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Nursing 1 > Exam 3 (w5&6) > Flashcards

Exam 3 (w5&6) Flashcards

1
Q

Chest Tube: purpose

A

Drain whatever is causing lungs to be collapsed that is causing pneumothorax

Tube is placed into plural space

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2
Q

Assessments for chest tube

A

Go watch youtube video on slide 55/79 in powerpoint

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3
Q

Describe the movement of water in the chest tube

A

Inspiration = water goes up (water goes down with inspiration if patient on vent)

Expiration = water goes down; always bubbling (water goes up with expiration if patient is on vent)

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4
Q

What is happening if the water seal chamber is always bubbling

A

Water seal chamber should never constantly be bubbling; if it is, it could be a sign of an air leak, so make sure it is connected to the patient

If you clamp the tubing and the bubbling stops, the leak is coming from the patient. If you clamp the tubing and the bubbling does not stop, the leak of coming from the system

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5
Q

What part of the chest tube system is always bubbling?

A

suction control chamber (?)

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6
Q

What should the nurse do if the chest tube comes out of the patient?

A

Put sterile gauze dressing out the hole in the patients chest; only tape it down on 3 sides

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7
Q

What should the nurse do if the pluravac comes disconnected?

A

The tube coming out of the patient should be put in a bottle/container of sterile saline or water (SHOULD HAVE THIS AT BEDSIDE JUST IN CASE)

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8
Q

Sternal and rib fracture: common cause

A

MVA - most are benign and treated conservatively

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9
Q

What ribs have the highest mortality if they become fractured and why?

A

they are closest to the subclavian artery or vein - can lacerate –> bleeding

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10
Q

Sternal and rub fracture: clinical manifestations and assessment

A

Pain increases with breathing resulting in hypoventilation

crepitus

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11
Q

Sternal and rib fractures: medical and nursing management

A

Pain management
Do not decrease respiratory drive
Chest binder to decrease pain

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12
Q

What is a common complication of sternal and rub fractures?

A

Pneumonia related to hypoventilation (slow breathing because it is painful)

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13
Q

What is flail chest?

A

Blunt chest trauma

Three or more adjacent ribs are fractures in two or more sites resulting in free floating rib segments

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14
Q

Flail chest: clinical manifestations and assessment

A

Hypoxia and respiratory acidosis

Asymmetrical chest wall movement (no intercostal or diaphragm support)

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15
Q

Flail chest: medical and nursing management

A 
Ventilatory support and pain management
Rib plating (surgery; metal put in rib to put back together to decrease complications with ventilator)
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16
Q

Pulmonary contusion: patho

A

Damage to lung tissues resulting in hemorrhage and edema

Abnormal accumulation of fluid in the interstitial and intra alveolar spaces result from the inflammatory process (leaking proteins change osmotic pressure, capillaries leak fluid which then interferes with gas exchange

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17
Q

Pulmonary contusion: clinical manifestations and assessment

A

Constant ineffective cough, unable to clear secretions

Hypoxia, respiratory acidosis

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18
Q

Pulmonary contusion: medical and nursing management

A

Hydration to mobilize secretions

May need antibiotics to treat infection r/t fluid leaking into the interstitial tissue

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19
Q

How can we prevent pulmonary contusions?

A

Pulmonary hygiene / toileting to prevent

  • cough, deep breath, incentive spirometry, chest
  • physiotherapy, postural drainage (affected side up)
  • Mobilize secretions
  • Pain management
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20
Q

What is a cardiac tamponade?

A

Compression of the heart resulting from fluid or blood within the pericardial sac; compresses ventricles –> decreased CO (hypotension)

High mortality rate

painful

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21
Q

Cardiac tamponade: complications

A

Narrowing pulse pressure & hypotension (complications)

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22
Q

Cardiac tamponate nursing management

A

teach to lean forward - Might be able to breath better if they lean forward

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23
Q

cardiac tamponade: cause

A

direct assault to chest: air bag, baseball bat, etc.

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24
Q

Pneumothorax: patho

A

Parietal or visceral pleura punctures and pleural space exposed to positive atmosphere pressure

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25
Q

Pneumothorax: clinical manifestations and assessment

A

Respiratory distress varies

Tracheal alignment (tension: trachea shifts Away from affected side)

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26
Q

Pneumothorax: medical and nursing management

A

Chest tube

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27
Q

Simple pneumothorax

A

Spontaneous: rupture of bleb on surface of lung or emphysema

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28
Q

Traumatic pneumothorax

A

Air escapes from a laceration in lung itself and enters the pleural space

May occur during a procedure (lung biopsy)

Barotrauma from mechanical ventilation

May be accompanied with a hemothorax

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29
Q

Tension pneumothorax

A

Air that enters the chest can not escape
Each breath increases pressure in the chest
May need decompressed emergently with a needle
Might see trachea deviateion
Put in needle and re-expand that lug

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30
Q

What should the nurse keep in mind about ABC with pneumothorax

A

circulation trumps airway and breathing because there is bleeding occurring in chest

(IV in, ready for fluid and blood replacement before we fix that airway)

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31
Q

Subcutaneous emphysema: what?

A

Air escapes into the subcutaneous tissue

Not an emergency unless enters neck area and airway may become compromised (then patient will need trach)

Can happen with any chest trauma

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32
Q

Aspiration: patho

A

Stomach contents into lung

Ph of stomach destructive to alveoli and capillaries

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33
Q

Aspiration risk factors

A

Altered level of consciousness
Ng feeding
dysphagia

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34
Q

Aspiration: medical and nursing management

A

Compensating for absent reflexes

Assessing feeding tube placement

  • Xray placement and document where the tube exits the nose and checked every medication or feeding
  • Air auscultation & ph EBP remains inconclusive
  • Must follow institution protocol
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35
Q

Where should the nurse listen if she believes someone has aspirated?

A

Right lower lobe

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36
Q

Aspiration: prevention

A

Prevention = key

Unconscious people –> on side
Tube feed –> bed 35 degrees or higher at all times

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37
Q

COPD: emphysema

A

abnormal enlargement of the airspaces (alveoli) beyond the terminal bronchioles with destruction of the walls of the alveoli

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38
Q

COPD: chronic bronchitis

A

presence of cough and sputum production for at least 3 months in each of 2 consecutive years (chronic infection)

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39
Q

What should we keep in mind about tracheostomy suctioning?

A

only apply suction coming out; sterile; only when needed;

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40
Q

COPD: risk factors

A

Alpha1-antitrypsin deficiency (genetic link)

Smoking

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41
Q

COPD: diagnosis

A

hx physical exam PFT

FEV1 lower

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42
Q

How do you calculate pack years?

A

packs per day x years smoked = pack years

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43
Q

COPD: teaching

A

Get to quit smoking
Modify teaching around their decision to quit or not
– not going to get 70 year old to quit

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44
Q

COPD (emphysema / chronic bronchitis): clinical manifestations and assessment

A

a. Easily fatigued
b. Frequent respiratory infections
c. Use of accessory muscles
d. Orthopneic
e. Cor Pulmonale (late in disease)
f. Thin appearance
g. Wheezing
H. Pursed-lip breathing
I. Chronic cough
j. Barrel chest
k. prolonged expiratory time
l. bronchitis - increased sputum
m. nail clubbing

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45
Q

COPD: tripod position

A

Promotes getting rid of CO2

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46
Q

COPS: RR high 20s-30

A

patient is in trouble

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47
Q

COPD: management

A 
Education
Bronchidilators 1st
Inhaled corticosteroids 2nd 
Pulmonary rehabilitation
O2
Surgery
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48
Q

COPD: Bronchodilators

A 
laba (long acting beta adrenergic) 
lama (long acting muscarinic agent) 
saba (short acting beta adrenergic)
sama ( short acting muscarinic agent)
MDI
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49
Q

COPD: corticosteroids

A

inhaled or Iv

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50
Q

COPD: Roflumilast

A

?

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51
Q

Go look at slide 71

A

Tells about bronchidilators for COPD

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52
Q

COPD: IV steroids and steroids in general

A

Chronic problems –> increase risk of adrenal insufficiency, not abruptly stop

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53
Q

COPD: nutritional concerns

A

Eating can be very tiring for these individuals

Frequent, small meals that are high in protein

No carb intake because byproduct of carb is co2

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54
Q

COPD: resting energy expenditure

A

10-15%

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55
Q

COPD: physical activity

A

Simple, small goals

Minimize weight loss d/t low lung reserve

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56
Q

Asthma: patho

A

complex and characterized by recurring and variable symptom and airflow obstruction and hyper-responsiveness

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57
Q

Asthma: inflammation is key in underlying feature - how?

A

leads to recurrent episodes

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58
Q

Asthma: clinical manifestations and assessment

A

cough, chest tightness, wheezing, dyspnea

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59
Q

Asthma: prevention

A

Patients should ID triggers and avoid them

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60
Q

Asthma: continuous attack

A

wheezing not breathing well tight – status asthmaticus (corticosteroids, bronchodilators, IV zanthene such as theophylline (10-20 is correct range)

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61
Q

Function and regulation of hormones

A

Directly released into blood and go to target tissue to initiate function of that target tissue

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62
Q

hypothalamus - connection

A

The hypothalamus is the connection between the nervous system and endocrine system. It controls the pituitary system gland which secretes stimulating hormones

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63
Q

Anterior pituitary gland releases what hormones

A 
Growth hormone 
Follicle stimulating hormone 
Lutenizing hormone 
Prolactin
Andrenocorticotropic hormone 
Thyroid stimulating hormine 
Melanocyte stimulating hormone
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64
Q

Growth hormone

A

Growth Hormone releasing hormone secreted from hypothalamus to stimulate pituitary to secrete growth hormone (somatotropin) (causes pain

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65
Q

Prolactin

A

Released by anterior pituitary gland

Control breast milk secretion

66
Q

Adrenocorticotropic hormone

A

Controlled by anterior pituitary gland

adrenal stimulating

67
Q

Melanocyte stimulating hormone

A

controlled by anterior pituitary glan

skin color

68
Q

Posterior pituitary gland releases what hormones?

A
  1. Vasopressin (ADH) - when released, decrease UOP

2. Oxytocin - uterine contractions during labor

69
Q

Thyroid gland releases what hormones?

A

a. TSH (thyrotropin) = pituitary, then to thyroid to release the hormones thyroxing, triiodothyonine, calcitonin

70
Q

Thyroxine (t4)

A

released by TSH (thyrotropin) - metabolism

71
Q

Calcitonin

A

released by TSH (thyrotropin) - lowers blood calcium and phosphate by pushing calcium back into the bone when someone is hypocalcemic

72
Q

Where are the parathyroid glands?

A

Sit on thyroid

73
Q

Parathyroid hormone releases what hormone?

A

PTH - regulates serum calcium and phosphate levels

secreted when someone is hypocalcemic

74
Q

What hormones are released from adrenal cortex

A

Androgens, mineralcorticoids, glucocorticoids

75
Q

Androgens

A

Released by adrenal glands; Sex hormones (mainly male)

76
Q

Mineralcorticoids

A

Released by adrenal glands - ex. is aldosterone; regulates electrolytes and metabolism

77
Q

Glucocorticoids

A

Released by adrenal glands; example is cortisol - regulates inflammation and glucose metabolism

78
Q

What hormones are released by the adrenal medulla

A

Catecholamines (epinephrine and NE)

- fight or flight response

79
Q

Insulin

A

Hormone released by the pancreas

Facilitates glucose transport INTO the cells

80
Q

Glucagon

A

Released by pancreas
increases BG
stimulates gluconeogenesis

81
Q

Somatostatin

A

Released by pancreas

Reduced rate food is absorbed from GI tract

82
Q

Gerontological considerations: thyroid

A

Decreased metabolic rate (not as hungry, cold)

83
Q

Gerontological considerations: parathyroid

A

Decreased absorption of vitamin D leading to..

Osteoporosis

84
Q

Gerontological considerations: adrenals

A 
Decreased androgens 
Decreased glucocorticoids (decreased inflammatory response)
85
Q

Gerontological considerations: pancreas

A

Decreased insulin secretion

Decreased cell sensitivity

86
Q

Gerontological considerations: pituitary

A

Decreases TSH, ACTH, FSH, LH (stimulating hormones)

87
Q

What is the main issue with DM

A

hyperglycemia - goal is to prevent complications by controlling hyperglycemia

88
Q

Type I Diabetes

A

Onset any age
Cause: genetics, environmental, immunologic
Pancreas producing little to no insulin
Will need life-long insulin

aka ketosis, DKA

89
Q

Why are most people diagnosed with Type I diabetes

A

patient goes to hospital because they developed DKA

90
Q

Characteristics of type II diabetes: patho

A

Decrease insulin production

Decrease cell sensitivity

91
Q

Type 2 diabetes cause

A

Obesity, genetics and environmental

pancreas = tired

92
Q

type 2 diabetes management

A

Oral antidiabetic agents may help
May need insulin (does not require)
May improve with weight loss and diet
Ketosis uncommon

93
Q

Type 2 diabetes: Hyperglycemic Hyperosmolar Non Ketotic Syndrome

A

idk

94
Q

Secondary diabetes: pancreatic diseases

A

Cancer of pancreas can lead to diabetes dx

medications such as corticosteroids and estrogen containing meds can lead to DM dx

95
Q

Gestational diabetes

A

Usually 2 or 3 trimester
Due to hormones secreted by placenta that inhibit the action of insulin
Macrosomia (unusually large babies)
30-40 % of mothers may develop DM II later
All women should be screened 24-28 weeks gestation

96
Q

Impaired glucose tolerance: oral glucose tolerance

A

test value between 140 mg/dL (7.7 mmol/L) and 200 mg/dL (11 mmol/L)

97
Q

Impaired glucose tolerance: impaired fasting glucose

A

a fasting plasma glucose between 110 mg/dL (6 mmol/L) and 126 mg/dL (7 mmol/L)

98
Q

Describe what happens to glucose tolerance is someone is on corticosteroids

A

Glucose tolerance is going to be artificially elevated if someone on corticosteroids

99
Q

Pathophysiology of diabetes

A

Insulin produced by the pancreas secreted by the beta cells

Transports and metabolizes glucose for energy

Stimulates storage of glucose as glycogen in the liver and muscle cells

Signals liver cells to stop the release of glucose

Enhances storage of dietary fat in adipose tissue

Accelerates transport of amino acids into cells

Facilitates the transport of potassium into the cells

Inhibits the breakdown of stored glucose, protein, and fat

100
Q

Insulin secretion

A

Approximately 50% of the total insulin secreted daily by the pancreas is secreted under basal conditions, and the remainder is in response to meals.

The estimated secretion rate of basal insulin in the average adult (assume a weight of 70 kg) ranges from 18 to 32 units/24 hours

Minutes after eating, the serum insulin level rises, peaking in 3 to 5 minutes and returning to baseline within 2 to 3 hours

To attain glycemic control, nurses may be required to manage insulin drips based upon the secretion rate of basal insulin.

101
Q

What does the body do if BG gets too low

A

glucagon, is secreted by the alpha cells

Glucagon stimulates the liver to release stored glucose, thereby increasing the blood sugar.

102
Q

How do insulin and glucagon work together

A

insulin promotes hypoglycemia; glucagon promotes hyperglycemia. They work in tandem to maintain a constant level of glucose in the blood.

103
Q

Why do we get confused when we are hypoglycemic?

A

Brain does not store supply of glucose for us

We have to have a constant steady supply of BG because our brain does not store it for us  why we get confused when we are hypoglycemic

104
Q

Liver role in diabetes

A

The liver assists with glucose control by storing glucose in the form of glycogen.

As the level of glucose in the blood begins to drop, the liver produces glucose through the breakdown of glycogen (glycogenolysis)

After 8 to 12 hours without food, the liver forms glucose from the breakdown of noncarbohydrate substances, including amino acids (gluconeogenesis)

105
Q

Clinical manifestations of diabetes

A 
Polyuria (most common w type 1)
Polydipsia (most common w type 1)
Polyphagia (most common w type 1)
Dehydration
Weight loss
Fatigue and weakness
Numbness and tingling hands and feet (type 2)
Vision changes (type 2)
Dry skin
Wounds that are slow to heal
Recurrent infections (particlarily yeast)
106
Q

Complications of hyperglycemia

A

Impairs immune function (decreases white blood cell function)

promotes inflammation

increases blood viscosity (increase risk for blood clot)

favors the growth of yeast organisms

associated with changes in the blood vessel walls

  • resulting in increased risk for infection
  • microvascular and macrovascular complications (eyes –> blind, kidney failure)
  • foot ulcers (neuropathy, cant feel)
107
Q

Criteria for diagnosis of DM

A

A1c of 6.5% or greateror

Symptoms of diabetes plus casual plasma glucose concentration equal to or greater than 200 mg/dL (11.1 mmol/L). “Casual” is defined as any time of day without regard to time since last meal. The classic symptoms of diabetes include polyuria, polydipsia, and unexplained weight loss.or

Fasting plasma glucose greater than or equal to 126 mg/dL (7.0 mmol/L). Fasting is defined as no caloric intake for at least 8 hours.or

Two-hour postload glucose equal to or greater than 200 mg/dL (11.1 mmol/L) during an oral glucose tolerance test. The test should be performed as described by the World Health Organization, using a glucose load containing the equivalent of 75 g anhydrous glucose dissolved in water.

108
Q

Gerontological considerations for DM

A

Almost 27% of people over 65 years of age have diabetes

Older patients with diabetes are likely to have coexisting illnesses

the goals of diabetes treatment may need to be altered when caring for elderly patients
- Quality not quantity

Focus is on quality of life

109
Q

DM medical management

A 
Nutrition
Exercise
Monitoring
Medication
Education
110
Q

Stress and BG

A

The stress response results in hyperglycemia because it activates the sympathetic nervous system. The ensuing increase in catecholamines, systemically derived from the adrenal gland or released locally at the level of the liver, increases hepatic glycogenolysis and the release of large quantities of glucose into the bloodstream while inhibiting the release of insulin. Thus, all patients who are stressed are at risk for hyperglycemia.

111
Q

BG and eating / nutrition

A

It is important to assess the patient’s blood sugar BEFORE meals when insulin coverage is ordered since the patient’s blood sugars will rise after ingesting food.

Promote eating patterns that help improve glucose, blood pressure, and lipid control.

Tailor therapy to each person’s individual cultural and behavioral needs.

Emphasize the pleasure of eating while changing eating
habits.

Provide practical tools for healthy eating.

Caloric requirements

Carbohydrates

Protein

112
Q

Alcohol and BG

A

Alcohol is absorbed before other nutrients
Large amounts can be converted to fats, increasing the risk for DKA
Hypoglycemia and drunk can mask each other

113
Q

What should the nurse do if she cannot tell if someone is drunk or hypoglycemic

A

Treat patient like they are hypoglycemic until she knows for certain

114
Q

Misleading food labels

A

Foods labeled “sugarless” or “sugar-free” may still provide calories equal to those of the equivalent sugar-containing products if they are made with nutritive sweeteners

Foods labeled “dietetic” still may contain significant amounts of sugar or fat

Read the labels of “health foods”—especially snacks—often contain carbohydrates, such as honey, brown sugar, and corn syrup

115
Q

Exercise benefits and education for DM

A

Exercise uses glucose, caution for hypoglycemia (teach about ss)

Should not get implement a big exercise regime after being diagnosed

116
Q

SS hypoglycemia

A

Tachycardia, agitation, confusion

117
Q

Monitoring glucose and keytones

A 
Self Monitoring of Glucose
Continuous monitoring (phone apps)
Measuring Glycated Hemoglobin
Urine Glucose
Ketone testing
118
Q

Insulin therapy: rapid

A

Meal coverage

Onset = 15 minutes

119
Q

insulin therapy: short

A

Regular is the only insulin that can be given IV (regular insulin is a form of short acting)

used for meal coverage

120
Q

slide 36/50

A

brush up on insulin types

121
Q

Insulin sites

A

Rotate sites but keep in same area
SQ is fastest absorbed because high vol. of vessels
Do not massage sites

122
Q

Complications from insulin therapy: Local vs systemic allergy

A 
Local = usually NBD 
Systemic = not allergic to insulin by allergic to the preservatives in it
123
Q

Insulin lipodystrophy

A

no clue

124
Q

Fasting hyperglycemia: Dawn phenomenon

A

someone who wakes w hyperglycemia

Intervention = give insulin later at night, no snacking before bed

125
Q

Fasting hyperglycemia: Somogyi effect

A

morning hyperglycemia because hyperglycemic episode in middle of the night (at 2 or 3 am BG is really low, body responds then you become hyperglycemia.

Intervention = giving long acting or insulin coverage earlier in evening, snack b4 bed

126
Q

Dawn phenomenon and somogyi effect require what?

A

middle of night BG checks

127
Q

Fast hypoglycemia: insulin waning

A

no idea

128
Q

Non-insulin anti diabetic agents: sulfonylureas

A

Sulfonylureas (glipazides)

Stimulate insulin release from pancreas, can cause hypoglycemia

Effective for type II only

These will sulfur antibiotics together increase risk of hypoglycemia

129
Q

Non Insulin Anti Diabetic Agents: Biguanides

A 
Metformin
Nephrotoxic
Can cause lactic acidosis
Does NOT cause hypoglycemia 
Discontinue in response to needing contrast dye for diagnostic testing
130
Q 
Non Insulin Anti Diabetic Agents: 
GLP-1 Agonists
SGLT-2 Inhibitors
Thiazolidinediones
Alpha-Glucosidase Inhibitors
Non sulfonylurea Insulin Secretagogues
A

Did not talk about these not sure if i need to know

131
Q

What does someone require if they have a pancreas transplant

A

Lifelong immunosuppressants = at risk for infection

132
Q

Diabetes: nursing management

A

Develop a Diabetic Teaching Plan

  • Assess readiness to learn
  • Determine teaching methods

Implementing the teaching plan

  • Teaching experienced patients
  • Teaching patients self care

Providing Continuing Care

133
Q

Acute complications of DM: hypoglycemia

A

we can over correct hyperglycemia and cause this. We need to know ss and hypoglycemia

134
Q

Acute Complications of DM: DKA

A

Causes metabolic acidosis

    • body can not use sugar and uses fat instead (?)
    • goal = gets BG down
    • losing a lot of fluid –> replace (fluids, IV, and hyperkalemia treatment)
135
Q

Acute Complications: Hyperglycemic Hyperosmolar Nonketotic Syndrome (HHNS)

A

Type II

Hyperglycemia that is not spilling ketones

136
Q

Long term complications of DM

A 
Macrovascular
Microvascular
Diabetic Neuropathy
 - peripheral and autonomic neuropathies 
- complications of legs and feets

Renal failure, blindness

137
Q

What is an example of autonomic neuropathy? And what is a treatment

A

Gastroparesis - stomach does not mTing

Metaclopromide can promote gastric mTing

138
Q

Adverse side effect of metaclopromide

A

Extrapyramidal symptoms

139
Q

Gigantism

A

Pituitary tumor
during puberty, our epiphysis on end of bones close NORMALLY - here, they stay open and grow LONGER

Growth hormone issues
Exessive secretion
Occurs pre-puberity

140
Q

Acromegaly

A

Pituitary tumor
Occurs post puberty

during puberty, our epiphysis on end of bones close NORMALLY - here, they stay open (?) and grow WIDER

141
Q

Diabetes insipidus

A

Pituitary disorder

Not enough ADH (large UOP, hypernatremia, dehydrated)

142
Q

Diabetes insipidus treatment

A

vasopressin (should see decrease in UOP), Na restriction, high fluids

143
Q

SIADH

A

Pituitary disorder

Syndrome of Inappropriate ADH (decrease UOP, edema, hyponatremia)

144
Q

SIADH intervention

A

Declamyacin – increase UOP

Increase NA and strict fluid restriction

145
Q

Most common surgery for when someone has pituitary tumor? What are important considerations before and after this surgery?

A

Most common surgery is hypophysectomy (incision in mouth above teeth, clip tumor, put face back to tumor) – MUST KEEP CLEAN TO DECREASE INCISION or patient could get meningitis

After surgery - no oral care bc they will break surgical scar (more opportunity for bacteria) and CSF can leak potential

146
Q

Hypothyriodism: what? treatment? complication?

A

Thyroid disorder - cold, fat, slow
Treatment: thyroid replacement
Complication: Myedema –> progress to coma

147
Q

Priapism

A

Hypothyroid as infant (mental delays / mentally challenged)

148
Q

Hyperthyroidism: what, treatment, goal, complication

A

Thyroid disorder - hot, fast, skinny
Treatment: PTU – suppress thyroid hormone until they get to surgery (will most likely need it)

Goal: get TSH down

Complication: thyroid storm – hypertensive, tachycardic, hot

149
Q

Considerations for Synthroid

A

can cause cardiac arrhythmia’s (monitor HR, esp. geriatric); most common A fib
- do not administer when someone having MI (increase metabolic rate, release of catecholamines)

150
Q

Hyperparathyroidism

A

Parathyroid Disorders - causes hypercalcemia

151
Q

Hypoparathyroidism

A

Parathyroid Disorders

causes hypocalcemia

152
Q

Things to consider with thyroidectomy

A

If we take out thyroid gland, parathyroids are disrupted because parathyroid sits on top of it, so after surgery asses pt for hypocalcemia (?)

Assess neck incision and back (blood and gravity)
Assess tracheal is midline (blood can move it)

153
Q

Pheochromocytoma

A

adrenal disorder

tumor of adrenal glands, benign  take it out

154
Q

PHEOCHROMOCYTOMA: considerations b4 surgery

A
  • before surgery, get HR and BP under control (Beta blocker, anti htn meds)
155
Q

PHEOCHROMOCYTOMA: s/s

A
  • causes excessive catecholamine release, HTN, headache , tachycardia
156
Q

PHEOCHROMOCYTOMA: post op considerations

A
  • in post-op , going to have significant HYPOTENSION problem (fluid replacement, vasopressors)
157
Q

Addison’s disease

A

Adrenal disorder
Hypoadrenalism
Not enough cortisol
Cause – daily steroid

158
Q

Addison’s disease: s/s

A

hypoglycemia, hypotension, hyperkalemia

159
Q

Addison’s disease: treatment

A

IV cortocosteroids

160
Q

Cushing Disease

Primary Aldosteronism

A

Adrenal disorders

Go look at these in the endocrine work document

Nursing 1 (6 decks)

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