Final Flashcards

(487 cards)

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
What do SSRIs do
Increase serotonin concentration in the synapse
26
What do MAOIs do
Inhibit the breakdown of serotonin
27
Side effects of SNRIs
Body weight decrease Anorexia Decrease blood pressure Suicidal thoughts Nausea and vomiting Reproductive- sexual dysfunction Insomnia
28
Patient teaching with SSRIs and SNRIs
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
29
Tricyclic antidepressants
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.
30
Indications for TCAS
Depression Neuropathic pain
31
Adverse reactions to TCAs
Anticholinergics ( dry out body ) Can’t see Can’t pee Can’t spit Can’t shit IOP Sedation Weight gain
32
Serious side effects of TCAS
In high doses of tca, Impair cardiac conduction can occur causing a widening of the QRS Complex and heart block, often following hypotension
33
Patient teaching for TCAs
Mood elevation can take 1-4wks Drowsiness and dizziness can occur Careful driving for few weeks, symptoms should subside Do not stop abruptly
34
Monoamine oxidase inhibitors
MAOIs Mechanism of action - Inhibit MAO enzymes
35
MAO-A
Degrades epinephrine,norepinephrine, and serotonin and dopamine
36
MAO-B
Degrades phenylethylamine and dopamine
37
Side effects to MAOIs
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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IS PATH WARM (intent to harm/ pass attempts)
Ideation Substance abuse Purposeless Anxiety Trapped Hopelessness Withdrawing Anger Recklessness Mood changes
39
CAGE questions are used for what?
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 )
40
What is psychosis?
Perception and thoughts through hallucinations and delusions
41
Psychosis
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
42
Definition of psychosis
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.
43
Definition of schizophrenia
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.
44
Schizophrenia =
Split mind
45
Symptoms of schizophrenia
DSM Criteria- delusions, hallucinations, disorganized speech You must have one of these three symptoms and must be present for at least one month
46
Etiology of schizophrenia
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
47
Epidemiology of schizophrenia
More common in males ages 15-25 Later onset for females 25-35
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Substance abuse
50% of patients with schizophrenia exhibits either alcohol or illicit drug dependence and more than 70% are nicotine dependent
49
Phases of schizophrenia
Prodrome phaser Phase 1 acute Phase 2 stabilization Phase 3 maintenance
50
Prodromal
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.
51
Assessment during the pre psychotic phase
General assessment includes: Positive symptoms Negative symptoms Cognitive symptoms Affective symptoms
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Positive symptoms
Hallucinations,delusions, disorganized speech (associative looseness), bizarre behaviour
53
Negative symptoms
Blunted affect, poverty of thought (alogia), loss of motivation ( avoliation), inability to experience pleasure or joy (aphedonia)
54
Affective symptoms
Dysphoria, suicidality, hopelessness
55
Cognitive symptoms
Easily distracted, impaired memory, poor problem solving, poor decision making skills, illogical thinking, impaired judgement
56
Phase 1
Acute phase, onset or exacerbation of symptoms
57
Phase 2
Stabilization, symptoms diminishing, movement toward previous level of functioning
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Phase 3
Maintenance, at or near baseline of functioning
59
Primary prevention
Consider environmental factors
60
Secondary prevention
Monitoring for sub clinical symptoms, screening high risk
61
EPS symptoms (typical antipsychotics)
AD- acute dystonia (days to weeks) AP- akathisia, Parkinsonism (weeks to months) T- tardive diskinesia (months to years)
62
FIRST-GENERATION ANTIPSYCHOTICS
•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
63
SECOND-GENERATION ANTIPSYCHOTICS
•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
64
THIRD-GENERATION ANTIPSYCHOTIC
•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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POTENTIALLY DANGEROUS RESPONSES TO ANTIPSYCHOTICS
•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.
66
Mild anxiety
•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).
67
Moderate anxiety
•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.
68
Severe anxiety
•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
69
Panic anxiety
•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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What is serotonin syndrome
Too much serotonin, muscle rigidity, high HR,BP, muscle tightness(rhabdo), mental changes
71
Benzodiazepines
•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
72
Therapeutic uses for benzodiazepines
•Therapeutic Uses •Treats anxiety •Sedation/ Muscle Relaxant •Treats seizures •Treats alcohol withdrawal
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Antidote for benzodiazepines
•Antidote à Flumazenil “ I FLU past the BENZ”
74
Side effects for benzodiazepines
•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
75
Buspirone
•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
76
Panic disorder
Recurrent unexpected panic attack, in the absence of triggers, persistent concern about additional panic attacks and or maladaptive change in behaviour related attacks.
77
Specific phobia
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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Obsessive compulsive disorder
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.
79
OCD
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.
80
Risk factors
Male, fam hx, late adolescence to early 20’s, stressful life events, pregnancy
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Panic disorder
•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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Risk factors of panic disorder
White ethnicity, other psychological factors, asthma, comorbid disorders
83
Investigations for panic disorder
Not typically required but may see a ECG, blood glucose, cbc and lytes, tox screen and thyroid test to rule out any comorbidities.
84
Management of panic disorders
•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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Phobia
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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Advanced practice interventions for phobia
˜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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What is delirium?
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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Epidemiology of delirium
Often unrecognized many casesundiagnosed and or misdiagnosed as depression geriatric patients at most risk.
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high risk patient for delirium
LTC, hip fracture, icu admits, palliative. ↓ Do to increase inflammation. circadian rhythm is affected.
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Can delirium fluctuate
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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Clinical features of delirium
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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Clinical features of delirium
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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Hyperactive (clinical variants)
Restless/agitated Autonomic arousal Aggressive/ hyperactive
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Hypoactive
Lethargic /drowsy Apathetic/ inactive Quiet/confused Often escapes diagnoses Mistaken for depression
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Mixed
Hypo and hyper symptoms
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Delirium vs dementia
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
97
To determine delirium?
Delirium = acute onset and fluctuating course and intention + either disorganized thinking oraltered loc
98
How to treat delirium
In form the medical team Identify common causes Institute treatment plan Identify safety concerns
99
1st generation meds are?
Typical
100
2nd generation meds are?
Atypical
101
Delirium can be caused by what in the brain?
Micro inflammation
102
Side effects of haldol?
Prolonged Q T, EPS, over sedation, NMS
103
Cholinergics help with?
Memory
104
What is consent?
Non negotiable component, consent is ongoing
105
Ages of consent?
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
106
Hypertensive disorders of pregnancy (hdp)
Leading cause of maternal morbidity and mortality
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Diagnosis of hypertension
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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Pre-existing hypertension
Pre pregnancy or appears 20 weeks gestation
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Gestational hypertension
Appearing at or after 20 weeks gestation
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Two subgroups of HTN
with co-morbid conditions (e.g. diabetes, cardiovascular or kidney disease) Preeclampsia
111
Transient HTN effect
Elevation r/t environmental stimuli
112
White coat HTN effect
Elevated in office/ normal outside
113
Masked HTN effect
Normal in office/ elevated outside
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How to identify preeclampsia
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
115
Risk factors for preeclampsia
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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Progression of preeclampsia
Begins @ conception, symptoms and adverse effects worsen as pregnancy advances Cure=delievery
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HELLP syndrome
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
118
Physiologic changes in preeclampsia
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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Adverse Conditions Associated with Preeclampsia → CNS
Headache Visual symptoms
120
Cardiac and RESPIRATORY
Chest pain Sob Sats under <97%
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Hematological
Increase WBC's Decrease platelets Increase INR and PTT
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Renal
Increase serum creatinine Increase serum uric acid
123
Hepatic
Nausea, vomiting, RUQ or epigastric pain Increase AST, alt,LDL, bili Decrease albumin
124
Fetal placental
Abnormal FHR IUGR Oligohydramnios Absent or reverse End diastolic flow by Doppler velocimetry
125
Severe complications
Eclampsia Stroke Pulmonary edema Abruption Severe organ dysfunction
126
Fetal complications
Abnormal FHR Oligohydramnios Intrauterine growth restriction (IUGR) Absent or reversed end-diastolic flow in umbilical artery (Doppler) Intrauterine fetal death (IUFD)
127
Caring for person with HDP
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
128
Guidelines for BP
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
129
Positioning for accurate BP
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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Accurate BP by auscultation
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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Fetal health surveillance
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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Treatment for hypertension
Labetolol Nifedipine Methyldopa
133
What is mag sulf ? (MgS04)
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
134
Caring for mom getting magsulf
Require close & ongoing monitoring: Vital signs Neurological evaluation – reflexes Strict Intake Output – minimum 25ml/hr
135
Antidote for mag self?
Calcium gluconate: 10ml of 10% calcium gluconate solution. IV over 3 minutes Must monitor mg blood levels
136
Signs of magnesium toxicity
Weakness Hyporeflexia ↓respiratory rate Hypotension Oliguria SOB Chest pains
137
If seizure occurs what do you do?
Call for help Promote lateral position Prepare MgSO4 bolus (and infusion if not already started)
138
What do you do post seizure?
ensure adequacy of airway check vital signs, O2 saturation, and FHR assess for signs of abruption
139
Labour and birth
Early anesthesia consultation Epidural/spinal anesthesia/analgesia is preferred, Blood product administration if necessary Antihypertensives are continued during labour
140
Postpartum hypertension
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
141
Pressure without co-morbid conditions
BP ↓: 130 – 155 mmHg / 80 – 105 mmHg
142
Pressure with co-morbid conditions
BP ↓: < 140 mmHg / <90 mmHg
143
Benign disorders
Red blood cell disorder, WBC disorders,platelet disorders, homeostasis and thrombosis
144
Malignant
Leukemias Lymphomas plasma cell neoplasm Myelodysplasia Myeloproliferative disorders
145
WBC lab value
4.5 - 11. 1
146
Hgb value
140 - 173 g/L
147
Platelets value
140 - 400
148
What is hematology?
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
149
Cellular regulation definition
“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”.
150
Cellular replication and growth
proliferation versus differentiation
151
Neoplasia
benign versus malignant
152
Dysplasia
loss of DNA control over differentiation
153
Neoplasia
cells growing independently with no physiological purpose
154
Process of cancer development
• Initiation • Promotion • Progression
155
Who is at risk?
• 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
156
7 warning signs of cancer
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
157
Neutropenia
• 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.
158
Side effects of neutropenia
• 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.***
159
Neutropenia
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.
160
Fever in cancer patient
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
161
Absolute neutrophil count (ANC) indicates?
• The degree of neutropenia or risk for infection.
162
Collaborative person Centered care
Goals: •Cure •Control •Palliation
163
Surgery
• 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
164
How to diagnose?
Biopsy
165
Chemotherapy goal
• 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
166
Cure
Burkitt's lymphoma, wilms tumour, neuroblastoma, ALL, hodgkins disease, testicular cancer
167
Control
Breast cancer, non-hodgkins lymphoma,small cell carcinoma of the lung, ovarian cancer
168
Palliation
Relieve pain, relieve obstruction, improve the sense of well being
169
Chemo considerations
• 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
170
Extravasation Injury
• Infiltration of medications into the tissues surrounding the infusion site.
171
What is Cytotoxic Waste?
•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
172
Occupational Health Risks?
No safe level of exposure has been established No exposure is safest
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What are the major routes of exposure?
•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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What is the risk for exposure for health care providers ?
• Handling chemotherapy medication • Handling cytotoxic waste & body fluids • Cleaning a spill • Inadequate cleaning of spill • Research
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Safe Handling of Oral Chemo
• 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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Cytotoxic Wastes: Body Fluids
• 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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Radiation Therapy: internal radiation
- Brachytherapy Implantation or insertion of radioactive materials into or close to tumor.
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External radiation
Most Common • Target tumor using imaging, exam, and surgical reports • External marks
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Common side effects of chemotherapy and radiation include:
• Bone marrow suppression • Fatigue • GI disturbances (N+V, Diarrhea, Constipation) • Integumentary and mucosal reactions • Pulmonary effects • Reproductive effects
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Hormonal Therapy
Hormonal agonist and antagonists – treat cancers that are responsive to hormones (prostate, breast, endometrial)
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Targeted therapy
• Targets specific cancer cells • Much reduced side effect profile • Rapidly growing area of anticancer agents
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Biologic therapy
Modifies immune response (activates immune system - ’biologic response modifiers’)
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Systemic cancer therapy
. 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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Targeted therapies
Target specific antigens found on the cell surface • Penetrate the cell membrane to interact with targets inside a cell
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Chemotherapy: target and adverse Events
Target: rapidly dividing tumour and normal cells Adverse events: diverse due to non specific nature of therapy
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Targeted therapies: target and adverse events
Target: specific molecules involved in tumour growth and progression Adverse events: reflect targeted nature
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I-O therapies: target and adverse events
Targets immune system Adverse events: unique events can occuras a result of immune system activity
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Types of Targeted Therapy
• 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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What's the target?
• 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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Gene therapy -FYI
• 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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Autologous stem cell transplant
Harvesting Stem Cells ▪ Stem cells from bone marrow ▪ Peripheral blood ▪ Umbilical cord blood (Can be stored and used later)
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Autologous stem cell transplant complications
▪ 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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Complications of cancer
• 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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Metabolic emergencies
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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Cancer pain
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
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Age related considerations
Be aware of late and long-term effects of cancer: • Secondary Cancers • Cognitive Changes • Cardiovascular / Sexual Dysfunction • Psychosocial Effects
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Common fears
Disfigurement, emaciation • Dependency • Disruption of relationships • Pain • Financial depletion • Abandonment • Death
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Coping with cancer
• 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
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Support patient and family
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
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Leukemia & Lymphoma
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
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Acute lymphoblastic leukemia (ALL)
potentially curable disease, with more than 80% of cases cured.
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The lymphomas of childhood are non-Hodgkin lymphoma and Hodgkin lymphoma.
• 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%.
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Splenomegaly
• Largest lymphatic organ. • Located on left side of abdomen just above the kidney. • Normal Spleen Size – approximately 11cm.
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Function of spleen
• 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
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Normal spleen
• 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.
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Disorders causing massive spleen
• Polycythemia Vera • Multiple Myeloma • POEMS Syndrome • Waldenstrom’s Macroglobulenemia • Chronic Lymphocytic Leukemia (CLL) • Myelofibrosis • Non-Hodgkin’s Lymphoma • Chronic Myeloid Leukemia (CML) • Thalassemia Major
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Massive splenomegaly
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.
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Lymphoma
• 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.
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Primary lymphoid organs
Bone marrow and thymus
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Secondary lymphoid organs
Spleen, lymph nodes, tonsils and peyers patches of small intestine
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Other lymphoid tissue
Appendix ,waldeyers Ring
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Hodgkins
• Classical Hodgkin Lymphoma (CHL) • Nodular Sclerosis (NSHL) • Mixed Cellularity (MCHL) • Lymphocyte-Rich (LRHL) • Lymphocyte – Depleted (LDHL) • Nodular Lymphocyte Predominant HL (NLPHL)
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Non hodgkins
• 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%)
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Non-hodgkins lymphoma characteristics
Multiple peripheral nodes Mesenteric nodes and Waldeyer’s ring commonly involved Non-contiguous B symptoms uncommon Rarely localized Extranodal involvement is common
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Hodgkins lymphoma characteristic
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
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Risk Factors of Hodgkin’s
• Epstein Barr Virus (EBV) • Family History • Genetic Abnormalities • Higher SES • Lifestyle Factors
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Signs & Symptoms
• 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%)
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General work up
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
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Diagnosis work up
Pretreatment • Lymph Node Biopsy (excisional) • Hematopathology review • Immunohistochemistry • FISH Studies • Molecular Studies • Cytogenetics • Ki-67 Proliferation Index
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Post treatment general work up
History including presence of B Symptoms • Physical examination including lymphoid regions, liver and spleen. • Labs: CBC with diff, CMP, LDH • ESR
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Staging
Pet/ct scan Bone marrow biopsy (greater than 1.6cm)
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Hodgkin’s Lymphoma
• 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%)
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Ards
Acute respiration distress syndrome
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what is ARDS
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
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Types of pneumocytes
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
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Gas exchange unit
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
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How is ARDS determined
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
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is ARDS a perfusion issues or ventilation issue
ARDS patients often get daily ABG’S, not a perfusion issue (shunting), a ventilation issue
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PEEP
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.
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What is the name of the time used for criteria of ARDS
Berlin
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Symptoms you may see with ARDS
Crackles, increased SOB, HR. Hypoxemia gets worse, you see them in tripod position trying to expand lung capacity as much as possible
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4 Things that happen in ARDS
1. diffusion- hypoxia 2. Shunting (V/Q mismatch) 3. Decrease surfactant=Decrease lung compliance (leading to scar tissue) 4.Fibrosis- macro attracts fibrin
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Acute respiratory failure
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
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Hypoxemic Respiratory Failure
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
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Hypercapnic Respiratory Failure
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)
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V/Q ratio
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
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A low V/Q is indicative of what?
less ventilation more perfusion An area with perfusion and no ventilation is referred to as shunting
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A high V/Q is indicative of what?
more ventilation and less perfusion an area with ventilation but no perfusion is referred to as dead space
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A PE is example of what?
A deadspace
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assessment for someone with ARDS
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.
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Early manifestation
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
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Late manisfestations
severe difficulty breathing, SOB, Tachycardia, cyanosis, thick frothy sputum, metabolic acidosis, abnormal breath sounds
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Is it possible to have respiratory issues or infection and not develop ARDS?
Some people never progress to ards, like pancreatitis will still do damage but not receive ards
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What are consequences of hypoxemia and hypoxia?
Metabolic acidosis and cell death Initially increased and then decreased cardiac output Impaired renal function GI alterations
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Diagnostic studies for ARDS
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)
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In the CT of ARDS patient what can you see?
Ground glass appearance
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Medical management of ards
Supplemental oxygen mechanical respirator fluid therapy
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what are positioning strategies?
Prone position to open up the airways, lateral rotation therapy
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Is there a specific therapy for ARDS?
No specific therapy exist you are treating the underlying cause
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What are the 5 P's of ARDS
Perfusion Position Protective lung ventilation Protocol weaning Preventing complications
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pharmacological treatment of ARDS
Steroids, vasodilators, surfactant, anti-inflammatory, DVT prophylaxis, Reflux Px and sedation
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Perfusion (5P's)
maximize perfusion in the pulmonary capillary system by increasing oxygen transport between the alveoli and pulmonary capillaries.
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Positioning
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.
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Protective Lung Ventilation
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.
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Protocol weaning
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.
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Preventing complications
VILI, DVT, T/P
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Nursing management of those caring for patients with ARDS
-Nursing assessment Health information Health history Medications Surgery Symptoms -Physical assessment General Integumentary Respiratory Cardiovascular Gastrointestinal Neurological -Laboratory findings
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Overall goals
-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
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Prevention
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.
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Mobilization of secretions
Hydration and humidification Chest physiotherapy Tracheal suctioning Effective coughing and positioning
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Medication therapy
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.
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IV therapy
IV antibiotics, such as vancomycin (Vancocin) or ceftriaxone, are frequently given to inhibit bacterial growth.
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sedation and analgesia medications
benzodiazepines (e.g., lorazepam) and narcotics (e.g., morphine, fentanyl) are used to decrease anxiety, agitation, and pain.
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Nutritional therapy
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.
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Age related considerations
Decreased ventilatory capacity Alveolar dilation Diminished elastic recoil Decreased respiratory muscle strength Decreased chest wall compliance
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What is RSV?
Respiratory Syncytial Virus
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what is affected in RSV
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
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Who is at most risk for RSV?
Children less than 2 years and those less than 12 months being at most risk peaking at 2-6 months
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Risk factors for severe RSV
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)
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RSV transmission
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)
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What day is the worst for RSV symptoms to arise?
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
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where do the majority of RSV deaths occur?
low- and middle-income countries, these places are less likely to have access to adequate health care
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RSV facts
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.
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RSV Pathophysiology
Airway obstruction may occur due to sloughed epithelium and inflammatory cells with mucus and fibrin that get into small airways.
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compound issues in small children
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
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what can RSV cause
asthma or COPD exacerbations and secondary infections such as bronchitis or pneumonia.
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RSV Symptoms for general population
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
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RSV Symptoms for under 2
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!!!
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Examples of children's WOB
Nasal flaring, trach tug, intercostal
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Supportive management for RSV
Hydration, fluid, nebs, oxygen
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Monoclonal antibody prevention
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
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vaccine prevention
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
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Management – Moderate to Severe BRONCHIOLITIS
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
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DO NOT USE what when treating bronchiolits
salbutamol ipratropium bromide inhaled corticosteroids abx oral bronchodilators systemic corticosteroids
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symptoms peak when? and can last how long?
5 day peak 21 days duration
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sats under what is indicative of admission to hospital
90%
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Nursing interventions
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. 3. Ensure that nurses caring for a child with RSV do not care for other high-risk children. 4. Use contact, droplet, and universal precautions during care; use of good handwashing techniques is necessary. 5. Monitor airway status and maintain a patent airway. 6. 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. 7. Provide cool, humidified oxygen as prescribed. 8. Monitor pulse oximetry levels. 9. Encourage fluids; fluids administered intravenously may be necessary until the acute stage has passed. 10. 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.
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viral pneumonia
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
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PVZ is offered to who?
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.
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PVZ is NOT offered to whom?
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. 
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Chemotherapy
Tradition → travels through bloodstream and destroys all rapidly dividing cells healthy and unhealthy
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Radiation
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
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Hodgkin's
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
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Non-hodgkins
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
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3 main type leukemia
ALL, CLL ,AML
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PEEP stands for what
Positive end expiratory pressure
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ALL
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.
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AML
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.
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Main difference between ALL and AML
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.
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AML
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.
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ALL
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.
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CLL
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.
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CML
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.
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Sepsis facts
Leading cause of death in Canada, 30 - 50% mortality rate higher among males than females
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Sepsis facts
Leading cause of death in Canada, 30 - 50% mortality rate higher among males than females
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What is shock?
Inadequate tissue perfusion, cellular and tissue hypoxia Due to: increase 02 delivery, increase 02 consumption, insufficient 02 utilization or a combo of them all
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3 main types of shock
Hypovolaemic, cardiogenic and distributive
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3 main types of shock
Hypovolaemic, cardiogenic and distributive
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Hypovolemic
Decreased preload due to intravascular volume loss. Diminished preload decreases CO so SVR increases in an effort to compensate and maintain perfusion
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Cardiogenic (includes obstructive)
Pump failure = decrease CO SVR increases in an effort to compensate for the diminished CO to maintain perfusion
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Cardiogenic (includes obstructive)
Pump failure = decrease CO SVR increases in an effort to compensate for the diminished CO to maintain perfusion
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Distributive= vasodilatory
Includes sepsis, anaphylaxis, neurogenic, cellular toxin Consequences of severely decreased SVR CO is increased in an effort to compensate for SVR
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Infection
pathological process caused by invasion of normally sterile tissue or fluid or body cavity by pathogenic or potentially pathogenic micro-organisms
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Sepsis
Infection plus 2 or more sirs
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Severe sepsis
Infection plus 2 or more sirs plus new organ dysfunction
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Septic shock
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)
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Pathophysiology of sepsis
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!!!
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When to suspect sepsis
The qsofa "hat" Hypovelemia - SBP22/min
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Signs of end organ dysfunction (hypo perfusion)
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
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3 key components to recognizing and responding to sepsis for inpatients
1.timely recognition of early infection 2. Early treatment with antibiotics: intravenous fluids 3. Appropriate escalation to high acuity or ICU care
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Disruptive shock:
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
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Distributive shock symptoms
Tachycardia Tachypnea/hyperventilation Temperature dysregulation Decreased urine output Altered neurological status GI dysfunction Respiratory failure is common.
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How to diagnose
Vitals Blood cultures Lactate ABG BUN Creatinine
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Treatment for shock
Quicker treatment = Decreased mortality Broad spectrum abx Fluid Resusitation 2 Large Bore Ivs Monitor Progress
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Why do ALL sepsis patients need volume need volume?
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
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when to give bolus
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.
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Do patients who have known heart failure, kidney disease or low EF?
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.
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what are the stages of shock
Initial Compensatory Progressive Refractory
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Initial
Cellular level Not clinically apparent Metabolism changes at the cellular level, from aerobic to anaerobic-lactic acid buildup
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Compensatory
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.
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Progressive
-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
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Multiple organ dysfunction syndrome
---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
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Refractory stage
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
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Diagnostic studies
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
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Primary therapy for sepsis is?
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.
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what to monitor when giving fluids?
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.
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If fluids do NOT work what do you give?
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.
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Is nutrition important in sepsis?
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.
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Steps for caring with someone with septic shock
Fluid replacement to restore perfusion (30 or more mL/kg) Hemodynamic monitoring Vasopressor medication therapy Vasopressin for patients refractory to vasopressor therapy
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why are IV corticosteroids recommended?
IV corticosteroids are recommended only for patients in septic shock who cannot maintain adequate BP with vasopressor therapy despite fluid resuscitation.
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When should antibiotics be started?
Antibiotics after cultures are obtained (e.g., blood, wound exudate, urine, stool, sputum) should be started within the first hour of septic shock.
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Glucose levels during septic shock
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.
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What is DIC?
Disseminated intravascular coagulation--- too much and too little clotting.
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DIC?
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
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Common findings of DIC
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.
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Immediate nursing interventions
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
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Lab findings
decreased platelets prolonged PT time fibrinogen decreased ddimer elevated aptt unpredictable
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DIC management
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
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Pathophysiology of DIC
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
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Generalized bleeding from how many unrelated sites is suggestive of DIC?
3
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Thrombus
A clot that form within a vessel, bad "blood clot"
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Thrombosis
Process of thrombus forming
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Emboli (embolus - singular)
General term for a foreign body free floating in blood stream (example: blood, air, fatty deposit)
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Tromboembolus
Clotted material
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Thromboembolism
Actually blocks artery
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Thrombin
Enzyme that ispart of coagulation cascade converting fibrinogen to fibrin
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Venous thrombolism
Most common disorder of the veins, can be either superficial or deep vein thrombosis.
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Superficial vein thrombosis (svt)
Formation of a thrombus in a superficial vein, usually the greater or lesser saphenous vein, generally a benign disorder.
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Deep vein thrombosis (dvt)
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.
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Characteristics of superficial vein thrombosis
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.
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VTE - superficial
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)
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Thrombophlebitis management
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)
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Deep vein Thrombosis
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.
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Risk factors for DVT
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
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Risk factors for DVT
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
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Goal for treatment of a confirmed DVT are to?
Prevent new clot development Prevent spread of the clot Prevent embolization
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Pharmacology for dvt's
Vitamin K antagonists Thrombin inhibitors (both indirect and direct) Factor xa inhibitors
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Antidote for warfarin
Vitamin K
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When does warfarin take effect?
48-72 hours and the level of anticoagulation is monitored daily with the INR
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Unfractionated heparin
Medication → heparin sodium can be given IV, subcut continuous measured by APTT by monitoring at regular intervals
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Low molecular weight heparin (lmwh)
Medications→ enoxaparin, dalteparin. Given subcut, typically tests are not required CBC may be ordered at regular interval
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Antidote for heparin
Protamine
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Factor xa inhibitors
Produce rapid anticoagulation Examples: fondaparinx, rivaroxaban ( xarelto) andapixaban (eliquis) All these are used for both VTE prevention and treatment Coagulation monitoring is not necessary
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What is HIT?
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.
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Physical findings of hit
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)
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Clinical features of DVT
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
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What is the name of criteria chart for dvt's
Well's criteria
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Investigations of dvt's
D dimer (for wells criteria under 2) Ultrasound (for wells criteria over 2)
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Assessment of hospitalized patients → prophylaxis
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
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Are compression stockings recommended if patient already has VTE?
No and they must be fitted correctly
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Nursing diagnoses
Acute-pain Ineffective health maintenance Impaired skin integrity Risk for bleeding related to anticoagulant therapy
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Overall goals For VTE
1. Pain relief 2. Decreased edema 3. No skin ulceration 4. No evidence of pulmonary embolism
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What should be educated to patient?
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
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Pulmonary embolism
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
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Other sites of origin of PE include
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
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Risk factors for PE
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
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Clinical manifestations of PE
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
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investigations for pe?
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%.
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Prophylaxis in management of pulmonary embolism
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
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What is cerebral palsy?
umbrella term referring to a non-progressive disease of the brain.
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Where does it originate?
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.
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What does it affect ?
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.
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Mild CP
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
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Is CP curable?
Non curable, life long condition, damage does not worsen, may be congenital or acquired
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Pathophysiology of CP
Premature neonatal brain is susceptible to two main pathologies: intraventricular hemorrhage (IVH) and periventricular 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 the corticospinal tracts, composed of descending motor axons, course through the periventricular region
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Intraventricular Hemorrhage (IVH) 
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.
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Periventricular Leukomalacia (PVL)
PVL is a separate pathological process. The pathogenesis of PVL arises from two important factors: (1) ischemia/hypoxia and (2) infection/inflammation.
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Ischemia/hypoxia
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), this watershed zone is 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.
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Autoregulation of cerebral blood flow 
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
Infection and inflammation
This process involves microglial (brain macrophage) cell activation and cytokine release, which causes damage to a specific cell type in the developing brain called the oligodendrocyte.
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Causes of Cerebral Palsy
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
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Protective factors
obstetrical care: magnesium sulfate, antibiotics, corticosteroids
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Motor types
Spastic Ataxic Dyskinetic Mixed types
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Spastic
70-80% most common form. muscle appear stiff and tight. arises from motor cortex damage. Cerebral cortex
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Ataxic
6%, characterized by shaky movements, affects balance and sense of positioning in space. Arises from cerebellum damage.
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Dyskinetic
6%, characterized by involuntary movements. arises from basal ganglia damage.
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Mixed types
combination damage, multiple parts of the brain.
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Monoplegia
Affecting one limb, usually lower limb
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Hemiplegia
affecting the upper and lower limbs on one side of the body, the upper limb is usually more affected than the lower limb.
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Diplegia
Affecting all limbs, but the lower limbs are much more affected that the upper limbs, which usually only show fine motor impairment.
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Triplegia
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.
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Quadriplegia
Affecting all four limbs and the trunk, also known as tetraplegia.
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SPASTIC (SPASTIC CEREBRAL PALSY)
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
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Non spastic CP
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.
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Dyskinetic Cerebral Palsy
separated further into two different groups; athetoid and dystonic
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Athetoid
Cerebral Palsy includes cases with involuntary movement, especially in the arms, legs, and hands.
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Dystonia/Dystonic 
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.
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Athetosis
slow, writhing movements that are often repetitive, sinuous, and rhythmic
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Chorea
irregular movements that are not repetitive or rhythmic, and tend to be more jerky and shaky
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Chorea 
irregular movements that are not repetitive or rhythmic, and tend to be more jerky and shaky
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Choreoathetoid 
a combination of chorea and athetosis; movements are irregular, but twisting and curving
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Dystonia 
involuntary movements accompanied by an abnormal, sustained posture
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Ataxic CP
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
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Cerebral Palsy Classifications
Mild, Moderate, Severe
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Mild CP
Mild Cerebral Palsy means a child can move without assistance; his or her daily activities are not limited.
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Moderate CP
Moderate Cerebral Palsy means a child will need braces, medications, and adaptive technology to accomplish daily activities
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Severe CP
Severe Cerebral Palsy means a child will require a wheelchair and will have significant challenges in accomplishing daily activities.
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General Assessment
Suspicions of CP are commonly based on a positive history of adverse perinatal or antenatal events. If no positive history, suspicions are often raised by parental or family observations 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 of degenerative diseases, metabolic disorders, spinal cord lesions/tumours, muscular dystrophy, and anomalies of the cervical spinal cord and skull.
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Children Assessment
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.
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Associated disorders
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.
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Diagnosis of CP
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
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Common Hospital Visit Concerns
Respiratory problems particularly pneumonia Uncontrolled seizures / status epilepticus Unexplained irritability - consider acute infections, oesophagitis, dental disease, hip subluxation, pathological fracture. Review medications.
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Communication Devices 
symbol boards voice synthesizers head sticks and keyguards for computers
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Mobility Devices 
wheelchairs (manual, power and sports) scooters specially made bicycles and tricylces walkers and crutches
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Daily Living Aids 
electronic door openers large-handled eating utensils grab sticks environmental control systems
435
What is ADHD?
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)
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ADD VS ADHD
They are the same, ADD Is the old term
437
Is ADHD highly hereditary
Yes, 75%
438
Who is diagnosed more?
Males see more hyperactivity
439
Hows ADHD diagnosed
Dsm-5
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How are you diagnosed
Starts between 6-12 years old and there's 2 types→ inattentive and hyperactive/impulsive and you can also have both
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Inattentive
Not paying attention, must have 6/9 symptoms for atleast 6 months Careless mistakes, not listening, easily distracted
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Hyperactive/ impulsive
Overly active and impulsive must have 6/9 symptoms for at least 6 months Fidget, squirm, get up often
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ADHD in girls
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
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ADHD is rarely by itself true or false?
True often have comorbid mental health disorders
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What is dysthymia?
Form of chronic depression
446
Preschool
Behavioural disturbances
447
School age
Behavioural disturbance, academic problems, difficulty with social interaction and self-esteem issues
448
Adolescence
Academic problems, difficulty with social interactions, self-esteem issues, legal issues, smoking, drugs, injury/accidents and risky sexual behaviour
449
College age
Academic problems, occupational difficulties, relationship, problems, self-esteem, issues, substance abuse, injuries/accidents, risky, sexual behaviour
450
Adult
Occupational failure, self-esteem issues, injury/accident, relationship, problems, substance, abuse, and risky sexual behaviour
451
ADH
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.
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Psychoeducation
Discover demystify and still hope educate emphasize encourage recognize, be sensitive, motivate, promote humor, and give resources
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First line options
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.
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Second line options
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
Ideology in pathophysiology of spinal cord injuries
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
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Spine consist of how many vertebrae
33
457
Spinal cord is wrapped in what?
DURA
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Spinal cord injuries due to cord compression by what
Bone displacement, tumour or abscess, interruption of blood supply to the cord, and tumor. Penetrating trauma, (gunshot wounds, or stab wound)
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Biphaphasic
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
Apoptosis
Cell death of tissue
461
C2 to C3 injuries
These injuries cut off breathing function and are usually fatal
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c4
Require a ventilator for breathing and typically result in quadriplegia (paralysis of both the arms and legs)
463
c5
Quadriplegia, but with some shoulder and elbow function
464
c6
Quadriplegia, with some shoulder, elbow, and wrist function
465
c7
Quadriplegia, with some shoulder, elbow, wrist, and hand function
466
c8
Quadriplegia, with arm function and hand weakness
467
T1-T6
Paraplegia (paralysis of the legs and lower body) with full function of arms but loss of function below mid-chest
468
T6-T12
Paraplegia with control of torso, but loss of function below waist
469
L1-L5
Paraplegia with varying control of muscles in the legs
470
Spinal shock
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
Neurogenic shock
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
complete injury
no sensory no motor
473
incomplete injury
some sensory and motor movement left
474
phrenic nerve
c3-c5 controls breathing
475
incomplete lesions
theres 6 syndromes
476
central cord syndrome
extension injury, damage to central spinal cord. more motor affected, upper extremities more affected, distal, more control in lower extremeties
477
anterior cord syndrome
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
Brown-Séquard Syndrome
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
Posterior Cord Syndrome
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
Conus Medullaris Syndrome and Cauda Equina Syndrome
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
ASIA
impairment scale
482
higher the injury?
more serious the sequelae, the proximity of cervical cord to medulla and brainstem
483
Immediate post injury conditions
Maintaining a patent airway Adequate ventilation Adequate circulating blood volume Preventing extension of cord damage (secondary injury)
484
Respiratory complications
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
cardiovascular complications
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
Urinary complications
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.