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CEN prep 2021 > Endocrine Emergencies > Flashcards

Endocrine Emergencies Flashcards

1
Q

what is the causal difference in type 1 and type 2 diabetes?

A

Diabetic Emergencies
Type 1; an absolute insulin deficiency
Type 2; impaired glucose secretion, peripheral insulin resistance, and increased hepatic glucose production

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2
Q

Diabetic Ketoacidosis has a __-__% mortality rate

A

3-10%

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3
Q

DKA; Infection, illness, pregnancy, or situational stressors can lead to ____. This creates insulin ____. In some patients, excess circulating glucose due to poor dietary management can overwhelm an already stressed system.

A

gluconeogenesis

insulin deficiency

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4
Q

Name four things that can lead to gluconeogenesis.

A

Infection, illness, pregnancy, or situational stressors

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5
Q

Insulin deficiency leads to the release of counterregulatory hormones (such as ____ and ____), which can lead to gluconeogenesis

A

glycogen and cortisol

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6
Q

After a prolonged insulin deficiency, the patient can present with four acute concurrent problems, what are they?

A

Hyperglycemia, dehydration, electrolyte depletion, and metabolic acidosis

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7
Q

Hyperglycemia increases serum ____ and leads to osmotic ____, which causes significant dehydration from urinary loses of water, and these five electrolytes

A

osmolarity
osmotic diuresis, which causes significant dehydration from urinary loses of water, sodium, potassium, magnesium, calcium, and phosphorus

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8
Q

With DKA, Hyperosmolarity further impairs ____ secretion and promotes insulin ____. Without insulin, the newly liberated ____ cannot be used, further increasing the blood glucose level, urine glucose concentration, and osmotic diuresis

A

insulin
resistance
glucose

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9
Q

With DKA, The body burns ____ and ____ ____ for energy. The ensuing lipolysis causes a buildup of fatty acids, which overcomes the body’s natural buffering system and leads to ____

A

fats and muscle proteins

ketoacidosis

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10
Q

Diabetic Ketoacidosis develops over this timeframe

A

2 to 3 days

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11
Q

The presenting signs of hyperglycemia include what? (5)

A

polydipsia, polyuria, fatigue, weakness, and weight loss in new diabetics

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12
Q

Ketoacidosis can cause additional signs and symptoms including
(8)

A

Nausea, vomiting,
hypotension and dehydration
Sinus tachycardia (most common) and possibly dysrhythmias caused by electrolyte disturbances,
Decreased appetite, abdominal cramping
Decreased LOC
Hyperthermia
Kussmaul respirations as the respiratory system compensates for metabolic acidosis
Fruity odor on the breath, which indicates worsening acidosis

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13
Q

Lab tests for DKA involve:
Blood glucose usually exceeds __,
Serum osmolarity greater than __ mOsm/kg
Serum acetone titrations that are ____
Serum ____ level that is increased
For diagnosis and monitoring, expect to use serum ketone testing based on the measurement of
____-____ (the main ketoacid in acidosis), which is recommended. A level greater than __ mmol/L is considered positive
ABG analysis with a decreased PCO2 and metabolic ____
UA with increased ketone and glucose levels

A 
250
310
positive 
ketone
Beta-hydroxybutyrate
1.5
acidosis
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14
Q

____-____ is the main ketoacid in acidosis, which is recommended. A level greater than __ mmol/L is considered positive

A

Beta-hydroxybutyrate (the main ketoacid in acidosis), which is recommended. A level greater than 1.5 mmol/L is considered positive

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15
Q

what are the steps in treating DKA?

  • Monitor mental status, VS, and urine output every ____ until it has improved, and then monitor q 2 to 4 hours
  • Monitor ____ q 1 to 2 hours while the patient is on an insulin drip
  • Check ___ q 2 to 4 hours
  • Bolus 1 to 2 L of NSS over the first __ to __ hours
A

hour
potassium
BMP
1 to 2

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16
Q

When treating DKA, after initiating the intravenous fluid replacement, be prepared to administer an initial loading IV bolus of __ units/kg regular insulin followed by a continuous infusion rate of __ units/kg/hr. To prevent life threatening hypokalemia, insulin replacement should generally not be started until serum ____ is greater than greater than __ mEq/L

A

0.1
0.1
potassium
3.3

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17
Q

In treating DKA, why is it important to decrease the blood glucose level gradually?

A

If the blood glucose level falls too rapidly, the resulting fluid shift can lead to cerebral edema, which is associated with a higher mortality rate.

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18
Q

How does insulin therapy correct metabolic acidosis?

A

Insulin therapy generally corrects metabolic acidosis because the energy is allowed into the cells leading to decreased protein lysis and lipolysis and ultimately resolving ketoacidosis.

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19
Q

When treating DKA, Continue with the insulin infusion until the ___ or serum ____ level returns to normal.

A

pH

bicarbonate

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20
Q

Potassium in DKA treatment; fluid replacement dilutes the serum potassium and promotes ____. In addition, ____ ____ exacerbates total body hypokalemia. Begin potassium replacement after infusing ____ ____ ____ of IV fluid, even when the initial electrolyte levels are ____. In the first few hours after treatment starts, expect the potassium level to ____ precipitously, why?

A 
diuresis
metabolic acidosis
the initial liter
normal 
because potassium moves back to the intracellular space along with the insulin and existing glucose.
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21
Q

HHS stands for what?

A

HHS; Hyperosmolar Hyperglycemic State

10-60% mortality rate

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22
Q

HHS; Hyperosmolar Hyperglycemic State has a __-__% mortality rate

A

10 - 60

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23
Q

HHS; Hyperosmolar Hyperglycemic State can result from

8

A

An underlying infection, acute MI, CVA, certain medications, medication and treatment noncompliance, undiagnosed diabetes, substance abuse, coexisting disease

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24
Q

what is the pathophysiology of Hyperosmolar Hyperglycemic State?
How does it cause dehydration?
How does Underlying renal disease increase the glucose level even further?
The loss of more water than sodium leads to ____
The metabolism of fat and muscle tissues as energy sources, which increases circulating fatty acid and amino acid levels
The resulting hepatic ____ compounds existing hyperglycemia

A

-Osmotic diuresis and an osmotic shift of fluids from the intravascular space can contribute to severe dehydration. The condition worsens because the patient cannot replace the lost fluids
-Underlying renal disease or decreased intravascular volume reduces the glomerular filtration rate and increases the glucose level even further.
hyperosmolarity
gluconeogenesis

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25
Q

For a patient with HHS, the SS can develop over how long?

A

days or weeks

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26
Q

How would you describe a Hyperosmolar Hyperglycemic State patient?
What can possibly be said about their medications?

A

The patient is typically over 50 and has undiagnosed diabetes mellitus that is managed by diet, oral medication, or both
The patient is likely to take a medications that aggravates the problem, such as a diuretic that causes mild dehydration

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27
Q

Hyperosmolar Hyperglycemic State Early SS

A

include decreased appetite and weight loss, polydipsia, polyuria, weakness, mental obtundation (can range from full alertness to coma), and signs of dehydration

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28
Q

Hyperosmolar Hyperglycemic State later S/S

A

Neurologic SS, such as HA, blurred vision, confusion, decreased LOC, seizures, or coma
Tachycardia, dysrhythmias, and hypotension
Increased respirations, but without the fruity smell associated with diabetic ketoacidosis
The decreased LOC is usually what brings the patient to the hospital

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29
Q

Hyperosmolar Hyperglycemic State Lab results to be expected
Blood Sugar greater than __mg/dl
Serum osmolarity greater than __ mOm/kg
pH greater than __
Mild or absent ____
Elevated ___ count if there is an infection present
Normal or increased serum ____ and ____ levels, depending on the degree of dehydration

A

BS greater than 600mg/dl
Serum osmolarity greater than 320 mOm/kg
pH greater than 7.3
Mild or absent ketonemia
Elevated WBC count is there is an infections present
Normal or increased sodium and potassium levels, depending on the degree of dehydration (the initial sodium levels are inaccurate due to the hyperglycemia.

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30
Q

Hyperosmolar Hyperglycemic State Treatment generally consists of (4)

A

IV rehydration, electrolyte correction, administration of intravenous insulin, diagnosis and management of the underlying illness or coexisting condition

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31
Q

Hyperosmolar Hyperglycemic State Treatment
Fluid replacement; isotonic solution rate may be as high as __ to __ liters in the first __ hours.
Continuous reassessments
Be alert for signs of ____ overload, given that most patients are over __
Consider a ____ ____ for accurate IO

A 
1 to 2 liters
2 hours
circulatory
65
urinary catheter
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32
Q

Hyperosmolar Hyperglycemic State Treatment
Insulin; begin regular insulin at __ unit/kg/hr after an initial bolus.
Reduce the BS level by about __ to __ mg/dl/hr
Reductions of BS that are greater than __ an hour may cause fluid shifts and lead to ____ ____

A

Insulin; begin regular insulin at 0.1 unit/kg/hr after an initial bolus.
Reduce the BS level by about 50 to 70 mg/dl/hr
Reductions of BS that are greater than 100 an hour may cause fluid shifts and lead to cerebral edema

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33
Q

Hyperosmolar Hyperglycemic State Treatment
Ongoing; after serum osmolarity begins to normalize or the blood glucose reaches __ to __ mg/dl, expect to switch the intravenous fluid to ____ __% in __ NSS

A

250 to 300 mg/dl

expect to switch the intravenous fluid to dextrose 5% in 0.45 NSS

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34
Q

Hyperosmolar Hyperglycemic State Treatment
ongoing
Expect to ____ the insulin infusion to between __ and __ unit/kg/hr to maintain the blood glucose level between __ and __ mg/dl until the plasma osmolarity is __ mOsm/kg or less and the patient is alert

A

Expect to decrease the insulin infusion to between 0.05 and 0.1 unit/kg/hr to maintain the blood glucose level between 250 and 300 mg/dl until the plasma osmolarity is 315 mOsm/kg or less and the patient is alert

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35
Q

Fun Quiz fact; HHS can put the patient at risk of what?

A

DVT

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36
Q

Hypoglycemia
Most common causes include
(11)

A
  • Iatrogenic insulin effects in patients with type 1 diabetes (most common cause)
  • Pancreatic tumors
  • adrenal insufficiency
  • sepsis
  • congenital metabolic disorders
  • lack of calorie intake
  • increased physical stress
  • liver disease
  • changes in the type of insulin or oral antidiabetic agents
  • pregnancy
  • alcohol ingestion
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37
Q

Hypoglycemia

Most common causes by medications include

A

NSAIDS
Phenytoin (Dilantin)
Thyroid hormones
Beta-blockers

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38
Q

Hypoglycemia
Pathophysiology
The release of ____ accounts for common signs and symptoms of hypoglycemia, such as (9)

A 
epinephrine 
1 shakiness 
2 anxiety 
3 palpitations 
4 sweating
5 dry mouth 
6 pallor,
7 pupil 
8 dilation
9 and hunger
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39
Q

A patient with known diabetes can usually recognize these symptoms and self treat them. However, ____-____ mask the sympathetic response, so a patient who takes a ____-____ may not recognize the onset of hypoglycemia

A

Beta-blockers

Beta-blockers

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40
Q

why are the most profound S/S of hypoglycemia neurological? what S/S can be expected (8)? What can it lead to (3)?

A

The brain cannot store or synthesize glucose so the most profound signs are neurological
Abnormal mentation, irritability, confusion, difficulty speaking, ataxia, paresthesia, headaches, and stupor
Without treatment this Neuroglycopenia can lead to seizures, coma, and even death

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41
Q

Hypoglycemia treatment
Ensure a ____ ____ is intact, and administer __ to __ grams of simple carbohydrate orally.
Wait __ minutes and repeat if necessary.

A

gag reflex
10 to 15
Do not delay oral treatment for lab results
15

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42
Q

Hypoglycemia treatment

what is the treatment of choice for an unconscious patient?

A

To treat a lethargic or unconscious patient, be prepared to rapidly administer 25 to 50 ml of 50% dextrose intravenously as the treatment of choice.

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43
Q

Hypoglycemia treatment

what is the treatment of choice for an unconscious patient with no IV access?

A

If IV access is not possible, administer 1 mg of glucagon intramuscularly

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44
Q

when giving glucagon IM, what should you keep in mind?

A

Because glucagon commonly causes vomiting, position the patient to prevent aspiration

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45
Q

What should you do with a hypoglycemic patient who has an insulin pump?

A

stop the pump immediately

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46
Q

what discharge considerations are there for a hypoglycemic patient?

A

If the cause is identified, you may discharge the patient after a meal.
If the patient takes an oral antidiabetic agent with a long half life, perform further observation.

47
Q

Alcoholic Ketoacidosis
Metabolic emergency that usually occurs __ to __ hours after a patient who has been ingesting large amounts of alcohol abruptly stops drinking. This disorder commonly effects adults with chronic alcohol abuse and a recent history of what (3)?

A

24 to 36

of binge drinking, persistent vomiting, and decreased food intake.

48
Q

Alcoholic Ketoacidosis

Although death is rare, illness typically results from complications such as (3)

A

rhabdomyolysis, liver dysfunction, seizures

49
Q

Alcoholic Ketoacidosis
Alcohol metabolism decreases ____ and worsens the metabolic state. Vomiting leads to ____. ____, ____, and ____ ____ levels increase due to volume depletion, which further alter glucose use.

A 
gluconeogenesis
dehydration
epinephrine
cortisol 
and growth hormone
50
Q

A patient with alcoholic ketoacidosis exhibits SS related to ____, ____ ____, ____ ____, and an accumulation of ____. Lab test reveal an increased serum ketone level and a high ____ ____.

A

dehydration, hormone imbalance, chronic malnutrition, and an accumulation of ketoacids
anion gap

51
Q 
Alcoholic Ketoacidosis lab results may include 
ABG that indicates metabolic \_\_\_\_ due to vomiting and volume depletion or respiratory \_\_\_\_ due to tachypnea, depending on how the patient is compensating.
\_\_\_\_ pH
Normal or increased \_\_\_\_
Increased \_\_\_\_ enzymes
Increased \_\_\_\_
Low or undetectable \_\_\_\_ level
Decreased \_\_\_\_
A 
ABG that indicates metabolic alkalosis due to vomiting and volume depletion or respiratory alkalosis due to tachypnea, depending on how the patient is compensating 
Decreased pH
Normal or increased K
Increased liver enzymes
Increased amylase 
Low or undetectable alcohol level
Decreased electrolytes
52
Q

Alcoholic Ketoacidosis treatment
Administer __% ____ in ___ (___). As rehydration progresses an adequate renal function is established, consider ____ replacement. If ordered, give ___ because fluid therapy and shifting glucose molecules can lead to ____.

A

5% dextrose in NSS (D5NS)
electrolyte
K
hypokalemia

53
Q

when treating Alcoholic Ketoacidosis, Give ____ and ____ to reverse underlying causes.
Avoid using ____ to reverse ketogenesis.

A

carbs
fluids
insulin

54
Q

when treating Alcoholic Ketoacidosis, Expect to administer ____ because ____ can increase the risk of seizures during alcohol withdrawal.

A

magnesium

hypomagnesemia

55
Q

when treating Alcoholic Ketoacidosis, Give ____ (vitamin __) before dextrose containing fluids. ____ depletion in the CNS may cause Wernicke’s encephalopathy, a syndrome characterized by (3). Chronic ____ deficiency may cause heart failure.

A

thiamine (vitamin B1)
Thiamine
ataxia, confusion, and impaired short term memory
thiamine

56
Q

Another name for Antidiuretic Hormone ADH is what?

In what part of the body is it made?

A

Vasopressin

Pituitary gland

57
Q

Neurogenic diabetes insipidus

Can occur when the secretion and release of antidiuretic hormone is impaired, this can result from (5)

A

Damage to the hypothalamus-neurohypophyseal region due to head trauma
Brain surgery
Intracranial tumor, aneurysm, or infarct
Idiopathic or genetic cause

58
Q

Neurogenic diabetes insipidus

what are three medications that can be used in treatment?

A

As prescribed, replace ADH with medications, such as desmopressin (DDAVP), chlorpropamide (diabinese), or carbamazepine (tegretol)

59
Q

Nephrogenic diabetes Insipidus

How can you describe this condition?

A

The amount of ADH is sufficient, but the kidneys cannot properly concentrate the urine. This type of diabetes insipidus usually results from a genetic or acquired disorder.
Acquired forms are more common and are characterized by changes in the kidneys structure or function. Kidney damage may be permanent or temporary.

60
Q

Nephrogenic diabetes Insipidus treatment
Does not respond to ___.
Correct ____ and ____ and discontinue drugs that may be the cause
Administer a ____ ____ and instruct the patient to follow a modest salt restriction to reduce filtrate delivery to the diluting portions of the nephrons

A

Does not respond to ADH.
Correct hypokalemia and hypercalcemia and discontinue drugs that may be the cause
Administer a thiazide diuretic and instruct the patient to follow a modest salt restriction to reduce filtrate delivery to the diluting portions of the nephrons

61
Q

Dipsogenic Diabetes Insipidus

what is it?

A

Occurs from excessive fluid intake that lowers the plasma osmolarity to a point well below ADH secretion thresholds. It is often associated with psychiatric disorders

62
Q

Dipsogenic Diabetes Insipidus

How is it diagnosed?

A

Dx is based on the measurement of urine osmolarity, which helps determine whether polyuria is caused by diabetes insipidus. A urine osmolarity of less than 200mOsm/kg in a patient with polyuria characterizes diabetes insipidus.

63
Q

SIADH
The patient is likely to report
(12) which are S/S of what secondary condition?

A

Weakness and fatigue nausea and vomiting, diarrhea, abdominal cramps, sudden weight gain without edema, HA, decreased urine output despite regular oral intake, impaired taste, thirst, dyspnea on exertion
Hyponatremia

64
Q

SIADH is likely to show what Neurologic function impairments?

A

As hyponatremia worsens, the patient appears confused and disoriented and may have seizures. Severe hyponatremia leads to fluid shifts, which can cause cerebral edema and hyponatremic encephalopathy
DTR’s are diminished

65
Q

SIADH stands for what?

A

syndrome of Inappropriate antidiuretic hormone

66
Q

SIADH lab tests may result as
Marked hyponatremia ___ or below
Low serum osmolarity (less than ___ mOsm/kg
____ to normal BUN and Creatinine
____ renal functions tests
Increased urine osmolarity, sodium levels, and specific gravity
Urine that is ____ compared to plasma

A

Marked hyponatremia 125 or below
Low serum osmolarity (less than 280 mOsm/kg
Low to normal BUN and Creatinine
Normal renal functions tests
Increased urine osmolarity, sodium levels, and specific gravity
Urine that is hyperosmolar compared to plasma

67
Q

SIADH Treatment fluid restrictions
If hyponatremia is mild, free water restriction is sufficient
__ to __ ml/day, however, the patient may need a restriction as severe as __ ml/day

A

800
1000
500

68
Q

SIADH Severe hyponatremia (less than __) is associated with neurologic problems such as ____. Treat urgently because of the high risk for what? (2)

A

124
seizures
cerebral edema and hyponatremic encephalopathy

69
Q

The majority of patients with SIADH have chronic hyponatremia. For these patients, avoid rapid rates of correction that can cause severe neurologic injury. Sodium correction rates should not exceed __ to __ mEq/L/day in chronic hyponatremia
Monitor for circulatory what?

A

6 to 8 mEq/L/day

overload, loop diuretic to increase urine output if needed.

70
Q

____ disease - responsible for for about __ % of all hyperthyroid cases

A

Graves

80 % of all hyperthyroid cases

71
Q

Certain drugs, especially iodine and iodin-containing agents, such as ____ (____), ____ (____), can cause hyperthyroidism.

A

amiodarone (cordarone) and lithium (lithobid)

72
Q

Thyroid storm; is a rare, life-threatening form of thyrotoxicosis. While a thyroid storm may be the result of unrecognized or undertreated thyrotoxicosis, it is usually an acute reaction from what? (8)

A

Hospitalization, surgery, infection, emotional stress, trauma, childbirth,
Sudden discontinuation of antithyroid medication
Over Manipulation of the thyroid gland
An iodine load (contrast media or amiodarone)

73
Q

Thyroid storm SS
Hyperthermia with a temp of __ to __F (__ to __C)
Restlessness, short attention span, agitation, possible ____ ____
Tachydysrhythmias, including rapid, new onset ____ in geriatric patients
Neurologic manifestations, such as (3)
Pulmonary crackles secondary to ____ ____
Warm, diaphoretic skin that becomes hot and dry as ____ worsens
Nausea, vomiting, and diarrhea caused by increased ____ ____

A 
105 to 106F (40.5 to 41C)
anxiety attack
a fib in geriatric patients 
delirium, syncope, or coma
cardiac failure
dehydration
gastric motility
74
Q

Thyroid storm
If untreated, mortality rate is about __%, however, prompt recognition and aggressive treatment can reduce mortality to between __ and __ percent.
Exhaustion, cardiac failure, and death can occur within hours

A

100%

10 and 30

75
Q

Thyroid storm treatment
Give ____ and ____ (____) orally or through a gastric tube to block hormone synthesis. The drugs onset of action occurs within __ hour, but the full effects take __ to __ weeks

A

propylthiouracil and methimazole (tapazole)
1
3
6

76
Q

Thyroid storm treatment
Administer iodides, as prescribed, to block the conversion of ____ to ____ and inhibit hormone release.
Do this at least one hour after giving antithyroid medications to slow the release of stored thyroid hormone from the thyroid gland. If given sooner, ____ may be used to create new thyroid hormone

A

thyroxine to triiodothyronine

iodine

77
Q

Thyroid storm treatment
Administer ____-____ to inhibit adrenergic effects. Use these drugs with caution in geriatric patients and those with preexisting heart disease, or asthma.

A

beta-blockers

78
Q

For patients with Graves disease and thyroid crisis, administer ____, which increase survival rates. (these patients metabolize and use ____ faster than normal)

A

glucocorticoids

cortisol

79
Q

Thyroid storm treatment
Avoid using ____ for temperature control because it can displace thyroid hormones from binding sites and worsen the problem

A

aspirin

80
Q

what radiology should you anticipate for the treatment of thyroid storm?

A

Radiography to rule out infection
Head and neck computed tomography to identify neoplasms or structural abnormalities
ABx if infection is the suspected cause

81
Q

what lab tests should you anticipate for the treatment of thyroid storm?

A 
C and S
Toxicology
TFS
Electrolyte levels
CBC
82
Q

What is Myxedema Coma?

A

Is an extreme complication of hypothyroidism in which the patient exhibits multiple organ dysfunctions and progressive mental deterioration.

83
Q

Myxedema Coma Effects more ____ then ____

Even with optimal treatment, mortality rate is ____

A

women than men

high

84
Q

Myxedema madness refers to associated psychiatric symptoms such as what? (5)

A

hallucinations, paranoia, depression, combativeness, and decreased concern for personal appearance

85
Q

Untreated ____ progresses over months or years before culminating in myxedema coma.

A

hypothyroidism

86
Q

All patients who develop myxedema coma have some type of ____
Primary ____ may result from autoimmune thyroiditis (such as ____ disease), ablation therapy (treatment of hyperthyroidism), iodine deficiency, tumor activity, or drug therapy

A

hypothyroidism
hypothyroidism
Hasimoto’s

87
Q

Secondary hypothyroidism stems from ____ dysfunction. Alterations in ____ function decrease the release of thyroid-stimulating hormone, which reduces thyroid hormone secretion.

A

pituitary

pituitary

88
Q

Tertiary hypothyroidism occurs when the ____ secretes too little thyrotropin-releasing hormone or when that hormone fails to reach the pituitary gland

A

hypothalamus

89
Q

SS myxedema coma
Because the patient does not have a fever, tachycardia, or diaphoresis, the crisis my go unnoticed at first. The patient may report (5)

A 
Pronounced fatigue
Puffy face with dull expression 
Decreased activity tolerance
Episodes of SOB
Weight gain
90
Q

describe the presentation of a myxedema coma patient

A

The patient may answer the questions slowly and become very confused. The patient may exhibit an AMS, including somnolence, depression, and lethargy. Rarely, these may progress to coma.

91
Q

How can myxedema coma affect the respiratory system?

5

A

Tongue swelling that may obstruct the airway
Weak respiratory effort and drive
Alveolar hypoventilation also leads to hypercarbia, which can worsen mental status
Obesity related sleep apnea
Respiratory failure is the usual cause of death

92
Q

How does myxedema coma affect the cardiovascular system?

A

Decreased HR, stroke volume, and cardiac output

EKG may show widespread ST-segment and T wave changes and prolonged QT intervals (as shown in the image)

93
Q

How can myxedema coma contribute to hypothermia?

A

When the body uses peripheral vasoconstriction to conserve heat, the skin becomes cool and pale, and the temperature usually falls below 96F or 35.5C

94
Q

Renal and other findings of myxedema coma
Renal blood flow, GFR, and sodium reabsorption rate ____
The patient cannot excrete the usual amount of fluid, and urine osmolarity does not reflect the ____ hypo-osmolarity
____ non pitting edema may be present
____ may result from increased insulin sensitivity and decreased oral intake.
Constipation
Oral drugs may not be absorbed adequately

A

decreased
serum
generalized
hypoglycemia

95
Q

Lab results found with myxedema coma
WBC count, hemoglobin, hematocrit, and thyroid hormone levels are ____
The creatine kinase and lactate dehydrogenase levels may be ____ due to increased muscle membrane permeability

A

decreased

elevated

96
Q

Treatment for myxedema coma
Synthroid, glucocorticoids, to prevent ____ crisis
Radiography and diagnostics
Warm the patient slowly. Why?
Analgesic
____ ____ ____ to decrease abdominal pressure and distension

A

adrenal
Warming too quickly can overstress the system
Gastric tube placement

97
Q

Acute adrenal insufficiency, which affects the ____ and ____ Is a rare, life threatening disorder characterized by the depletion of adrenal (same answer)

A

glucocorticoids and mineralocorticoids

98
Q

Acute adrenal insufficiency can occur with ____ disease or may result from
The sudden withdrawal of what?
Adrenal removal or injury
Injury or destruction of the ____ gland

A

Addison’s
long term steroid therapy
pituitary

99
Q

Massive bilateral adrenal hemorrhage can occur under severe physiological stress such as what?

A

MI, septic shock, or complicated pregnancy.

100
Q

Acute adrenal insufficiency
Normally, stress increases ____ output from the adrenal glands. The inability to meet the increased demand begins a sequence of events that leads to a crisis.

A

cortisol

101
Q

Acute adrenal insufficiency Pathophysiology
When the adrenal system fails, the resulting decrease in ____ and ____ levels lead to sodium and water loss from the kidneys and gastrointestinal tract.
Water loss causes ____ and ____, which can progress to cardiovascular collapse, coma, and death

A

cortisol and aldosterone

hypotension and hypovolemia

102
Q

Acute adrenal insufficiency Pathophysiology

Without sufficient cortisol, ____ (the normal hepatic response to stress) fails, which can cause hypoglycemia.

A

gluconeogenesis

103
Q

Acute adrenal insufficiency Pathophysiology
The decreased cortisol level also alters the actions of the adrenal ____, which normally responds to stress by releasing ____ to increase the heart rate and blood glucose levels. The lack of ____ response magnifies the severity of the hypoglycemia and hypotension

A

medulla
catecholamines
catecholamine

104
Q

Acute adrenal insufficiency can result from recent changes such as

A

Prior illness, such as asthma with steroid therapy
Recent medication changes
Recent surgery
Recent injury

105
Q

Acute adrenal insufficiency findings include

A

HA, fatigue, weakness, weight loss, palpitations,
gastro problems such as N/V, anorexia, abd pain, chronic diarrhea
High fever due to infection
Resting tachycardia
Hypotension or orthostatic hypotension
Signs of dehydration

106
Q

Acute adrenal insufficiency treatments include

A

Glucocorticoid replacement to stimulate gluconeogenesis, inhibit inflammation, and increase the body’s response to stress
Correction of electrolytes
Cardiac monitoring

107
Q 
Pheochromocytoma, which affects the \_\_\_\_ 
SS include (8)
A

catecholamines

fatigue, anxiety, pallor, tremors, fever, chest and abdominal pain, mental status changes

108
Q

Pheochromocytoma can cause Severe hypertension accompanied by a triade of what (3)?
Vision disturbances related to hypertensive retinopathy

A

HA, palpitations, and diaphoresis

109
Q

Pheochromocytoma can cause Cardiovascular symptoms such as (8)

A

Atrial and ventricular fibrillation, MI, cardiomyopathy, pulmonary edema, CVA, pulmonary edema, hypertensive encephalopathy

110
Q

Suspect Pheochromocytoma based on the patients Hx. Prepare patient for what tests, which may detect adrenal mass.
Initiate __ ____ urine test for catecholamines

A

abdominal CT or MRI

24 hour

111
Q

Treatments for Pheochromocytoma include
Emergent care that controls effects of excess ____. To manage hypertensive crisis, expect to administer an intravenous ____-____, such as ____ (Regitine) or ____ (Nitropress)
Cardiac monitoring
IV fluids to maintain a normal circulating volume

A

catecholamines
alpha-blocker
phentolamine
Nitroprusside

112
Q

Cushing’s syndrome affects the ____ is caused by what?

A

glucocorticoids

prolonged exposure to elevated or exogenous glucocorticoids

113
Q

In most patients, Cushing’s syndrome results from the administration of ____ ____

A

exogenous steroids

CEN prep 2021 (36 decks)

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