Endocrine

Question 1

DKA

Multiple risk factors are associate with DKA and include: illness, trauma, surgery, non-compliance with medication regimen, or myocardial infarction.

Question 2

DKA
* Results from a deficiency in insulin.

• Insulin is necessary to decreased glucose levels in the body.
• Patient becomes hyperglycemic which ignites several metabolic changes within the body.
• Intracellular dehydration occurs that causes the body to burn fatty acid and produce ketones.
• Signs and symptoms of DKA include: polyuria, polydipsia, polyphagia, nausea and vomiting, abdominal pain, changes in LOC, and weight loss.
• On exam, the patient could have the following: Kussmaul respirations, tachycardia, altered level of consciousness, and a fruity smell to the breath.

Question 3

DKA
Laboratory studies and patient presentation are key in making a diagnosis of DKA.

pH: <7.30
Bicarbonate: < 15
Blood sugar:> 250
Urinalysis: Ketones and glucose present
Elevated K+
BUN/Creatinine elevation
AGAP- elevation> 17 ( higher AGAP, higher patient acuity) Barkley, 2021

Question 4

IVF in DKA

Patient usually have a fluid deficit of 4-8L.

0.9% saline is the solution of choice. Infuse 0.9% saline at 1L/hr over the first 1-2 hours. The rate should be adjusted to 300-500ml/hr after the initial fluid replacement.
Rate after dehydration is corrected- 250 cc/hr.
F
luid can be changed to to ½ NS if hemodynamically stable. Close monitoring of electrolytes and volume status are important in adjusting fluid therapy.

Fluids should be changed to D5 ½ normal saline once glucose reaches 250 to prevent hypoglycemia.

Monitor potassium levels and add K+ therapy as indicated. K+ up to 30 meq maybe necessary during the first 3 hours of managing DKA.

Always monitor patient lab values and EKG to determine patient’s needs. Remember peak T waves is an indicator of hyperkalemia, flat T waves with associated U waves indicates hypokalemia. Bicarbonate is indicated with pH values < 7.0.

Question 5

Insulin-in DKA

Loading dose: 0.1 - 0.15 units/kg then a continuous insulin drip at 0.1 units/kg/hr (Barkley, 2021).

When the blood sugars is < 200 decrease drip to 0.02- 0.05 units/kg/hr.

Change from IV to SQ- give basal dose 2-4 hours prior to stopping drip (Barkley, 2021).

Glucose should be lowered by 50-70 mg/dL/hr.

The patient can be transitioned to SQ insulin after resolution of acidosis.

Question 6

HbA1C should be 8.5%-9% for older patients with diabetes who have very complex health
problems.
4. HbA1c of 8% to 8.9% is associated with better functional outcomes for older adults after 2
years.

Question 7

For patients who are insulin naive, insulin can safely be initiated at a TDD of 0.3–0.6 units/kg body weight.

The lower starting dose is recommended for leaner patients and for those with renal insufficiency, and the higher starting dose is recommended for obese patients and those on glucocorticoids

Question 8

HYPEROSMOLAR HYPERGLYCEMIC NONKETOSIS
Hyperosmolar Hyperglycemic Nonketosis or HHNK is primarily seen in Type II diabetics.

Patients have extremely elevated blood glucose levels due to osmotic diuresis.

HHNK does not produce ketosis and patients have severe dehydration.

Risk factors associated with HHNK are the same as those for DKA. Patients typically present with altered mental status (confusion, seizures, coma), weakness, increased heart rate and shallow respirations. Signs of dehydration will also be present and include poor skin turgor and dry mucous membranes.

Question 9

DIAGNOSIS for HHNK

Blood glucose> 600, most of the time it will be >1000

Serum Hyperosmolality: > 320(leads to coma)

BUN/Creatinine elevation

Hypernatremia

pH is normal

Bicarbonate> 15

Question 10

MANAGEMENT of HHNK
Admission to ICU
FLUIDS ARE THE KEY: IVF: Normal saline up to 6 liters in the first 8-10 hours.
If BP and NA are normalizing- 1/2 NS
Add fluid containing dextrose once glucose is down to 250

Question 10

DI
is a condition in which there is a deficient amount of ADH released from the pituitary gland resulting in excessive dilute urine.

The primary types of DI include:

Central - results from damage to the pituitary gland or hypothalamus. Damage can be the result of injury, infections and cancers.

Nephrogenic - results from issues with the renal tubules. The issues can result from specific medications, renal disease, and inherited traits.

Psychogenic - specialist referral necessary

Regardless of the type, there is not enough ADH secreted, which results in excessive urinary output and increased fluid intake.

Question 11

DI
Individuals with DI present with increased thirst and a fluid intake of up to 20 liters per day.

Additional symptoms include: excessive urination, increased heart rate, altered level of consciousness, decreased blood pressure, and dizziness. (Barkely, 2021)

Question 11

DIAGNOSIS for DI

Laboratory data and patient presentation are essential components related to diagnosing DI.

Central DI is diagnosed by the clinical symptoms and with with the administration of a Desmopressin challenge test.

Labs will reveal: hypernatremia, increased serum osmolality, decreased urine osmolality and specific gravity.

24-hour urine collection may also be used as a diagnostic indicator of DI.

Question 12

Tx of DI

The hallmark of treatment is to replace fluid volume. The NA+ levels should be monitored closely.

NA+ levels should not be lowered more than 15 meq/L/day to decrease the risk of cerebral edema which can be fatal.

NA+ > 150- D5W, replace half of deficit in 12-24 hours

NA+ < 150 normal saline or half normal saline

Central DI- Desmopressin SQ/IV every 12-24 hours (Barkley, 2021)

Question 13

SIADH
results from excessive release of ADH which causes water retention and the dilution of NA+.

risk factors for SIADH include: cancers, pulmonary conditions, CNS disorders and certain drugs.

Patients will present with a wide range of symptoms depending on the severity of the conditions. Mild symptoms include: thirst, headache, nausea/vomiting, decreased reflexes, decreased urine output, edema and cramps.

In more severe cases, the patient maybe agitated, have no urine output, and more pronounced CNS involvement ranging from seizures to coma.

Question 13

SIADH
Laboratory data and patient presentation are essential components related to diagnosing SIADH.

Patients typically have normal volume states; however, the NA+ levels will be low. The serum osmolality will be decreased while urine osmolality is increased. Urine NA + will be increased.

MANAGEMENT
The goal of management is to identify and correct to cause of the problem. NA+ levels should be monitored and treatment accordingly. Close monitoring of NA+ and K+ is necessary.

NA+ > 120- fluid restrictions 1000ml/24 hours

NA+ 110-120 & no CNS involvement- restrict fluid intake to 500 ml /24 hours

NA< 110/ CNS involvement- fluid replacement hypertonic fluid add Lasix 1-2 mEq/hr.

Question 14

ADDISON’S DISEASE
Addison’s disease is also known as primary adrenal insufficiency. Addison’s is the result of insufficient cortisol, androgens, and aldosterone.

The condition typically develops in the 4th decade of life and can be caused by: cancers and destruction of the adrenal gland.

Patient presentation includes the following symptoms: hyperpigmentation of various aspects of the body (elbows, buccal mucosa, knuckles, etc.), fever, headache, abdominal pain, weight loss, decreased blood pressure, fatigue, and altered levels of consciousness.

Question 15

Addisons Disease Primary Adrenal insufficiency

Lab values: Increased potassium, calcium, decreased sodium and glucose, ESR elevated. The cortisol level will be < 5 mg/dL at 8 am.

Cosyntropin test-patients are administered this medication intravenously and cortisol level are checked within an hour. Under normal circumstances the levels are expected to rise. Cortisol levels that remain unchanged are indicative of Addison’s.

Question 16

MANAGEMENT for Addison’s Disease

Specialist referral is necessary in the outpatient management.

Patients are typically places on S-sugar Glucocorticoid(Hydrocortisone)
S-salt
Mineralocorticoid (Florinef).

Patients who are hospitalized in crisis should be started on Solu-Cortef IV with normal saline.

Hydrocortisone phosphate or hydrocortisone sodium succinate should be started after the above dose and tapered over depending on the patient’s condition. A mineralocorticoid is typically added by day 4 of therapy.

IVF- D5NS @ 500 cc/hr for 4 hours then decrease
Antibiotics maybe needed if a bacterial cause of the crisis is suspected

Convert to PO hydrocortisone once patient is stable.

Question 17

Cushing’s syndrome

of hypercortisolism results from various factors including: increased secretion of ACTH, tumors of the adrenal glands and excessive use of glucocorticoids.

The following are some of the characteristics of Cushing’s syndrome: central obesity, purple striae, moon face, buffalo hump, increased blood pressure, irritability weakness, excessive hair and amenorrhea in female patients.

Question 18

Cushings

DIAGNOSIS
Lab values: elevated glucose and sodium, decreased potassium. Serum and urine cortisol levels will be increased.

*Urine Free Cortisol - 24-hour urine collection
Normal - UFC< 50 mcg/24 hrs. , if it is above the normal range the results are considered diagnostic

Dexamethasone Suppression Test - Dexamethasone administered at 11 pm, cortisol levels checked at 8 am. Diagnostic if cortisol levels > 1.8

MANAGEMENT
The management of Cushing’s is cause specific. Glucocorticoids should be decreased or weaned totally. Patients can also undergo surgical interventions such as: resection of pituitary adenomas, cortisol secreting tumors, and removal of removal of adrenal tumors. Patient will need a specialist referral.

Question 19

MANAGEMENT of Cushings

The management of Cushing’s is cause specific. Glucocorticoids should be decreased or weaned totally. Patients can also undergo surgical interventions such as: resection of pituitary adenomas, cortisol secreting tumors, and removal of removal of adrenal tumors. Patient will need a specialist referral.

Question 20

CUSHINGS SYNDROME

Leukocytosis with the body trying to produce inflammation

hyperglycemia with the body moving glucose

hypernatremia and hypokalemia from volume depletion

Question 21

PHEOCHROMOCYTOMA
Pheochromocytoma is a tumor that secretes excessive amounts of the catecholamines, epinephrine, and norepinephrine, which ultimately causes the patient’s blood pressure to reach extremely high levels.

10% of these tumors are malignant. Signs and symptoms include but are not limited to: increased perspirations, headache, flushing, palpitations, chest pain, and nausea.

Question 22

DIAGNOSIS of Pheochromocytoma

24-hour urine checking for:

Urine and serum metanephrines
Catecholamines
Vanillylmandelie acid (VMA)
Creatinine
Results:

> 2.2 mcg metanephrine/mg of creatinine
135 mcg catecholamines/gram of creatinine
5.5 mcg VMA/mg creatinine
CT/MRI of the adrenal glands confirm diagnosis.