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4th Semester Nursing > MedSurg2 - Exam 3 > Flashcards

MedSurg2 - Exam 3 Flashcards

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1
Q

Why would you worry if a head injury patient suddenly developed a runny nose?

A

Because it could be a CSF leak

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2
Q

Why might you see eye bruising in a head trauma patient?

A

It’s a sign of a skull fracture (to the orbital bone). You’d want to send them to CT/X-ray.

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3
Q

What action would you want to avoid with a patient who has a Basilar fracture?

A

Insertion of an NG tube

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4
Q

What is Battle’s sign? What is it indicative of?

A

Bruising behind the ear. Indicative of a skull fracture (basilar fracture?)

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5
Q

What are the two types of Focal Brain injuries?

A

Contusion and Coup Contrecoup

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6
Q

Describe a contusion. Is it visible or invisible? Microscopic or macroscopic?

A

A contusion is like a bruise of the brain.
Localized and deep.
Visible on a CT scan
Occurs at a macroscopic level.

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7
Q

Describe a coup contrecoup injury.

A

It’s a contusion that happens on both front and back (or side to side) of the brain.

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8
Q

What are two Diffuse Brain Injuries?

A

Concussion and Diffuse Axonal Injury

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9
Q

Describe a concussion. Is it macroscopic or microscopic? Visible or invisible?

A

A concussion is microscopic damage to the neurons of the brain.
Invisible on imagery
Widespread and diffuse
Disruptive to the physiology rather than the anatomy.

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10
Q

Describe a Diffuse Axonal Injury

A 
Damage to axons that occurs from rotational acceleration. 
Axons stretch, shear and twist 
—> swelling and damage to axons
—> disruption to neuronal functioning. 
(Very severe concussion)
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11
Q

Which brain injury is the #1 cause of morbidity? What happens to this patient?

A

Diffuse Axonal Injury - many patients don’t survive
Electrical signals can’t transmit effectively
Mood disturbances in the long run.

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12
Q

True or False - ALL brain injury types can lead to:
A) disruption in functioning of neurons
B) increased ICP

A

True to both

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13
Q

3 layers of meninges, from outer to inner

A

Dura Mater
Arachnoid Mater
Pita Mater

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14
Q

Epidural Hematoma - cause? Problems? Speed of progression?

A

Typically caused by rupture of the meningeal artery (above the dura).

Arterial bleed = fast with rapid growth (pressure against brain increases quickly).

Can go from lucid to unconscious in a few hours - very fast.

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15
Q

Subdural Hematoma - typical cause? Speed? Different levels?

A
  • Rupture of the bridging vein (between the two hemispheres) in the subdural space
  • Venous bleed means it’s slower to develop (s/s will be headaches and confusion)

-Levels:
Acute: takes 24-48h to develop symptoms
Subacute: takes 2-14 days to develop symptoms
Chronic: takes weeks to months to develop symptoms.

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16
Q

What are the components involved in the regulation of ICP?

A

Cerebrospinal Fluid (CSF)
Cerebral Blood Flow (CBF)
Brain Tissue

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17
Q

Why is it important to keep the head and neck aligned with a patient who’s at risk of increased ICP? What’s the best HOB position?

A

If there’s an obstruction/kink in the venous outflow, it can create a buildup of ICP, especially in heart failure patients.

Place HOB at 30-45 degrees.

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18
Q

What range of MAP is needed to regulate intracranial pressure effectively?

A

50-150mmHg

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19
Q

If you have a MAP below 50, what is the effect on the brain tissue?

A

Cerebral ischemia d/t decreased cerebral blood flow

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20
Q

If you have a MAP over 150, what is the effect on the brain tissue?

A

Increased ICP due to excess CBF

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21
Q

What is the effect of Acidosis on the vasculature of the brain?

A

Vasodilation and increased blood flow

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22
Q

What is the effect of Increased CO2 on the vasculature of the brain?

A

Vasodilation and increased blood flow

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23
Q

What is the effect of hypoxemia on the vasculature of the brain?

A

Increased blood flow and vasodilation

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24
Q

Why might you hyperventilate a patient with increased ICP?

A

To blow off excess CO2 (decrease vasodilation in brain)

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25
Q

Why do you have to be concerned about coughing, sneezing, vomiting and ascites in patients with increased ICP? What do we do about this?

A

Because increases in intra-thoracic and intra-abdominal pressure will increase ICP.

We’ll make sure to provide bowel meds, cough suppressants, anti-emetics, paracentesis (ascites)

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26
Q

If the body can’t compensate for increased ICP, what is the order of decompensated actions?

A
  • Compression of Ventricles (CSF)
  • Compression of Blood Vessels
  • Decreased blood flow d/t blood vessel compression (tissue death and subsequent ICP increases)
  • Swelling and compression of brainstem and respiratory center
  • Increase in CO2, vasodilation and more blood flow/brain volume.
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27
Q

When does the risk for herniation occur? What directions can the brain herniate?

A

When tiny changes in volume leads to big changes in pressure.
Once the brain can’t compensate, brain goes from Poor compensatory reserve to Deranged compensatory reserve.

Brain will herniate Inwards, Outwards or Downwards

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28
Q

What is the most sensitive and earliest indicator of increased ICP?

A

Behavioral changes / Deteriorating LOC

Ex: restlessness, irritability, decreased attention, slowed speech, lethargy.

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29
Q

What are non-LOC indicators of increased ICP?

A 
Severe Headache, Seizures, N/V
Abnormal pupils
Altered/irregular breathing pattern
Nuchal Rigidity
Posturing (decorticate/decerebrate)
Cushing’s Triad
Halo’s sign
Deteriorating GCS
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30
Q

What is Cushing’s Triad?

A

Severe HTN with widening pulse pressure
Bradycardia
Irregular respirations

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31
Q

What is Halo’s sign?

A

Tests for CSF leakage in pt’s blood (From head). Dried blood with a “halo” around it.

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32
Q

What are the levels of Glasgow Coma Scale?

A

Mild: 13-15
Moderate: 9-12
Severe: 3-8
Vegetative: less than 3

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33
Q

Range for normal ICP? At what level does it get treated?

A

5-15 mmHg

Gets treated at 20mmHg

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34
Q

What is a ventriculostomy (intraventricular catheter)? What are the pros and cons?

A

-Probe through the skull and into the ventricles (not the brain tissue)
-Measures ventricular pressure
-Allows for therapeutic drainage of CSF
-Allows for delivery of drugs into intraventricular space
Most accurate and Most common.

Cons: HUGE infection risk, risk of bleeding and overdrainage.

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35
Q

What is a fiber optic catheter for? What are the pros and cons?

A

Catheter that’s placed in the brain tissue (not as deep as a ventriculostomy).

Provides monitoring only. (Second most accurate method) Lower risk of brain infection or bleed.

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36
Q

What is a subarachnoid bolt/screw? Pros/cons?

A

Screws in just below the arachnoid layer (not the brain tissue).

Easier insertion, faster measurement, lower risk of bleed or infection.

Monitoring only, less accuracy.
Risk of obstruction.
Can be done in the ED.

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37
Q

What is an epidural catheter? Pros/cons?

A

Placed between the dura and the skull to measure ICP.

Least invasive but least accurate method.

Can be done in the ED.

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38
Q

What are the indications for ICP monitoring?

A

1) A moderate head injury (9-12 GCS) and some reason the patient can’t be adequately assessed (sedated) OR they have an abnormal CT scan.
2) . A severe head injury (less than 8 GCS) with an abnormal CT
3) A severe head injury (less than 8 GCS) and over 40 y/o OR abnormal posturing.

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39
Q

What two parts of the body do you want to be certain to align with a pt with a head injury?

A

Neck and Hips

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40
Q

What is the most effective way to administer Mannitol to someone with increased ICP?

A

IV boluses (not a slow drip)

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41
Q

What electrolyte is important to know about when administering Mannitol?

A

Sodium - you cannot give mannitol if sodium is over 145

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42
Q

What medication is often given alongside Mannitol?

A

Lasix

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43
Q

Which IV fluid acts like Mannitol?

A

Hypertonic Saline (3% NS)

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44
Q

How would you decide whether to give 3% NS or Isotonic fluids (NS, LR) to a head injury patient?

A

If there is cerebral edema and increased ICP, give 3% NS

If brain ischemia is happening due to decreased volume (or if you need to maintain adequate volume), give NS or LR

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45
Q

In what situation would you give Hypotonic fluids to a patient with a brain injury?

A

You wouldn’t - EVER

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46
Q

What does the P-wave represent?

A

Firing of the SA node in the R atrium

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47
Q

What does the flat line after the p-wave (in an ECG) represent?

A

The contraction of both atria

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48
Q

What does the Q-wave (in an ECG) represent?

A

The electrical impulse traveling through the bundle of His and the L&R bundle branches (center of the ventricles)

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49
Q

What does the portion from Q to R (in an ECG) represent?

A

The impulse moving around the outside of the ventricles via the Purkjinke fibers

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50
Q

What does the portion between R and S (in an ECG) represent?

A

The impulse traveling across and through the ventricles from the Purjinke fibers

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51
Q

What does the flat part after the QRS complex (in an ECG) represent?

A

Contraction of the left and right ventricles

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52
Q

What does the T-wave represent (in an ECG)

A

Repolarization of the ventricles

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53
Q

What does the flat part after the T wave (in an ECG) represent?

A

Resting polarized period before the SA node fires again.

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54
Q

What is the distribution of electrolytes at polarization?

A

K is inside the cell, Na and C are outside

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55
Q

Depolarization and Repolarization - which is contraction and which is relaxation?

A

Depolarization is contraction

Repolarization is relaxation

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56
Q

How long should the p-wave last?

This is the time it takes for _____

A

0.06-0.12s

… firing of the SA note to depolarization & atrial contraction

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57
Q

The PR interval should take ______ to _____ seconds

This is the time it takes for __________

It’s measured from P to _______

A

0.12-0.20s

…the impulse to spread through the atria, the AV node, the bundle of His and the bundle branches to the Purjinke fibers

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58
Q

The QRS complex should last _____

This represents….

A

Less than 0.12s

…the time from depolarization of the ventricles to ventricular contraction

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59
Q

The ST segment should last _____

What shape is it?

This represents….

A

0.12s

It should be flat (isoelectric)

It represents the time between ventricular depolarization and repolarization (refractory period)

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60
Q

The T wave should last _____

It represents….

A

0.16s

…repolarization of the ventricles

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61
Q

The QT interval should last _______

It’s measured from_____

It represents_____

A

0.34-0.43s

measured from the start of Q to the end of T

Represents the TOTAL time for depolarization and repolarization of the ventricles.

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62
Q

Which interval (in an ECG) is most likely to be affected by antipsychotics, antiepileptics, antibiotics, etc?

What two medications combined with antibiotics will increase this risk further?

A

QT interval

Warfarin and Methadone combined with antibiotics increase the risk

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63
Q

A thick fuzzy isoelectric line on an ECG likely has what problem?

A

Problem with the ground lead

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64
Q

An ECG that is all over the place with shaky artifacts likely has what problem?

A

Poor electrode contact with the skin (dry them, shave, change electrodes)

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65
Q

How many seconds does each “tab” at the top of an ECG strip represent?

How do you use this to determine heart rate?

A

3 seconds.

Count the beats in two of them and multiply by ten

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66
Q

What are the dimensions of a large box in an ECG (height in millivolts, length in seconds)?

A
  1. 5 millivolt high

0. 2 seconds long

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67
Q

What are the dimensions of a small box in an ECG (height in millivolts, length in seconds)?

A
  1. 04s long

0. 1 millivolts high

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68
Q

How to treat symptomatic sinus bradycardia (less than 60bpm)

(Medication and non-medication)

A

IV atropine (increases heart rate)

Transcutaneous pacing or permanent pacemaker

69
Q

How to treat symptomatic tachycardia? (What would you see on the ECG in addition to a HR over 100bpm)?

A

QT interval would be shortened (less than 0.34)

Would treat the cause if it’s transient (anxiety, pain, etc)

If it’s a long-term problem, MD would probably prescribe beta-blockers or calcium channel blockers.

70
Q

What is the first step when you notice a patient has an abnormal ECG.

A

Assess the patient (maybe an electrode fell off - don’t assume)

71
Q

How do the ABC’s change when a patient is unresponsive?

A

Order of operations is CAB in an unresponsive patient.

Responsive patient is still ABC

72
Q

How would you treat Premature Atrial Contractions if the patient is symptomatic?

(How would you recognize them on an ECG?)

A

1st, treat the cause (might be drinking too much caffeine)

If necessary, Beta Blockers can help control heart rate.

On an ECG, a Premature Atrial Contraction will show up as an extra beat with no relaxation between T and P.

73
Q

How would you treat Paraoxysmal Superventricular Tachycardia (PSVT) or SVT if the patient is symptomatic?

How would you recognize this on an ECG?

A

1 step is Carotid massage or Valsalva maneuver (but don’t do this if the patient is over 65 b/c of the risk of plaque breaking off)

On ECG,
Rate 150-220
P-wave will likely be hidden and PR interval (if there is one) might be shorter (less than 0.12)

74
Q

Above what heart rate (tachycardic) will decreased cardiac output occur?

A

180bpm

75
Q

How would you prevent thrombus formation in someone with Atrial Flutter or Atrial Fibrillation? How does this relate to synchronized cardioversion?

A

Warfarin

If someone has been in Afib or Aflutter for more than 48h, they must be on warfarin (or other anticoagulant) for 3-4 weeks before synchronized cardioversion can happen.

76
Q

How would you treat Afib or Aflutter (aside from anti-coagulation)?

(Medication and non-medication)

A

Beta Blockers (propranolol)
Calcium Channel Blockers (Verapamil or Diltiazem)
(Goal is to slow AV conduction and control ventricular response)

Synchronized conversion is also an option

77
Q

How would you differentiate Aflutter from Afib on an ECG?

A

Aflutter has sawtooth waves (atrial BPM of 200-350) whereas Afib is more of a wiggly line (atrial BPM of 350-500).

Neither will have distinguishable p-waves - only QRS complexes.

78
Q

What is the AV block poem?

A

If the R is far from P, then you have a first degree

Longer, longer, longer, drop! Then you have a Wenkebach

If some Ps do not get through, then you have a Mobitz II.

If Ps and Qs do not agree, then you have a third degree

79
Q

What is the basic problem in all types of AV block?

A

The electrical impulse is not effectively making it through the AV node

80
Q

How do you identify a 1st degree AV block? How do you treat it?

A

PR interval longer than 0.20 seconds.

No treatment necessary.

81
Q

How do you identify a second degree AV block type I (Wenkebach)? How do you treat it?

A

When the PR interval gets longer and longer until a QRS complex is skipped.

This is usually asymptomatic - we just watch it.

82
Q

How do you identify a second degree AV block type II (Mobitz)? How do you treat it?

A

PR intervals constant
QRS complexes are skipped randomly

This is somewhat dangerous. Treatment - possibly a temporary pacemaker.

83
Q

How do you identify a third degree AV block? What is the treatment?

A

No relationship between p-waves and Q-waves.

This pt needs a pacemaker (temporary one will be placed until a permanent one is possible).

84
Q

How would you recognize PVCs on an ECG? What are the possible variations?

A

Regular rhythm with randomly occurring PVCs.
-the PVC itself will have a wide QRS complex and QT interval will be distorted.

Variations:

  • Ventricular Bigeminy (every other beat is a PVC)
  • Ventricular Trigeminy (every 3rd beat is a PVC)
  • Multifocal: PVCs look different from one another (different foci/origins)
  • Unifocal: all PVCs look the same (single origin)
85
Q

How do you classify a rhythm with more than 3 PVCs in a row?

A

This is ventricular tachycardia.

86
Q

What is the treatment for a patient with PVCs?

A

Sodium Channel Blockers (Procainamide, Lidocaine)

Potassium Channel Blockers (Amiodarone)

87
Q

How do Sodium Channel Blockers help with PVCs?

A

They slow conduction and increase the duration of the AP. Prevent ventricular depolarization and suppress ectopic activity.

88
Q

How do potassium channel blockers help with PVCs?

A

The prolong the refractory period, slowing the heart rate and reducing automaticity. This prevents ventricular contractions.

89
Q

How would you identify VTach on an ECG? What is the treatment (pulse vs no pulse)?

A

Looks like a fairly symmetrical continued series of V’s (or 4+ PVCs in a row). 150-250 bpm.

With a pulse: synchronized conversion
Without a pulse: Call a code. Start CPR. Then, defibrillate.

90
Q

How would you identify Torsades de Pointes on an ECG? What’s the most common cause?

What’s the treatment?

A

VTach with multiple focal points: looks like a twisty, zig-zag line.

Most common cause: drugs that prolong the QT interval (methadone, antidysrhythmic drugs).

Treatment:
Treat underlying cause (TAPER meds)
IV Magnesium (to relax heart)
Synchronized cardioversion

91
Q

VFib - how to recognize? Treatment?

A

No rhythm/rate. Ventricles just quivering. No Cardiac output.

Call code, start CPR, defibrillate.

92
Q

How does the defibrillator work?

A

The shock passing through the heart depolarizes the myocardial cells. The hope is that the SA node will pick back up as a pacemaker after repolarization occurs.

93
Q

What are the two types of defibrillators?

A

Monophasic: full dose of energy in one direction. (360 joules)

Biphasic: bidirectional charge (100-200 joules each direction)

94
Q

What are the two heart rhythms you can defibrillate?

A

Pulseless Ventricular Tachycardia

Ventricular Fibrillation

95
Q

What are the four heart rhythms you can do synchronized cardioversion with?

A

V.Tach with a pulse
Afib
Aflutter
PSVT (if unresponsive to therapy)

96
Q

How does synchronized cardioversion work?

A

Lower energy shock that’s delivered on the R wave of the QRS complex.

Use sedation if non-emergent.

97
Q

What rhythms might you use a pacemaker for?

A

Bradyarrythmias
Tachyarrythmias
AV block

98
Q

What should we know about MRIs and pacemakers?

A

It’s best if this patient can avoid MRIs.

99
Q

What should we know about MRIs and implantable defibrillators?

A

This patient absolutely cannot ever go in an MRI.

100
Q

How can a pacemaker help with VTach?

A

Pacemakers can be programmed to give a stimulus to the ventricle to end VTach.

101
Q

What education is necessary for patients with implantable cardioverter defibrillators?

A
  • No driving until cleared by HCP
  • Caregiver must learn CPR
  • No sex until after incision has healed.
  • Call HCP if ICD fires once
  • Call 911 if ICD fires more than once
  • Call 911 if you feel sick/off
102
Q

Difference between Chronic Stable Angina and Acute Coronary Syndrome?

A

Chronic Stable Angina goes away with rest and feels the same every time. It happens with increased workload of the heart and temporarily decreased O2 supply/perfusion.

Acute Coronary Syndrome: can either be Unstable Angina, an NSTEMI or a STEMI. Worry when a patient has any chest pain that occurs for the first time, or is different than the norm in any way.

103
Q

At what percentage of vessel blockage does Atherosclerosis lead to symptoms?

A

50% or more

104
Q

Quick summary of the patho behind atherosclerosis?

A
  • Damage to endothelium
  • Platelets attach
  • Macrophages get deposited in the endothelium, consume lipids and become fat-filled-foam cells
  • Collagen cap forms over top.
105
Q

When does plaque in the veins become a complicated lesion?

A

When damage to the collagen cap occurs and has the potential to form a thrombus.

106
Q

Why might 80 year-olds have a higher survival rate from MIs than 30 year-olds?

A

collateral circulation (angiogenesis of new pathways) forms when there is long-term decreased blood flow due to blockages.

107
Q

What’s the patho behind the chest pain of Chronic Stable Angina?

A

Myocardial cells at work become hypoxic and have to use anaerobic metabolism

Lactic acid forms and irritates the nerve cells, which leads to pain messages.

Stopping activity leads to the dissipation of lactic acid and the relief of pain as perfusion can keep up with demand.

108
Q

What do PQRST stand for?

A 
Precipitating factor
Quality
Radiation
Severity 
Timing
109
Q

What are some non-chest locations of chest pain for a patient with Angina or an MI?

A 
Down both arms
Left Shoulder
Epigastric
Btw Shoulder blades
Jaw
Neck
110
Q

How long are Nitro SL tabs good for?

A

6m-1y (if not kept in a warm place)

111
Q

What drugs would you use for antiplatelet therapy (to keep a thrombus from forming)?

A

Aspirin

Clopidogrel

112
Q

Aside from Nitro and antiplatelet meds, what other sorts of meds might be used to treat Chronic Stable Angina?

A

ACEs/ARBs
Beta-blockers
Calcium Channel Blockers
Lipid-lowering drugs

113
Q

What is a Percutaneous Coronary Intervention (PCI) and when would you use it?

A

Guidewire is fed through the femoral or radial artery to the heart. Dye is used to locate the blockage.
Balloon inflated multiple times to open artery/compress plaque.
Stent may or may not be left in place.

May be used for CSA or ACS.

114
Q

What is the nurse looking for after a patient has come back from a PCI?

A

The existence of any chest pain (PCI should have taken care of this)

Bleeding at the placement site (artery!)

115
Q

Basics of a Coronary Artery Bypass Graft (CABG)? When would one be used?

A

Sternotomy
Cardiopulmonary bypass while heart is stopped and an artery or vein is grafted from aorta to the coronary artery (distal to the occlusion)

Might use it for a STEMI or NSTEMI, but PCI is more likely.

116
Q

What will the nurse want to be careful about when her patient comes back from a CABG?

A

Monitoring the airway (patient will be intubated for a few hours)

Ensuring sufficient circulation (fluids to maintain volume)

Managing pain (pain = SNS stimulation)

117
Q

Acute Coronary Syndrome consists of Unstable Angina, Non-STEMIs and STEMIs. Which of these is an emergency?

A

All three of these!

Take an ambulance to the hospital for all.

118
Q

Cardiovascular manifestations of MIs? (Early and late)

A

Early: Increased BP and increased HR (as the body is trying to push blood past the clot)

Late: Drop in both BP (and HR, eventually)

119
Q

If a patient has ischemia (from a NSTEMI or Unstable Angina), what would you see on the ECG?

A

T-wave inversion or ST-segment depression

This might happen with USA, but also might not

120
Q

If a patient has a heart injury from a STEMI, what would you see on the ECG?

A

ST segment elevation

121
Q

If a patient has necrosis from a STEMI, what would you see on an ECG?

A

An abnormal Q-wave (This is an ominous sign)

122
Q

What would Troponin results be (+/-) for USA, NSTEMI and STEMI?

How long will it take for Troponin to be released? What cardiac marker might be helpful to check in the meantime?

A

(-) for USA
(+) for STEMI and NSTEMI

It takes about 5 hours for Troponin to begin to elevate, and 20h for it to peak.

Myoglobin will peak before 5 hours and is a helpful marker to check (though not specific to heart muscle). CKMB ratio, too.

123
Q

How could a Coronary Angiography be helpful in diagnosing Unstable Angina, a STEMI or NSTEMI?

A

In addition to opening vessels, it is used as a diagnostic tool to visualize the blockage (uses dye).

124
Q

How does management of an NSTEMI differ from management of a STEMI?

A

NSTEMI:
Meds: Nitro, antiplatelet, anticoagulation.
PCI or CABG could happen, but they would wait 12-72h to do it.

STEMI:
-Oxygen (always indicated with a STEMI), Nitro, Antiplatelet and Anticoagulation (maybe morphine) AND:

-Priority PCI/reperfusion therapy within 90 minutes (if in facility) or 120m (if needing a transfer)
OR - Thrombolytic therapy (only if PCI is not available) w/in 30m.

125
Q

Difference between an anticoagulant and a thrombolytic?

A

Anticoagulants decrease active clotting but don’t break up clots.

Thrombolytics break down fibrin in order to lose the clot.

126
Q

How soon do thrombolytics need to be given in order to work?

A

Recommendation is to give within 30minutes of arrival to the ED (if PCI therapy is not available)

Must give within 3-6 hours to be effective.

127
Q

Aspirin therapy can be continued indefinitely after an MI, but Plavix/Clopidogrel cannot - how long will Clopidogrel therapy last?

A

14d-1y

128
Q

How long with Anticoagulant therapy last for after an MI?

A

48h-8d.

129
Q

5 characteristics of cancer cells

A 
Don’t stop dividing
Don’t stay within boundaries of tissue
Don’t stick together
Don’t specialize (won’t do the job of the cell)
Develop their own blood supply
130
Q

Brief description of the staging of cancer?

A

Stage I: Limited to tissue of origin
Stage II: Limited local spread
Stage III: Extensive local and regional spread
Stage IV: metastasis to distant tissues

131
Q

TNM classification - what’s this all about?

A

Simple classification for the size of the tumor (0-4), the number of lymph nodes involved (0-3), and how many organs the cancer has metastasized to (0-4).

132
Q

What are breast cancer screening guidelines and how does the ACS differ from USPSTF?

A

USPSTF: Screen every other year from 50-74.

ACS thinks you should start screening EVERY year starting at a younger age (at 45), and that at 55, you should screen every other year (for forever).

133
Q

What are the cervical cancer screening guidelines and how does the USPSTF differ from ACS?

A

USPSTF and ACS have the same recommendations.

21-29, Pap smear every 3 years

30-65 same as above, OR, you can add an HPV test and have it done every 5 years.

134
Q

What are the colorectal cancer screening guidelines and how does USPSTF differ from ACS?

A

USPSTF: Screening from 55-75 (different frequencies for different tests)

ACS: 45-75

135
Q

What are the screening guidelines for Prostate cancer and how does ACS differ from the USPSTF?

A

Prostate cancer screenings no longer recommended routinely (individual choice)

(Both agencies say this)

136
Q

What are the three types of stool tests (for colon cancer screening) and how often should they be done?

A

Fecal Immunochemical test: sample from 1BM to lab, every year

Hi-Sensitivity Guaiac-based FOBT: sample from 3BMs to lab, every year

Multi-target Stool DNA: whole BM to lab, Q3y

137
Q

What are the dietary restrictions for FOBT testing

A 
Raw turnips
Radishes
Broccoli
Horseradish
Red Meat
138
Q

What are the medication restrictions for FOBT testing?

A

7 days before test, no:
Aspirin
Anti-inflammatories
Vitamin C

(If pt must be on aspirin, they can’t take this type of test)

139
Q

What are the types of visual screenings for colon cancer and how often are they necessary?

A

Colonoscopy: every 10y (best). Probe w/ camera, both colon and rectum.

CT colonography: every 5y. Still needs bowel prep.

Flexible sigmoidoscopy: every 5 years. Only needs enemas.

140
Q

Difference between Cell-Cycle Specific chemo and Cell-Cycle Non-Specific chemo?

A

Cell-cycle Specific chemo attacks the cell at a particular point in the cell cycle (mitosis, replication, etc)

Cell-cycle non-specific chemo attacks at all/any phases of the cell cycle.

141
Q

What factors can have an effect on a cancer’s response to chemo?

A

Mitotic rate of the cancer (higher the rate = better response)
Tumor size (smaller tumor = better response)
Location of tumor (bone cancer and cancer in cavities especially hard)
Resistance of the tumor to chemo (can be inherent or can develop)

142
Q

Possible treatments for Mucositis/Stomatitis from chemo?

A

Magic Mouthwash (lidocaine)
Salt Water rinses
Baking soda rinses

Soft-bristle brush and soft-foods
(No alcohol-based rinses)

143
Q

Why does chemo make you vomit?

What’s the recommended timing for anti-emetic treatment?

A

It triggers the CTZ (Chemotherapy Trigger Zone) and releases serotonin and dopamine (which also trigger the CTZ).

Anti-emetic (Zofran or Reglan) should be given before chemo (30m?) during and after.

144
Q

How to manage diarrhea related to chemo? (Why does it occur?)

A

Low-fiber diet.

Occurs because of high mitotic rate of cells in gut. Intestines can’t absorb properly.

145
Q

How to manage anorexia from chemo? (Why does it occur?)

A

Small, high-protein, high-calorie meals.
Food diary.

Chemo is an appetite suppressant. (Plus the N/V/D effects)

146
Q

Why does fatigue occur with chemo?

A

Accumulation of metabolites from cell breakdown.

Anemia

147
Q

What level of platelets is risky in thrombocytopenia?

A

Under 20k.

148
Q

How often are gloves good for when you’re handling chemo?

A

Only 30m. Make sure you double-glove (unless they’re chemo-specific).

149
Q

T/F - Linens of chemo patients are considered biohazards

A

True

150
Q

Why might extravasion occur?

A

If the chemo punctures the vein, the fluid can enter the SQ and subdermal tissue.

Both an irritant and a vessicant (causes tissue death)

151
Q

How to avoid extravasion when placing IV site?

A

Flush IV quickly with 30ml saline (3 flushes). If edema occurs, your vein isnt’ intact.

152
Q

Order of operations when you notice signs of extravasion?

A
  1. Stop IV
  2. Disconnect IV from device
  3. Aspirate residual chemo drug from IV site
  4. Remove line from pt
  5. Assess site
  6. Notify MD
  7. Give Antidote (Ice pack? Elevate? Warm pack? Check protocol).
153
Q

MOA of radiation?

A

DNA damage to cancer cells, that is passed on as cells divide (new cells have dysfunctional DNA).

154
Q

Describe wet and dry desquamation.

A

Both are inflammatory reactions that occur in response to radiation.

Dry desquamation: dry, flaky, itchy skin

Wet desquamation: occurs in high-friction areas (typically a cumulative effect). Redness, pain and serous drainage.

155
Q

Care of radiation-damaged skin - basics?

A 
No chemicals
Protect from sun 
Loose clothing
Avoid ice or heat to site
Use a moisture barrier/cream
Keep clean and dry
156
Q

What is brachytherapy? Is there a radiation risk to people nearby?

A

Internal radiation - placed either via a tube or radioactive seeds.

No radiation risk for the general public, but avoid prolonged contact with infants and pregnant women.

157
Q

What is interleuken therapy? What are SEs?

A

A type of biological response modifier.

Pt is given interleukens, which activate parts of the immune system (T cells, NK cells, macrophages).

SEs: Flu-like symptoms (tired, n/v, anorexia, headaches)

158
Q

What is interferon therapy?

A

A type of biological response modifier.

Slow or stop division of cells.
Stimulate NK cells, T cells and macrophages.
Make cancer cells more vulnerable to attack by body’s immune system.

159
Q

What do you call it when you get a hemapoetic stem cell transplant from a donor? What about from yourself?

What is this treatment for? What do you need to be cautious of in this patient?

A

From donor: Allogenic
From self: Autologous

Treatment is to re-establish the body’s blood cell production (transplant goes to bone marrow).
This pit will be severely immunocompromised - be careful of infection.

160
Q

Pathophysiology behind myasthenia gravis?

A

Autoimmune condition where antibodies block ACh receptors, preventing the transmission of ACh in neuromuscular junctions (especially in facial areas - swallowing and breathing muscles).

Chronic condition characterized by exacerbations and remissions, with muscle weakness occurring after periods of activity and as the day progresses.

161
Q

Which gland is theorized to be responsible for MG? How?

A

It’s thought that the thymus gives incorrect instructions to developing T cells, leading to ACh antibody production.

(MG patients often have thymus gland hypertrophy and thymic tumors)

162
Q

What muscles are commonly weakened with MG?

A 
Eyelids (ptosis: drooping eyelids)
Chewing
Swallowing
Speaking 
Breathing
163
Q

What triggers MG symptoms? If a myasthenic crisis were to be triggered, what would you expect to see?

A

Triggers: Physical or emotional stressors, infection

Myasthenic crisis: Dysphagia, weakness, incontinence, respiratory muscle weakness (biggest risk - decreased RR and possible respiratory failure).

164
Q

What is a Tensilon test and what is it used for? What’s the antidote (and why would you give it)?

A

A short-acting AChE is given: if the symptoms of MG go away, then it can indicate that a patient has MG (or that they’re in a myasthenic crisis).

Antidote: Atropine
Give for too much PNS activation (salivation, bradycardia and increased GI motility can occur - give atropine if this compromises the pt’s airway/safety)

165
Q

What do you need to know when meal-planning for an MG patient?

A

High Calorie, soft foods, small meals.

Breakfast should be the largest meal of the day with progressively smaller meals.

166
Q

What are the long-term treatment options for MG?

A
  1. Cholinesterase inhibitors (Pyridostigmine & Neostigmine)
    - long-acting AChE’s only give 6h of relief - take on time!
  2. Immunosuppressants
    -Corticosteroids (prednisone - first line)
    Or, Cytotoxic agents (methotrexate) to decrease T cell production
  3. IV immunoglobulin to overwhelm defective T cells
    - ONLY if other meds fail or a myasthenic crisis
  4. Thymectomy
    - but this will take years to see results b/c of long life of T cells
167
Q

What are the treatment options for a myasthenic crisis?

A

IV immunoglobulin

Plasmapheresis (like dialysis but for antibodies)

168
Q

What is a cholinergic crisis, why does it usually happen and what is the treatment?

A

We typically cause a cholinergic crisis by giving too much AChE (Tensilon test), but it can be caused by the removal of the thymus.

Symptoms: Bradycardia, Increased salivation, GI hypermotility, N/D, respiratory impairment (be aware of impaired breathing and possible respiratory failure).

Treatment: Atropine

4th Semester Nursing (8 decks)

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