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Nurs 726 Med Surg 2 > Test 4: Neuro, Onc and Endocrine > Flashcards

Test 4: Neuro, Onc and Endocrine Flashcards

1
Q

What type of meningitis is more severe, and what causes it?

A

Bacterial-Neisseria meningitidis which causes meningococcal meningitis

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2
Q

What are the causes of viral meningitis?

A

Mumps
Measles
Herpes
Arboviruses

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3
Q

How is viral meningitis prevented?

A

MMR Vaccine

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4
Q

What is the vaccine schedule for MMR vaccination?

A

1st vaccine at 12-15 months and 2nd at 4-6 years of age

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5
Q

How can bacterial meningitis be prevented?

A

Hib vaccine given at 2 months, 4 months, (6 months) and 12 to 15 months of age

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6
Q

What is the hallmark symptom of bacterial meningitis?

A

Excruciating constant headache

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7
Q

What are the subjective signs of bacterial meningitis?

A

Excruciating, constant headache (HALLMARK)
Nuchal Rigidity (stiff neck)
Photophobia
Altered mental status (patient is deteriorating)

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8
Q

What are the objective symptoms of bacterial meningitis?

A

Pallor, cold extremities with high fever, signs of shock (early s/s)
Fever, Chills
N/V
Stomach/joint/muscle pain
LOC (confusion, disorientation, lethargy, difficulty swallowing, coma)
+ Kernig’s Sign
+ Brudzinski’s Sign
May not be very obvious due to nucal rigidity
Hyperactive deep tendon reflexes
Tachycardia
Tachypnea
Seizures
Red Macular Rash
Restlessness, irritability

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9
Q

What are Kernigs and Brudzinki’s signs?

A

Kernig’s: Knee cannot fully extend when patient is supine and hip is flexed 90 degrees

Brudzinki’s Neck sign: passive flexion of the neck causes flexion of both legs and thighs

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10
Q

What is the ‘glass test’ in regards to meningitis?

A

Macular red rash from meningitis will not blanche when glass is pressed against it

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11
Q

Meningitis, when exhibited in older adults, immunocompromised patients, or patients on antibiotics may not exhibit what symptom?

A

A fever

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12
Q

What labs should you collect on a patient with meningitis?

A

Urine
Throat
Nose
Blood Culture and Sensitivity

**Basically you are trying to identify the possible infectious bacteria asap to be able to administer antibiotic

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13
Q

What is the most definitive diagnostics for meningitis?

A

A lumber puncture for CSF analysis

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14
Q

What is the alternative diagnostic measure if there is a delay in a lumbar puncture?

A

Blood Culture and Sensitivity

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15
Q

What is a lumbar puncture for CSF analyzed for?

A

Cell Count
Differential Cell Count
Glucose concentrations
Culture/sensitivity/gram stain

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16
Q

How many tubes of CSF will be collected during the lumbar puncture?

A

3-5

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17
Q

If the meningitis is bacterial, what results will we see on a CSF?

A

Cloudy
Increased protein, WBC, CSF Pressure
Decreased glucose

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18
Q

If the meningitis is viral, what results will we see on a CSF?

A

Clear
Increased protein, CSF Pressure
Normal Glucose

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19
Q

Inability to move the eyes to the left (6th cranial nerve defect) can indicate?

A

The development of hydrocephalus

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20
Q

In older patients with meningitis, what should you also monitor for?

A

Pneumonia

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21
Q

Meningitis Medications:
Antibiotic:

A

Ceftriaxone or Cefotaxime

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22
Q

Meningitis Medications:
Anticonvulsant:

A

Phenytoin

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23
Q

Meningitis Medications:
Antipyretic:

A

Acetaminophen

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24
Q

Meningitis Medications:
Analgesic:

A

Non-opioid because you do not want to alter mental status

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25
Q

What is a normal ICP pressure?

A

5-15mmHg

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26
Q

A hallmark of a transient ischemic attack is that if there are any deficits/symptoms, they typically resolve within?

A

24 hours

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27
Q

What are the causes of a hemorrhagic stroke?

A

HTN
Aneurysm
AV malformation
head injury
subarachnoid hemorrhage

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28
Q

What are the three causes of ischemic strokes?

A

Thrombotic
Embolic
Infarct and pneumbra

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29
Q

What is the difference between an embolic cause and a thrombotic cause of an ischemic stroke?

A

Thrombotic: atherosclerotic plaque in cerebral artery
Embolic: Embolus travels from a distant location to the cerebral artery

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30
Q

The most common reason for an embolic cause of ischemic stroke is?

A

A-Fib

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31
Q

What is the goal of stroke management?

A

To save the ischemic penumbra before it becomes an infarction

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32
Q

What are the risk factors for ischemic stroke?

A

A-Fib
Smoking
Oral Contraceptives
HTN
Sleep Apnea
Carotid Stenosis
Hyperlipidemia
Substance/cocaine use
Obesity

A Snake Originally Had Super Creepy Old Slimy Hands

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33
Q

What is the most common cause of a hemorrhagic stroke?

A

HTN/cocaine use

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34
Q

Cranial Nerves:
1
2
3
4
5
6
7
8
9
10
11
12

A

1) Olfactory (Smell)
2) Optic
3) Oculomotor (Ability to move or blink)
4) Trochlear (ability to move eyes up/down and back and forth
5) Trigeminal (sensation in face/cheeks, taste)
6) Abducens (ability to move your eyes)
7) Facial Nerve (facial expressions and taste)
8) Auditory/vestibular (Sense of hearing/balance)
9) Glossopharyngeal nerve (Ability to taste and swallow)
10) Vagus nerve (Digestion and heart rate)
11) Accessory nerve (or spinal accessory nerve (
Shoulder and neck muscle movement)
12) Hypoglossal nerve: Ability to move your tongue.

Only Owls Often Taste Tacos And Fresh Guacamole Very Aloofly, Huh?

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35
Q

What is the treatment for ischemic stroke?

A

Initiate ASA or antiplatelet to prevent stroke
-DAT (dual antiplatelet therapy-aspirin and clopidogrel)
Txt Between 3 and 4.5 hours from onset of symptoms
Control of blood glucose
Decrease HTN (MAP goals)
Control of lipids

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36
Q

In cerebral autoregulation, hypoxia and hypercapnia cause?

A

Vasodilation

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37
Q

In cerebral autoregulation, hypocapnia causes?

A

Vasoconstriction

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38
Q

What is the formula for cerebral perfusion pressure?

A

CPP=MAP-ICP

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39
Q

What is a normal cerebral perfusion pressure?

A

Normal CPP: 60-80 mmHg

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40
Q

What MAP do we want to see to insure cerebral perfusion?

A

MAP > 60 mmHg to maintain perfusion
Normal is between 70 and 110

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41
Q

What are the common s/sx of a stroke?

A

Common s/s include:
Facial weakness, droop, or numbness
Arm/leg weakness, drift, or numbness
Slurred speech confusion , or trouble
understanding others
Sudden change in vision
Dizziness, trouble walking, loss or balance or coordination
Sudden severe HA with no known cause (hemorrhagic; worst headache ever)

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42
Q

How is the NIH Stroke scale scored?

A

Range of 0 (no deficits) to 42 (significant deficits)
Lower the number the better the outcome
< 4 = highly likely to have good clinical outcomes (minor stroke)
21-42 = severe stroke

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43
Q

A rapid bedside assessment for a stroke includes?

A

Cognitive changes (LOC and commands)
Drift of eyes in direction of stroke
Motor Changes (facial palsy, arm and leg drift, ataxia via heel-shin)
Sensory changes (Numbness, tingling)
Language/aphasia/Dysarthria
Neglect (Innattention)

Cats Literally Don’t Make Sense Normally

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44
Q

What is Dysarthria?

A

Tongue, mouth and lips no longer functional to produce speech
Impaired articulation, slurred speech

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45
Q

What is hemianopia?

A

Hemianopia– loss of vision in either R or L sides of both eyes
Ensure to ask patient’s to read or ask what they see

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46
Q

What is agnosia?

A

Agnosia– loss of ability to recognize objects, persons, sounds, shapes

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47
Q

What is apraxia?

A

Apraxia– unable to perform tasks or movements when asked (command understood)

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48
Q

What is hemiparesis?

A

Hemiparesis– weakness on one side of body

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49
Q

What is hemiplegia?

A

Hemiplegia– total paralysis of one side of body (arm, trunk, leg)

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50
Q

What is Broca’s aphasia?

A

Expressive (Broca’s)– comprehension, but unable to express thoughts coherently
They know it’s cup but they can’t say its a cup

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51
Q

What is Wenicke’s aphasia?

A

Receptive (Wernicke’s)– inability to understand spoke or written language

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52
Q

Right-sided or frontal lobe strokes may exhibit what types of symptoms?

A

Impulsivity, impaired judgment, impaired attention span

(Might get out of bed when told not to, or drink out of the urinal)

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53
Q

What labs should you run for a stroke patient?

A

CBC
BMP
Platelets
PT/INR, aPTT
Glucose (to rule out hypoglycemia)

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54
Q

What are the different types of diagnostics for strokes?

A

CT without contrast***
MRI (Superior to CT for ischemic lesions within first 24 hours)
Carotid Duplex/Vascular Study
Cerebral angiogram
Lumbar Puncture
Myelogram

*You need to determine whether the suspected stroke is not hemorrhagic in nature, Add contrast AFTER without

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55
Q

If a stroke patient suddenly has an increase in blood pressure, what is the nursing priority?

A

Notify the provider
If BP>185mmHg call Rapid Response

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56
Q

To what O2 saturation should you keep a stroke patient above?

A

94%

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57
Q

If one side of a stroke patient is affected, what are the nursing actions?

A

Dress affected side first
Do not use affected arm for BP readings, to move up in bed, etc.

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58
Q

What are the preventative medications for strokes?
Ischemic:
Hemorrhagic:

A

Ischemic: antiplatelets (ASA, clopidogrel)
Hemorrhagic: HTN management

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59
Q

What are the medications for acute ischemic stroke treatment?

A

Fibrinolytic therapy: tPA (tissue plasminogen activator)
Newer: Tenecteplase TNK (recombinant fibrinolytic agent)
Anticoagulants: Heparin, warfarin
Anticonvulsants: Phenytoin
Meds to ↓ ICP: Mannitol, loop diuretics

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60
Q

How is tPA (tissue plasminogen activator) administered?

What about TNK?

A

tPA: given within 3-4.5 hours of onset of symptoms
Bolused and given over 60 minutes; weight-based

TNK: Given as a one-time bolus; weight-based

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61
Q

What type of stroke should tPA NOT be used?

A

Hemorrhagic

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62
Q

What levels do we want to see prealbumin at for stroke patients?

A

Prealbumin 16-30 mg/dL

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63
Q

What does FAST stand for?

A

Rapid recognition and response to early warning signs (FAST)
Facial droop, Arm weakness, Speech difficulty, Time is critical

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64
Q

What is the negative feedback loop for thyroid hormones?

A

Hypothalamus signals anterior pituitary to release TSH (thyroid stimulating hormone) which then stimulates the thyroid to produce T3 and T4. T4 is then converted to T3 in the peripheral tissue. If too much T3, the hypothalamus is signaled to stop sending messages to the anterior pituitary.

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65
Q

What is Thyrocalcitonin?

A

Inhibits calcium reabsorption from bone

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66
Q

What are the normal levels of thyroid stimulating hormone?

A

~4 (0.5 to 5.0 mIU/L)

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67
Q

What is the difference between a primary and secondary alterations in the thyroid hormone system?

A

Primary Alterations: Disease of thyroid
Secondary: Disease of Pituitary

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68
Q

What types of medication can cause hypothyroidism?

A

Lithium
Amiodarone
Sulfonylureas

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69
Q

What are the laboratory trends for hypothyroidism?

A

↑ TSH (primary)
↓ or normal TSH (secondary)
↓ T3- Triiodothyronine
↓ T4- Thyroxine

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70
Q

What would be the results of a thyroid scan– radioisotope uptake?

A

Determines whether or not the thyroid is working
Uptake will be low in hypo and high in hyperthyroid

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71
Q

Serum Cholesterol levels will be high in what type of thyroid disorder?

A

Hypothyroidism because they are not able to use fatty acids properly

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72
Q

Patients with hypothyroidism will have to do what for the rest of their lives?

A

Lifelong thyroid hormone replacement– T4
Normally in form of Levothyroxine

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73
Q

What is the hallmark disease for hypothyroidism?

A

Hashimotos

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74
Q

How long will it take levothyroxine to reach therapeutic levels?

A

Will take approx. 4 weeks to achieve steady state blood level of medication

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75
Q

What is the hallmark disease for hyperthyroidism?

A

Grave’s disease

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76
Q

Besides Graves Disease, what other disorders could cause hyperthyroidism?

A

Goiter
Hyperfunctioning Thyroid Nodules
Thyroiditis
Postpartum (inflammation)
Excessive Exogenous Thyroid Hormone Replacement
Excessive Intake of Dietary Iodine

77
Q

What are the laboratory trends for someone with hyperthyroidism?

A

↓ TSH
↑ T3 levels
↑ T4 levels

78
Q

What would you see on an ECG of a patient with hyperthyroidism?

A

ECG– tachycardia, atrial fibrillation, dysrhythmias

79
Q

What is the nursing priority when caring for a patient with hyperthyroidism?

A

Report temperature ↑ of ≥ 1° F (possible impending thyroid crisis)

80
Q

What are some of the nursing actions for a patient with hyperthoidism?

A

Pace activity with rest periods
↓ stimulation (avoid palpation)
Monitor ECG for dysrhythmias-There should be a telemetry order for these patients. If there is not, you as the nurse need to ask for one
↑ HOB to ↓ eye pressure
Keep environment cool

81
Q

What are the risks for a Thyroidectomy surgery?

A

Normally used as a treatment for hyperthyroidism, it presents a risk for laryngeal nerve damage and parathyroid damage.

82
Q

What is a complication of damage to the parathyroid gland?

A

The parathyroid gland is responsible for calcium balance

83
Q

Besides a Thyroidectomy, what other treatment options are there for hyperthyroidism?

A

Radioactive Iodine (RAI) treatment
Anti-thyroid medications
Ablation surgery

84
Q

Before a patient can have any type of thyroid surgery, what needs to occur?

A

euthyroid state required before

85
Q

What is the nutritional guidelines for patients with hyperthyroidism?

A

↑ Calories (high protein)
↑ Vitamin supplements
Calcium supplements to combat bone demineralization
Small, frequent meals
Avoid excessive iodine intake

86
Q

What is the nursing guidance for patients undergoing Radioactive Iodine therapy for hyperthyroidism?

A

Avoid pregnant women and children for approx. 7 days s/p tx
Keep > 3 ft away from others
Avoid use of same bathroom for 2 weeks; flush toilet twice
Rinse washing machine before washing other family members’ clothes
Sleep alone for up to 7 days
Avoid public transportation for 7 days
Can trigger radiation monitors at airports for up to 3 mos s/p tx
↑ fluid intake and urinate frequently

87
Q

What medication is the synthetic T4 replacement?

A

Levothyroxine (Synthroid)

88
Q

What is the nursing guidance for patients taking levothyroxine?

A

Small difference between generic and brand name
Maintain the same Rx inpatient/discharge
Start with small dose (112mcg) and increase slowly
Take 1 hr before meals or 3 hours after meals
Do not take within 4 hours of antacids, iron, calcium, PPIs

89
Q

What two drugs can Levothyroxine affect?

A

Can increase the effects of Warfarin, and digoxin

90
Q

What are the two thioamide drugs used to treat hyperthyroidism?

A

Methimazole (Tapazole)
Propylthiouracil (PTU)

91
Q

What does Methimazole do?

A

For hyperthyroidism– inhibits production of thyroid hormone, and is often given before radioactive iodine treatment

92
Q

What are the nursing considerations for methimazole?

A

Fewer side effects than PTU
Taken 1x/day (Better adherence)
Itching, rash, hives, joint pain, change in taste
Agranulocytosis– Report fever, sore throat, jaundice, bruising
Pancreatitis
Avoid during early pregnancy

93
Q

What does Propylthiouracil do?

A

For hyperthyroidism– inhibits production of thyroid hormone AND blocks conversion of T4 to T3 in periphery
Often drug of choice for thyrotoxicosis

94
Q

What are the nursing considerations for Propylthiouracil?

A

Taken 3-4x/day
Itching, rash, hives, joint pain, change in taste
Agranulocytosis– Report fever, sore throat, jaundice, bruising
Liver damage, vasculitis
Okay in pregnancy

95
Q

How can propanol help to treat hyperthyroidism?

A

Control symptoms of adrenergic activation (HR, BP, tremors)
May help prevent peripheral conversion of T4 to T3

96
Q

What is Thyrotoxicosis (Thyroid Storm)?

A

Increased release of thyroid hormones
Precipitated by sudden worsening of hyperthyroid symptoms like surgery or severe illness or caused by digoxin toxicity, DKA, trauma, infection

97
Q

What are the symptoms of thyrotoxicosis?

A

Profound hyperthermia (40.5°C, 105°F)
Severe tachycardia, dysrhythmias, HTN → hypotension & ↓ CO, HF
Restlessness, agitation, tremors, unconsciousness, coma

98
Q

What are the priority nursing interventions for thyrotoxicosis?

A

place on monitor, O2, fluids, high doses of iodine and propylthiouracil, propranolol
Immediate endocrine consult

99
Q

What is a Myxedema Coma?

A

Severe deficiency in thyroid hormone
Precipitated by abrupt cessation in exogenous hormone, severe illness

100
Q

What are the symptoms of a Myxedema Coma?

A

Profound hypotension, bradycardia, ↓ CO, hypothermia, hypoglycemia

101
Q

What are the nursing priority interventions for myxedema coma?

A

IV thyroid hormone (T4)
O2
Temp control
Cardiac monitoring
Fluids

102
Q

What do these symptoms indicate??
Hypocalcemia, Chvostek’s Sign, Trousseau’s Sign, tingling of fingers, toes, or mouth, tetany, seizures

A

Damage to the parathyroid gland

103
Q

What are the nursing priority interventions for a damaged parathyroid gland?

A

Institute seizure precautions, prepare for calcium replacement, constipation prevention, fall & injury risk precautions

104
Q

What are the symptoms of Hypoparathyroidism?

A

hypocalcemia
hyperphosphatemia
paresthesia, muscle cramps, fatigue

105
Q

What can cause hypoparathyroidism?

A

neck surgery radiation, autoimmune, hereditary, hypomagnesemia

106
Q

What are the nursing interventions for hypoparathyroidism?

A

calcium replacement, Vit D replacement, magnesium replacement, stool softeners

107
Q

Why are calcium supplements and stool softeners often given together?

A

Calcium supplements can often cause constipation, hence the stool softeners

108
Q

What are the symptoms of Hyperparathyroidism?

A

hypercalcemia
hypophosphatemia
osteoporosis
renal calculi
bone pain
nausea
anorexia
abdominal pain

“Disease of bones, groans and moans”

109
Q

What can cause hyperparathyroidism?

A

parathyroid hyperplasia, CKD, calcium and vit D deficiency

110
Q

What are the nursing interventions for hyperparathyroidism?

A

hydration
diuretics (to help with fluid volume retention)
parathyroidectomy
fall & injury precautions

111
Q

What is one of the main functions of the posterior pituitary gland?

A

secretion of Antidiuretic Hormone (ADH)/Vasopressin
Controls serum osmolarity & water balance via effecting water reabsorption in distal renal tubules

112
Q

What is diabetes insipidus?

A

ADH deficiency or inability of kidneys to respond to ADH
Excretion of large amounts of dilute urine

113
Q

What are the two different origins of diabetes insipidus?

A

Neurogenic: Head injury/TBI, Tumor, Surgery or irradiation near pituitary, meningitis

Nephrogenic: Lithium, Renal Damage

114
Q

What are some of the signs and symptoms of diabetes insipidus?

A

Hypovolemia
Excessive water excretion & dehydration
Dilute urine
Polyuria (5-30 L/day)
Nocturia
Polydipsia (2-20 L/day)
Acute weight loss
S/s of dehydration
S/s of hypernatremia
S/s of hyperkalemia

115
Q

What are these symptoms a sign of?
Hypotension, tachycardia, weak pulses, thirst, dry mucous membranes, decreased skin turgor

A

Dehydration

116
Q

What are these symptoms of?
Muscle irritability and twitching, ↑ DTRs, restlessness progressing to confusion

A

Hypernatremia

117
Q

What are these symptoms of?
Peaked T waves, dysrhythmias, diarrhea, metabolic acidosis

A

Hyperkalemia

118
Q

What trends would you see in the serum chemistry for diabetes insipidus?

A

↑ Sodium (> 145 mEq/L)
↑ Potassium (> 5.0 mEq/L)
↑ Osmolality (> 295 mOsm/kg)
↓ ADH

119
Q

What trends would you see in the urine chemistry for diabetes insipidus?

A

↓ Sodium
↓ Potassium
↓ Osmolality (↓ specific gravity, < 1.005)

120
Q

What is the Water Deprivation Test?

A

+ for DI if polyuria persists in presence of dehydration (kidneys cannot concentrate urine)
If DI is present, there will be no concentration of urine

121
Q

What are the two diagnostic tests for diabetes insipidus?

A

Water Deprivation Test
Vasopressin Challenge Test

122
Q

What is the Vasopressin Challenge Test?

A

+ for DI if urine specific gravity ↑ after administration of vasopressin

123
Q

Diabetes Insipidus is also known as ________ insufficiency.

A

ADH insufficiency

124
Q

What are signs of water intoxication?

A

Headache
Confusion

125
Q

Why should someone with DI avoid caffeine?

A

Because caffeine exhibits a diuretic effect

126
Q

What is Desmopressin?

A

A synthetic ADH that can be given to patients with DI

127
Q

Which form of desmopressin is stronger? IV or PO

A

The IV (parental) form of desmopressin is 10x stronger than the oral form and the dosage must be reduced

128
Q

What medications would be expected on the MAR for a patient with diabetes insipidous?

A

Desmopressin
Thiazide Diuretic
Insulin/Kayexelate

129
Q

Why would you administer a thiazide diuretic to a patient with DI?

A

To facilitate ADH action and potassium wasting

130
Q

What are the complications from DI?

A

Dehydration
Circulatory Collapse
Seizures

131
Q

What is a disorder of ADH excess?

A

SIADH
Syndrome of Inappropriate Antidiuretic Hormone

132
Q

What normally inhibits ADH production and secretion?

A

Decreases in plasma osmolarity

133
Q

What things can cause SIADH?

A

Tumors
Increased intrathoracic pressure (mechanical ventilation)
Head injury
Stroke
Medications

134
Q

What are the types of medications that can cause SIADH?

A

Chemotherapeutic Agents
TCAs
SSRIs
Opioids
Fluoroquinolone antibiotics

135
Q

What are the early SSAs for SIADH?

A

Hypervolemia
Fluid Retention
Concentrated urine
Oliguria
Anorexia
Headache
Muscle cramps
Acute weight gain
S/S of fluid volume overload
S/S of hyponatermia
S/S of hypokalemia

136
Q

What are the late SSAs for SIADH?

A

Decreased deep tendon reflexes
N/V
Seizures
Diarrhea
Change in personality

137
Q

What are the signs/symptoms of hyponatremia?

A

Muscle weakness
Decreased DTR
Confusion
Lethargy
Seizures

138
Q

What are the signs/symptoms of hypokalemia?

A

Flat or inverted T-waves
Dysrythmias
Irregular Pulse
Paresthesia
Constipation
Metabolic Acidosis

139
Q

What trends would you see in the serum chemistry for SIADH?

A

↓ Sodium (< 135 mEq/L)
↓ Potassium (< 3.5 mEq/L)
↓ Osmolality (< 275 mOsm/kg)
↑ ADH

140
Q

What trends would you see in the urine chemistry for SIADH?

A

↑ Sodium
↑ Potassium
↑ Osmolality (↑ specific gravity)

141
Q

What are the first-do priorities for SIADH?

A

Fluid restriction <1 L a day
Daily weights
s/s of heart failure from fluid volume overload
s/s of pulmonary edema
Monitor for altered mental status
Cardiac Dysrythmias
Flush enteral tubes w/NS instead of water

142
Q

What medications are used to treat SIADH?

A

Loop Diuretics (furosemide)
Vasopressin Antagonists
Hypertonic 3% NaCL administered through a central line

143
Q

What are the complications of SIADH?

A

Water intoxication
Cerebral edema
Cheyne-Stokes Ventilation Pattern
Pulmonary edema
Severe Hyponatremia
Seizures
Coma
Central pontine myelinolysis

144
Q

What is a glucocorticoid?

A

Known more as Cortisol, it diverts amino acids from the metabolism from building into supplying energy to deal with stress

145
Q

Increased glucocorticoid ______ gluconeogenesis and __________ peripheral glucose utilization.

A

Increased glucocorticoid increases gluconeogenesis and decreases peripheral glucose utilization.

146
Q

What occurs to protein breakdown when the levels of glucocorticoids are increased?

A

Protein synthesis is suppressed which can lead to a loss in muscle mass from the extremities

147
Q

In patients with increased glucocorticoids, why do we see a pot belly, moon face, and buffalo hump?

A

Glucocorticoids stimulated lipolysis and fat redistribution

148
Q

What effect do glucocorticoids have on bone?

A

It increases osteoclast activity and decreases osteoblast activity

149
Q

What does mineralocorticoid do?

A

Also known as Aldosterone, it regulated Na+ and K+ balance by promoting reabsorption of sodium and renal excretion of potassium

150
Q

What effect does mineralocorticoid Aldosterone have on blood volume and pressure?

A

It increases blood volume and increases blood pressure by decreasing urine output

151
Q

Why is Addison’s disease also known as ‘double d’?

A

Decreased cortisol
Decreased aldosterone

The disease of ‘not enough’

152
Q

What causes Addison’s disease?

A

Hypofunction of the adrenal gland normally autoimmune in origin

153
Q

What are the endogenous risk factors for Addison’s Disease?

A

Auto-Immune mediated destruction of the adrenal glands
Deficiency in ACTH secretion
Adrenal Infarction
Infection
Metastatic Cancer
Bilateral adrenalectomy
Adrenal Hemorrhage

154
Q

What are the exogenous risk factors for Addison’s Disease?

A

Abrupt discontinuation of chronic pharmacological steroids that can cause adrenal shock

155
Q

What are some of the stand out SSAs of Addison’s disease?

A

Hyperpigmentation
Thinning of public and axillary hair
Hypoglycemia
Hypotension
Hyperkalemia
Hyponatremia

156
Q

What trend will you see in the lab values for sodium, potassium, calcium and glucose in a patient with Addison’s Disease?

A

Decreased sodium and glucose
Increased potassium and calcium

157
Q

What are the diagnostic tests for Addison’s Disease?

A

Adernocorticotropic hormone test
Stimulation test
ECG
CT
MRI

158
Q

What are the nutritional needs of a patient with Addison’s Disease?

A

Increased calories, carbohydrates, and sodium

Decreased potassium

159
Q

What will you administer to a patient with Addison’s disease at the lowest level first?

A

Exogenous glucocorticoid

You administer it slowly so that the pendulum does not swing in the other direction

160
Q

What is an “Addisonian Crisis” or adrenal crisis?

A

A life-threatening event in which the need for cortisol and aldosterone is greater than the body’s supply and normally results from an abrupt discontinuation of pharmacological steroids

161
Q

What are the signs and symptoms of an Addisonian Crisis?

A

Severe hypotension
Hyponatremia
Hyperkalemia
Dehydration->circulatory shock
Hypoglycemia

162
Q

What is the treatment of an Addisonian Crisis?

A

Fast-Acting IV glucocorticoid replacement
(May require a mineralocorticoid as well)
Dextrose IV
Loop Durietics/kayexalate/dextrose+insulin (Potassium wasting drugs)
Seizure precautions

163
Q

What is Cushing’s Syndrome?

A

Hyperfunction of the adrenal gland that causes adrenocortical excess resulting in increased glucocorticoids and mineralocorticoids

164
Q

What are the endogenous risk factors for Cushing’s syndrome?

A

ACTH-secreting pituitary tumor
Adrenal Tumors
ACTH-secreting tumors of lungs or pancreas

165
Q

What are the exogenous risk factors for Cushing’s syndrome?

A

High-dose, chronic administration of pharmacological steroids (for autoimmune diseases, asthma, cancer tx, etc) for more than 2 weeks

166
Q

What are some of the physical SSAs of Cushings syndrome?

A

Changes in fat distribution:
Moon face
Buffalo hump
Abdominal adiposity
Muscle wasting
Ecchymosis
Petechiae
Weight gain
Hirsutism

167
Q

What are some of the metabolic SSAs of Cushing’s syndrome?

A

Hyperglycemia
Glucosuria
Increased appetite
Peptic ulcers

168
Q

What are some of the physiological symptoms of Cushing’s syndrome?

A

Osteoporosis
Irritability
HTN
Arrythmias
Cardiac Hypertrophy
Infection from excess glucose

169
Q

What trend in the lab values for sodium, potassium, calcium and glucose would you see in Cushing’s Syndrome?

A

Increased sodium and glucose
Decreased potassium and calcium

170
Q

What are some of the diagnostics to test for Cushing’s Syndrome?

A

Blood and Salivary cortisol levels
24hr urine for free cortisol level
Dexamethasone suppression test
ECG
CT
MRI

171
Q

What is the dexamethasone suppression test for Cushing’s syndrome?

A

Administration of dexamethasone in the evening at bedtime, then collect a 24 hr urine.

If the patient does not have Cushing’s, then the cortisol levels will not go up.

If cortisol excretion continues despite administration of dexamethasone, Cushing’s is present

172
Q

What should you be monitoring in a patient with Cushing’s syndrome?

A

VS
Neuro
S/S of infection
GI Bleed (Dark, tary stools)
Blood glucose
S/S of fluid overload

173
Q

Because GI bleeds can be common due to peptic ulcer formation in Cushing’s syndrome, what medication should you administer?

A

H2 receptor Blocker

174
Q

What are the nutritional recommendations for Cushing’s Syndrome>

A

Low sodium
Low Fat
High potassium
High Calcium

ADA diet if hyperglycemic

175
Q

What are the potential complications of Cushing’s syndrome?

A

Severe:
Hypernatremia
Hypokalemia
Hypocalcemia
Seizures (secondary to hypokalemia)

176
Q

Why are patient’s with Cushing’s sydrome at an increased risk for peptic ulcer development?

A

Increased cortisol=loss of gastric mucosal protection

177
Q

Addison’s Patients will require lifelong?

A

Lifelong physiological glucocorticoid replacement

178
Q

Both Addison’s and Cushing’s patient should wear?

A

A medical alert bracelet

179
Q

What is a pheochromocytoma?

A

A tumor in the adrenal medulla that produces excess catecholamines (epi, norepi)

180
Q

What are the signs and symptoms of a pheochromocytoma?

A

Tachycardia
HTN
HA
Angina/palpitations/dysrythmias
Increased temperature, diaphoresis, heat intolerance
N/V

181
Q

If a patient has uncontrolled hypertension, even after the administration of anti-hypertensive medication, what could be suspected?

A

A pheochromocytoma

182
Q

What should you monitor for a patient with pheochromocytoma?

A

VS
Neuro
Development of HTN crisis

183
Q

What can you expect to administer to a patient with a pheochromocytoma?

A

Antihypertensives
Alpha Adreneric Blockers
Beta Blockers

184
Q

What is the treatment for a pheochromocytoma?

A

Adrenalectomy

185
Q

What are the adverse effects of chemotherapy?

A

NAUSEA*
N: Non-productive cough/fever/tachypnea/pneumonia
A: Anemia
U: Uricemia
S: Stomatitis
E: Elimination problems (anorexia, nausea, vomiting, constipation)
A: Alopecia

186
Q

Can a patient undergoing internal radiation have visitors?

A

Yes for under 30 minutes and they must stay 6 feet away

187
Q

What is Superior Vena Cava Syndrome?

A

MEDICAL EMERGENCY
Compression of the superior vena cava results in swelling from the shoulders up, and the patient turns bright red and cannot breathe

188
Q

How is superior vena cava syndrome treated?

A

Radiation, Steroids and Chemo

189
Q
A

Nurs 726 Med Surg 2 (6 decks)

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