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Health And Illness 3 Denas Final > Final > Flashcards

Final Flashcards

1
Q

What is mood?

A

Subjective data, states: grief, happy, sad, melancholy

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2
Q

What is affect?

A

Objective observation, what emotions is the client expressing.. client appears…?

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3
Q

Major Depressive disorder

A

Characterized as a persistent depressed mood for at least 2 weeks, can be chronic, higher prevalence rates in lower income, unemployed and unmarried or divorced people

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4
Q

Who is at most risk for MDD?

A

Females, teenage years due to increase hormone levels

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5
Q

What is disruptive mood dysregulation disorder?

A

Severe and recurrent outburst NOT consistent with development level

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6
Q

Risk factors for depression

A

Female gender, early childhood trauma, stressful life events, family hx, chronic or disabling medical condition

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7
Q

How is MDD diagnosed

A

The DSM-5

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8
Q

Psychotic features

A

Disorganized thinking, delusions, hallucinations

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9
Q

Melancholic features

A

Severe apathy, weight loss, profound guilt, symptoms worse in morning & early morning awakening

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10
Q

Atypical features

A

Vegetative state ( overeating, oversleeping), onset is younger, psychomotor activities are slow and anxiety is often accompanying problem, can see a improved mood when exposed to pleasurable events

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11
Q

Catatonic features

A

Non responsiveness, withdrawal, negativity, retardation ( may seem paralyzed)

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12
Q

Post partum onset

A

Within first 4 weeks after birth but can last up until 1 year after

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13
Q

Seasonal depression

A

SAD- mostly begins in fall remit in spring, characterized by lack of Anergia (lack energy) hypersomnia ( excessive daytime sleep), weight gain, overeating, crave carbs. Responds well to daylight therapy.

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14
Q

What does SIGE CAP stand for

A

Sleep
Interest
Guilt
Energy
Concentration
Appetite
Psychomotor activity
Suicidal ideation

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15
Q

Lab studies for mood disorders

A

No lab studies for mood disorders, thorough work up to rule out underlying conditions.

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16
Q

Anti depressants

A

Increase risk of suicide and suicidal thoughts first few weeks of treatment, particularly in ages 18-24, sudden changes in mood, there’s a slow onset and slow taper… you should never stop abruptly

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17
Q

What meds should not be mixed

A

SSRI, St. John’s warts
MAOIs and other depressants

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18
Q

What does the monoamine hypothesis suggest

A

Deficiency of synaptic neurotransmitters such as serotonin, norepinephrine, and dopamine.
Serotonin being one that is associated with mood

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19
Q

SSRIs

A

Selective serotonin reuptake inhibitors, they are the first line of therapy

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20
Q

Common SSRIs used

A

Fluoxetine- Prozac
Paroxetine-Paxil
Sertraline- Zoloft
Citalopram- celexa
Escitalopram- cipralex

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21
Q

Pharmacokinetics of SSRIs

A

Typically have long half-life (24 hours plus) this allows for once daily dosing

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22
Q

Side effects of SSRIs

A

Insomnia, weight gain, postural hypotension, sexual disturbances

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23
Q

Contraindications with meds

A

SSRIs and MAOIs
There must be a one to two week washout period if switching between the two

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24
Q

What do SNRIs do

A

Reuptake inhibitors that increase the concentration of both serotonin and noradrenaline in the synaptic cleft

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25
Q

What do SSRIs do

A

Increase serotonin concentration in the synapse

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26
Q

What do MAOIs do

A

Inhibit the breakdown of serotonin

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27
Q

Side effects of SNRIs

A

Body weight decrease
Anorexia
Decrease blood pressure
Suicidal thoughts
Nausea and vomiting
Reproductive- sexual dysfunction
Insomnia

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28
Q

Patient teaching with SSRIs and SNRIs

A

May cause low sex drive
May cause insomnia anxiety nervousness
No OTC meds without reviewing with a pharmacist
Avoid alcohol
Do not stop abruptly
Report increase in depression or suicidal thoughts, increase HR, difficulty urinating, fever,hyperactive behaviour and severe headache

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29
Q

Tricyclic antidepressants

A

TCAs, inhibits the reuptake of serotonin (5HT), and NA into the presynaptic cell body, which increases the amount of 5HT AND NA availible to bind to post synaptic receptors.

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30
Q

Indications for TCAS

A

Depression
Neuropathic pain

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31
Q

Adverse reactions to TCAs

A

Anticholinergics ( dry out body )
Can’t see
Can’t pee
Can’t spit
Can’t shit
IOP
Sedation
Weight gain

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32
Q

Serious side effects of TCAS

A

In high doses of tca, Impair cardiac conduction can occur causing a widening of the QRS Complex and heart block, often following hypotension

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33
Q

Patient teaching for TCAs

A

Mood elevation can take 1-4wks
Drowsiness and dizziness can occur
Careful driving for few weeks, symptoms should subside
Do not stop abruptly

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34
Q

Monoamine oxidase inhibitors

A

MAOIs
Mechanism of action - Inhibit MAO enzymes

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35
Q

MAO-A

A

Degrades epinephrine,norepinephrine, and serotonin and dopamine

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36
Q

MAO-B

A

Degrades phenylethylamine and dopamine

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37
Q

Side effects to MAOIs

A

Avoid foods with tyramine
- no wine, cheese, pickled foods
Sleep disturbances
Postural hypotension
Weight gain
Breakdown of norepinephrine is inhibited leading hypertensive crisis

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38
Q

IS PATH WARM (intent to harm/ pass attempts)

A

Ideation
Substance abuse
Purposeless
Anxiety
Trapped
Hopelessness
Withdrawing
Anger
Recklessness
Mood changes

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39
Q

CAGE questions are used for what?

A

Alcohol consumption
C- cut down on drinking
A- have people annoyed you by criticizing drinking
G- have you ever felt guilty about your drinking
E- have you ever had a drink in the am to calm your nerves or cure hangover ( eye opener )

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40
Q

What is psychosis?

A

Perception and thoughts through hallucinations and delusions

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41
Q

Psychosis

A

It is a symptom not a mental illness, it is referred to altered cognition, altered perception, and impaired ability to determine what is or is not real

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42
Q

Definition of psychosis

A

Episode where one is detached from reality, can be a symptom of sleep deprivation, substance use and mental illness. Signs may include hallucinations, delusions, agitation, disorganized thoughts and behaviours.

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43
Q

Definition of schizophrenia

A

A mental illness that impacts thought processes, emotions and behaviours, to be diagnosed you must experience at least two symptoms for six months. Symptoms are : delusions, hallucinations, disorganized speech, catatonic behaviour and negative symptoms.

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44
Q

Schizophrenia =

A

Split mind

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45
Q

Symptoms of schizophrenia

A

DSM Criteria- delusions, hallucinations, disorganized speech
You must have one of these three symptoms and must be present for at least one month

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46
Q

Etiology of schizophrenia

A

Biological factors such as parent
Neurobiological- over abundance of dopamine or too many dopamine receptors.
Brain structure abnormalities- enlarged ventricles and brain cavities contain CSF, Reduction in grey matter and less frontal lobe activity
MARIJUANA USE

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47
Q

Epidemiology of schizophrenia

A

More common in males ages 15-25
Later onset for females 25-35

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48
Q

Substance abuse

A

50% of patients with schizophrenia exhibits either alcohol or illicit drug dependence and more than 70% are nicotine dependent

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49
Q

Phases of schizophrenia

A

Prodrome phaser
Phase 1 acute
Phase 2 stabilization
Phase 3 maintenance

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50
Q

Prodromal

A

First symptoms may manifest a year prior to a full blown manifestation of symptoms. Initially decreased function then improve.
Anxiety, phobias, obsessions, dissociative features and compulsions may be noted.

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51
Q

Assessment during the pre psychotic phase

A

General assessment includes:
Positive symptoms
Negative symptoms
Cognitive symptoms
Affective symptoms

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52
Q

Positive symptoms

A

Hallucinations,delusions, disorganized speech (associative looseness), bizarre behaviour

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53
Q

Negative symptoms

A

Blunted affect, poverty of thought (alogia), loss of motivation ( avoliation), inability to experience pleasure or joy (aphedonia)

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54
Q

Affective symptoms

A

Dysphoria, suicidality, hopelessness

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55
Q

Cognitive symptoms

A

Easily distracted, impaired memory, poor problem solving, poor decision making skills, illogical thinking, impaired judgement

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56
Q

Phase 1

A

Acute phase, onset or exacerbation of symptoms

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57
Q

Phase 2

A

Stabilization, symptoms diminishing, movement toward previous level of functioning

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58
Q

Phase 3

A

Maintenance, at or near baseline of functioning

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59
Q

Primary prevention

A

Consider environmental factors

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60
Q

Secondary prevention

A

Monitoring for sub clinical symptoms, screening high risk

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61
Q

EPS symptoms (typical antipsychotics)

A

AD- acute dystonia (days to weeks)
AP- akathisia, Parkinsonism (weeks to months)
T- tardive diskinesia (months to years)

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62
Q

FIRST-GENERATION ANTIPSYCHOTICS

A

•Dopamine antagonists (D2 receptor antagonists)
•Target positive symptoms of schizophrenia
•Advantage
•Less expensive than second generation
•Disadvantages
•Extrapyramidal side effects (EPS)
•Anticholinergic (ACh) adverse effects
•Tardive dyskinesia
•Weight gain, sexual dysfunction, endocrine disturbances
•Risk of Neuroleptic Malignant Syndrome
•Haldol / Loxapine

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63
Q

SECOND-GENERATION ANTIPSYCHOTICS

A

•Treat both positive and negative symptoms
•Minimal to no extrapyramidal side effects (EPS) or tardive dyskinesia
•Disadvantage—tendency to cause significant weight gain
•Olanzapine
•Clozapine
•Risperidone
•Quetiapine

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64
Q

THIRD-GENERATION ANTIPSYCHOTIC

A

•Aripiprazole (Abilify)
•Brexpiprazole (Rexulti),
•Cariprazine (Vraylar)
•Dopamine system stabilizer
•Improves positive and negative symptoms and cognitive function
•Little risk of EPS or tardive dyskinesia

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65
Q

POTENTIALLY DANGEROUS RESPONSES TO ANTIPSYCHOTICS

A

•Anticholinergic toxicity- anhidrosis, anhidrotic hyperthermia, vasodilation-induced flushing, mydriasis, urinary retention, and neurological symptoms, including delirium, agitation, and hallucinations.

•Neuroleptic malignant syndrome (NMS)-Neuroleptic malignant syndrome (NMS) is a life-threatening neurologic emergency associated with the use of antipsychotic (neuroleptic) agents and characterized by a distinctive clinical syndrome of mental status change, rigidity, fever, and dysautonomia.

•Agranulocytosis- Agranulocytosis refers to having severely low neutrophil levels. Neutrophils are a type of white blood cell. They fight germs that make you sick.

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66
Q

Mild anxiety

A

•Individual sees, hears and grasp more information
•Problem solving more effective
•i.e. Taking a quiz
•Physical symptoms may include slight discomfort, restlessness, irritability, impatience or mild tension-relieving behaviours (i.e. nail biting, foot or finger tapping, fidgeting, wringing of hands).

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67
Q

Moderate anxiety

A

•Individuals sees, hears, and grasps less information
• May have selective inattention
•Information or environment events are not heard or seen
•Ability to process information is impaired.
•Problem solving less effective, although may still occur
•Physical symptoms
• Tension, pounding heart, increased pulse and respiratory rate, perspiration, and mild somatic symptoms (gastric discomfort, headache, urinary urgency).
• Voice tremors and shaking may be noticed.
•Constructive mechanism as these manifestations may indicate that something in the person’s life needs attention or is dangerous.

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68
Q

Severe anxiety

A

•Perceptual field of individual becomes quite decreased
•Individual may focus on one particular detail or many scattered details
•Individual may have difficulty noticing his or her environment, even when it is pointed out by another.
•Learning and problem solving are not possible.
•Individual may appear dazed and confused.
•Purposeless activity
•Hyperventilation

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69
Q

Panic anxiety

A

•Unable to focus on environment
•May have hallucinations or delusions
•Disorganized or
•Irrational reasoning
•Feeling of terror
•Unintelligible communication or inability to speak
•Insomnia
•Hallucinations or delusions

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70
Q

What is serotonin syndrome

A

Too much serotonin, muscle rigidity, high HR,BP, muscle tightness(rhabdo), mental changes

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71
Q

Benzodiazepines

A

•Benzos work to increase the ability of Gamma Aminobutyric Acid (GABA), an inhibitory neurotransmitter in the central nervous system.
•Slows down nervous system (why we use for seizures), causes sedation, anxiolytic and muscle relaxant properties

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72
Q

Therapeutic uses for benzodiazepines

A

•Therapeutic Uses
•Treats anxiety
•Sedation/ Muscle Relaxant
•Treats seizures
•Treats alcohol withdrawal

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73
Q

Antidote for benzodiazepines

A

•Antidote à Flumazenil
“ I FLU past the BENZ”

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74
Q

Side effects for benzodiazepines

A

•Hypotension, RESPIRATORY ARREST, Apnea, Airway occlusion, dizziness, somnolence
•High risk of dependence, not meant for long term
•Long term use leads to TOLERANCE, larger amounts needed for desired outcome
•Must be tapered
•Take at bedtime

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75
Q

Buspirone

A

•Partial agonist of serotonin receptors in brain
•Used as anti-anxiety medication
•SLOW onset à Not for acute anxiety! (May take 2-4 weeks to work)
•Not for acute anxiety or panic attacks
•Does NOT cause CNS depression
•No risk of physical dependence or withdrawal symptoms

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76
Q

Panic disorder

A

Recurrent unexpected panic attack, in the absence of triggers, persistent concern about additional panic attacks and or maladaptive change in behaviour related attacks.

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77
Q

Specific phobia

A

Unreasonable fear or anxiety about a specific object or situation, which is actively avoided. I.e flying, heights, animals, seeing blood.

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78
Q

Obsessive compulsive disorder

A

Obsession: recurrent and persistent thoughts, urges, or images that are experienced as intrusive and unwanted and that cause marked anxiety or distress.
Compulsion: repetitive behaviours (hand washing), or mental acts (counting), that the individual feels driven to perform to reduce the anxiety generated by obsession.

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79
Q

OCD

A

Can exist independently but most often seen together.
•These are time consuming (e.g., take more than 1 hour per day) and/or cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.
•Cognitive behavioural therapy in the form of exposure and response prevention, alone or in combination with a selective serotonin-reuptake inhibitor (SSRI) or clomipramine, is a first-line therapy.

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80
Q

Risk factors

A

Male, fam hx, late adolescence to early 20’s, stressful life events, pregnancy

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81
Q

Panic disorder

A

•When an individual experiences a constellation of anxiety based symptoms that approximate panic.
•A fear of impending disaster or of losing control in the absence of an actual threat
•Can become recurrent and effect one’s life so it is debilitating
Most common in women, developing in mid 20’s

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82
Q

Risk factors of panic disorder

A

White ethnicity, other psychological factors, asthma, comorbid disorders

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83
Q

Investigations for panic disorder

A

Not typically required but may see a ECG, blood glucose, cbc and lytes, tox screen and thyroid test to rule out any comorbidities.

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84
Q

Management of panic disorders

A

•Cognitive behavioural therapy (CBT)
•Medication
•SSRI / SNRI typically

•Good sleep
•Regular exercise
•Reduced use of caffeine, tobacco, and alcohol
Healthy diet
Staying engaged with meaningful activities and healthy social supports.

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85
Q

Phobia

A

Intense, persistent irrational fear of a simple thing or situation that causes the person to avoid at all cost.
•Reaction is disproportionate and excessive and goes against rational thinking
•Some individuals develop a phobia as a result of a physical or psychological traumatic exposure.
•I.e. Being bit by dog or trapped in closed space
•Treatment looks at desensitization, self-help group therapy
•Journaling
•Exercise
•SSRI’s

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86
Q

Advanced practice interventions for phobia

A

˜Cognitive therapy
˜Behavioural therapy
•Modelling – demonstrate appropriate behavior and patient imitates it
•Systematic desensitization – Patient is gradually introduced to feared object
•Flooding – Exposes patient to a large amount of undesirable stimulus at once
•Response prevention – patient not allowed to perfor compulsive ritual
•Thought stopping – Negative thought of obsession is interrupted

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87
Q

What is delirium?

A

An acute change in mental status leading to fluctuating course ) inattention disorganized thinking and altered loc. Very common in hospitalized settings. Often a sign of serious disease in older patients that should not be ignored.

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88
Q

Epidemiology of delirium

A

Often unrecognized many casesundiagnosed and or misdiagnosed as depression geriatric patients at most risk.

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89
Q

high risk patient for delirium

A

LTC, hip fracture, icu admits, palliative.

           ↓ Do to increase inflammation. circadian rhythm is affected.
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90
Q

Can delirium fluctuate

A

Yes, comes on fast. Serious change in mental abilities, it is confused thinking and lack of awareness. Change must be abrupt.

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91
Q

Clinical features of delirium

A

Acute onset usually develops over hours todays onset may be abrupt
Prodromal phase initial symptoms can be mild transient if onset is more gradual (fatigue/daytime , decrease concentration, irritability, restless and anxiety, and mild cognitive impairment.

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92
Q

Clinical features of delirium

A

Fluctuation-unpredictable, over the course of interview and 1 or more days, intermittent and is worse at night, can have psychomotor disturbances I.e restless and agitated and lethargic and inactive.
And have normal level function.

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93
Q

Hyperactive (clinical variants)

A

Restless/agitated
Autonomic arousal
Aggressive/ hyperactive

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94
Q

Hypoactive

A

Lethargic /drowsy
Apathetic/ inactive
Quiet/confused
Often escapes diagnoses
Mistaken for depression

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95
Q

Mixed

A

Hypo and hyper symptoms

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96
Q

Delirium vs dementia

A

Delirium - acute onset, fluctuates, always inattentive (wandering gaze,staring into space, not able to recite things back to nurse).deviates from the
Patients typical benaviour, often occurs with patients with dementia
Dementia- chronic, insidious onset and progressive, sundowning

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97
Q

To determine delirium?

A

Delirium = acute onset and fluctuating course and intention + either disorganized thinking oraltered loc

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98
Q

How to treat delirium

A

In form the medical team
Identify common causes
Institute treatment plan
Identify safety concerns

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99
Q

1st generation meds are?

A

Typical

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100
Q

2nd generation meds are?

A

Atypical

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101
Q

Delirium can be caused by what in the brain?

A

Micro inflammation

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102
Q

Side effects of haldol?

A

Prolonged Q T, EPS, over sedation, NMS

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103
Q

Cholinergics help with?

A

Memory

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104
Q

What is consent?

A

Non negotiable component, consent is ongoing

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105
Q

Ages of consent?

A

A person under 12 cannot consent
12-13 can consent with someone less than2 years
14-15 can consent with someone less than 5 years
16 years old is legal consent

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106
Q

Hypertensive disorders of pregnancy (hdp)

A

Leading cause of maternal morbidity and mortality

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107
Q

Diagnosis of hypertension

A

Hypertension = SBP>_140 mmhg and or DBP >_90
Severe hypertension=SBP >160mmhg or DBP> 110mmhg

Average of 2 measurements taken 15 minutes apart, on the same arm

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108
Q

Pre-existing hypertension

A

Pre pregnancy or appears 20 weeks gestation

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109
Q

Gestational hypertension

A

Appearing at or after 20 weeks gestation

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110
Q

Two subgroups of HTN

A

with co-morbid conditions (e.g. diabetes, cardiovascular or kidney disease)
Preeclampsia

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111
Q

Transient HTN effect

A

Elevation r/t environmental stimuli

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112
Q

White coat HTN effect

A

Elevated in office/ normal outside

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113
Q

Masked HTN effect

A

Normal in office/ elevated outside

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114
Q

How to identify preeclampsia

A

Hypertension AND one or more of the following:
New onset proteinuria
One/more adverse condition(s)

With preexisting hypertension be aware of resistant hypertension or new/worsening proteinuria

Severe preeclampsia includes
One/more severe complications

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115
Q

Risk factors for preeclampsia

A

1st pregnancy
Previous history
Age ≥ 40
Obesity (BMI ≥ 35)
Pre-existing HTN, DM
Multiple pregnancy
Inter-pregnancy interval < 2 years or ≥ 10 years
Ethnicity: Nordic, African Canadian, South Asian
Excessive weight gain
Family history
New partner

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116
Q

Progression of preeclampsia

A

Begins @ conception, symptoms and adverse effects worsen as pregnancy advances
Cure=delievery

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117
Q

HELLP syndrome

A

variant of preeclampsia
Acronym for:
Hemolysis- increase Hgb, increase LDH resulting from RBCs damaged by fibrin
Elevated Liver enzymes – increase AST, increase ALT from liver edema and damage from fibrin
Low Platelets – Thrombocytopenia < 150 x 109/L from increase consumption of platelets due to damaged vascular endothelium

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118
Q

Physiologic changes in preeclampsia

A

Decreased volume
- Hemoconcentration,
Vasoconstriction and increased resistance
- Hypertension
Vasospasms
Decrease in GFR and RPF
- Increased BUN, serum creatinine and uric acid
Impaired Coagulation
- Increased INR / PTT

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119
Q

Adverse Conditions Associated with Preeclampsia → CNS

A

Headache
Visual symptoms

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120
Q

Cardiac and RESPIRATORY

A

Chest pain
Sob
Sats under <97%

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121
Q

Hematological

A

Increase WBC’s
Decrease platelets
Increase INR and PTT

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122
Q

Renal

A

Increase serum creatinine
Increase serum uric acid

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123
Q

Hepatic

A

Nausea, vomiting, RUQ or epigastric pain
Increase AST, alt,LDL, bili
Decrease albumin

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124
Q

Fetal placental

A

Abnormal FHR
IUGR
Oligohydramnios
Absent or reverse
End diastolic flow by Doppler velocimetry

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125
Q

Severe complications

A

Eclampsia
Stroke
Pulmonary edema
Abruption
Severe organ dysfunction

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126
Q

Fetal complications

A

Abnormal FHR
Oligohydramnios
Intrauterine growth restriction (IUGR)
Absent or reversed end-diastolic flow in umbilical artery (Doppler)
Intrauterine fetal death (IUFD)

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127
Q

Caring for person with HDP

A

Dietary and Lifestyle Modification- not supported by evidence
Bedrest- not supported by evidence
Ongoing monitoring- Accurate BP monitoring,
Clinical Test – urine & blood testing, Fetal Health Surveillance
Anti-hypertensive therapy

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128
Q

Guidelines for BP

A

BP Measurement Methods
- Auscultation (mercury, calibrated aneroid)
- Validated Automated Device
Appropriately sized cuff
At rest prior to measurement
First measurement discarded
Average of two measurements

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129
Q

Positioning for accurate BP

A

Sitting with feet resting on floor (or other)
legs uncrossed
cuff positioned on bare arm at the level of the heart
with arm well supported
should not be talking during the assessment

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130
Q

Accurate BP by auscultation

A

Rapidly increase cuff pressure – 30mmHg above disappearance of radial pulse
Stethoscope over brachial artery
Open the control valve – deflation rate of approx. 2 mmHg per heart beat

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131
Q

Fetal health surveillance

A

Antepartum:
Fetal Movement counts
Daily with risk factors
Goal: 6 or more movements in 2 hours
↓ movement warrants further assessment
Ultrasound for fetal growth, AFV or BPP
Umbilical Artery Doppler

Intrapartum:
Electronic Fetal Monitoring
Admission FHR tracing
Continuous EFM in labour

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132
Q

Treatment for hypertension

A

Labetolol
Nifedipine
Methyldopa

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133
Q

What is mag sulf ? (MgS04)

A

Given to prevent or treat eclampsia
-Administration:
IV loading dose - usually 4g over 20-30min
IV maintenance dose - 1g/hr
-If a seizure occurs while on MgSO4:
Another bolus dose – 2g IV over 20-30 min
Followed by maintenance dose – 1g/hr
-Neuroprotection
Imminent preterm deliveries <32 wks
Do not delay emergency delivery
Typically nurse is 1:1 ratio
Patient is in quiet area and dark room

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134
Q

Caring for mom getting magsulf

A

Require close & ongoing monitoring:
Vital signs
Neurological evaluation – reflexes
Strict Intake
Output – minimum 25ml/hr

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135
Q

Antidote for mag self?

A

Calcium gluconate: 10ml of 10% calcium gluconate solution. IV over 3 minutes
Must monitor mg blood levels

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136
Q

Signs of magnesium toxicity

A

Weakness
Hyporeflexia
↓respiratory rate
Hypotension
Oliguria
SOB
Chest pains

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137
Q

If seizure occurs what do you do?

A

Call for help
Promote lateral position
Prepare MgSO4 bolus (and infusion if not already started)

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138
Q

What do you do post seizure?

A

ensure adequacy of airway
check vital signs, O2 saturation, and FHR
assess for signs of abruption

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139
Q

Labour and birth

A

Early anesthesia consultation
Epidural/spinal anesthesia/analgesia is preferred,
Blood product administration if necessary
Antihypertensives are continued during labour

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140
Q

Postpartum hypertension

A

May first appear, or symptoms worsen following birth
Most common at 3 to 6 days
Can occur up to 3 weeks
Isolated or with pre-eclampsia
MgSO4 will be continued – usually 24 hours
Antihypertensive therapy – initiated or continued
Caution with NSAIDs for analgesia

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141
Q

Pressure without co-morbid conditions

A

BP ↓: 130 – 155 mmHg / 80 – 105 mmHg

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142
Q

Pressure with co-morbid conditions

A

BP ↓: < 140 mmHg / <90 mmHg

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143
Q

Benign disorders

A

Red blood cell disorder, WBC disorders,platelet disorders, homeostasis and thrombosis

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144
Q

Malignant

A

Leukemias
Lymphomas
plasma cell neoplasm
Myelodysplasia
Myeloproliferative disorders

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145
Q

WBC lab value

A

4.5 - 11. 1

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146
Q

Hgb value

A

140 - 173 g/L

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147
Q

Platelets value

A

140 - 400

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148
Q

What is hematology?

A

Branch of medicine that is concerned with the study, teaching, prevention, diagnosis, and treatment of diseases related to the blood
Includes bone marrow, immune system, hemostatic, vascular system

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149
Q

Cellular regulation definition

A

“All functions carried out within a cell to maintain homeostasis, including its responses to extracellular signals (e.g., hormones, cytokines, and neurotransmitters) and the way each cell produces an intracellular response”.

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150
Q

Cellular replication and growth

A

proliferation versus differentiation

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151
Q

Neoplasia

A

benign versus malignant

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152
Q

Dysplasia

A

loss of DNA control over differentiation

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153
Q

Neoplasia

A

cells growing independently with no physiological purpose

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154
Q

Process of cancer development

A

• Initiation
• Promotion
• Progression

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155
Q

Who is at risk?

A

• Populations
• Age (males > females in age groups <20 and >60; more Cancer in women 20-59)
• Smoking / Tobacco
• Infectious Agents
• Genetic Risk
• Radiation
• Carcinogens
• Nutrition and Physical Activity

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156
Q

7 warning signs of cancer

A

Change in bowel or bladder habits
A sore that does not heal
Usual bleeding or discharge from any body orifice
Thickening or a lump in the breast or elsewhere
Indigestion or difficulty swallowing
Obvious change in a wart or mole
Nagging cough or hoarseness

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157
Q

Neutropenia

A

• Reduction in neutrophils (type of granulocyte) = granulocytopenia.
• Neutrophilic granulocytes are closely monitored - Risk for infection
indicator.
• A clinical consequence that occurs with a variety of conditions or
diseases - it can be a predictable or unanticipated side effect of taking
certain drugs.

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158
Q

Side effects of neutropenia

A

• Side effects are sometimes a necessary
step in therapy (chemotherapy,
radiation).
• Monitor the neutropenic patient
for signs and symptoms of infection
and early septic shock.

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159
Q

Neutropenia

A

The risk of infection increases with neutrophil
count < 1.0 x 109/L or ANC 1000
• Markedly increases at < .5 x 109/L or ANC 500,
particularly when due to impaired production
(e.g. after chemotherapy).
• Patients should be aware that they need
to seek medical attention if they have fever
or other symptoms of infection.

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160
Q

Fever in cancer patient

A

Do not take any meds to lower fever
Go to Er right away, need treatment within 50 mins
Triaged CTAS level ll
CBC and blood culturesx2
Lytes, bun, Cr, UA and UC, CXR

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161
Q

Absolute neutrophil count (ANC) indicates?

A

• The degree of neutropenia or risk for infection.

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162
Q

Collaborative person Centered care

A

Goals:
•Cure
•Control
•Palliation

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163
Q

Surgery

A

• May consist of removal of the entire
tumor or metastasis, resection of
tumor or mets, palliation, or
reconstructive surgery or during an
oncological emergency (i.e., spinal
cord compression or SVCS)
• Oldest treatment modality for cancer
• Used alone, or in combination with
other modalities

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164
Q

How to diagnose?

A

Biopsy

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165
Q

Chemotherapy goal

A

• Goal: Reduce number of malignant cancer cells in tumor sites
• Acts on all dividing cells (++ side effects), allows body’s
immune system to act.
• IV, Oral, SC, IM, Topical, Arterial, Intrathecal,
Intraperitoneally, Intracavitarily
• Classified by molecular structure and mechanism of action

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166
Q

Cure

A

Burkitt’s lymphoma, wilms tumour, neuroblastoma, ALL, hodgkins disease, testicular cancer

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167
Q

Control

A

Breast cancer, non-hodgkins lymphoma,small cell carcinoma of the lung, ovarian cancer

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168
Q

Palliation

A

Relieve pain, relieve obstruction, improve the sense of well being

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169
Q

Chemo considerations

A

• Preparation / handling – irritants versus vesicants
• May pose an occupational hazard
• Drugs may be absorbed through skin and inhalation
during preparation, transportation, and administration
• Only properly trained personnel should handle drugs.
• Must differentiate between tolerable and toxic side effects

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170
Q

Extravasation Injury

A

• Infiltration of medications into the tissues surrounding the infusion site.

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171
Q

What is Cytotoxic Waste?

A

•All materials used for prep and admin of cytotoxic
drugs
•patient’s body fluids
•Separated from general waste
•Disposed of according to provincial/institutional
guidelines

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172
Q

Occupational Health Risks?

A

No safe level of exposure has been established
No exposure is safest

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173
Q

What are the major routes of exposure?

A

•Inhalation of vapors of drug from uncovered waste
container or Spill
•By contact with skin or mucous membranes
•Ingestion of drug by eating or drinking in administration area

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174
Q

What is the risk for exposure for
health care providers ?

A

• Handling chemotherapy medication
• Handling cytotoxic waste & body fluids
• Cleaning a spill
• Inadequate cleaning of spill
• Research

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175
Q

Safe Handling of Oral Chemo

A

• Always wear gloves – Avoid
touching tablets
• Always prepared in Pharmacy
• Never alter medication – crush,
split, open
• Always give as directed
• Store separately in leak proof
container with lid and labeled as
cytotoxic
• Dispose of equipment used to
administer in cytotoxic waste ie;
med cup, gloves

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176
Q

Cytotoxic Wastes: Body Fluids

A

• Cytotoxic waste can be excreted
thru patient body fluids:
• Urine, emesis, feces, saliva, semen,
vaginal fluid
• Cytotoxic precautions during and
for at least 48 hours after last dose
of chemotherapy. Some drugs
take longer than 48 hours. Your
chemo nurse will notify you length of time

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177
Q

Radiation Therapy: internal radiation

A
  • Brachytherapy

Implantation or insertion of
radioactive materials into or
close to tumor.

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178
Q

External radiation

A

Most Common
• Target tumor using imaging,
exam, and surgical reports
• External marks

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179
Q

Common side effects of chemotherapy and radiation include:

A

• Bone marrow suppression
• Fatigue
• GI disturbances (N+V, Diarrhea, Constipation)
• Integumentary and mucosal reactions
• Pulmonary effects
• Reproductive effects

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180
Q

Hormonal Therapy

A

Hormonal agonist and antagonists – treat cancers that are responsive to hormones
(prostate, breast, endometrial)

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181
Q

Targeted therapy

A

• Targets specific cancer cells
• Much reduced side effect profile
• Rapidly growing area of anticancer agents

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182
Q

Biologic therapy

A

Modifies immune response (activates immune system - ’biologic response
modifiers’)

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183
Q

Systemic cancer therapy

A

. Chemotherapy- attacks rapidly dividing cells
• Targeted Therapy- involves with specific molecules involved with tumor
growth
• Immunotherapy (I-O)- utilizes the body’s own immune system to attack tumor
cells
• Biologic (i.e. endocrine)

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184
Q

Targeted therapies

A

Target specific antigens found
on the cell surface
• Penetrate the cell membrane
to interact with targets inside
a cell

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185
Q

Chemotherapy: target and adverse Events

A

Target: rapidly dividing tumour and normal cells
Adverse events: diverse due to non specific nature of therapy

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186
Q

Targeted therapies: target and adverse events

A

Target: specific molecules involved in tumour growth and progression
Adverse events: reflect targeted nature

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187
Q

I-O therapies: target and adverse events

A

Targets immune system
Adverse events: unique events can occuras a result of immune system activity

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188
Q

Types of Targeted Therapy

A

• Small-Molecule Drugs are small enough to enter
cells easily, so they are used for targets that are
inside cells. (-nib)
• They block the process that helps cancer cells
multiply and spread.

• Monoclonal Antibodies are drugs that are not able
to enter cells easily. Instead, they attach to specific
targets on the outer surface of cancer cells. (-mab)
• they block a specific target on the outside of
cancer

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189
Q

What’s the target?

A

• Not all cancers have the same targets
• Pathology review and molecular testing is done to determine the presence
or absence of certain targets
• Most used targets are:
• Human epidermal growth factor (HER2)-Breast & Gastric
• Epidermal growth factor receptor (EGFR)- Colorectal, head & Neck ca
• Vascular Endothelial growth factor (VEGF)-Colorectal, Neuro, Gyne

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190
Q

Gene therapy -FYI

A

• Missing or altered genes may lead to cancer.
• Transfer of exogenous genes into cells of patients in an effort to correct
defective gene
• Gene therapy is an experimental therapy that involves introducing genetic
material into a person’s cells to fight disease.
•Some approaches target healthy cells to enhance their ability to fight cancer.
•Other approaches target cancer cells to destroy them or prevent their growth.
•Currently investigational

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191
Q

Autologous stem cell transplant

A

Harvesting Stem Cells
▪ Stem cells from bone marrow
▪ Peripheral blood
▪ Umbilical cord blood (Can be stored
and used later)

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192
Q

Autologous stem cell transplant complications

A

▪ Bacterial, viral, and fungal infections
are common.
▪ Graft-versus-host disease
▪ Peripheral blood stem cells cause
fewer and less severe complications.

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193
Q

Complications of cancer

A

• Nutrition Problems Malnutrition, Altered taste sensation
• Infection
• Oncological Emergencies:
Obstructive, metabolic,
infiltrative
• Superior vena cava
syndrome
• Spinal cord compression
• Third space syndrom

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194
Q

Metabolic emergencies

A

Syndrome of Inappropriate Anti Diuretic Hormone
(SIADH)
• Malignant Hypercalcemia
• Tumor Lysis Syndrome
• Watch hypocalcemia, renal failure
• Hyperuricemia, hyperphosphatemia,
hyperkalemia, hypocalcemia
• Septic Shock
• Disseminated Intravascular Coagulation (DIC)

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195
Q

Cancer pain

A

Patient report should always be believed accepted as primary source for pain assessment data. Drug therapy should be used to control pain. Fear of addiction is unwarranted.numerous drug options for painmanagement. Non pharmacological intervention including relaxation techniques and imagery

196
Q

Age related considerations

A

Be aware of late and long-term effects of cancer:
• Secondary Cancers
• Cognitive Changes
• Cardiovascular / Sexual Dysfunction
• Psychosocial Effects

197
Q

Common fears

A

Disfigurement, emaciation
• Dependency
• Disruption of relationships
• Pain
• Financial depletion
• Abandonment
• Death

198
Q

Coping with cancer

A

• Coping with stress in the past
• Availability of significant others
• Ability to express feelings/concerns
• Age at time of diagnosis
• Extent of disease
• Disruption of body image
Presence of symptoms

199
Q

Support patient and family

A

Being available
• Exhibiting a caring attitude
• Listening actively to fears/concerns
• Providing relief from distressing symptoms
• Being honest
• Assist to setting realistic goals
• Maintain hope

200
Q

Leukemia & Lymphoma

A

The types of childhood leukemia include, in order of their rate of incidence, ALL, AML, and
CML.
• Cause unknown; likely the result of interactions between hereditary or genetic predisposition +
environment

201
Q

Acute lymphoblastic leukemia (ALL)

A

potentially curable disease, with more than 80%
of cases cured.

202
Q

The lymphomas of childhood are non-Hodgkin lymphoma and Hodgkin lymphoma.

A

• The origin of non-Hodgkin lymphoma is unknown.
• Factors that have been implicated include defective host immunity, a viral agent, chronic immuno-
stimulation, and genetic predisposition.
• Non-Hodgkin lymphoma has a favorable prognosis, with a 70% to 80% cure rate.
• The risk of Hodgkin lymphoma is associated in part with infectious diseases, immune deficits, and
genetic susceptibility.
• Hodgkin lymphoma is a readily curable disease with long-term cure rates of 90% to 95%.

203
Q

Splenomegaly

A

• Largest lymphatic organ.
• Located on left side of abdomen just above the kidney.
• Normal Spleen Size – approximately 11cm.

204
Q

Function of spleen

A

• Site of fetal hematopoiesis
• Phagocytes filter and cleanse the blood. Removes old or
damaged cells.
• Lymphocytes start an immune response to blood-borne
microorganisms.
• Acts as a blood reservoir

205
Q

Normal spleen

A

• Located Along: 9, 10 , 11 ribs - Mid Axillary Line
• Spleen should be twice the size in order to be PALPABLE
• Palpable spleens are not always ABNORMAL
• 3 % of the population has a palpable spleen.

206
Q

Disorders causing massive spleen

A

• Polycythemia Vera
• Multiple Myeloma
• POEMS Syndrome
• Waldenstrom’s Macroglobulenemia
• Chronic Lymphocytic Leukemia (CLL)
• Myelofibrosis
• Non-Hodgkin’s Lymphoma
• Chronic Myeloid Leukemia (CML)
• Thalassemia Major

207
Q

Massive splenomegaly

A

Symptoms Include:
• Pain - a sense of fullness,
or discomfort in the LUQ
• Pain- referred to the Left
Shoulder
• Early Satiety - due to
encroachment on the
adjacent stomach.

208
Q

Lymphoma

A

• Heterogeneous group of malignancies that originates in B-Lymphocytes, T-
Lymphocytes, or natural killer (NK) cells.
• Lymphocytes are found in the organs of the lymphatic system.
• Lymphomas develop because of an unregulated proliferation of monoclonal
lymphocyte as a result of accumulated mutations.
• As the lymphoid cells develop from stem cells to mature cells, malignancies
can occur at any stage of development.
• The disease that results depends on the point during the lymphocyte
maturation cycle the when malignancy occurs.

209
Q

Primary lymphoid organs

A

Bone marrow and thymus

210
Q

Secondary lymphoid organs

A

Spleen, lymph nodes, tonsils and peyers patches of small intestine

211
Q

Other lymphoid tissue

A

Appendix ,waldeyers Ring

212
Q

Hodgkins

A

• Classical Hodgkin Lymphoma (CHL)
• Nodular Sclerosis (NSHL)
• Mixed Cellularity (MCHL)
• Lymphocyte-Rich (LRHL)
• Lymphocyte – Depleted (LDHL)
• Nodular Lymphocyte Predominant HL
(NLPHL)

213
Q

Non hodgkins

A

• B-Cell Non-Hodgkin Lymphoma (85%)
• Aggressive “Fast Growing”
• Diffuse Large B Cell Lymphoma
• Indolent “Slow Growing”
• Follicular Lymphoma
• T-Cell Non – Hodgkin Lymphoma (15%)

214
Q

Non-hodgkins lymphoma characteristics

A

Multiple peripheral nodes
Mesenteric nodes and Waldeyer’s ring commonly involved
Non-contiguous
B symptoms uncommon
Rarely localized
Extranodal involvement is common

215
Q

Hodgkins lymphoma characteristic

A

Localized to single axial group of nodes
(i.e., cervical, mediastinal, para-aortic)
Mesenteric nodes and Waldeyer’s ring rarely involved
Orderly spread by contiguity
Symptoms common
Extranodal involvement is rare
Extent of disease is often localized

216
Q

Risk Factors of Hodgkin’s

A

• Epstein Barr Virus (EBV)
• Family History
• Genetic Abnormalities
• Higher SES
• Lifestyle Factors

217
Q

Signs & Symptoms

A

• There are approx. 600 lymph nodes in the body.
• The most common early sign of NHL is painless swelling of one or two lymph node areas. (Most Commonly: Cervical, mediastinal, and axillary)
• Splenic or liver involvement. Bone marrow involvement (anemia, bleeding,
infection)
• B symptoms: Unexplained fever (>38 during prior month), chills, drenching /
recurring night sweats, weight loss (> 10% BMI in less than 6 mth).
• B symptoms are significant indicators for disease progression.
• Unique Clinical Features: Pruritis (85%), Alcohol induced pain (5%)

218
Q

General work up

A

Pre treatment: History, Including presence of B symptoms.
• Physical Exam Including
Lymphoid regions, liver, spleen.
• Performance Status (ECOG)
• Labs: CBC with diff, CMP, LDH,
Uric Acid, ESR

219
Q

Diagnosis work up

A

Pretreatment
• Lymph Node Biopsy (excisional)
• Hematopathology review
• Immunohistochemistry
• FISH Studies
• Molecular Studies
• Cytogenetics
• Ki-67 Proliferation Index

220
Q

Post treatment general work up

A

History including presence of B Symptoms
• Physical examination including lymphoid
regions, liver and spleen.
• Labs: CBC with diff, CMP, LDH
• ESR

221
Q

Staging

A

Pet/ct scan
Bone marrow biopsy (greater than 1.6cm)

222
Q

Hodgkin’s Lymphoma

A

• Lymphoma: malignant neoplasms originating in the bone marrow and
lymphatic structures resulting from proliferation of lymphocytes.
• Hodgkin’s: proliferation of abnormal giant, multinucleated cells (Reed-
Sternberg cells) located in the lymph nodes.
• Causes unknown - ? Epstein-Barr, ?genetics, ?occupational toxins
• Increased in patients with HIV
• Nursing Management – focused on problem management – pain,
pancytopenia, side effects of therapy.
• Prognosis is good (>90%)

223
Q

Ards

A

Acute respiration distress syndrome

224
Q

what is ARDS

A

Form of respiratory failure (acute)- not a primary disease it happens because of something, and it cannot come from the heart. It can come two ways direct or indirect.
-drownings, sepsis, pancreatitis, house fire, covid patients- things that affect the lung and damage the alveoli
-40% death rate 4/10 will die
Major site of injury is alveolar capillary membrane

225
Q

Types of pneumocytes

A

Alveoli are made up of PNEUMOCYTES. There are TWO types
Type I : cells that align the alveoli – thin and large surface area

Type II: makes surfactant that coats the alveoli- smaller, thicker, and proliferate in lung injury- GREATER the damage to type 2 we will see collapsed alveoli
No surfactant = alveolar collapse

226
Q

Gas exchange unit

A

Results from inadequate gas exchange at alveolar capillary membrane. Membrane becomes more permeable resulting in pulmonary edema

1. Insufficient O2 transferred to the  blood Hypoxemia
2. Inadequate CO2 removal Hypercapnia

Fluid also washed away surfactant= alveoli collapse dead cells and fluid build up forming waxy image called waxy hyaline membrane

227
Q

How is ARDS determined

A

Needs to be acute in nature- see within a week. Secondary drowning- days go on and symptoms appear
Or new or worsening symptoms within the week (sepsis), patient decompensating

228
Q

is ARDS a perfusion issues or ventilation issue

A

ARDS patients often get daily ABG’S, not a perfusion issue (shunting), a ventilation issue

229
Q

PEEP

A

PEEP: setting on vent that pushes air into the lungs that expands the alveoli. Fibrin in the lungs will have scarring in lungs and not be able to expand lungs having chronic lung issues.

230
Q

What is the name of the time used for criteria of ARDS

A

Berlin

231
Q

Symptoms you may see with ARDS

A

Crackles, increased SOB, HR. Hypoxemia gets worse, you see them in tripod position trying to expand lung capacity as much as possible

232
Q

4 Things that happen in ARDS

A
  1. diffusion- hypoxia
  2. Shunting (V/Q mismatch)
  3. Decrease surfactant=Decrease lung compliance (leading to scar tissue)
    4.Fibrosis- macro attracts fibrin
233
Q

Acute respiratory failure

A

Not a disease but a condition
Result of one or more diseases involving the lungs or other body systems
Causes include sepsis, overload, shock, trauma, toxic substances and inflammation

234
Q

Hypoxemic Respiratory Failure

A

Causes:
Hypoxemic
Acute respiratory distress syndrome (ARDS)
Pneumonia
Toxic inhalation
Hepatopulmonary syndrome
Massive pulmonary embolism
Anatomical shunt
Cardiogenic pulmonary edema
Shock
Ventilation–perfusion (VQ) mismatch
Many disease and conditions alter overall VQ mismatching
Most common COPD, atelectasis and pain

235
Q

Hypercapnic Respiratory Failure

A

Airways and alveoli:
Asthma
Emphysema
Chronic bronchitis
Cystic fibrosis
Central nervous system:
Opioid or other CNS depressant medication overdose
Brainstem infarction
High-level spinal cord injury
Chest wall:
Flail chest
Kyphoscoliosis
Massive obesity
Neuromuscular conditions:
Muscular dystrophy
Guillain–Barré syndrome
Multiple sclerosis
Myasthenia gravis (acute exacerbation)

236
Q

V/Q ratio

A

The amount of air that reaches the alveoli per minute
DIVIDED BY
The amount of blood that reaches the alveoli per minute
RATIO SHOULD EQUAL 1.0

237
Q

A low V/Q is indicative of what?

A

less ventilation more perfusion
An area with perfusion and no ventilation is referred to as shunting

238
Q

A high V/Q is indicative of what?

A

more ventilation and less perfusion
an area with ventilation but no perfusion is referred to as dead space

239
Q

A PE is example of what?

A

A deadspace

240
Q

assessment for someone with ARDS

A
  1. Tachypnea- rapid shallow breathing, tripod postions
  2. Dyspnea – paradoxical breathing, retraction, accessory muscle use
  3. Decreased breath sounds
  4. Deteriorating ABG levels
  5. Hypoxemia despite high concentrations of delivered oxygen
  6. Decreased pulmonary compliance
  7. Pulmonary infiltrates
    Severe morning headache

Sudden or gradual onset

** A sudden decrease in PaO2 or a rapid increase in PaCO2 indicates a serious condition.

241
Q

Early manifestation

A

Restless, dyspnea, low bp, confusion, extreme tiredness, change in pt behaviour (mood swings, disorientation, change in LOC)
If pneumonia is causing ARDS then client may have fever and cough

242
Q

Late manisfestations

A

severe difficulty breathing, SOB, Tachycardia, cyanosis, thick frothy sputum, metabolic acidosis, abnormal breath sounds

243
Q

Is it possible to have respiratory issues or infection and not develop ARDS?

A

Some people never progress to ards, like pancreatitis will still do damage but not receive ards

244
Q

What are consequences of hypoxemia and hypoxia?

A

Metabolic acidosis and cell death
Initially increased and then decreased cardiac output
Impaired renal function
GI alterations

245
Q

Diagnostic studies for ARDS

A

History and physical assessment
ABG analysis
Chest radiograph DAILY (to not progression of the lungs)
CBC, sputum/blood cultures (determining the source of possible infections), electrolytes
ECG
Urinalysis (detecting potential kidney damage)
CT Chest (contrast may be given and hard on kidneys)
V/Q lung scan
Pulmonary artery catheter (severe cases)

246
Q

In the CT of ARDS patient what can you see?

A

Ground glass appearance

247
Q

Medical management of ards

A

Supplemental oxygen
mechanical respirator
fluid therapy

248
Q

what are positioning strategies?

A

Prone position to open up the airways, lateral rotation therapy

249
Q

Is there a specific therapy for ARDS?

A

No specific therapy exist
you are treating the underlying cause

250
Q

What are the 5 P’s of ARDS

A

Perfusion
Position
Protective lung ventilation
Protocol weaning
Preventing complications

251
Q

pharmacological treatment of ARDS

A

Steroids, vasodilators, surfactant, anti-inflammatory,
DVT prophylaxis, Reflux Px and sedation

252
Q

Perfusion (5P’s)

A

maximize perfusion in the pulmonary capillary system by increasing oxygen transport between the alveoli and pulmonary capillaries.

253
Q

Positioning

A

Change from supine to prone position generates a more even distribution of the gas–tissue ratios along the dependent–nondependent axis and a more homogeneous distribution of lung stress and strain.

254
Q

Protective Lung Ventilation

A

During the early stages of ARDS, use mechanical ventilation to open collapsed alveoli. The primary goal of ventilation is to support organ function by providing adequate ventilation and oxygenation while decreasing the patients work of breathing. But mechanical ventilation itself can damage alveoli, making protective lung ventilation necessary.

255
Q

Protocol weaning

A

Weaning protocols can reduce the time and cost of care while improving outcomes for ARDS patients. The rule of thumb: the patient either needs full ventilatory support or should be weaning.

256
Q

Preventing complications

A

VILI, DVT, T/P

257
Q

Nursing management of those caring for patients with ARDS

A

-Nursing assessment
Health information
Health history
Medications
Surgery
Symptoms
-Physical assessment
General
Integumentary
Respiratory
Cardiovascular
Gastrointestinal
Neurological
-Laboratory findings

258
Q

Overall goals

A

-ABG values within patient’s baseline
-Breath sounds within patient’s baseline
-No dyspnea or have breathing patterns within patient’s baseline
-Effective cough and ability to clear secretions

259
Q

Prevention

A

the nurse will need to teach a patient at risk for respiratory failure about coughing, deep breathing, incentive spirometry, and ambulation.
Prevention of atelectasis, pneumonia, and complications of immobility, as well as optimizing hydration and nutrition, can potentially decrease the risk of respiratory failure in the acutely or critically ill patient.

260
Q

Mobilization of secretions

A

Hydration and humidification
Chest physiotherapy
Tracheal suctioning
Effective coughing and positioning

261
Q

Medication therapy

A

Short-acting bronchodilators, such as fenoterol hydrobromide and salbutamol, reverse bronchospasm.
If severe bronchospasm continues, IV aminophylline may be administered.
Corticosteroids (e.g., methylprednisolone [Solu-Medrol]) may be used in conjunction with bronchodilating agents when bronchospasm and inflammation are present.
Because long-term oral steroids are associated with systemic adverse effects, their use should be avoided if possible. Instead, inhaled steroids such as fluticasone (Flovent) or budesonide (Pulmicort) are used to reduce the risk of those systemic adverse effects.
IV diuretics (e.g., furosemide [Lasix]) and nitroglycerin are used to decrease pulmonary congestion caused by heart failure. If atrial fibrillation is also present, calcium channel blockers (e.g., diltiazem) and β-adrenergic blockers (e.g., metoprolol) are used to decrease heart rate and improve CO.

262
Q

IV therapy

A

IV antibiotics, such as vancomycin (Vancocin) or ceftriaxone, are frequently given to inhibit bacterial growth.

263
Q

sedation and analgesia medications

A

benzodiazepines (e.g., lorazepam) and narcotics (e.g., morphine, fentanyl) are used to decrease anxiety, agitation, and pain.

264
Q

Nutritional therapy

A

Maintain protein and energy stores.
Enteral or parenteral nutrition
Nutritional supplements
The patient may be prescribed a high-carbohydrate diet, depending on individual patient needs.

265
Q

Age related considerations

A

Decreased ventilatory capacity
Alveolar dilation
Diminished elastic recoil
Decreased respiratory muscle strength
Decreased chest wall compliance

266
Q

What is RSV?

A

Respiratory Syncytial Virus

267
Q

what is affected in RSV

A

The leading cause of lower respiratory tract infections in young children
Almost all children have experience RSV by the age of 2 years.
1-3% of all infants are hospitalized with RSV infection in Canada
The two most common complications from RSV are bronchiolitis and viral pneumonia
The most common cause of hospitalization in children less than 2 years of age (bronchiolitis)
Typically begins, nov-dec and lasts 4-5 months- typically April

268
Q

Who is at most risk for RSV?

A

Children less than 2 years
and those less than 12 months being at most risk peaking at 2-6 months

269
Q

Risk factors for severe RSV

A

Being less than 6 weeks old
Prematurity
Crowded Housing
Lower SES
Down syndrome
Immunocompromised infants
Daycare
Exposure to smoking
Genetics
? Asthma
Young children with congenital (from birth) heart or chronic lung disease
Young children with compromised (weakened) immune systems due to a medical condition or medical treatment
Immunocompromised adults (particularly older adults)

270
Q

RSV transmission

A

RSV transmission occurs from respiratory particles containing the virus and from direct contact with contaminated surfaces.
Direct person to person contact – saliva, mucus or nasal discharge
Close contact like sharing utensils, kissing, nasal discharge)

The infectious period is about 8 days on avg, with range 1-21days
RSV can survive for up to 6 hours on hard surfaces such as tables and crib rails
Typically lives on soft surfaces for 30mins (hands)

271
Q

What day is the worst for RSV symptoms to arise?

A

Days 4-5 biggest, increase SOB, accessory muscle use, nasal flaring, harsh cough, hyperinflation of the lungs.

target is the bronchioles in the lungs that are connected to the alveoli. Wheezing in RSV.
Rhinorrhea, sneezing (cold)
Abx are not helpful

272
Q

where do the majority of RSV deaths occur?

A

low- and middle-income countries, these places are less likely to have access to adequate health care

273
Q

RSV facts

A

Virtually everyone gets RSV at some point in their lives, usually by two years of age.
RSV disease is often mild, like a cold, but can be severe (or deadly) for infants.
Transmission can occur through sneezing or coughing and transference from contaminated surfaces.
Repeated infections can occur over a lifespan.
Although any child can get severely ill or hospitalized due to RSV, children are at highest risk if they are under 6 months of age, have co-infections, or live in a socioeconomically disadvantaged area.

274
Q

RSV Pathophysiology

A

Airway obstruction may occur due to sloughed epithelium and inflammatory cells with mucus and fibrin that get into small airways.

275
Q

compound issues in small children

A

Airway is smaller in diameter and also shorter, which allows pathogens to more easily enter the deeper areas of the respiratory tract.
Why RSV often causes bronchiolitis in children

276
Q

what can RSV cause

A

asthma or COPD exacerbations and secondary infections such as bronchitis or pneumonia.

277
Q

RSV Symptoms for general population

A

Headache, low grade fever and muscle aches
Cough and sore throat
Runny nose, congestion, sneezing
Conjunctivitis and/or ear infection
Vomiting, diarrhea, loss of appetite
Wheezing due to a narrow space

278
Q

RSV Symptoms for under 2

A

Early – runny nose, sneezing, maybe coughing
Rhonchi, wheezing, crackles, diminished breath sounds
Fever
Tachypnea and increased WOB (look for accessory muscle use)
Periods of apnea
Cyanosis
*** A fever in a child less than 2 months is ALWAYS a concern!!!

279
Q

Examples of children’s WOB

A

Nasal flaring, trach tug, intercostal

280
Q

Supportive management for RSV

A

Hydration, fluid, nebs, oxygen

281
Q

Monoclonal antibody prevention

A

PALIVIZUMAB (EXISTING)Short-lasting mAb that can prevent severe RSV in high-risk infants
Use is limited to high-income countries
Requires up to 5 monthly doses
Expensive/ impractical for low- and middle-income markets

NIRSEVIMAB (NEW)Long-acting mAb given at birth or soon thereafter (approved in Europe in late 2022)
Price and supply may be early barriers to access, requiring market shaping to overcome
IM Injection to vastus lateralis
Likely good for full RSV season
79% effective

282
Q

vaccine prevention

A

Only approved for > 60 year olds and individuals 32-36 weeks pregnant as of now
One time injection of vaccine
Not publicly funded in Nova Scotia but is in certain provinces based on criteria

283
Q

Management – Moderate to Severe BRONCHIOLITIS

A

oxygenation
hydration
MEDICATIONS
» The majority of evidence for bronchiolitis treatment is for infants less than 12 months of age with a first episode of wheezing in the winter months. The following treatment recommendations are intended for this population.
EPINEPHRINE AND HYPERTONIC SALINE

284
Q

DO NOT USE what when treating bronchiolits

A

salbutamol
ipratropium bromide
inhaled corticosteroids
abx
oral bronchodilators
systemic corticosteroids

285
Q

symptoms peak when? and can last how long?

A

5 day peak
21 days duration

286
Q

sats under what is indicative of admission to hospital

A

90%

287
Q

Nursing interventions

A
  1. For a child with bronchiolitis, interventions are aimed at treating symptoms and include airway maintenance, cool humidified air and oxygen, adequate fluid intake, and medications.
    2.For a hospitalized child with RSV, the child should be admitted to a single room to prevent transmission of the virus.
  2. Ensure that nurses caring for a child with RSV do not care for other high-risk children.
  3. Use contact, droplet, and universal precautions during care; use of good handwashing techniques is necessary.
  4. Monitor airway status and maintain a patent airway.
  5. For the most effective airway maintenance, position the child at a 30- to 40-degree angle with their neck slightly extended to maintain an open airway and decrease pressure on the diaphragm.
  6. Provide cool, humidified oxygen as prescribed.
  7. Monitor pulse oximetry levels.
  8. Encourage fluids; fluids administered intravenously may be necessary until the acute stage has passed.
  9. Periodic suctioning may be necessary if nasal secretions are copious; use of a bulb syringe for suctioning infants may be effective. Suctioning should be done before feeding to promote comfort and adequate intake.
288
Q

viral pneumonia

A

a. Acute or insidious onset
b. Symptoms range from mild fever, slight cough, and malaise to high fever, severe cough, and diaphoresis.
c. Nonproductive or productive cough of small amounts of whitish sputum
d. Wheezes or fine crackles—audible high-pitched crackling or popping sounds heard during lung auscultation; result from fluid in the airways and are not cleared by coughing

289
Q

PVZ is offered to who?

A

premature infants of < 30 weeks gestational age (wGA) and < 6 months of age at onset of or during the RSV season;
Children aged < 24 months with chronic lung disease of prematurity who require ongoing oxygen therapy within the 6 months preceding or during the RSV season
Infants aged < 12 months with haemodynamically significant CHD and infants born at < 36 wGA and age < 6 months old living in remote northern Inuit communities who would require air transport for hospitalization. For children with both CHD and chronic lung disease, recommendations for chronic lung disease should be followed.

290
Q

PVZ is NOT offered to whom?

A

PVZ should not be offered to otherwise healthy infants born at or after 33 wGA; or to siblings in multiple births who do not otherwise qualify for prophylaxis. It should not be offered routinely for children <24 months of age with cystic fibrosis; for children <24 months of age with Down syndrome without other criteria for PVZ; or for healthy term infants living in remote northern Inuit communities, unless hospitalization rates for RSV are very high.

291
Q

Chemotherapy

A

Tradition → travels through bloodstream and destroys all rapidly dividing cells healthy and unhealthy

292
Q

Radiation

A

High energy waves or particles sent to the site of cancer and destroys DNA of cells so they can no longer grow and divide
Given through internal (brachytherapy) and external and systemic

293
Q

Hodgkin’s

A

Localized, single group of nodes
Patients nave relatively good prognosis
Reed sternbergcells
Young adult hood and >55 years
Associated with EBV
Low grade fever, severe night sweats, weight loss

294
Q

Non-hodgkins

A

Multiple lymph nodes involved
Majority beers involved a few are T cell lineage
can occur in children and adults
Maybe associated with HIV and autoimmune disorders

295
Q

3 main type leukemia

A

ALL, CLL ,AML

296
Q

PEEP stands for what

A

Positive end expiratory pressure

297
Q

ALL

A

In ALL, the bone marrow makes too many immature lymphocytes (a type of white blood cell).
It’s most common in children, but adults can get it too.
Symptoms can include fatigue, easy bruising or bleeding, fever, and bone pain.
Treatment usually involves chemotherapy, and sometimes a bone marrow transplant.

298
Q

AML

A

In AML, the bone marrow makes too many immature myeloid cells (another type of white blood cell).
It can affect both adults and children, but it’s more common in older adults.
Symptoms can be similar to ALL, like fatigue, bruising, and fever.
Treatment also typically involves chemotherapy, sometimes followed by a bone marrow transplant.

299
Q

Main difference between ALL and AML

A

the main difference lies in the type of immature cells that are overproduced in the bone marrow. In ALL, it’s immature lymphocytes, and in AML, it’s immature myeloid cells. Both require prompt medical attention and treatment.

300
Q

AML

A

AML involves the rapid growth of abnormal myeloid cells in the bone marrow.
It can occur in both adults and children but is more common in older adults.

301
Q

ALL

A

This is a type of leukemia where too many immature lymphocytes (a type of white blood cell) are produced in the bone marrow.
ALL is more common in children but can also affect adults.

302
Q

CLL

A

CLL is characterized by the accumulation of abnormal lymphocytes in the blood, bone marrow, and lymph nodes.
It usually progresses slowly and is more common in older adults.

303
Q

CML

A

CML is marked by the excessive production of mature and immature granulocytes (a type of myeloid cell) in the bone marrow.
It typically progresses slowly but can accelerate into a more aggressive phase.

304
Q

Sepsis facts

A

Leading cause of death in Canada, 30 - 50% mortality rate higher among males than females

305
Q

Sepsis facts

A

Leading cause of death in Canada, 30 - 50% mortality rate higher among males than females

306
Q

What is shock?

A

Inadequate tissue perfusion, cellular and tissue hypoxia
Due to: increase 02 delivery, increase 02 consumption, insufficient 02 utilization or a combo of them all

307
Q

3 main types of shock

A

Hypovolaemic, cardiogenic and distributive

308
Q

3 main types of shock

A

Hypovolaemic, cardiogenic and distributive

309
Q

Hypovolemic

A

Decreased preload due to intravascular volume loss. Diminished preload decreases CO so SVR increases in an effort to compensate and maintain perfusion

310
Q

Cardiogenic (includes obstructive)

A

Pump failure = decrease CO
SVR increases in an effort to compensate for the diminished CO to maintain perfusion

311
Q

Cardiogenic (includes obstructive)

A

Pump failure = decrease CO
SVR increases in an effort to compensate for the diminished CO to maintain perfusion

312
Q

Distributive= vasodilatory

A

Includes sepsis, anaphylaxis, neurogenic, cellular toxin
Consequences of severely decreased SVR
CO is increased in an effort to compensate for SVR

313
Q

Infection

A

pathological process caused by invasion of normally sterile tissue or fluid or body cavity by pathogenic or potentially pathogenic micro-organisms

314
Q

Sepsis

A

Infection plus 2 or more sirs

315
Q

Severe sepsis

A

Infection plus 2 or more sirs plus new organ dysfunction

316
Q

Septic shock

A

severe sepsis with a lactate greater than or equal to 4 mmol/L OR continued hypotension (systolic BP < 90, MAP < 65 or 40 mmHg decrease from their baseline) after initial fluid bolus (30 mL/kg)

317
Q

Pathophysiology of sepsis

A

Septic Shock = “Rotten” “decreased tissue perfusion”
Infective material invades blood stream (bacterial, viral or fungal)
WBC fight off in vasculature
Fibrinolysis
Inflammatory state
WBC release nitrous oxide, cytokines and other molecules that interact with vessel and cause endothelial injury
Vasodilation
Increase permeability
Difficult for cells to receive O2 from RBC due to increased fluids leaving vasculature
Cells deprives of oxygen and “starve”
WBC release lytic enzymes that damage pathogens but also damage vasculature (happening through whole body!)
Clotting factors activated
Increased coagulation
DIC or ARDS are serious complications that carry high mortality
CO originally increased to compensate for dec. SVR but fatigues. CO will lower and BP lower
Early infection – skins may be warm  Cool and clammy CONCERNING!!!

318
Q

When to suspect sepsis

A

The qsofa “hat”
Hypovelemia - SBP</=100mmhg
Altered mentatation - GCS less than 15
Tachypnea - RR >22/min

319
Q

Signs of end organ dysfunction (hypo perfusion)

A

Altered mental status
• Cardiac dysfunction
• Acute respiratory distress/hypoxia
Decreased urine output (normal output is 0.5-1 mL/kg/hr)
Serum lactate (lactic acid) > 2.2 mmol/L
Coagulopathy (INR >1.5 or aPTT >60 secs) ¨ Bilirubin > 34.2 µmol/L
Platelet count < 100,000

320
Q

3 key components to recognizing and responding to sepsis for inpatients

A

1.timely recognition of early infection
2. Early treatment with antibiotics: intravenous fluids
3. Appropriate escalation to high acuity or ICU care

321
Q

Disruptive shock:

A

Increased coagulation and inflammation
Decreased fibrinolysis
Formation of microthrombi
Obstruction of microvasculature
Clinical presentation of sepsis is complex
Current clinical criteria are hypotension, elevated lactate level, and a sustained need for vasopressor therapy.
Hyperdynamic state: increased CO and decreased SVR

322
Q

Distributive shock symptoms

A

Tachycardia
Tachypnea/hyperventilation
Temperature dysregulation
Decreased urine output
Altered neurological status
GI dysfunction
Respiratory failure is common.

323
Q

How to diagnose

A

Vitals
Blood cultures
Lactate
ABG
BUN
Creatinine

324
Q

Treatment for shock

A

Quicker treatment = Decreased mortality
Broad spectrum abx
Fluid Resusitation
2 Large Bore Ivs
Monitor Progress

325
Q

Why do ALL sepsis patients need volume need volume?

A

Vascular volume is lost into interstitial space do to diffuse capillary leaking from cytokine release
Both venous and arteriolar tone is reduced and blood volume occupies a larger intravascular space than normal
Many patients also have GI and skin losses

326
Q

when to give bolus

A

Aggressive fluid resuscitation is a vital component of initial management of a patient with severe sepsis with either hypotension or a lactate greater than or equal to four.

Fluid should be given very fast, using gravity or a pressure bag—not by an infusion pump. The goal is to provide 500 mL every 15-30 minutes until the 30 mL/kg bolus is achieved.

327
Q

Do patients who have known heart failure, kidney disease or low EF?

A

Yes, still require the fluid for the same reasons other patients in severe sepsis need the fluid. In this population we might just need to provide the fluid a little slower with more frequent reassessments.

328
Q

what are the stages of shock

A

Initial
Compensatory
Progressive
Refractory

329
Q

Initial

A

Cellular level
Not clinically apparent
Metabolism changes at the cellular level, from aerobic to anaerobic-lactic acid buildup

330
Q

Compensatory

A

Baroreceptors in Body activates neural, hormonal, and biochemical compensatory mechanisms.
-Attempt to overcome the increasing consequences of anaerobic metabolism and to maintain homeostasis.
-Clinical presentation begins to reflect the body’s responses to the imbalance in oxygen supply and demand
-Classic sign hypotension
carotid and aortic bodies activate SNS ….. Norepi, epi
-Blood flow to heart and brain preserved and BF to other organs is diverted or shunted
-Inspired air cannot participate in gas exchange in certain areas of lung due to dead space
-During the compensatory stage, the body can compensate for the changes in tissue perfusion.
-Perfusion deficit is corrected and patient recovers with few or no residual consequences.
AND IF Perfusion deficit is not corrected and the body is unable to compensate, the patient enters the progressive stage of shock.

331
Q

Progressive

A

-Changes in mental status important to assess here
-Continued decreased cellular perfusion and resulting altered capillary permeability are the distinguishing features of this stage.
-As a result of altered capillary permeability, fluid and protein leak out of the vascular space into the surrounding interstitial space.
-Fluid leakage from the vascular space also affects the solid organs (e.g., liver, spleen, GI tract, lungs) and peripheral tissues by further decreasing perfusion.
-Aggressive interventions to prevent multiple organ dysfunction syndrome

332
Q

Multiple organ dysfunction syndrome

A

—Fluid moves into alveoli
Alveolar edema
Decreased surfactant production
Worsening V/Q mismatch
Tachypnea
Crackles
Increased work of breathing
—CO begins to fall
Decreased artery, cerebral and peripheral perfusion
Hypoperfusion
Weak peripheral pulses
Ischemia of distal extremities
—Myocardial dysfunction results in
Dysrhythmias
Ischemia
Myocardial infarction (MI)
—Mucosal barrier of GI system becomes ischemic
Ulcers
Bleeding
Risk of translocation of bacteria
Decreased ability to absorb nutrients
—Liver fails to metabolize medications and waste.
Jaundice
Elevated enzymes
Loss of immune function
Risk for DIC and significant bleeding

333
Q

Refractory stage

A

Increased capillary permeability allows fluid and plasma proteins to leave the vascular space and move to the interstitial space.
Blood pools in the capillary beds secondary to the constricted venules and dilated arterioles.
Loss of intravascular volume worsens hypotension and tachycardia and decreases coronary blood flow.
Decreased coronary blood flow leads to worsening myocardial depression and a further decline in CO.
Profound hypotension and hypoxemia
Tachycardia worsens.
Failure of one organ system affects others.
Recovery unlikely

334
Q

Diagnostic studies

A

Thorough history and physical examination
No single study to determine shock
Blood studies
Elevation of lactate
Base deficit
12-lead ECG
Chest radiograph
Continuous pulse oximetry
Hemodynamic monitoring

335
Q

Primary therapy for sepsis is?

A

Cornerstone of therapy for septic, hypovolemic, and anaphylactic shock = volume expansion
Crystalloids (e.g., normal saline); exact fluid is controversial
Colloids (e.g., albumin) have not been shown to improve patient outcomes except for packed red blood cells (PRBCs) to correct for hypovolemia due to exsanguination.
Before beginning fluid resuscitation, the nurse should insert two large-bore (e.g., 14–69-gauge) intravenous (IV) catheters, preferably into the antecubital veins.

336
Q

what to monitor when giving fluids?

A

Fluid responsiveness:
Determined by clinical assessment
Hemodynamic parameters
Monitor trends in BP
In-dwelling urinary catheter to monitor urine output
The goal for fluid resuscitation is to restore tissue perfusion.

337
Q

If fluids do NOT work what do you give?

A

Vasopressor medications (e.g., norepinephrine)
Achieve/maintain mean arterial pressure (MAP) >65 mm Hg
Reserved for patients unresponsive to fluid resuscitation
** NB: Medications used to improve perfusion in shock are administered intravenously via an infusion pump and a central venous line.

338
Q

Is nutrition important in sepsis?

A

Protein-calorie malnutrition is one of the main manifestations of hypermetabolism in shock.
Start the patient on a slow, continuous drip of very small amounts of enteral feedings.
Early enteral feedings enhance perfusion of the GI tract and help maintain the integrity of the gut mucosa.
Initiate parenteral nutrition if enteral feedings are contraindicated or fail to meet caloric requirements.
Monitor weight, protein, nitrogen balance, blood urea nitrogen (BUN), glucose, and electrolytes.
Large weight gains are common because of third spacing of fluids.

339
Q

Steps for caring with someone with septic shock

A

Fluid replacement to restore perfusion (30 or more mL/kg)
Hemodynamic monitoring
Vasopressor medication therapy
Vasopressin for patients refractory to vasopressor therapy

340
Q

why are IV corticosteroids recommended?

A

IV corticosteroids are recommended only for patients in septic shock who cannot maintain adequate BP with vasopressor therapy despite fluid resuscitation.

341
Q

When should antibiotics be started?

A

Antibiotics after cultures are obtained (e.g., blood, wound exudate, urine, stool, sputum)
should be started within the first hour of septic shock.

342
Q

Glucose levels during septic shock

A

Early research showed improved survival rates when continuous infusions of insulin and glucose were used to keep glucose levels between 4.44 and 6.11 mmol/L.
However, recent studies have shown lower mortality rates and fewer episodes of severe hypoglycemia when glucose levels were kept at <10.0 mmol/L.

343
Q

What is DIC?

A

Disseminated intravascular coagulation— too much and too little clotting.

344
Q

DIC?

A

Characterized by activation and malfunctioning of coagulation pathways, resulting in formation of intravascular thrombi and depletion of platelets and coagulation factors.
AND
Activated pathways produce multiple fibrin clots in small blood vessels. Reduction of coagulation factors and platelets results in increased bleeding risk

345
Q

Common findings of DIC

A

Petechiae or purpura
thrombosis, bleeding, or both.
Microvascular thrombosis often results in multi-organ ischemia and failure.

Hypotension
Tachycardia
Circulatory collapse
Dyspneal/hypoxia
Gastrointestinal ulcers
Adrenal dysfunction.

Hemorrhagic findings include petechiae/ecchymosis, oozing, intracranial bleeding, hematuria, and massive gastrointestinal bleeding.

Ischaemic findings include purpura fulminans/gangrene/acrocyanosis, delirium/coma
In general, ischemic findings are considered earlier signs of DIC, while bleeding findings are late overt signs.

346
Q

Immediate nursing interventions

A

First initiate intravenous fluid resuscitation to support blood pressure
* Control active bleeding
* Apply oxygen
* Assess, monitor and document sites of bleeding or cyanosis
* Place the patient in the Trendelenburg position (elevate legs)
* Establish immediate venous and /or arterial access
* Include supportive measures as directed by the Primary Care Provider
* Communicate and educate the patient, and family

347
Q

Lab findings

A

decreased platelets
prolonged PT time
fibrinogen decreased
ddimer elevated
aptt unpredictable

348
Q

DIC management

A

First treat the underlying cause. After the underlying disease has been identified and therapy initiated, symptomatic treatment of thrombosis, hemorrhage, hypotension, acidosis, and hypoxia can also be directed.
The four key medical management aims are:
1. Remove the trigger or treat the underlying cause.
2. Maintain organ perfusion.
3. Restore the balance of normal homeostasis.
4. Provide supportive management of complications.
Oxygen – IV fluids

349
Q

Pathophysiology of DIC

A

In major injury, there is a release of procoagulants, tissue factors and enzymes - excessive activation of coagulation cascase - thrombosis of small and medium vessels occurs
Ischemia, necrosis and organ damage can occur
Kidneys, liver, lungs and brain are particularly susceptible
Massive formation of clots throughout body deplete platelets and clotting factors.
Infection/sepsis, trauma, malignancy, obstetrical complications, burn victims, snake bites, anaphylaxis are some examples

350
Q

Generalized bleeding from how many unrelated sites is suggestive of DIC?

A

3

351
Q

Thrombus

A

A clot that form within a vessel, bad “blood clot”

352
Q

Thrombosis

A

Process of thrombus forming

353
Q

Emboli (embolus - singular)

A

General term for a foreign body free floating in blood stream (example: blood, air, fatty deposit)

354
Q

Tromboembolus

A

Clotted material

355
Q

Thromboembolism

A

Actually blocks artery

356
Q

Thrombin

A

Enzyme that ispart of coagulation cascade converting fibrinogen to fibrin

357
Q

Venous thrombolism

A

Most common disorder of the veins, can be either superficial or deep vein thrombosis.

358
Q

Superficial vein thrombosis (svt)

A

Formation of a thrombus in a superficial vein, usually the greater or lesser saphenous vein, generally a benign disorder.

359
Q

Deep vein thrombosis (dvt)

A

Involving a thrombus in a deep vein, most common in iliac and femoral vein.
VTE represents the spectrum of pathology from DVT to pulmonary embolis.

360
Q

Characteristics of superficial vein thrombosis

A

Varicosities →tenderness, rubourwarmth, pain, inflammation and induration along the course of the superficial vein, vein appears as palpable cord. Edema rarely occurs. If let untreated clot may extend to deeper veins and VTE may occur.

361
Q

VTE - superficial

A

Often a palpable, form, cordlike vein
Surrounding area tender, warm, red
May have low grade temp and leukocytosis
May have edema to affected extremity
Most common cause is from IV cannulation ( particularly >48 hours)

362
Q

Thrombophlebitis management

A

Initial treatment of infusion-related SVT involves the immediate removal of the IV catheter, ultrasounds is used to confirm the diagnosis (clot 5cm or larger) and to rule out clot extension to a deep
Interventions: wear graduated compression stockings or bandages, apply warm compresses, elevate affected limb above the heart, apply topical NSAIDS and perform mild exercise (walking)

363
Q

Deep vein Thrombosis

A

Development of a blood clot in a major deep vein in the leg, thigh, pelvis or abdomen canalso happen arms, the portal, mesenteric, ovarian, or retinal veins and venous sinuses of the brain. DVT results in impaired venous blood flow
There is a genetic predisposition as 1st degree relative with history of PE or DVT.

364
Q

Risk factors for DVT

A

Advanced age
Obesity
Recent surgery
Major trauma
Active cancer
Acute medical illness
Stroke or immobilization
Previous clot
Congenital venous malformation
Varicose veins
Central venous catheter or IVC filter
Long distance travel
Oral contraceptives
Pregnancy
Antiphospholipid syndrome
Inherited thrombophilia

365
Q

Risk factors for DVT

A

Advanced age
Obesity
Recent surgery
Major trauma
Active cancer
Acute medical illness
Stroke or immobilization
Previous clot
Congenital venous malformation
Varicose veins
Central venous catheter or IVC filter
Long distance travel
Oral contraceptives
Pregnancy
Antiphospholipid syndrome
Inherited thrombophilia

366
Q

Goal for treatment of a confirmed DVT are to?

A

Prevent new clot development
Prevent spread of the clot
Prevent embolization

367
Q

Pharmacology for dvt’s

A

Vitamin K antagonists
Thrombin inhibitors (both indirect and direct)
Factor xa inhibitors

368
Q

Antidote for warfarin

A

Vitamin K

369
Q

When does warfarin take effect?

A

48-72 hours and the level of anticoagulation is monitored daily with the INR

370
Q

Unfractionated heparin

A

Medication → heparin sodium can be given IV, subcut continuous measured by APTT by monitoring at regular intervals

371
Q

Low molecular weight heparin (lmwh)

A

Medications→ enoxaparin, dalteparin. Given subcut, typically tests are not required CBC may be ordered at regular interval

372
Q

Antidote for heparin

A

Protamine

373
Q

Factor xa inhibitors

A

Produce rapid anticoagulation
Examples: fondaparinx, rivaroxaban ( xarelto) andapixaban (eliquis)
All these are used for both VTE prevention and treatment
Coagulation monitoring is not necessary

374
Q

What is HIT?

A

Serious adverse effect of heparin induced thrombocytopenia (HIT)
This is an immune reaction to heparin in which the platelet count diminishes severely and suddenly along with a paradoxical increase in venous or arterial thrombosis
Diagnosed by measurements for the presence of heparin antibodies in the blood
Treatment requires immediate stopping and if further anticoagulation is required use a nonheparin anticoagulant.

375
Q

Physical findings of hit

A

Signs of PE
Signs of use-dvt
Ischemic limb necrosis
Necrotic skin lesions
Signs of DVT
Abdominal tenderness (venous thrombosis)
Hypotension (adrenal insufficiency)
CNS findings (dural venous sinus thrombosis)

376
Q

Clinical features of DVT

A

Unilateral leg edema (larger calf diameter)
Erythema
Warmth
Tenderness
Homans sign (unreliable)
Pitting e demo may be present
Superficial venous dilatation
80% of clots are in great saphenous vein
Measure calves at 10cm
Below tibial tuberosity

377
Q

What is the name of criteria chart for dvt’s

A

Well’s criteria

378
Q

Investigations of dvt’s

A

D dimer (for wells criteria under 2)
Ultrasound (for wells criteria over 2)

379
Q

Assessment of hospitalized patients → prophylaxis

A

Low SX → minor: mobilize patient
Moderate sx→ general, gyne, urology, surgery and bedrest
High → hip/knee sx, major trauma, spinal cord injury and cancer surgery

380
Q

Are compression stockings recommended if patient already has VTE?

A

No and they must be fitted correctly

381
Q

Nursing diagnoses

A

Acute-pain
Ineffective health maintenance
Impaired skin integrity
Risk for bleeding related to anticoagulant therapy

382
Q

Overall goals For VTE

A
  1. Pain relief
  2. Decreased edema
  3. No skin ulceration
  4. No evidence of pulmonary embolism
383
Q

What should be educated to patient?

A

Avoid takin aspirin NSAIDS fish oil supplements garlic supplements ginkgo biloba and certain abx
Report any bleeding excessive bruising coffee ground vomit excessive menstrual bleeding

384
Q

Pulmonary embolism

A

Blockage of pulmonary arteries by a thrombus,fat or air embolus or tumor tissue
Mortality rate 30.% when left untreated when treated with therapy reduced to 6-8%
Lethal PE’s most commonly originates in the femoral or illiac veins

385
Q

Other sites of origin of PE include

A

right side of the heart, especially with atrial fibrillation
Upper extremities, which is rare sometimes though from the presence of central venous catheters or cardiac pacing wires
The pelvic veins, especially after surgery or childbirth
Risk factors are from virchows triad

386
Q

Risk factors for PE

A

Prior DVT or PE, congestive heart failure, malignancy, obesity, smoking, pregnancy, lower, limb injury, orthopaedic surgery, prolong mobilization, travel, surgery requiring 30 minutes greater under general anaesthesia

387
Q

Clinical manifestations of PE

A

Varied and non-specific, making diagnosis difficult
Classic triad, such as dyspnea, chest pain, hemoptysis
Syncope, tachypnea, hypotension may be present and may begin slow or sudden
ECG → changes such as RBBB or T wave inversion
Mild to moderate hypoxemia with a low pressure of C02

388
Q

investigations for pe?

A

VQ scan can be done if CT Angio should not be done for example, Patient with severe kidney disease, a young patient pregnancy or contrast allergy. Consider echo if very unstable compression ultrasound for proximal DVT and provoked PE risk factors from virchows triad unprovoked idiopathic is 50%.

389
Q

Prophylaxis in management of pulmonary embolism

A

Management oxygen therapy
Pharmacology needs to continue at least three months after PE sometimes this becomes lifelong reoccurring emboli always treated, lifelong sometimes thrombolic medication‘s will be given

390
Q

What is cerebral palsy?

A

umbrella term referring to a non-progressive disease of the brain.

391
Q

Where does it originate?

A

Originates during the antenatal, neonatal, or early postnatal period.
when brain neuronal connections are still evolving and results in disorders of movement and posture development.

392
Q

What does it affect ?

A

Brain injury interferes with messages from the brain to the body affecting body movement and muscle coordination.
CP does not damage a child’s muscles or the nerves connecting them to the spinal cord—only the brain’s ability to control the muscles.
Depending on how much of the brain was affected, the effects of CP vary widely from individual to individual.

393
Q

Mild CP

A

may result in a slight awkwardness of movement or hand control.
At its most severe, CP may result in virtually no muscle control, profoundly affecting movement and speech

394
Q

Is CP curable?

A

Non curable, life long condition, damage does not worsen, may be congenital or acquired

395
Q

Pathophysiology of CP

A

Premature neonatal brain is susceptible to two main pathologies:intraventricular hemorrhage (IVH)andperiventricular leukomalacia (PVL).
Both pathologies increase the risk of CP, PVL is more closely related to CP and is the leading underlying etiology in preterm infants.
The term PVL describes white matter in the periventricular region that is underdeveloped or damaged (“leukomalacia”).
Both IVH and PVL cause CP because thecorticospinal tracts, composed of descending motor axons, course through the periventricular region

396
Q

Intraventricular Hemorrhage (IVH)

A

IVH describes bleeding from the subependymal matrix (the origin of fetal brain cells) into the ventricles of the brain.
Blood vessels around the ventricles develop late in the third trimester, thus preterm infants have underdeveloped periventricular blood vessels, predisposing them to increased risk of IVH. The risk of CP increases with the severity of IVH.

397
Q

Periventricular Leukomalacia (PVL)

A

PVL is a separate pathological process. The pathogenesis of PVL arises from two important factors: (1)ischemia/hypoxiaand (2)infection/inflammation.

398
Q

Ischemia/hypoxia

A

The periventricular white matter of the neonatal brain is supplied by the distal segments of adjacent cerebral arteries.
Although collateral blood flow from two arterial sources protects the area when one artery is blocked (e.g., thromboembolic stroke), thiswatershed zoneis susceptible to damage from cerebral hypoperfusion (i.e., decreased cerebral blood flow in the brain overall). Since preterm and even term neonates have low cerebral blood flow, the periventricular white matter is susceptible to ischemic damage.

399
Q

Autoregulation of cerebral blood flow

A

usually protects the fetal brain from hypoperfusion, however, it is limited in preterm infants due to immature vasoregulatory mechanisms and underdevelopment of arteriolar smooth muscles.

400
Q

Infection and inflammation

A

This process involvesmicroglial (brain macrophage) cell activation and cytokine release, which causes damage to a specific cell type in the developing brain called the oligodendrocyte.

401
Q

Causes of Cerebral Palsy

A

Antenatal: Prematurity and low birth weight, intrauterine infections, multiple gestation, pregnancy complications.
Perinatal: Birth asphyxia, complicated labor delivery.
Postnatal: non accidental injury, head trauma, meningitis, encephalitis, cardiopulmonary arrest

402
Q

Protective factors

A

obstetrical care: magnesium sulfate, antibiotics, corticosteroids

403
Q

Motor types

A

Spastic
Ataxic
Dyskinetic
Mixed types

404
Q

Spastic

A

70-80% most common form. muscle appear stiff and tight. arises from motor cortex damage.
Cerebral cortex

405
Q

Ataxic

A

6%, characterized by shaky movements, affects balance and sense of positioning in space. Arises from cerebellum damage.

406
Q

Dyskinetic

A

6%, characterized by involuntary movements. arises from basal ganglia damage.

407
Q

Mixed types

A

combination damage, multiple parts of the brain.

408
Q

Monoplegia

A

Affecting one limb, usually lower limb

409
Q

Hemiplegia

A

affecting the upper and lower limbs on one side of the body, the upper limb is usually more affected than the lower limb.

410
Q

Diplegia

A

Affecting all limbs, but the lower limbs are much more affected that the upper limbs, which usually only show fine motor impairment.

411
Q

Triplegia

A

affecting all limbs, usually the two lower limbs and one upper limb. the lower limb is usually more affected on the side of the upper-limb involvement.

412
Q

Quadriplegia

A

Affecting all four limbs and the trunk, also known as tetraplegia.

413
Q

SPASTIC (SPASTIC CEREBRAL PALSY)

A

Increased muscle tone.
Muscles continually contract, making limbs stiff, rigid, and resistant to flexing or relaxing.
Reflexes can be exaggerated, movements tend to be jerky and awkward.
Often, the arms and legs are affected.
The tongue, mouth, and pharynx can be affected, as well, impairing speech, eating, breathing, and swallowing.
The injury to the brain occurs in the cerebral cortex and is referred to as upper motor neuron damage.
Stress on body can result in associated conditions such as hip dislocation, scoliosis, and limb deformities. Concern with the constant contracting of muscles (contracture) that results in painful joint deformities.
Spastic Cerebral Palsy is often named in combination with a topographical method that describes which limbs are affected, such as spastic diplegia, spastic hemiparesis, and spastic quadriplegia

414
Q

Non spastic CP

A

An injury in the brain outside the pyramidal tract causes non-spastic Cerebral Palsy.
Due to the location of the injury, mental impairment and seizures are less likely.
Non-spastic Cerebral Palsy lowers the likelihood of joint and limb deformities.
The ability to speak may be impaired as a result of physical, not intellectual, impairment.
Non-spastic Cerebral Palsy is divided into two groups, ataxic and dyskinetic. Together they make up 11% of Cerebral Palsy cases.

415
Q

Dyskinetic Cerebral Palsy

A

separated further into two different groups; athetoid and dystonic

416
Q

Athetoid

A

Cerebral Palsy includes cases with involuntary movement, especially in the arms, legs, and hands.

417
Q

Dystonia/Dystonic

A

Cerebral Palsy encompasses cases that affect the trunk muscles more than the limbs and results in fixed, twisted posture.
Because non-spastic Cerebral Palsy is predominantly associated with involuntary movements, some may classify Cerebral Palsy by the specific movement dysfunction.

418
Q

Athetosis

A

slow, writhing movements that are often repetitive, sinuous, and rhythmic

419
Q

Chorea

A

irregular movements that are not repetitive or rhythmic, and tend to be more jerky and shaky

420
Q

Chorea

A

irregular movements that are not repetitive or rhythmic, and tend to be more jerky and shaky

421
Q

Choreoathetoid

A

a combination of chorea and athetosis; movements are irregular, but twisting and curving

422
Q

Dystonia

A

involuntary movements accompanied by an abnormal, sustained posture

423
Q

Ataxic CP

A

Ataxic Cerebral Palsy affects coordinated movements.
Balance and posture are involved.
Walking gait is often very wide and sometimes irregular.
Control of eye movements and depth perception can be impaired.
Often, fine motor skills requiring coordination of the eyes and hands, such as writing, are difficult.
Does not produce involuntary movements, but instead indicates impaired balance and coordination

424
Q

Cerebral Palsy Classifications

A

Mild, Moderate, Severe

425
Q

Mild CP

A

Mild Cerebral Palsy means a child can move without assistance; his or her daily activities are not limited.

426
Q

Moderate CP

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Moderate Cerebral Palsy means a child will need braces, medications, and adaptive technology to accomplish daily activities

427
Q

Severe CP

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Severe Cerebral Palsy means a child will require a wheelchair and will have significant challenges in accomplishing daily activities.

428
Q

General Assessment

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Suspicions of CP are commonly based on a positive history ofadverse perinatal or antenatal events.
If no positive history, suspicions are often raised by parental or familyobservations of developmental delays.
Observations of the child while being held by their caregiver include: movements, posture, dysmorphic features, etc.
Growth curves: crossing major percentile lines raises concerns for growth and developmental disorder
CP is non-progressive but can change its clinical manifestations throughout childhood. Therefore, such changes are important to discuss with parents.
Examine and rule out the possibility ofdegenerative diseases, metabolic disorders, spinal cord lesions/tumours, muscular dystrophy, and anomalies of the cervical spinal cord and skull.

429
Q

Children Assessment

A
  1. Extreme irritability and crying
  2. Feeding difficulties
  3. Abnormal motor performance
  4. Alterations of muscle tone; stiff and rigid arms or legs
  5. Delayed developmental milestones
  6. Persistence of primitive infantile reflexes (Moro, tonic neck) after 6 months (most primitive reflexes disappear by 3 to 4 months of age)
  7. Abnormal posturing, such as opisthotonos (exaggerated arching of the back)
  8. Seizures may occur.
430
Q

Associated disorders

A

Hearing deficits, visual deficits, speech and language problems, intellectual disability, growth and development, spinal deformities and osteoarthritis, incontinence, infections and long term illness, malnutrition, contractures.

431
Q

Diagnosis of CP

A

Brain imaging is one of the most useful diagnostic tools
Confirmation of brain/spinal cord lesion via MRI.
Location and extent of lesion.
May reveal periventricular leukomalacia, congenital malformation, stroke, or haemorrhage. Cystic lesions may be present, and are not unusual in cases of hemiplegia as a result of antenatal or perinatal vascular accidents.
Can at times be ‘normal’ in the face of clear clinical findings.
Severe disease can be diagnosed shortly after birth but mild disease may not be picked up until after up to years of age

432
Q

Common Hospital Visit Concerns

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Respiratory problems particularly pneumonia
Uncontrolled seizures / status epilepticus
Unexplained irritability - consider acute infections, oesophagitis, dental disease, hip subluxation, pathological fracture. Review medications.

433
Q

Communication Devices

A

symbol boards
voice synthesizers
head sticks and keyguards for computers

433
Q

Mobility Devices

A

wheelchairs (manual, power and sports)
scooters
specially made bicycles and tricylces
walkers and crutches

434
Q

Daily Living Aids

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electronic door openers
large-handled eating utensils
grab sticks
environmental control systems

435
Q

What is ADHD?

A

ADHD is a chronic neurodevelopmental disorder that affects approximately 5%-9% of children and 3%-5% of adults.
ADHD is highly hereditary ~ 75% – comparable to heritability of height
A medical condition characterized by inattention and hyperactivity – impulsivity.
An individual with ADHD finds it more difficult to focus without becoming distracted
Individuals with ADHD not only have difficulty focusing but sometimes have difficulty breaking focus on certain behaviors (i.e. playing video games)

436
Q

ADD VS ADHD

A

They are the same, ADD Is the old term

437
Q

Is ADHD highly hereditary

A

Yes, 75%

438
Q

Who is diagnosed more?

A

Males see more hyperactivity

439
Q

Hows ADHD diagnosed

A

Dsm-5

440
Q

How are you diagnosed

A

Starts between 6-12 years old and there’s 2 types→ inattentive and hyperactive/impulsive and you can also have both

441
Q

Inattentive

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Not paying attention, must have 6/9 symptoms for atleast 6 months
Careless mistakes, not listening, easily distracted

442
Q

Hyperactive/ impulsive

A

Overly active and impulsive must have 6/9 symptoms for at least 6 months
Fidget, squirm, get up often

443
Q

ADHD in girls

A

Not always present with the inattentive presentation therefore less noticeable in school
Less likely to show disruptive behaviour
Hyperactivity can sometimes be seen verbally
Girls are as impaired as boys in social skills and academic achievement although they are under diagnosed

444
Q

ADHD is rarely by itself true or false?

A

True often have comorbid mental health disorders

445
Q

What is dysthymia?

A

Form of chronic depression

446
Q

Preschool

A

Behavioural disturbances

447
Q

School age

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Behavioural disturbance, academic problems, difficulty with social interaction and self-esteem issues

448
Q

Adolescence

A

Academic problems, difficulty with social interactions, self-esteem issues, legal issues, smoking, drugs, injury/accidents and risky sexual behaviour

449
Q

College age

A

Academic problems, occupational difficulties, relationship, problems, self-esteem, issues, substance abuse, injuries/accidents, risky, sexual behaviour

450
Q

Adult

A

Occupational failure, self-esteem issues, injury/accident, relationship, problems, substance, abuse, and risky sexual behaviour

451
Q

ADH

A

Focus is on pharmacological and nonpharmacological options behavioural psychotherapy is also an option to use be used as an adjunct. This focusses on teaching time management and organizational skills rewards when sticking to routine and involving teachers and parents is important.

452
Q

Psychoeducation

A

Discover demystify and still hope educate emphasize encourage recognize, be sensitive, motivate, promote humor, and give resources

453
Q

First line options

A

stimulants that we use for ADHD there is methylphenidate and amphetamines so methylphenidate been around since the 50s. prefer to use long acting methylphenidate, which is also known as Concerta in Canada. Options both of these work, they both work to stimulate the neurotransmitters to be more readily available in the brain so they both work similar ways and they have the same efficacy, but some people tolerate trial and error, knowing what’s gonna work best for people stimulants to increase the dopamine and epinephrin in the brain and it diminishes the need for multiple dosing so medication’s need to be given several times a day. They also have a higher abuse potential short acting cycle. Stimulants are often used, as as like upper type drugs, so they kinda give that upper feeling typically they’re in a lot higher doses than what we prescribe for ADHD or they’re also crushed it snorted or inject it which gives the effect in a lot quicker of a manner than I’m just giving someone an oral medication that takes longer amount of time to work so do it using something like Adderall or Concerta that is longer acting there’s less risk of snorting and crashing.

454
Q

Second line options

A

Second line treatments are medication approved by health Canada for the treatment of ADHD, but may have lower effect sizes, sub, optimal, duration of action compared to the first line treatment or reduce tolerate ability and risk benefit profile. They can be used for patients who experience significant side effects, have had sub optimal response with birth line medication, or do not have access to first line medication‘s. Non-stimulants may also be used in combination with first line agents as a potential augmentation for the first line treatment, sub optimal responders. Second line non-stimulant agents also are appropriate winter stimulants agents are contraindicated such as in cases where there is high risk of stimulant issues.

455
Q

Ideology in pathophysiology of spinal cord injuries

A

Most seen and peaks in third and eighth generation so 20-year-olds and seven-year-olds most common causes are motor vehicle accidents and others such as diving into shallow water infection falls work related injuries

456
Q

Spine consist of how many vertebrae

A

33

457
Q

Spinal cord is wrapped in what?

A

DURA

458
Q

Spinal cord injuries due to cord compression by what

A

Bone displacement, tumour or abscess, interruption of blood supply to the cord, and tumor. Penetrating trauma, (gunshot wounds, or stab wound)

459
Q

Biphaphasic

A

primary injury is the initial mechanical disruption of the axons as a result of the stretch or laceration to the spinal cord
Secondary injury is vascular dysfunction, edema, ischemia, electrolyte shift, inflammation, free, radical production, and apoptic death and ongoing progressive damage that occurs after the initial injury so this may be seen a few days to a week later

460
Q

Apoptosis

A

Cell death of tissue

461
Q

C2 to C3 injuries

A

These injuries cut off breathing function and are usually fatal

462
Q

c4

A

Require a ventilator for breathing and typically result in quadriplegia (paralysis of both the arms and legs)

463
Q

c5

A

Quadriplegia, but with some shoulder and elbow function

464
Q

c6

A

Quadriplegia, with some shoulder, elbow, and wrist function

465
Q

c7

A

Quadriplegia, with some shoulder, elbow, wrist, and hand function

466
Q

c8

A

Quadriplegia, with arm function and hand weakness

467
Q

T1-T6

A

Paraplegia (paralysis of the legs and lower body) with full function of arms but loss of function below mid-chest

468
Q

T6-T12

A

Paraplegia with control of torso, but loss of function below waist

469
Q

L1-L5

A

Paraplegia with varying control of muscles in the legs

470
Q

Spinal shock

A

Temporary neurological syndrome
Characterized by
Decreased reflexes
Loss of sensation
Flaccid paralysis below level of injury
Experienced by about 50% of people with acute spinal cord injury
lasts days to months and may mask postinjury neurological function
active rehabilitation may begin in presence of spinal shock

471
Q

Neurogenic shock

A

Loss of vasomotor tone caused by injury leading to pooling of peripheral blood
Characterized by hypotension, hypothermia, and bradycardia (important clinical cues)
Arteries and veins become “floppy”

Loss of sympathetic nervous system innervation causes
Peripheral vasodilation
Venous pooling
Decreased cardiac output

These effects are generally associated with a cervical or high thoracic injury (T5 or higher).

472
Q

complete injury

A

no sensory no motor

473
Q

incomplete injury

A

some sensory and motor movement left

474
Q

phrenic nerve

A

c3-c5 controls breathing

475
Q

incomplete lesions

A

theres 6 syndromes

476
Q

central cord syndrome

A

extension injury, damage to central spinal cord. more motor affected, upper extremities more affected, distal, more control in lower extremeties

477
Q

anterior cord syndrome

A

Manifestations include motor paralysis and loss of pain and temperature sensation below the level of injury.
Because the posterior cord tracts are not injured, sensations of touch, position, vibration, and motion remain intact.
complete loss of motor, compromised blood flow.
Flexion injury of the neck.
temp lost below place of injury
Anterior portion of spinal column affected = tend to have bilateral loss of motor function, light touch, pain and temperature below the level of the lesion/injur
Because the posterior cord tracts are not injured, sensations of touch, position, vibration, and motion remain intact.

478
Q

Brown-Séquard Syndrome

A

Result of damage to one-half of spinal cord
Characterized by loss of motor function and position and vibration sense
Vasomotor paralysis on the same side (ipsilateral) as lesion
The opposite (contralateral) side has loss of pain and temperature sensation below the level of the lesion.

479
Q

Posterior Cord Syndrome

A

Better prognosis
Results from compression or damage to posterior spinal artery
Very rare condition
Usually dorsal columns are damaged.
Results in loss of proprioception
Pain, temperature sensation, and motor function below level of lesion remain intact.

480
Q

Conus Medullaris Syndrome and Cauda Equina Syndrome

A

Result from damage to very lowest portion of spinal cord (conus) and lumbar and sacral nerve roots (cauda equina)
Injury to these areas produces flaccid paralysis of lower limbs and bladder and bowel dysfunction.

481
Q

ASIA

A

impairment scale

482
Q

higher the injury?

A

more serious the sequelae, the proximity of cervical cord to medulla and brainstem

483
Q

Immediate post injury conditions

A

Maintaining a patent airway
Adequate ventilation
Adequate circulating blood volume
Preventing extension of cord damage (secondary injury)

484
Q

Respiratory complications

A

Above level of C4
Presents special problems because of total loss of respiratory muscle function
Mechanical ventilation is required to keep the patient alive.

485
Q

cardiovascular complications

A

Cardiac monitoring is necessary.
Peripheral vasodilation
Decreased venous return of blood to heart
Decreased cardiac output
IV fluids or vasopressor medications may be required to support blood pressure (BP).
In marked bradycardia (heart rate <40 beats/minute), appropriate medications (atropine) are necessary to increase heart rate.

486
Q

Urinary complications

A

Urinary retention is common.
The bladder is atonic and overdistended.
In-dwelling catheter inserted
Increased risk of infection
The bladder may become hyperirritable.
Loss of inhibition from brain
Reflex emptying

Chronic in-dwelling catheterization increases the risk of infection.
Once the patient is medically stable and large quantities of IV fluids are no longer required, remove the in-dwelling catheter, and intermittent catheterization should begin as early as possible. This helps to maintain bladder tone and decreases the risk of infection.

Health And Illness 3 Denas Final (1 decks)

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