RESPIRATORY-HEMATOLOGY

→ Unequal lung expansion → Unequal chest

RESPIRATORY (decreased/absent expansion (decreased
affected side) in the affected region)
RESPIRATORY SYSTEM • Wheezing/stridor is → Unequal lung expansion
→ Purpose: To perform gas exchange r/t bronchospasm (decreased affected
→ Goal: To get oxygen (cellular processes) and remove (asthma) side, atelectasis)
carbon dioxide (neurotoxic) → Chest percussion - → Chest percussion - dull
• CO2 is dangerous to the body hyperresonant (d/t d/t too much fluid
alveolar collapse)
• High levels of CO2 can lead to brain damage
• N: resonant (part
→ Main trigger for breathing: elevated carbon dioxide air, part space)
levels • Dull-
• Controlled by brain stem/chemoreceptors (pons fluid/mass/organ
varolii & medulla oblongata: controls vagal • Flat- bone
stimulation) → Compensatory hypoxia-
→ Pathology ↑HR, ↑RR
• COPD patients→ too much CO2→ the body
becomes dependent on the presence of CO2→ Management: CTT or Thoracentesis
defective trigger→ replacement trigger- low
oxygen levels (hypoxic drive) THORACENTESIS
• Management → Removal of air/fluid at the pleura to reestablish the
o Low flow oxygen (1-2 LMP) via venturi mask negative pressure→ allow air entry→ alveolar
o Most accurate/precise delivery system expansion→ lung reexpansion
▪ Rationale: too much oxygen for COPD • Lungs are capable of regeneration
patients, will inhibit the hypoxic drive → Short term
(defective)- destroy both triggers for → Centesis- direct removal of air fluid at the third space
breathing→ respiratory cessation (edema, ascites, pleura pericardium)
o E.g. Pneumonia patient is ordered 10L/min of • Diuretics remove fluid from the blood vessels only
O2
▪ Follow the order because the problem is
not COPD thus high flow is okay to give
o E.g. Emphysema patient is ordered with
5L/min
→ Question the order, because emphysema
is an example of COPD

High flow oxygen is not contraindicated for patients without

COPD (e.g., COVID patients, etc.)

Types of Respiration (External and Internal)

→ External/Ventilation- between the environment (positive → The bag is placed at the bottom to allow drainage via
pressure) towards the lungs (negative pressure) gravity
• The normal pressure of the lungs is negative → Prevent mediastinal shifting- occurs when the pressure
• Pathology: Air/fluid in the pleura→ abnormal gets so high that it pushes the heart and great vessels
pressure will cause positive pressure→ prevent air into the unaffected side of the chest. These structures
entry→ alveolar collapse/atelectasis→ lung are compressed from external pressure and cannot
collapse expand to accept blood flow
• This causes pressure to the heart resulting in
Pneumothorax Pleural effusion cardiac tamponade
o Decreased contractility→ CHF
Too much air → positive Too much fluid → causes • Removal of air/fluid in the affected side will re-
pressure→ prevent air entry positive pressure → expand the lungs and will bring back the airways to
→ atelectasis preventing air entry → their position
atelectasis

Types:
→ Open - caused by a
stabbed wound, GSW,
or penetrating wound
(trauma) → air entry→
pneumothorax
→ Closed - r/t air trapping
that leads to
overinflated alveoli
(bleb)→ bleb rupture→
air exit→ pneumothorax;
no opening;
overdistended and over
inflated alveoli related to
emphysema
• CPT needs doctors
order → might
cause rupture of the
bleb
Causes:
→ Water → caused by
hydrothorax → d/t renal
failure → fluid volume
excess → fluids may
accumulate in the lungs
→ Pus
(Pyothorax/Empyema)
→ d/t infection
→ Blood (hemothorax) →
caused by trauma or
metastasis (spread of
cancer)
→ Site
• Air (pneumothorax)- 2nd-3rd ICS
• Fluid (pleural effusion)- 7th- above 9th ICS
o Avoid puncture of other organs (R: liver, L:
spleen)

Signs and symptoms: Signs and Symptoms: Nursing Considerations BEFORE the procedure
→ Unequal breath sounds → SOB → Check consent
• Doctors obtain consent, nurses witness consent
→ Position of choice: orthopneic/tripod position
→ Pain medications 30 minutes before insertion
(abortive/anticipatory)
• Abortive- abort pain before it happens
• Anticipatory- anticipate pain
→ Orient the patient (insertion)
• Stay still
• Exhale and hold (prevent accidental puncture)
Nursing Considerations AFTER the procedure
→ Removal- confirm lung re-expansion via CXR
→ Upon removal, instruct the client to perform valsalva
maneuver (bearing down)
• Rationale: transient increase in thoracic pressure
that will prevent air entry
• Cover with vaselinized sterile gauze, occlusive
dressing; tape at 4 sides (done already, lungs go
back to normal)
o 3 sides are done to allow release of air
→ WOF pneumothorax
• Check breath sounds 30 minutes after
• Sign: unequal breath sounds
• Report to the doctor
• Confirmed via CXR
• Thoracentesis will be done again
CHEST TUBE DRAINAGE
→ Long term (takes days to complete)
→ Bottle system (old)- fragile, hard to transfer
→ Pleur Evac (new)- made from fiberglass (durable), easy
to transfer
• Both have the same drainage duration
Types of Respiration (External and Internal cont.)
→ Internal/Perfusion- It is the exchange of gasses between
the alveoli and the blood (oxygenated blood)
• Gas moves via diffusion (higher to lower
concentration)
o Blood going to lungs is deoxygenated →
should have water
o Alveoli has many O2, less CO2; deoxygenated
blood has many CO2, less O2
o Alveoli (O2) → Blood (CO2); Blood (CO2) →
Alveoli (O2)
o Osmosis- lower to higher concentration (this is
how fluid moves)
• Alveoli- increased oxygen, decreased carbon
dioxide
• Deoxygenated blood- decreased oxygen,
increased carbon dioxide
• Oxygen will go to the blood; carbon dioxide will go
to the alveoli to be expelled via respiration
Types of Internal Respiration
→ Aerobic- sufficient oxygen; byproduct: heat
• Perspire as a form of thermoregulation (heat is
removed through perspiration)
→ Anaerobic- insufficient oxygen; byproduct: lactic acid
(toxic to the tissues); causing damage or injury
• E.g., myocardial ischemia→ decreased oxygen→
anaerobic→ lactic acid→ inflammation of the
cardiac muscles→ pain→ angina pectoris
• Bleomycin - toxic to the lungs (SE)
Additional Notes:
→ Pneumonectomy
• There is presence of air inside the lungs
o (X) CPT → release of air → mediastinal shifting
→ Best position for pneumonia, emphysema or any
respiratory disease: Orthopneic
Protective Structures of the Respiratory System
→ Ribs- mechanical protection/structure of the lungs and
heart
→ Cilia- filters and humidifies air (hair-like structures)
→ Mucus- trap foreign body
→ Pseudostratified Columnar with Goblet Cells- lines up
the airways; most important
• Cough production- protective structure to remove
foreign body (remove foreign body via cough
production)
• Mucus production- trap foreign body
• If goblet cells are affected → cough and mucus
production will increase (productive cough)
• Any pollutant can cause obstruction or damage in
the goblet cells
• Part of immune system, in elderly → lesser cough
→ stasis of secretions
❖ Chronic bronchitis→ bronchus (airway)→ goblet cells
are affected→ chronic productive cough (suction)
❖ Emphysema→ overinflated alveoli→ goblet cells are not
affected→ dry cough (Quiet chest/ no adventitious
breath sounds)
→ Alveolar Type 1 Cells: Alpha 1 Antitrypsin- protects
alveoli from trypsin action (dissolves protein)
• Bacteria and viruses are made from protein→
destroyed by trypsin once it enters the lungs
• Pathology: genetic→ decreased levels of alpha 1
antitrypsin→ decreased protection of the alveoli→
alveolar damage→ emphysema
o Emphysema may also be d/t genetic
predisposition
• The mucosal lining serves as a protection of the
stomach from the hydrochloric acid which is vital for
digestion
o HCl → for digestion → if excessive, could
cause problems in the mucosal lining → ulcers
→ Alveolar Type 2: Surfactant- promote surface tension
preventing alveolar collapse/atelectasis
• Pathology: decreased surfactant→ premature
babies→ atelectasis (RDS)
o Safest to deliver in 7 months (stable). During
the 8th month, lung problems arise
MUSCLES OF BREATHING
INHALATION
Normal inhalation- effortless
→ Diaphragm
• Strongest respiratory muscle
• Controlled by the phrenic nerve (C3-C4)
o Immobilize the neck in vehicular accidents
• Effortless breathing → lesser O2 consumption
(better)
Accessory muscles for inhalation (DOB: priority)- more
muscles are used for respiration→ increased effort→
increased oxygen use→ can cause father hypoxia→ fatigue
→ Sternocleidomastoid
→ Upper Trapezius
→ Pectoralis Major and Minor
→ Anterior Scalenes
→ Serratus Major

→ Pathology: DOB→ increased accessory muscle use→
hypertrophy of chest muscle→ barrel chest (clinical
symptom of emphysema; APL ratio- 1:1)
• Normal APL (anterior post lateral) ratio- 2:1
EXHALATION
Normal Exhalation- effortless; chest recoil, no muscle
movement → effortless → lesser O2 consumption
Accessory muscles for exhalation (DOB)- more oxygen
use→ fatigue, hypoxia, hypertrophy of muscles
→ Abdominals – core muscles
→ Serratus minor
→ Intercostals
RESPIRATORY DISTRESS SYNDROME
→ Premature, GDM, LBW babies are affected
→ Atelectasis d/t decreased surfactant
• Decreased surfactant→ alveolar collapse→
decreased gas exchange
• The lungs are still capable for reexpansion
→ Early symptoms: compensatory mechanisms
• Increased HR, RR
• Altered LOC - d/t cerebral hypoxia
• Intercostal retractions - accessory muscle use →
increased effort (ABN) → hypoxia
• Poor, weak cry
→ Late symptoms:
• Blue colored lips, fingers and toes (acrocyanosis)
• Rapid, shallow breathing seen at the belly
• Flaring nostrils- no benefit for breathing; done d/t
weak compensation
• Grunting sound when breathing
Additional Note:
→ Pedia: Sign of normal breathing: Crying
→ The surfactant is not decreasing in adults d/t mature
lungs
Diagnostics
→ Chest x ray- scattered atelectasis
• Late: white lung (massive atelectasis)
→ ABG: Respiratory acidosis
• CO2 is increased d/t decreased gas exchange
(atelectasis)
Management
→ Before birth: corticosteroids IM (betamethasone/
dexamethasone) to the mother to promote lung
maturity
→ After birth: synthetic surfactant (Survanta) inhalation
via advanced airway, direct to the alveoli (ET tube,
laryngeal tube, tracheostomy)
ADULT RESPIRATORY DISTRESS SYNDROME (ARDS)
→ Atelectasis d/t (+) pressure
• Main cause: trauma → open pneumothorax
• Severe respiratory disorder - COVID (whole lungs
is white → massive alveolar collapse)
• Mechanical ventilator → tension pneumothorax
• Shock/Emboli → decreased blood flow to the
heart → atelectasis
→ Reversible (lung is able to regenerate)
→ Trauma/ severe respiratory disorder→ alveolar
collapse→ prolonged mech vent→ tension
pneumothorax→ positive pressure at the lungs→
atelectasis, fat emboli/ shock/ sepsis→ decreased
perfusion→ alveolar collapse
→ Early symptoms:
• Increased HR, RR
• Intercostal retractions
→ Late symptoms:
• Dyspnea/DOB
• Hypoxia
• Crackles Sign of pulmonary congestion
Diagnostics Management: Patent Airway (Immunocompromised →
→ Chest xray- white lung massive phlegm build up → no cough → stasis of phlegm
→ ABG- respiratory acidosis (↓pH ↑CO2) → decreased ventilation)
→ Chest physiotherapy/ pulmonary toilet (indirect
Management removal of secretions)
→ Thoracentesis (minor case) • Post drainage
→ CTT (chest tube drainage)- done if there is too much • Percussion/ back clapping
air • Vibration
→ Suctioning (direct removal)
Additional Note:
→ Increase fluid intake - liquefy secretions
→ Drowning: → Nebulization- liquefy secretions
• Problem - Atelectasis/Alveolar collapse → Antibiotics (after sputum exam- determine the
• Management: Remove fluids causative agent first before giving antibiotics)

Types of Pneumonia
PNEUMONIA
1. Hospital acquired- post 48hrs of hospitalization
2. Community acquired- from outside; <48hrs of
hospitalization
3. Immunocompromised- r/t HIV, AIDS, cancer,
undergoing chemotherapy patients

Community Acquired Pneumonia

→ More dangerous in elderly d/t low immune system

→ Non-productive cough → Causative Agent: Streptococcus pneumoniae
→ Obstruction of the bronchioles by exudates and (pneumococcus)
secretions → Lobar consolidation- increased secretions
→ Thickened alveolar membrane→ decreased • Egophony upon auscultation (the finding that when
diffusion→ decreased gas exchange→ hypoxia and the patient says E it sounds like A or “ah”, like the
hypercapnia bleating of a goat.)
→ Increased secretions→ ineffective airway clearance→ • Whispered pectoriloquy- increased loudness of
decreased ventilation→ decreased gas exchange→ whispering noted during auscultation
hypoxia, increased carbon dioxide o Normal: Muffled Sound
→ Cause: exposure to causative agents o Abnormal: Clear Sound = (+) secretions
→ Immunocompromised are commonly affected • Increased tactile fremitus- increased at the affected
• Geria site d/t accumulation of secretions
• Pedia o Abnormal: If the vibration is not equal = (+)
• HIV, AIDS phlegm
• Chemotherapy, cancer o (tres-tres)
People with pneumonia can recover without hospitalization as
long as the immune system is good Hospital Acquired Pneumonia (Nosocomial)
→ Streptococcus pneumoniae
→ Early symptoms: → Staphylococcus aureus (including methicillin-resistant
• Chills staphylococcus aureus [MRSA])
• Fever → Gram-negative bacteria such as Pseudomonas
• Increased HR, RR aeruginosa and Haemophilus influenzae
• Productive cough (yellow, blood streaked/rusty • HIB- vaccine for haemophilus influenzae (flu
sputum) vaccine)
→ Late symptoms: o Done once a year because the bacteria is
• Dyspnea (DOB) evolving
→ Clinical symptoms: → Other gram-negative intestinal bacteria
• Pleural pain/Pleuritic friction rub- chest pain that
increases upon inhalation (the chest becomes Immunocompromised Pneumonia
bigger upon inhalation, creating friction) → Pneumocystis jirovecii/ Pneumocystis carinii
• Yellow, blood streaked (rusty sputum) - only seen
in pneumonia Jirovecii and carinii are caused by HIV/AIDS
→ <30 years old/middle aged; possible for HIV
• Subject the patient to ELISA testing or western blot
Diagnostics to check for possible of pneumonia d/t HIV
→ CX-ray o Confirmatory test: Western Blot
→ Sputum gram stain (GS)/Culture sensitivity (CS) o Screening test: ELISA
• Sterile sample to be accurate; no alteration in the
sample → CMV- cytomegalovirus (teratogenic)
• Sample is obtained in the morning before → Gram-negative bacteria- Pseudomonas aeruginosa
breakfast → Mycobacteria
• Water may be gargled
• Instruct the patient to cough out
BRONCHIAL ASTHMA •Late symptom: Bronchospasm → RESPIRATORY
ACIDOSIS
→ Chest Xray

Management for Acute Asthma (OSHIIT)

→ Bronchospasm (reactive airway disease) manifested

by wheezes/ stridor
• Wheezes and stridor are both heard during → Bronchospasm is present (emergency)
inhalation and exhalation → Oxygen- high flow
o WhEEzEs- more heard in Exhalation than → Salbutamol (sympathomimetic bronchodilator)
inhalation • Safe to cardio patients because it does not cause
o StrIdor- more heard in Inhalation than tachycardia as a side effect but have palpitations
exhalation and tremors as a side effect
• But if bronchospasm is >6 months → ASTHMA → Hydrocortisone (steroid; -sone)- depress the immune
(disorder) system
→ Affects males, onset before 12 years old • WOF: infection
→ Intrinsic- autoimmune disorder (genetic, from an → Immediate acting bronchodilator
asthmatic mother) • Albuterol sulfate (short acting [for emergencies]
• Mother is the carrier, manifested by males adrenergic receptor agonist)- promote sympathetic
• A pregnant woman can have asthma responses causing bronchodilation
→ Extrinsic- allergens trigger mast cells (part of immune o SE: increased HR, RR, BP, nervousness,
system) palpitations, tremors
• Pollen, dust, fur, good governance (dito lang dapat o Contraindicated to cardio patients because it
to) increases the workload of the heart
• Anaphylaxis can occur d/t airway obstruction → Beta blocker → <HR → rest of heart
caused by severe allergy ❖ SE: Bronchoconstriction
❖ (X) asthma patient
Pathophysiology o AE: Chest pain (myocardial ischemia)
→ Autoimmune/allergens→ trigger mast cells→ o Antagonist- prevent
precursor: → Ipratropium Bromide (anticholinergic/ sympa
A. Histamine bronchodilator)
o urticaria • tiotropium (atrovent, duavent)
o inflammation of the airways→ inflammation of • SE: increase HR, RR, palpitations
goblet cells→ increased cough production→ • Contraindicated to cardio patients
DOB/accessory muscle use→ increase → Theophylline/Aminophylline- methyl xanthine
oxygen consumption→ fatigue→ hypoxia derivatives/ bronchodilator
o increased mucus production→ ineffective • Action: Makes CNS more sensitive to CO2 levels
airway clearance→ decreased ventilation→ stimulating respiratory drive→ increase RR →
decreased gas exchange→ hypoxia, increase CO2 elimination
hypercapnia; → Suction is allowed → decreased secretions → goblet
B. Leukotriene→ bronchospasm→ decreased cells → patent airway
ventilation→ decreased gas exchange→ hypoxia,
hypercapnia Management to Prevent Asthma Attack
In acute asthma, steroids are the drug of choice because 1. Avoid allergens
antihistamine blocks histamine but not leukotriene therefore 2. Antihistamine- Cetirizine, Diphenhydramine
bronchospasm is still present, while steroids decrease the • SE: drowsiness [management: safety]
immune system therefore blocking both histamine and o Avoid driving
leukotriene o Avoid operating heavy machineries/
automobile/ car
Signs and Symptoms: o Avoid drinking alcohol
→ Early Sign: ▪ Bacardi 151 contains 75.5% (151 proof)
• Restlessness - sign of cerebral hypoxia alcohol causing alcohol toxicity. This is
• Altered LOC - sign of cerebral hypoxia discontinued and only available in the
• Increased RR - compensatory mechanism black market 👀
→ Late sign: • SE: oral and nasal dryness [prone to injury]
• Bronchospasm (whEEzEs) - reason of death o Oral dryness: Increase fluid intake, promote
• Decreased airway clearance d/t secretions oral care, ice chips
• Increased O2 levels o Nasal dryness: Nasal saline spray (contains
sodium that attracts water → lubrication)
Diagnostics: 3. Leukotriene Receptor Antagonist- prevent
→ Incentive spirometry - to check for lung capacity bronchospasm
→ ABG • Montelukast- can cause mental retardation (long
• Early symptom: Hyperventilation → term)
RESPIRATORY ALKALOSIS • Zafirlukast
 Diagnosis
→ ABGs- respiratory acidosis (ph down, co2 up)

Management
1. Maintain patent airway (CPT, suctioning, nebulization)
2. Low flow oxygen via venturi mask (inhibit hypoxic drive
if too much O2)
• Nasal cannula - alternative for venturi mask
3. Promote rest/ schedule activities
4. (X) OFI - possible of heart failure
5. WOF complication: Bronchiectasis- permanent
dilatation and necrosis of the bronchus
• Halitosis
• Foul-smelling sputum

CHRONIC OBSTRUCTIVE PULMONARY DISORDER EMPHYSEMA

(COPD)

→ ↓oxygen, ↑carbon dioxide
→ Chronic in nature - non toxic
→ No cure, only symptomatic management
→ Smoking is the number one risk factor
→ Chronic Bronchitis (blue bloater)
• Airway is affected→ goblet cells are affected→
secretions
→ Emphysema (pink puffer)
• Alveoli is the problem→ no secretions (quiet chest)
CHRONIC BRONCHITIS
→ Overdistended, over inflated alveoli (bleb) d/t short
expiratory phase→ air trapping→ over inflated alveoli:
• Ineffective gas exchange→ accessory muscle
use→ hypertrophy of chest muscles→ barrel chest
(APL ratio- 1:1)
• Bleb→ risk for rupture→ air exit→ closed
pneumothorax→ atelectasis →lung collapse
→ Clinical symptom: barrel chest
Problem with oxygenation→ anaerobic metabolism→ lactic
acid→ failure of the heart d/t workload

Symptoms (PINK PUFFER)

→ Pink- no cyanosis; d/t CO2 retention
• Main problem: hypercapnia→ DOB, ineffective
cough
→ Puffer
• Pursed-lip breathing
o Exhalation is longer than inhalation
o Goal: remove carbon dioxide
• No secretions - ineffective cough
• Hyperresonance on percussion d/t air
accumulation
• Orthopneic position
• Accessory muscle use d/t DOB
→ Chronic inflammation of the bronchus d/t smoking, • Short jerky sentences (hinihingal) and anxious - r/t
environment pollutants→ injury to the bronchioles→ to high levels of O2
inflammation of airways→ inflammation of the goblet • Possible of RHF - d/t overwork of the heart
cells: • Exertional dyspnea
• Increased cough production→ accessory muscle
use/DOB→ fatigue→ hypoxia Diagnostic:
• Increased mucus production→ ineffective airway → Clinical symptom: Barrel chest
clearance→ obstruction→ decreased gas → ABGs: Respiratory Acidosis
exchange→ hypoxia and hypercapnia
→ Clinical symptom: chronic productive cough for 3 Management
months in 2 consecutive years 1. Avoid:
• Suctioning (further increase hypoxia and further
Symptoms (BLUE BLOATER) remove O2)
→ Blue d/t dusky cyanosis • Chest physiotherapy (bleb rupture → closed
• Main problem: hypoxia pneumothorax)
• Clubbing of fingernails (chronic hypoxia) • Nebulization (not needed)
→ Bloater 2. Low flow oxygen via venturi mask
• Overweight 3. Promote rest/ schedule activities
• Edematous 4. Prevent complication: closed pneumothorax
• Diaphragmatic breather (inhalation is longer than 5. WOF complication: Status Asthmaticus
exhalation) • Madalas ka inaasthma
o Goal: get oxygen
o Lumalaki ang tiyan during inhalation = bloated
 ABG Analysis (with Lyrics)
• ↓MCV→ microcytic RBCs (iron deficiency anemia,
Performed and composed by: Lianmuel De Guzman sickle cell anemia, thalassemia)
→ Male- 79-103 fl
→ Female- 78-102 fl

White Blood Cells (WBC)

→ 5000-10000/mm3 (5-10 x 109/L)
→ For immune system
• >WBC - current infection
Nobody • <WBC - immunocompromised/risk for infection
by Wonder Girls o Management:
RESPIRATORY ACIDOSIS (PH DOWN, CO2 UP)
▪ Teach patient handwashing
🎵 COPD TOOHHH ATELECTASISSSS RESPI FAILURE
▪ Use of PPEs
ASPIRAAAaaAaaAaTTTttttIIIIooonNNNNN 🎵
▪ (+) pressure room
Binibirocha
▪ No fresh flowers, potted plants,
By Andrew E vegetables, crowded places
RESPIRATORY ALKALOSIS (PH UP, CO2 DOWN) ▪ Neupogen
🎵 HYPOXEMIA HYPERVENT VENTILATOR (excessive → Segmented neutrophils: 62-68% (3.5-7.5 x 109/L)
mech vent use) SAKA PAIN (increase RR) YAN ANG • Kills bacteria and viruses
CAUSES NG RESPI ALKALOSIS BIRIBIROCHAAAA 2X 🎵 → Band neutrophils: 0.9% (0-1 x 109/L)
→ Lymphocytes: 1000-4000/mm3 - 20-40% (0.1-0.4 x
Don’t Stop the Music 109/L)
by Rihanna • Kills bacteria and viruses
METABOLIC ACIDOSIS (PH AND HCO3 - both low)
→ Monocytes: 100-700/mm3 - 2-8% (0.1-0.7 x 109/L)
🎵 DIARRHEA DIABETES MELLITUS RENAL FAILURE
• First responders; for phagocytosis
SHOCK 2X 🎵
→ Eosinophils: 50-100/mm3 - 1-4% (0.00-0.5 x 109/L)
Chichi Wo Motomete • Kills parasites
by Voltes V → Basophils: 15-50/mm3 - 0.5-1% (0.0200.05 x 109/L)
METABOLIC ALKALOSIS (PH AND HCO3 - both high) • For allergic reaction
🎵 TENENEN 2X VOMITING (release of acid) ANTACIDS
NASOGASTRIC SUCTION DIURETICS EXCESSIVE BICARB Platelets
→ 150,000-400,000/mm3 (150-400 x 109/L)
• ↓platelet- risk for bleeding
ADMINISTRATION (hinga lyk dis oh ) TENENEN
2X 🎵 → >Platelet - polycythemia vera (viscous blood) →?
Decreased perfusion status
→ <Platelet - risk for bleeding
HEMATOLOGY • Management/Bleeding precautions :
o Use soft
Red Blood Cells (RBC) o Avoid contact sports
→ Male- 4.7-6.2 x 1012/L o Avoid dark colored foods, electric razors,
→ Female- 4.2-5.4 x 1012/L injections
→ Increased RBC → Viscous blood (polycythemia vera) o Smallest gauge possible
→ decrease blood flow o Padded side rails
• All blood components are increased - o (X) vaginal/rectal routes
polycythemia vera
→ Decreased RBC → Anemia → pallor, easy fatigability, APLASTIC ANEMIA
weakness d/t lack of O2 → Pancytopenia- decreased RBC, WBC, platelet d/t bone
• Management: marrow suppression/myelosuppression related to
• Promote rest chemo drugs, cancer
• Promote high flow oxygen • Pan means all
• Epogen (SQ) → Signs and symptoms:
o Stimulate production of RBC • Early:
• Blood transfusion (for severe cases) o Pallor
o Easy fatigability
Hemoglobin o Altered loc
→ Oxygen carrying capacity of the blood o weakness
• < HgB → anemia • Late:
→ Male- 14-18 g/dl (140-180 mmol/L) o Immunocompromised
→ Female- 12-16 g/dl (120-160 mmol/L) o Bleeding tendency

Hematocrit Symptoms of decreased RBC

→ Concentration of RBC in the blood → Weakness
• ↑HCT- concentrated blood→ dehydrated → Easy fatigability
• ↓HCT- diluted blood→ overhydrated → Dizziness
→ Male- 42-52% (0.42-0.52 volume fraction) → Pallor
→ Female- 37-47% (0.37-0.47 volume fraction) → Activity intolerance
→ Management for anemia
↓RBC, HGB- the problem is oxygen • Blood transfusion for severe cases
↓HCT- fluid imbalances • Promote rest
• Oxygen
• Epogen/erythropoietin (SQ route)- increases RBC
Mean Corpuscular Volume (MCV) production (Php 4,500 per tusok) 😩
→ Determines the size of RBC
• ↑MCV→ megaloblastic RBCs (pernicious anemia/ Symptoms of decreased WBC
folic acid deficiency anemia) → Body malaise
→ Weakness
→ Management for neutropenia → Pernicious Anemia
• Avoid crowds → Folic Acid Deficiency Anemia
• Limit visitors
• Avoid fresh flowers and potted plants (opportunistic IRON DEFICIENCY ANEMIA
infection) → Microcytic and hypochromic (maputla) RBCs
• Avoid raw/fresh foods • Iron gives color to the RBCs
• Promote hand washing → D/t severe bleeding
• Use PPEs • Females → excessive menstruation/hormonal
problems → anemia
Symptoms of decreased Platelets (bleeding tendencies) → Clinical symptoms
→ Bruises • Angular cheilitis (ulceration at the corner of the
→ Petechiae mouth)
→ Hematoma
→ Management for thrombocytopenia
• Use electric razors
• Use soft bristle toothbrush • Spoon shaped nails (koilonychia)
• Avoid IM route, vaginal, rectal
• Avoid contact sports
• Raise and pad side rails
• Avoid dark colored foods in the diet
• Minimize infection- use smallest gauge possible • Smooth sore tongue

Diagnostic
→ Complete blood count
→ MRI/CT scan- to determine problem in the bone
marrow
Management:
Medical Treatment → Iron supplement
→ Stem cell therapy • Absorbed at acidic environment (given before
→ Bone marrow transplant meals)
• Give epogen, neupogen, platelet = BONE • Can be given with Vitamin C/citrus juice
MARROW TRANSPLANT (but low success rates • Not taken with milk, cereal (removes acidity of the
d/t HIGH REJECTION) stomach)
• To prevent rejection: give steroids • Oral SE: constipation. black tarry stool
(immunosuppressant) - azathioprine • Liquid SE: teeth staining (use straw)
o To decrease immune system and prevent • IM SE: skin staining (Z track method)
rejection o Retract the skin first→ wait for 10 seconds after
→ Promote rest injection→ remove the hand after withdrawing
the needle→ seals the medicine in the
POLYCYTHEMIA VERA muscular layer for it not to stain the skin
→ Increased RBC, WBC, platelet→ viscous blood flow→
decreased perfusion status
→ D/t overreacted bone marrow functioning
→ Idiopathic/ autoimmune disorder
→ Common to middle aged group

Symptoms (RED)
→ Ruddy complexion (clinical symptom)
→ Elevated RBC, WBC, platelet; enlarged liver d/t → Promote rest
overwork (r/t RBC production) → Promote oxygen
→ Decreased blood flow [headache, blurry vision, gout,
painful joints, pruritus] (viscous) THALASSEMIA
→ Microcytic RBCs with short RBC lifespan (10-12 days)
Diagnostic • N: 90-120 days
→ CBC- elevated RBC, WBC, platelet → Thalassea means near the sea (mediterraneans: Greek,
Italian, Syrian)
Management
→ Avoid iron such as green leafy vegetables Management: Thalassemia Minor
→ Avoid purine foods for gout → Asymptomatic, carrier- no management
→ Phlebotomy- withdraw blood
• Cannot be donated since it is infected Management: Thalassemia Minor
• (X) plasmapheresis - used in px with autoimmune → Symptomatic- lifetime blood transfusion as often as
disorders (inaalis antibodies); not effective for every week
polycythemia vera → (WOF: iron overload → bloody vomitus)
• (X) iron - there's too much RBC • Antidote for Iron Overload: Deferoxamine/Desferal
• At bedside: Desferal
TYPES OF ANEMIA
Beta Thalassemia/Cooley's Anemia (common in pedia: beta
Microcytic Anemia- small RBCs→ ↓MCV levels = bata)
→ Iron Deficiency Anemia
→ Thalassemia SICKLE CELL ANEMIA
→ Sickle Cell Anemia → Genetic disorder x-linked
• Mother (XX) carrier → transfers to son (XY)
Macrocytic Anemia- large RBCs (obstructs blood flow)→ • Father (XY) carrier → transfers to daughter (XX)
↑MCV levels→ paresthesia- numbness and tingling → Sickle cells can obstruct the blood flow→ problems with
sensation & claudication- painful walking oxygenation→ necrosis can occur→ amputation
 o First scenario: (+) pernicious anemia → no
intrinsic factor → <20% vitamin B12 (injectable
absorbed, oral not absorbed) → plenty of
vitamine B12 in feces (because oral is not
absorbed ); less vitamin B12 in urine
o Second scenario: no pernicious anemia → (+)
intrinsic factor (oral absorbed, injectable not
absorbed) → >20% vitamin B12 → plenty of
vitamin B12 in urine (Vit B12 is water soluble)

FOLIC ACID DEFICIENCY ANEMIA

→ D/t alcoholism, jejunum (vitamin B9 absorption site)
resection
→ No clinical symptom (no specific symptom but there
→ Vaso-occlusive crisis→ obstruct blood flow→ may be presence of pallor, easy fatigability)
decreased O2→ necrosis→ organ death/extremity → Diagnostics:
death→ amputation • CBC
• Vitamin B9 Blood test
→ Management: Vitamin B9 Supplements (injectable),
Vitamin B9-rich foods
• Oats
• Wheat
• Rice
• Grains

HEMOPHILIA

→ Priority nursing diagnosis: pain (crisis is already

present; sign of vaso-occlusive crisis)
→ Priority nursing management: Prevent/manage triggers
of the crisis
1. Dehydration- fluids
2. Hypoxia
3. Stress/ Infection
→ Priority Nursing Management:
• 1st: Hydration (to prevent crisis)
• 2nd: Oxygen → Philia - love for blood
• 3rd: Pain management → Genetic, recessive trait (rare disorder)
• (X) altitude places d/t less oxygen • Recessive trait needs 2 genes
→ Can ride an airplane (since there is O2 in the cabin) • X-linked disorder
→ DOC: hydroxyurea/hydrea- decreases HGB S levels → Generalized bleeding d/t absent clotting factors
• HGB S causes the sickling of cells • Epistaxis
• Bleeding in joints
PERNICIOUS ANEMIA • Melena
→ Vitamin B12 deficiency • Hematuria
→ Clinical symptom: red beefy tongue • Hematemesis
→ Affects vegetarians (no meat/dairy sources) → Management
• Meat and dairy are the highest source of vitamin • Clotting factor
B12 • Cryoprecipitate (contains clotting factors + fresh
• Management: oral vitamin B12 frozen plasma (volume expander) → manages
o Vegetarians have intrinsic factor shock)
→ People with absent/decreased intrinsic factor • If no FFP, use Desmopressin/Vasopressin (ADH)
(requirement of vitamin B12 to be absorbed in the small o Priority: Check nasal patency (it is
intestine) administered nasally)
• Intrinsic factor is produced in the stomach via ▪ 2nd priority: Check for water toxicity d/t
parietal cells fluid volume excess (headache, dizziness,
• Peptic ulcer, gastrectomy, antrectomy (removal of pulmonary congestion, crackles)
lower part of stomach)→ less stomach tissue→ o For DI
less intrinsic factor→ less vitamin B12 absorption ▪ Problem: Fluid volume deficit
• Management: injectable vitamin B12 (monthly, ▪ To increase antidiuretic hormone
lifetime)- directly to the blood o For Hemophilia: For transient increase of factor
o Oral route would not be absorbed since VIII (for hemophilia A)
intrinsic factor is absent/decreased
o Water soluble (no toxic reaction) Types
→ Diagnostics: Schilling’s test - 24 H urine collection
A B C
• with doctor’s order
• First (discard) → Second (save) It is the most common It is the second most Is is a mild
• Missed 1 hour: repeat the test type of hemophilia common type of form of
• 2 ways to give: (severe) hemophilia hemophilia
o Oral Vitamin B12 - radioactive (moderate)
o IV Vitamin B12
It is also known as It was originally Deficiency
factor VIII deficiency names “christmas of factor XI
or classic hemophilia disease”

Caused by factor IX
deficiency
X-linked gene
X-linked gene Autosomal

➢ X-linked ➢ X-linked
recessive recessive
➢ Decreased ➢ Decreased
synthesis of synthesis of
factor VIII (8) factor IX (9)
➢ Treat with ➢ Treat with
recombinant recombinant
factor VIII factor IX
➢ Christmas
disease