient with hyperosmolar non-ketotic state (HNS) is admitted to your service. You understand that the most important part of her management is:
a. Quickly administering insulin
b. Managing electrolyte imbalances
c. Administering D5W solution
d. Replacing lost fluids
d. Replacing lost fluids
D is correct because: the biggest piece of HNS is the osmotic diuresis
A 45-year-old male patient who is admitted to the hospital is unresponsive with a blood glucose of 35 mg/dL. The nurse reports there is no patient IV access. The first-line intervention for this patient is to order:
a. Oral glucose gel to be massaged into the patient’s gums
b. Sublingual administration of crushed glucose tablets
c. Glucagon 1mg IM
d. Glucagon 2mg subq
c. Glucagon 1mg IM
A and B are incorrect because: Patient is unresponsive, don’t put anything in their mouth
D is incorrect because: this route doesn’t work
While reviewing a patient’s daily glucose readings the AGACNP notes that the patient has 4 glucose readings less than 80 mg/dL in the last 24 hours. What would be the most appropriate intervention?
a. Decrease the total daily dose by 10%
b. Decrease the total daily dose by 20%
c. Decrease the basal dose by 10%
d. Decrease the basal dose by 20%
b. Decrease the total daily dose by 20%
While on call, you are paged to the ED to evaluate a 37-year-old female with a history of Graves’ disease. She has been non-compliant with controller therapy and now presents with tachycardia, HTN, palpitations, and overt anxiety. Immediate treatment should include:
a. Surgical intervention
b. Propyltiouracil (PTU) 450 mg PO
c. Dexamethasone (Decadron) 2 mg PO
d. Propranolol (Inderal) 80 mg PO
d. Propranolol (Inderal) 80 mg PO
A is incorrect because: it is not initial treatment
A 54-year-old male patient has a low TSH and elevated T4. Which signs and symptoms do you expect to find?
a. Exophthalmos, tachycardia, hyperreflexia
b. Bradycardia, weight gain, lid lag
c. Constipation, tremor, pale skin
d. Nausea, decreased visual acuity, polyuria
a. Exophthalmos, tachycardia, hyperreflexia
A is correct because: Labs indicate hyperthyroidism and these are the correct s/s
A 28-year-old female presents complaining of failure to conceive for 15 months and irregular menses. Further questioning reveals a history of chronic headache. Based upon the most likely cause of these symptoms, the AGACNP would order a:
a. Serum prolactin
b. Serum metanephrines
c. Serum cortisol
d. Serum TSH
a. Serum prolactin
A is correct because: this is describing a prolactinoma
You are evaluating a patient who was admitted to the step-down unit yesterday for a syncopal episode secondary to orthostatic hypotension. The patient arrived with complaints of weakness, fatigue, and anorexia. Lab studies reveal hyponatremia, hyperkalemia, and mild hypoglycemia. You order a cosyntropin stimulation test and the serum cortisol results at 2 mcg/dL. You note the patient is now consistently hypotensive with a SBP 75-85 mmHg and appears confused. In addition to NS infusion, which treatment is most appropriate for this patient?
a. Phenoxybenazmine (Dibenzyline) 10 mg IV q12h
b. Norepinephrine (Levophed) 8 mcg/min IV infusion
c. Hydrocortisone 75 mg IV q6-8h
d. Fludrocortisone (Florinef) 50 mg IV daily
c. Hydrocortisone 75 mg IV q6-8h
C is correct because: this patient has Addison’s disease; has already had the ACTH stimulation test so doesn’t need the dexamethasone or Florinef anymore
D is incorrect because: this is given prior to the ACTH stimulation test, is not treatment
Your patient has hypothyroidism. You are treating him with levothyroxine. Which lab value would you follow to determine if his treatment is adequate?
a. Thyroxine index
b. TSH
c. T3
d. T4
b. TSH
Diabetes insipidus would be most likely characterized by which of the following sets of lab values?
a. Serum glucose > 200 mg/dL; urine osmo 330 mOsm/L; serum K 6
b. Serum Na 125; serum K 2.9; serum glucose > 200
c. Serum osmo 330; serum Na 160; urine Na 5
d. Serum K 3, urine Na > 20; serum osmo 250
c. Serum osmo 330; serum Na 160; urine Na 5
C is correct because: Hypernatremic serum, hyponatremic urine (thick serum, thin urine)
A is incorrect because: DI has a low urine osmo
B is incorrect because: should see hypernatremia with DI
D is incorrect because: should see low urine Na in DI
A patient in ventricular fibrillation is failing to convert despite repeat attempts at defibrillation. Which of the following underlying endocrine abnormalities is most likely?
a. Type 2 DM
b. Addison’s disease
c. Hypothyroidism
d. Cushing’s syndrome
d. Cushing’s syndrome
D is correct because: Cushing’s produces hypokalemia and hypokalemia is a common cause of V-fib
The definitive treatment of choice for patients with pheochromocytoma is:
a. Phenoxybenzamine (Dibenzyline)
b. Propranolol (Inderal)
c. Tumor removal
d. Levothyroxine (Synthroid)
c. Tumor removal
A is incorrect because: this is an alpha blocker and is initial treatment
B is incorrect because: this is an beta blocker and is initial treatment
A CT scan of the adrenal glands would most likely identify abnormalities in a patient with:
a. Acromegaly
b. Kawasaki disease
c. Addison’s disease
d. Prolactinoma
c. Addison’s disease
C is correct because: this is an adrenal cortex problem
A is incorrect because: this is a pituitary problem
B is incorrect because: this is an autoimmune vascular disease
D is incorrect because: this is a pituitary tumor
Diabetes insipidus is caused by dysfunction of the:
a. Adrenal medulla
b. Adrenal cortex
c. Pituitary
d. Thyroid
c. Pituitary
C is correct because: DI is a lack of ADH from the pituitary
A 65-year-old male patient with a history of small cell lung cancer is sent to the ER from an infusion center wih a serum sodium of 130. The patient is awake, alert, and oriented. The patient reports a sudden decrease in his urine output over the last few days. Further lab analysis reveals a serum osmo of 260 and a urine Na of 35. Which of the following interventions would be most appropriate for this patient?
a. Fluid restriction of 1.5 L/day
b. Loop diuretics with NS infusion
c. 3% NS infusion
d. Insert a Foley catheter and monitor urine output for 24 hours
a. Fluid restriction of 1.5 L/day
A is correct because: Hyponatremic serum, hypoosmolality serum, hypernatremic urine – labs + decreased urine output are pointing us towards SIADH
C is incorrect because: Patient is asymptomatic, too aggressive
D is incorrect because: this is the equivalent of “doing nothing”
