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Med/Surg > EXAM 6 > Flashcards

EXAM 6 Flashcards

1
Q

Onset of DKA

A

SUDDEN

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2
Q

ONSET of HHS

A

GRADUAL

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3
Q

Precipitating factors of DKA

A

Infection
Stress
INADEQUATE INSULIN DOSAGE

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4
Q

Precipitating factors of HHS

A

Infection/Stress

INADEQUATE FLUID INTAKE

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5
Q

Manifestations of DKA

A

Ketosis: Kussmaul respirations: “rotting fruit” breath Nausea/ ABD pain.
DEHYDRATION or electrolyte loss: Polyuria/Polydipsia/ Weight loss/Dry Skin/Sunken eyes/Soft eyeballs/lethargy/ Coma.

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6
Q

Manifestations of HHS

A

Altered CNS function with neurologic symptoms.

DEHYDRATION or ELECTROLYTE LOSS.

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7
Q

Glucose for DKA

A

Greater than 300

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8
Q

Glucose for HHS

A

Greater than 600

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9
Q

Osmolarity DKA

A

HIGH or NORMAL

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10
Q

Osmolarity of HHS

A

GREATER than 320

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11
Q

SERUM KETONES IN DKA

A

POSITIVE at 1:2 dilutions

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12
Q

SERUM KETONES IN HHS

A

NEGATIVE

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13
Q

SERUM PH in DKA

A

LESS than 7.5

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14
Q

SERUM PH in HHS

A

GREATER THAN 7.35

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15
Q

HCO3 in DKA

A

LESS than 15

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16
Q

HCO3 in HHS

A

GREATER than 20

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17
Q

Serum SODIUM for DKA

A

Low/NORMAL/high

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18
Q

Serum SODIUM HHS

A

Normal or LOW

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19
Q

BUN in DKA

A

Greater than 30

ELEVATED because of DEHYDRATION

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20
Q

BUN in DKA

A

ELEVATED

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21
Q

CREATinine in DKA

A

GREATER than 1.5

Because of DEHYDRATION

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22
Q

Creatinine of HHS

A

ELEVATED

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23
Q

Urine ketones for DKA

A

POSITIVE

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24
Q

Urine Ketones for HHS

A

Negative

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25
Q

DKA occurs in what type of diabetic?

A

Type 1

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26
Q

What is the most common precipitating factor of DKA?

A

Infection

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27
Q

What is the mortality rate even with treatment?

A

10%

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28
Q

What is the onset time of DKA?

A

4-10hrs

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29
Q

What will be your potassium levels with DKA?

A

HIGH

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30
Q

What will be you VS with DKA?

A 
Tachycardia
Hypotension
Tachypnea (Kussmaul Respirations)
Normal to low O2
Abdominal Pain
Normal to slightly high Temp
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31
Q

What will be the assessment findings of DKA?

A 
Dry skin
Flushed skin
Polyuria
Polydipsia
Polyphagia
Decreased LOC
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32
Q

What will the H&H be for DKA?

A

Hemoconcentration= HIGH H&H
HEMATOCRIT
GREATER than 45-52% for men
Greater than 37-48% women

       HEMOGLOBIN GREATER than 13.5-17.5 for men Greater than 12.0-15.5 for women
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33
Q

Will people with DKA experience vomiting?

A

YES

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34
Q

What will a patients CVP be in DKA?

A

Below 9

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35
Q

What will a patient in DKA ABG’s be?

A

PH LOW less than 7.3
CO2 LOW less than 35
Bicarbonate LOW less than 22

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36
Q

What are the four priorities for a patient with DKA?

A

AIRWAY
HYDRATION
ELECTROLYTES
GLUCOSE

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37
Q

What are nursing interventions with a patient who has DKA?

A 
AIRWAY & Breathing
Cardiac monitoring & VS
Chest X-ray
Hourly BS
Comfort
Fluid&Insulin 
Patent IVs 
Safety
Nutrition (slow-clear liquids to start)
LOC
Simple explanations reassurance
2-4hr BMPs
VS Q15min
Accurate I&O QHR
LOC QHR
CVP measurement 
Foley catheter
Labs- WBC/CHEM/UA/ABGs
2 large bore IV's or central line.
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38
Q

What underlying diagnosis might elderly have to change nursing interventions for DKA?

A

CVD

RF

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39
Q

How do you restore volume and maintain perfusion for DKA?

A

0.9% NS 15-20mL/kg/hr for 1 HR BOLUS
0.45% NS 4-14 mL/kg/hr until glucose drops to 250
D5W 1/2NS as maintenance

Fluids need to replace volume loss 6-10 LITERS !!!!!

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40
Q

What is the drug therapy for DKA?

A

IV BOLUS 0.1U/kg
Continuous infusion 0.1U/kg/hr
SQ insulin when PO food/water returns

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41
Q

When is DKA considered an end point?

A

BS 200mg/mL
Serum bicarbonate: 18
Venous PH: 7.3 or greater
Anion gap less than 12

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42
Q

What are precautions when administering insulin for DKA?

A

ALWAYS use and insulin syringe

Insulin has to be PIGGYBACKED so it doesn’t clot off.

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43
Q

When is bicarbonate needed in DKA?

A

With a PH level below 7.0 or a bicarbonate level below 5.

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44
Q

What is important to assess before giving IV potassium solutions?

A

URRINE output is AT LEAST 30ml/HR.

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45
Q

What are s/s of HYPOKALEMIA?

A 
Fatigue
Malaise 
Confusion
Muscle Weakness
Shallow respirations 
Abdominal distention
Paralytic ileus
Hypotension
Weak pulse
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46
Q

What is a common cause of death with DKA treatment?

A

Hypokalemia

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47
Q

What are the “sick day” rules for a patient with diabetes to monitor for DKA?

A

Monitor BG levels Q4HR
Test urine for ketones when BS is greater than 240.
Continue Insulin regimen.
Drink 8-12oz of SUGAR FREE fluid per hour of awakens.
If BS is low drink sugar drinks.
Continue to eat.
Get plenty of rest.

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48
Q

What are the danger signals that a diabetic need to notify HCP about?

A

Persistent N/V
Moderate or large Ketones
BG high after 2 dose of insulin.
Temp above 101.5 or fever for longer than 24hrs.

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49
Q

How do you perform an anion gap?

A

SODIUM minus the result of your CL added to your Bicarbonate.

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50
Q

What is the normal anion gap?

A

7-9

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51
Q

What is the goal for insulin therapy?

A

Drop the glucose by 50-75 units PER HOUR.

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52
Q

What does the anion gap need to be to represent metabolic acidosis?

A

GREATER than 10-12.

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53
Q

What do you do to prevent hypokalemia with insulin treatment for DKA?

A

Potassium replacement is initiated after serum levels fall below 5.0.

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54
Q

When nausea is present with a patient that is ill and has diabetics what is the intervention?

A

Take liquids that contains both glucose and electrolytes: Soda pop/ diluted fruit juice/Gatorade

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55
Q

What is the most common manifestations of HHS?

A 
BS above 600
Dehydration
Hyper osmolarity 
Hypokalemia
Decrease renal perfusion 
ELDERLY
TYPE 2 diabetics
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56
Q

What are the causes of HHS?

A 
Infection
Stress
Environment
MI
Sepsis
Pancreatitis
Stroke
Medications
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57
Q

Are there ketones in HHS? WHY?

A

NO KETONES.

Because there is just enough insulin production to prevent ketoacidosis

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58
Q

Why does HHS happen more often in the elderly?

A

Decreased kidney function which leads to decreased ability for the kidneys to re absorb the glucose which leads to increased glucose levels or HHS. DEHYDRATION also leads to decreased volume which further reduces glomerular filtration rate and casing glucose levels to rise.

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59
Q

What is the mortality rate for the orderly population that have HHS?

A

40-70%

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60
Q

Will HHS occur in adequately hydrated patients?

A

NO

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61
Q

What types of drugs can lead to HHS?

A 
Glucocorticoids
Diuretics
Phenytoin (Dilantin)
Beta Blockers
Calcium Channel Blockers
62
Q

What might people with HHS have that people with DKA wont have?

A

Seizures

Reversible Paralysis

63
Q

When will a coma occur with someone who has HHS?

A

When serum osmolarity is greater than 350

64
Q

What does the severity of hyperglycemia cause with patients who have HHS?

A

Extreme diuresis
Sever DEHYDRATION
Severe electrolyte loss

65
Q

What is the expected outcome with a patient who has HHS?

A

Restore glucose levels within 36-72hrs

REHYDRATE

66
Q

When does CNS function return with a patient who has HHS?

A

Hours after blood glucose levels have returned to normal.

67
Q

What is the first priority for someone with HHS?

A

FLUID REPLACEMENT.

68
Q

What is used for sever shock or hypotension for HHS?

A

Normal saline

69
Q

What is used to treat HHS w/o shock or hypotension?

A

Half normal saline (0.45% chloride)
Infuse at 1hr/L until CVP or pulmonary capillary wedge pressure begins to rise OR until BP and urine output are adequate.
Then reduced to 100-200ml/hr
1/2 fluid deficit is replaced in 12hrs and the rest is given in the next 36hrs.

70
Q

What is used to determine the rate of infusion for HHS AFTER fluid deficit (12hrs) is replaced?

A

Body weight
Urine Output
Kidney function
Presence or absence of of pulmonary congestion and jugular venous distention.

71
Q

What do you need to monitor in patients with CHF, Kidney disease, or acute kidney injury?

A

Central Venous Pressure

72
Q

How often do you assess the patient, and what for?

A 
Hourly 
Signs of cerebral edema
Abrupt changes in mental status
Abnormal neurologic signs
Coma
73
Q

What can lack of improvement of LOC mean in a pt with HHS?

A

May indicate inadequate rates of fluid replacement OR reduction in plasma(blood) osmolarity.

74
Q

What can a regression after initial improvement of HHS mean?

A

TOO rapid reduction in blood osmolarity.

75
Q

What is best evidence in fluid management of HHS?

A

SLOW BUT STAEDY.

76
Q

What will you immediately report if seen in a patient with HHS during treatment?

A

Changes in LOC
Changes in pupil size or reaction
Seizures

77
Q

When is IV insulin therapy administered?

A

AFTER adequate fluids have been replaced.

78
Q

What is the the typical insulin intervention for HHS?

A

BLOUS dose of 0.15u/kg IV followed by an infusion of 0.1u/kg/hr until blood glucose levels fall to 250.

79
Q

What d you want to reduce the blood glucose levels by for HHS?

A

50-70 per hour.

80
Q

What do you need to monitor when a patient with HHS is receiving insulin therapy? And what are the signs&symptoms?

A 
Hypokalemia 
Sx/S:
Muscle weakness
Hypotension
Weak pulses
Fatigue 
Malaise 
Paralytic Ileus
Confusion
Abdominal distention
81
Q

When is potassium therapy initiated for HHS?

A

When urine output is adequate

82
Q

How after are serum electrolytes assessed with HHS?

A

Every one to two hours until stable.

83
Q

Why is continuous cardiac monitoring needed during HHS and DKA?

A

Hypokalemia or Hyperkalemia

84
Q

Who participates in education for a patient with diabetics and diabetic control? SIX

A 
Nurses
Physicians
Pharmacists
Social Worker
Psychologist 
Registered dietician
85
Q

What is is DI? And what is it caused by?

A

A WATER LOSS PROBLEM

Caused by either and ADH deficiency OR an inability of the kidneys to respond to ADH.

86
Q

What are the manifestations of DI?

A 
Decreased ADH
Dehydration
Increased urination
Increased serum NA (pulling out of cells)
Decreased urine NA (diluted)
Decreased specific gravity 
Increased Solute (dehydration/hemoconcentration) 
Decreased Solution (dehydration)
Decreased Plasma Osmolarity
87
Q

What is the most common electrolyte imbalance of DI?

A

Increased Sodium levels.

88
Q

What can lead to death in DI?

A

If thirst mechanism is poor or absent or if the person is unable to obtain water, DEHYDRATION becomes more severe and can lead to DEATH.

89
Q

What do you have to ensure that no patient is deprived of for DI?

A

DON’T DEPRIVE fluids any longer than 4 hours because they can not reduce urine output.

90
Q

What is nephrogenic diabetes insipidus? What gene is most commonly inherited?

A

A genetic disorder caused in which the kidney tubules do not respond to the actions of ADH.
Most commonly inherited as an X-linked recessive disorder AVPR2 gene.

91
Q

What is primary diabetes insipidus?

A

Defect of the hypothalamus gland or posterior pituitary gland, resulting in a lack of ADH production or release.

92
Q

What is secondary diabetes insipidus?

A

Most often results in tumors in or near the PPG or the hypothalamus
Also can be from head trauma, infectious process, brain surgery, or metastatic tumors.

93
Q

What is drug-related diabetes insipidus?

A

Usually caused by lithium carbonate and demeclocycline. These drugs can interfere with the response of the kidneys to ADH.

94
Q

What are the manifestations of DI?

A

DEHYDRATION
Increased urination
Excessive thirst

95
Q

What are the manifestations of DEHYDRATION?

A 
Poor skin turgor 
Dry or cracked mucous membranes 
Tachycardia 
Weak peripheral pulses
Decreased BP
Decreased pulse pressure
Orthostatic hypotension
Distended Neck Veins (supine position)
Increased RR
Dry skin
Decreased LOC
Concentrated dark urine with high SG
96
Q

What are the key features of DI?

A 
Hypotension
Tachycardia
Weak peripheral pulses
Hemonconcentration
Increased urine output
Dilute urine, low specific gravity
Poor turgor
Dry mucous membranes
Decreased cognition
Ataxia
Increased thirst
Irritability
97
Q

What is the first step in diagnosis to DI?

A

Measure a 24hr fluid intake and output without restrictions.
DI is considered if output is more than 4L during this period and is greater than the volume ingested.
Urine is dilute with a SG LESS than 1.005 and low osmolarity (50-200)

98
Q

What is the drug of choice for DI?

A

Desmopressin ( a synthetic for of vasopressin) given orally or intranasally in a metered spray.
Each spray delivered 10mcg
Mild 2-3 sprays daily
Severe ADH IV or IM

99
Q

What are side effects of intranasal form of desmopressin?

A 
Ulceration of mucous membranes 
Allergy 
Sensation of chest tightness 
Lung inhalation of the spray 
If these occur or if the patient has a URI an oral or subQ vasopressin is used instead.
100
Q

What is the difference between the parenteral and oral or intranasal desmopressin forms?

A

Parenteral from is 10x stronger.

101
Q

What is the nursing management for a patient with DI?

A 
Early detection of dehydration 
Maintaining adequate hydration
Accurately measuring I&O
Checking urine specific gravity 
Daily weight 
Urge pt to drink oral fluids
Ensure potency of IV and catheter
102
Q

What is the management for lifelong DI?

A

Polyuria or polydipsia are indications of the needle for another dose.
Drugs for DI can cause fluid overload so teach patients to weigh themselves daily.
Signs of fluid overload include weight gain of 2.2lbs or other signs of water toxicity (headache, acute confusion) CALL 911

103
Q

What is syndrome of inappropriate antidiuretic hormone (SIADH) or Schwartz-Bartter syndrome?

A

A problem in which vasopressin(antidiuretic hormone) is secreted even when plasma osmolarity is low or normal.

104
Q

When does SIAHD occur?

A 
Cancer 
Pneumonia 
Lung abscesses 
Active TB
PNEUMOTHORAX 
Chronic lung disease 
Mycoses
Positive pressure ventilation 
Trauma 
Infection
Tumors
Strokes
Porphyria
Lupus
Vincrisitne
Cyclophosphamide 
Carbamazepine
Opioids 
Tricyclics antidepressants 
General anesthetic
Fluoroquinolone
105
Q

What are the manifestations of SIADH?

A 
Early= water retention, N/V, anorexia 
Recent weight gain. 
Free water (not salt) is retained so no edema
HYPONATREMIA 
Lethargy 
Headaches
Hostility 
Disorientation
Change in LOC
Late: decreased responsiveness/seizure/coma
Full bundling pulse
Hypothermia
Decrease in urine volume
Urine osmolarity INCREASE 
Plasma Volume Increase
Plasma Osmolarity DECREASE 
Increased urine NA levels
Increased urine SG
Increased urine concentration
106
Q

What can help diagnose SIADH?

A

Radioimmunoassay of ADH along with clinical manifestations.

107
Q

What are the medical interventions for SIADH?

A

Restricting fluid intake.
Promoting excretion of water.
Replacing lost NA
Interfering with the action of ADH

108
Q

What are nursing interventions for SIADH?

A

Monitoring response to therapy
Preventing complications
Teaching the patient about fluid restrictions and drug therapy
Preventing injury
Measure I&O
Daily weight greater than 2.2lbs(1L/1000mL of fluid) is concern
Frequent oral rinses

109
Q

Why is fluid restriction essential for SIADH?

A

Fluid intake further dilutes plasma NA levels. In some cases fluid intake may be kept as low as 500 to 1000mL per day.
USE SALINE INSTEAD OF WATER FOR EVERYTHING

110
Q

What is drug therapy with patient who have hyponatremia with SIADH?

A

Tolvaptan ORAL or conivaptan IV
VASOPRESSIN ANTAGONISTS
Promote water excretion WITHOUT NA loss.
TOLVAPTAN BBW: rapid INCREASE in NA levels greater than 12/24hr can cause CNS demyelination that can lead to death. ALSO high doses or doses longer than 30 days SIGNIFICANT risk for liver failure and death.
ONLY ADMINISTER IN HOSPITAL SETTING

111
Q

What is the drug therapy for patient who have near normal NA levels or heart failure and SIADH?

A

Diuretics: be careful for further NA loss.
Demeclocycline: oral antibiotic may also help correct disturbed fluid and electrolytes

112
Q

What solution is used to treat SIADH when NA levels are very low?

A 
HYPERTONIC SALINE (3% NaCL) 
Give IV cautiously because my add to existing fluid overload and promote heart failure.
113
Q

What can ANY patients response to therapy lead to?

A

Fluid overload which leads to pulmonary edema and heart failure.

114
Q

What is the older adult with SIADH at risk for with these ________ secondary diseases?

A

With cardiac problems, kidney problems, or liver problems, the older adult is at great risk for fluid overload.

115
Q

What are the s/sx of fluid overload? How often do you assess?

A 
Bounding pulse
Distended neck veins
Crackles in lungs
Increasing peripheral edema
Reduced urine output 
 AT LEAST EVERY 2hrs

Pulmonary edema can occur VERY QUICKLY and can lead to death.

If these signs are present NOTIFY THE HCP IMMEDIATELY

116
Q

What is critical when serum NA levels fall below 120 in patients with SIADH?

A

PROVIDING SAFE ENVIRONMENT
Possible neurological changes and risk for seizures increases.
assess neuro changes and subtle changes such as muscle twitching.
Check A&Ox3 EVERY 2 HOURS
Reduce environmental noise and lightening to prevent overstimulation.

117
Q

What is an addisonian crisis?

A

LIFE THREATENING EVENT in which the need for cortisol and aldosterone is GREATER than the available supply.
Often occurs to a stressful event: (surgery/ trauma/ severe infection)

118
Q

What is the emergency care HORMONE REPLACEMENT regimen for and addisonian crisis?

A

RAPID INFUSION OF NS OR DEXTROSE 5% in NS

Initial dose of EITHER hydrocortisone sodium 100-300mg OR dexamethasone 4-12mg IV BOLUS

Administer an additional 100mg of hydrocortisone sodium by continuous IV infusion over next 8hrs

Give hydrocortisone 50mg IM concomitantly every 12hrs

Initiate an H2 histamine blocker (ranitidine) IV for ulcer prevention

119
Q

What is the emergency care HYPERKALEMIA regimen for and addisonian crisis?

A

Administer insulin (20-50 units) with dextrose (20-50mg) in NS to shift K into cells

Administer KAYEXALATE

Give lord or thiazide diuretic

AVIOD Ksparing diuretics

K restrictions no avocado/spinach/banana/whitebeans/sweetato

Monitor I&Os

Monitor HR/rhythm/and ECG for manifestations of hyperkalemia: bradycardia/heart block/tall peaked Twaves/fibrillation/asystole

120
Q

What is the emergency care HYPOGLYCEMIA regimen for and addisonian crisis?

A

ADMINISTER PRESCRIBED IV GLUCOSE

ADMINISTER GLUCAGON

MAINTAIN IV ACCESS

MONITOR BLOOD GLUCOSE LEVELS HOURLY

CONTINUOUS ECG

121
Q

WHAT IS PRIMARY ADDISONS DISEASE or adrenal hypofunction?

A 
Autoimmune 
TB
Metastatic Cancer
AIDS
Hemorrhage
Gram- SEPSIS
Adrenalectomy 
Abdominal radiation therapy
Mitotane drug and toxins
122
Q

What is the cause of secondary causes of Addison’s disease or adrenal hypofunction?

A

Pituitary Tumors
Postpartum Pituitary necrosis
Hypophysectomy
High dose pituitary or whole brain radiation

123
Q

What are manifestations of Addison’s disease?

A 
Lethargy (depressed/confused/psychotic)
Fatigue
Muscle/joint weakness
Salt craving
Anorexia
N/V/D/Constipation
Abdominal pain
Weight loss
Women:menstrual changes
Men: impotence 
Vitiligo
Hyperpigmentation 
Hypotension
124
Q

What are the lab values with Addison’s disease of adrenal hypofunction? And the manifestations of each?

A

Hypoglycemia (sweating/headaches/tachycardia/&tremors)
Hyponatremia
Hyperkalemia (dysrhythmias/ irregular HR=cardiac arrest)
Hypercalcemia
Low serum cortisol
Elevated BUN

125
Q

What is the most definitive test for adrenal insufficiency?

A

ACTH stimulation (provocation) test.
ACTH is given IV and plasma cortisol levels are obtained in 30min intervals.
PRIMARY: absent or decreased
SECONDARY: increased

126
Q

What are imaging testing to assess for Adrenal insufficiency or Addison’s disease?

A

Skull X-ray/CT/MRI and arteriography may determine the cause of pituitary problems.

CT may also show adrenal atrophy

127
Q

What are the nursing interventions for Addison’s Disease?

A

Because of hyperkalemia CARIAC FUNCTION is a nursing priority.

Promoting fluid balance

Monitoring for fluid deficit

Preventing poor glucose regulation with hypoglycemia

VS 1-4hrs

Weight pt daily

Record I&O

Monitor lab values (identify hemconcentration=^Hematocrit or BUN)

128
Q

What is the common drug regimen for Addison’s disease?

A

Cortisone 25-50mg orally WTH MEALS (GI irritation can occur)

Hydrocortisone 20-50mg orally S/Sx of excessive drug therapy: rapid weight gain/round face/fluid retention=Cushing Syndrome

Prednisone 5-10mg orally daily REPORT: sever diarrhea/vomiting/fever. May need to ^during illness

Fludrocortisone 0.5-0.2mg orally MONITOR: BP (hypertension is s/e) REPORT: weight gain or edema. (Na/retention is possible)

129
Q

What is Cushing Disease (hypercortisolism)and what is it caused by?

A

Excess secretion of cortisol from the adrenal cortex.

Problem with the adrenal cortex itself OR problem in the ANTERIOR pituitary gland OR problem with the hypothalamus.

130
Q

Who does Cushing’s DISEASE effect more often?

A

WOMEN

131
Q

What is Cushing SYNDROME?

A

GLUCOCORTICOID therapy can also lead to problems of hypercortisolism= CUSHINGS SYNDROME

132
Q

Endogenous secretion= Cushing’s Disease Causes?

A

Bilateral adrenal hyperplasia
Pituitary increase production of ACIH
Malignancies of lung/GI/pancreas
Adrenal carcinomas

133
Q

Exogenous Administration= Cushings SYNDROME Causes?

A 
Use of Glucocorticoids in treatment of:
Asthma
Autoimmune disorders
Organ transplantation
Cancer chemotherapy 
Allergic responses 
Chronic fibrosis
134
Q

Is Cushing’s Syndrome or Cushing’s Disease more common?

A

SYNDROME

135
Q

What are the key features of a patient with Cushing’s Disease/Syndrome?

A 
Moon face
Edema
Acne
Buffalo Hump
Truncal Obesity 
Weight Gain
Hypertension
Frequent Dependent Edema
Bruising 
Petechiae
Muscle Atrophy (extremities)
Osteoporosis 
    Pathologic features
    Decreased height to vertebral collapse
    Aseptic necrosis of the femur head
    Slow or poor healing of bone fractures 
Thinnning skin
Striae (stretch marks) and increased skin pigmentation
^risk for infection
Decreased immune function
Decreased inflammatory responses 
Manifestations of infection/inflammation may be masked.
136
Q

What are the cardiac changes that occur with Cushing’s disease?

A

Water and Na are retained leading to hypervolemia and edema formation. BP is elevated Pulses are full and bounding

137
Q

What is glucose levels with Cushing’s syndrome?

A

HIGH

138
Q

what are some emotional changes related to Cushing’s disease?

A 
"Don't feel like themselves"
Mood swings
Irritability
Confusion
Depression
Crying/laughing inappropriately 
Difficulties concentrating 
Sleep difficulties/ fatigue
139
Q

what are the lab tests for Cushing’s Disease?

A

Blood/Salivary/Urine cortisol levels
24hr urine for ^CALCIUM/^cortisol/^androgens/^K+/^Glucose.

ACTH levels are elevated in PITUITARY
ACTH levels are low in STEROID USE

140
Q

what is a normal salivary cortisol level?

A

2.0

141
Q

What is dexamethasone suppression testing?

A

Over night or 3-day period set doses of dexamethasone are given. A 24hr urine collection follows the drug.
If cortisol levels are SUPPRESSED by the drug Cushing’s is not present.

142
Q

What are some addition lab findings for Cushing’s disease?

A

Increased Blood GLUCOSE levels
Decreased Lymphocyte count
Increased Sodium levels
Decreased Serum Calcium levels

143
Q

What are imaging tests that can be performed for Cushing’s disease?

A 
X-ray
CT scan
MRI
Arteriography 
Identify leasions of adrenal/lung/pituitary/GI/or pancreas
144
Q

What are priority nursing diagnosis for Cushing’s disease?

A

SAFTEY: skin integrity/bleeding/intact skeleton
Fluid overload: pulmonary edema/heart failure
INJURY: think skin/poor wound healing/bone density loss.
Risk for INFECTION
Change positions Q2hr

145
Q

What is the drug therapy for a patient with Cushing’s disease?

A

DRUG that INTERFERE’s with ACTH production: Cyproheptadine

DECREASE IN CORTISOL PRODUCTION: Metyrapone/aminoglutethimide/ketoconazole

TUMORS: Mitotane

Type 2 diabetes: Korlym= BBW= don’t use in pregnancy

Pituitary: Signifor

146
Q

What is nutrition therapy for patients with Cushing’s Disease?

A

Fluid and Na restrictions.

Monitoring I&O

Daily weight 1lb=500mL of retained water

Urine Specific gravity below 1.005=fluid overload

147
Q

What is the possible surgical management of Cushing’s Disease?

A

Hypophysectomy: removal of Pituitary Gland

Adrenalectomy: removal of adrenal gland

Removal of tumors.

148
Q

What is POST/OP care for Cushing’s disease?

A 
Correct fluid&electrolyte balance BEFORE surgery.
Monitor blood Na/K+/Chloride levels.
Cardiac monitoring
Hyperglycemia controlled before surgery.
Hand washing
Side rails up
High calorie/high protein diet
Glucocorticoid preparations are given before surgery.
Adrenalectomy:
Assess for Shock q15min (hypotension/weak pulse/decrease in urine output.
Monitor VS
CVP
Serum electrolytes
149
Q

What are priority nursing interventions for a patient with Cushing’s disease?

A

Injury Prevention: Skin assessment/ protection/gentle handling

Assess skin for reddened areas/excoriation/breakdown/edema
Pad bony prominences/turn Q2hr

Avoid activities that can result in skin trauma

Soft toothbrush/electric razor

Keep skin clean&dry

excessive dryness use lotion

150
Q

What is diets for Cushing’s Disease?

A

Generous amounts of Milk/cheese/yogurt/green leafy root vegetables/

AVOID caffeine/alcohol=increase risk for GI ulcers/promote bone density loss.

Med/Surg (4 decks)

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