Final Flashcards by Meghan Hayes (2024)

What is mood?

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

What is affect?

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

Major Depressive disorder

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

Who is at most risk for MDD?

Females, teenage years due to increase hormone levels

What is disruptive mood dysregulation disorder?

Severe and recurrent outburst NOT consistent with development level

Risk factors for depression

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

How is MDD diagnosed

The DSM-5

Psychotic features

Disorganized thinking, delusions, hallucinations

Melancholic features

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

Atypical features

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

Catatonic features

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

Post partum onset

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

Seasonal depression

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.

What does SIGE CAP stand for

Sleep
Interest
Guilt
Energy
Concentration
Appetite
Psychom*otor activity
Suicidal ideation

Lab studies for mood disorders

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

Anti depressants

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

What meds should not be mixed

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

What does the monoamine hypothesis suggest

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

SSRIs

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

Common SSRIs used

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

Pharmaco*kinetics of SSRIs

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

Side effects of SSRIs

Insomnia, weight gain, postural hypotension, sexual disturbances

Contraindications with meds

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

What do SNRIs do

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

What do SSRIs do

Increase serotonin concentration in the synapse

What do MAOIs do

Inhibit the breakdown of serotonin

Side effects of SNRIs

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

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

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.

Indications for TCAS

Depression
Neuropathic pain

Adverse reactions to TCAs

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

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

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

Monoamine oxidase inhibitors

MAOIs
Mechanism of action - Inhibit MAO enzymes

MAO-A

Degrades epinephrine,norepinephrine, and serotonin and dopamine

MAO-B

Degrades phenylethylamine and dopamine

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

IS PATH WARM (intent to harm/ pass attempts)

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

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 )

What is psychosis?

Perception and thoughts through hallucinations and delusions

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

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.

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.

Schizophrenia =

Split mind

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

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

Epidemiology of schizophrenia

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

Substance abuse

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

Phases of schizophrenia

Prodrome phaser
Phase 1 acute
Phase 2 stabilization
Phase 3 maintenance

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.

Assessment during the pre psychotic phase

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

Positive symptoms

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

Negative symptoms

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

Affective symptoms

Dysphoria, suicidality, hopelessness

Cognitive symptoms

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

Phase 1

Acute phase, onset or exacerbation of symptoms

Phase 2

Stabilization, symptoms diminishing, movement toward previous level of functioning

Phase 3

Maintenance, at or near baseline of functioning

Primary prevention

Consider environmental factors

Secondary prevention

Monitoring for sub clinical symptoms, screening high risk

EPS symptoms (typical antipsychotics)

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

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

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

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

POTENTIALLY DANGEROUS RESPONSES TO ANTIPSYCHOTICS

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).

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.

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

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

What is serotonin syndrome

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

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

Therapeutic uses for benzodiazepines

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

Antidote for benzodiazepines

•Antidote à Flumazenil
“ I FLU past the BENZ”

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

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

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.

Specific phobia

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

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.

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.

Risk factors

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

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

Risk factors of panic disorder

White ethnicity, other psychological factors, asthma, comorbid disorders

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.

Management of panic disorders

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

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

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.

Epidemiology of delirium

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

high risk patient for delirium

Can delirium fluctuate

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

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.

Clinical features of delirium

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

Hyperactive (clinical variants)

Restless/agitated
Autonomic arousal
Aggressive/ hyperactive

Hypoactive

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

Mixed

Hypo and hyper symptoms

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

To determine delirium?

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

How to treat delirium

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

1st generation meds are?

Typical

2nd generation meds are?

Atypical

Delirium can be caused by what in the brain?

Micro inflammation

Side effects of haldol?

Prolonged Q T, EPS, over sedation, NMS

Cholinergics help with?

Memory

What is consent?

Non negotiable component, consent is ongoing

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

Hypertensive disorders of pregnancy (hdp)

Leading cause of maternal morbidity and mortality

Diagnosis of hypertension

Pre-existing hypertension

Pre pregnancy or appears 20 weeks gestation

Gestational hypertension

Appearing at or after 20 weeks gestation

Two subgroups of HTN

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

Transient HTN effect

Elevation r/t environmental stimuli

White coat HTN effect

Elevated in office/ normal outside

Masked HTN effect

Normal in office/ elevated outside

How to identify preeclampsia

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

Progression of preeclampsia

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

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

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

Adverse Conditions Associated with Preeclampsia → CNS

Headache
Visual symptoms

Cardiac and RESPIRATORY

Chest pain
Sob
Sats under <97%

Hematological

Increase WBC’s
Decrease platelets
Increase INR and PTT

Renal

Increase serum creatinine
Increase serum uric acid

Hepatic

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

Fetal placental

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

Severe complications

Eclampsia
Stroke
Pulmonary edema
Abruption
Severe organ dysfunction

Fetal complications

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

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

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

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

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

Fetal health surveillance

Treatment for hypertension

Labetolol
Nifedipine
Methyldopa

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

Caring for mom getting magsulf

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

Antidote for mag self?

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

Signs of magnesium toxicity

Weakness
Hyporeflexia
↓respiratory rate
Hypotension
Oliguria
SOB
Chest pains

If seizure occurs what do you do?

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

What do you do post seizure?

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

Labour and birth

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

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

Pressure without co-morbid conditions

BP ↓: 130 – 155 mmHg / 80 – 105 mmHg

Pressure with co-morbid conditions

BP ↓: < 140 mmHg / <90 mmHg

Benign disorders

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

Malignant

Leukemias
Lymphomas
plasma cell neoplasm
Myelodysplasia
Myeloproliferative disorders

WBC lab value

4.5 - 11. 1

Hgb value

140 - 173 g/L

Platelets value

140 - 400

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

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”.

Cellular replication and growth

proliferation versus differentiation

Neoplasia

benign versus malignant

Dysplasia

loss of DNA control over differentiation

Neoplasia

cells growing independently with no physiological purpose

Process of cancer development

• Initiation
• Promotion
• Progression

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

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

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.

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.

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.

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

Absolute neutrophil count (ANC) indicates?

• The degree of neutropenia or risk for infection.

Collaborative person Centered care

Goals:
•Cure
•Control
•Palliation

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

How to diagnose?

Biopsy

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

Cure

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

Control

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

Palliation

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

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

Extravasation Injury

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

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

Occupational Health Risks?

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

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

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

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

Cytotoxic Wastes: Body Fluids

• Cytotoxic waste can be excreted
thru patient body fluids:
• Urine, emesis, feces, saliva, sem*n,
vagin*l 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

Radiation Therapy: internal radiation

External radiation

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

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

Hormonal Therapy

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

Targeted therapy

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

Biologic therapy

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

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)

Targeted therapies

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

Chemotherapy: target and adverse Events

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

Targeted therapies: target and adverse events

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

I-O therapies: target and adverse events

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

Types of Targeted Therapy

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

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

Autologous stem cell transplant

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

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.

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

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)

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

Age related considerations

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

Common fears

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

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

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

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

Acute lymphoblastic leukemia (ALL)

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

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%.

Splenomegaly

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

Splenomegaly

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

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

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.

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

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.

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.

Primary lymphoid organs

Bone marrow and thymus

Secondary lymphoid organs

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

Other lymphoid tissue

Appendix ,waldeyers Ring

Hodgkins

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

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%)

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

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

Risk Factors of Hodgkin’s

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

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%)

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

Diagnosis work up

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

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

Staging

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

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%)

Ards

Acute respiration distress syndrome

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

Types of pneumocytes

Gas exchange unit

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

is ARDS a perfusion issues or ventilation issue

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

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.

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

Berlin

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

4 Things that happen in ARDS

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

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

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)

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

A low V/Q is indicative of what?

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

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

A PE is example of what?

A deadspace

assessment for someone with ARDS

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

Late manisfestations

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

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

What are consequences of hypoxemia and hypoxia?

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

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)

In the CT of ARDS patient what can you see?

Ground glass appearance

Medical management of ards

Supplemental oxygen
mechanical respirator
fluid therapy

what are positioning strategies?

Prone position to open up the airways, lateral rotation therapy

Is there a specific therapy for ARDS?

No specific therapy exist
you are treating the underlying cause

What are the 5 P’s of ARDS

Perfusion
Position
Protective lung ventilation
Protocol weaning
Preventing complications

pharmacological treatment of ARDS

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

Perfusion (5P’s)

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

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 hom*ogeneous distribution of lung stress and strain.

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.

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.

Preventing complications

VILI, DVT, T/P

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

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

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.

Mobilization of secretions

Hydration and humidification
Chest physiotherapy
Tracheal suctioning
Effective coughing and positioning

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.

IV therapy

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

sedation and analgesia medications

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

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.

Age related considerations

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

What is RSV?

Respiratory Syncytial Virus

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

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

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)

RSV transmission

What day is the worst for RSV symptoms to arise?

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

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.

RSV Pathophysiology

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

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

what can RSV cause

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

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

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!!!

Examples of children’s WOB

Nasal flaring, trach tug, intercostal

Supportive management for RSV

Hydration, fluid, nebs, oxygen

Monoclonal antibody prevention

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

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

DO NOT USE what when treating bronchiolits

salbutamol
ipratropium bromide
inhaled corticosteroids
abx
oral bronchodilators
systemic corticosteroids

symptoms peak when? and can last how long?

5 day peak
21 days duration

sats under what is indicative of admission to hospital

90%

Nursing interventions

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

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.

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.

Chemotherapy

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

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

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

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

3 main type leukemia

ALL, CLL ,AML

PEEP stands for what

Positive end expiratory pressure

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.

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.

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.

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.

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.

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.

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.