RESPIRATORY SYSTEM

Respiratory Function: for gas exchange; get oxygen (cellular THORACENTESIS

processes) and remove carbon dioxide (neurotoxic) → Removal of air/fluid at the pleura to reestablish the
→ Main trigger for breathing: elevated carbon dioxide negative pressure→ allow air entry→ alveolar
levels expansion→ lung reexpansion
• Controlled by chemoreceptors (pons & medulla • Lungs are capable of regeneration
oblongata) → Short term
→ Centesis- direct removal of air fluid at the third space
Types of Respiration (External and Internal) (edema, ascites, pleura pericardium)
→ External/Ventilation- between the environment (positive • Diuretics remove fluid from the blood vessels only
pressure) towards the lungs (negative pressure)
• The normal pressure of the lungs is negative
• Pathology: Air/fluid in the pleura→ abnormal
pressure will cause positive pressure→ prevent air
entry→ alveolar collapse/atelectasis→ lung
collapse

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

(COPD)

Pathology
→ COPD patients→ too much CO2→ defective trigger→
replacement trigger- low oxygen levels (hypoxic drive)
→ The bag is placed at the bottom to allow drainage via
Management gravity
→ Low flow oxygen (1-2 LMP) via venturi mask → Prevent mediastinal shifting- occurs when the pressure
• Most accurate/precise delivery system gets so high that it pushes the heart and great vessels
• Rationale: too much oxygen for COPD patients, will into the unaffected side of the chest. These structures
inhibit the hypoxic drive (defective)- destroy both are compressed from external pressure and cannot
triggers for breathing→ respiratory cessation expand to accept blood flow
• This causes pressure to the heart resulting in
cardiac tamponade
High flow oxygen is not contraindicated for patients without o Decreased contractility→ CHF
COPD (e.g., COVID patients, etc.) • Removal of air/fluid in the affected side will re-
expand the lungs and will bring back the airways to
PNEUMOTHORAX their position
→ Too much air at the pleural cavity causes
pneumothorax

Cause
→ Open pneumothorax- trauma (stab wound, GSW)→ air
entry→ pneumothorax
→ Closed pneumothorax- r/t air trapping that leads to
overinflated alveoli (bleb)→ bleb rupture→ air exit→
pneumothorax

Symptoms
→ Shortness of breath
→ Unequal breath sounds (decreased/absent at the
→ Site
affected side)
• Air (pneumothorax)- 2nd-3rd ICS
• Wheezing/stridor is r/t bronchospasm (asthma)
• Fluid (pleural effusion)- 7th- above 9th ICS
→ Unequal chest expansion (d/t alveolar collapse)
o Avoid puncture of other organs (R: liver, L:
→ Hyperresonant upon percussion (too much air)
spleen)
• N: resonant (part air, part space)
• Dull- fluid/mass/organ Nursing Considerations
• Flat- bone → Check consent
→ Compensatory hypoxia- ↑HR, ↑RR • Doctors obtain consent, nurses witness consent
→ Position of choice: orthopneic/tripod position
PLEURAL EFFUSION → Pain medications 30 minutes before insertion
→ Fluid in the pleura (abortive/anticipatory)
• Abortive- abort pain before it happens
Types:
• Anticipatory- anticipate pain
→ Hydrothorax- water
→ Orient the patient (insertion)
→ Hemothorax- blood
• Stay still
→ Empyema/Pyothorax- pus
• Exhale and hold (prevent accidental puncture)
→ Removal- confirm lung re-expansion via CXR
Signs
→ Upon removal, instruct the client to perform valsalva
→ SOB
maneuver (bearing down)
→ Unequal chest expansion (decreased in the affected
• Rationale: transient increase in thoracic pressure
region)
that will prevent air entry
→ Unequal breath sounds (decreased in the affected
• Cover with vaselinized sterile gauze, occlusive
region, atelectasis)
dressing; tape at 4 sides
→ Dullness on percussion
→ WOF pneumothorax
• Check breath sounds 30 minutes after
 • Sign: unequal breath sounds • Pathology: decreased surfactant→ premature
• Report to the doctor babies→ atelectasis (RDS)
• Confirmed via CXR o Safest to deliver in 7 months (stable). During
• Thoracentesis will be done again the 8th month, lung problems arise

CHEST TUBE DRAINAGE Muscles of Breathing

→ Long term (takes days to complete)
→ Bottle system (old)- fragile, hard to transfer INHALATION
→ Pleur Evac (new)- made from fiberglass (durable), easy Normal inhalation- effortless
to transfer → Diaphragm
• Both have the same drainage duration • Strongest respiratory muscle
• Controlled by the phrenic nerve (C3-C4)

Accessory muscles for inhalation (DOB: priority)- more

muscles are used for respiration→ increased effort→
increased oxygen use→ fatigue and oxygen
→ Sternocleidomastoid
→ Upper Trapezius
→ Pectoralis Major and Minor
→ Anterior Scalenes
→ Serratus Major

Types of Respiration (External and Internal cont.)

→ Internal/Perfusion- between alveoli and deoxygenated
blood
• Gas moves via diffusion (higher to lower
concentration)
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) → Pathology: DOB→ increased accessory muscle use→
• E.g., myocardial ischemia→ decreased oxygen→ hypertrophy of chest muscle→ barrel chest (clinical
anaerobic→ lactic acid→ inflammation of the symptom of emphysema; APL ratio- 1:1)
cardiac muscles→ pain→ angina pectoris • Normal APL (anterior post lateral) ratio- 2:1

Protective Structures of the Respiratory System

→ Ribs- mechanical structure of the lungs and heart
→ Cilia- filters and humidifies air
→ Mucus- trap foreign body
→ Pseudostratified Columnar with Goblet Cells- lines up
the airways
• Cough production- protective structure to remove
foreign body (remove foreign body via cough
production)
• Mucus production- trap foreign body
❖ 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 EXHALATION
• Pathology: genetic→ decreased levels of alpha 1
antitrypsin→ decreased protection of the alveoli→ Normal Exhalation- effortless; chest recoil, no muscles
alveolar damage→ emphysema movement
o Emphysema may also be d/t genetic Accessory muscles for exhalation (DOB)- more oxygen
predisposition use→ fatigue, hypoxia, hypertrophy of muscles
• The mucosal lining serves as a protection of the → Abdominals
stomach from the hydrochloric acid which is vital for → Serratus minor
digestion → Intercostals
→ Alveolar Type 2: Surfactant- promote surface tension
preventing alveolar collapse
 PNEUMONIA
→ Thickened alveolar membrane→ decreased
diffusion→ decreased gas exchange→ hypoxia and
hypercapnia
→ Increased secretions→ ineffective airway clearance→
decreased ventilation→ decreased gas exchange→
hypoxia, increased carbon dioxide
→ Immunocompromised are commonly affected
• Geria
RESPIRATORY DISTRESS SYNDROME • Pedia
→ Premature, GDM, LBW babies are affected • HIV, AIDS
→ Atelectasis d/t decreased surfactant • Chemotherapy, cancer
• Decreased surfactant→ alveolar collapse→ People with pneumonia can recover without hospitalization as
decreased gas exchange long as the immune system is good
→ Early symptoms:
→ Early symptoms:
• Poor, weak cry
• Chills
• Intercostal retractions (accessory muscle use)
• Fever
→ Late symptoms:
• Increased HR, RR
• Blue colored lips, fingers and toes (acracyanosis)
• Productive cough (yellow, blood streaked/rusty
• Rapid, shallow breathing seen at the belly
sputum)
• Flaring nostrils- no benefit for breathing; done d/t
→ Late symptoms:
weak compensation
• Dyspnea (DOB)
• Grunting sound when breathing
• Pleural pain/Pleuritic friction rub- chest pain that
• Increased HR, RR
increases upon inhalation (the chest becomes
bigger upon inhalation, creating friction)
Diagnostics
→ Chest x ray- scattered atelectasis
Diagnostics
• Late: white lung
→ Sputum gram stain (GS)/Culture sensitivity (CS)
• Sample is obtained in the morning before
Management
breakfast
→ Before birth: corticosteroids Im to the mother to
• Water may be gargled
promote lung maturity
• Instruct the patient to cough out
→ After birth: synthetic surfactant (Survanta) via
advanced airway, direct to the alveoli (ET tube,
Management: Patent Airway
laryngeal tube, tracheostomy)
→ Chest physiotherapy/ pulmonary toilet (indirect
removal of secretions)
ADULT RESPIRATORY DISTRESS SYNDROME (ARDS)
• Post drainage
→ Atelectasis d/t trauma (main cause)
• Percussion/ back clapping
→ Trauma/ severe respiratory disorder→ alveolar
• Vibration
collapse→ prolonged mech vent→ tension
pneumothorax→ positive pressure at the lungs→ → Suctioning (direct removal)
atelectasis, fat emboli/ shock/ sepsis→ decreased → Increase fluid intake
perfusion→ alveolar collapse → Nebulization- liquefy secretions
→ Early symptoms: → Antibiotics (after sputum exam- determine the
• Increased HR, RR causative agent first before giving antibiotics)
• Intercostal retractions
→ Late symptoms:
• Dyspnea/DOB
• Hypoxia
• Crackles

Diagnostics
→ Chest xray- white lung
→ ABG- respiratory acidosis (↓pH ↑CO2)

Management
→ Thoracentesis (minor case)
→ CTT (chest tube drainage)- done if there is too much
air
Types of Pneumonia o increased mucus production→ ineffective
1. Hospital acquired- post 48hrs of hospitalization airway clearance→ decreased ventilation→
2. Community acquired- from outside; <48hrs of decreased gas exchange→ hypoxia,
hospitalization hypercapnia;
3. Immunocompromised- r/t HIV, AIDS, cancer, B. Leukotriene→ bronchospasm→ decreased
undergoing chemotherapy patients ventilation→ decreased gas exchange→ hypoxia,
hypercapnia
Community Acquired Pneumonia
In acute asthma, steroids are the drug of choice because
antihistamine blocks histamine but not leukotriene therefore
bronchospasm is still present, while steroids decrease the
immune system therefore blocking both histamine and
leukotriene

Management for Acute Asthma (OSHIIT)

→ Bronchospasm is present (emergency)
→ Oxygen- high flow
→ Salbutamol (sympathomimetic bronchodilator)
• Safe to cardio patients because it does not cause
→ Causative Agent: Streptococcus pneumoniae tachycardia as a side effect
(pneumococcus) → Hydrocortisone (steroid; -sone)- depress the immune
→ Lobar consolidation- increased secretions system
• Egophony upon auscultation (the finding that when • WOF: infection
the patient says E it sounds like A or “ah”, like the → Immediate acting bronchodilator
bleating of a goat.) • Albuterol sulfate (short acting adrenergic receptor
• Whispered pectoriloquy- increased loudness of agonist)- promote sympathetic responses causing
whispering noted during auscultation bronchodilation
• Increased tactile fremitus- increased at the affected o SE: increased HR, RR, BP, nervousness,
site d/t accumulation of secretions palpitations
o Contraindicated to cardio patients because it
Hospital Acquired Pneumonia (Nosocomial) increases the workload of the heart
→ Streptococcus pneumoniae o Antagonist- prevent
→ Staphylococcus aureus (including methicillin-resistant → Ipratropium Bromide (anticholinergic/ sympa
staphylococcus aureus [MRSA]) bronchodilator)
→ Gram-negative bacteria such as Pseudomonas • SE: increase HR, RR
aeruginosa and Haemophilus influenzae • Contraindicated to cardio patients
• HIB- vaccine for haemophilus influenzae (flu → Theophylline/Aminophylline- xanthine bronchodilator
vaccine) • Action: Makes CNS more sensitive to CO2 levels
o Done once a year because the bacteria is stimulating respiratory drive→ increase CO2
evolving elimination
→ Other gram-negative intestinal bacteria
Management to Prevent Asthma Attack
Immunocompromised Pneumonia 1. Avoid allergens
→ Pneumocystis jirovecii 2. Antihistamine- Cetirizine, Diphenhydramine
→ Pneumocystis carinii • SE: drowsiness
Jirovecii and carinii are caused by HIV/AIDS o Avoid driving
o Avoid operating heavy machineries/
→ CMV- cytomegalovirus automobile/ car
→ Gram-negative bacteria- Pseudomonas aeruginosa o Avoid drinking alcohol
→ Mycobacteria ▪ Bacardi 151 contains 75.5% (151 proof)
alcohol causing alcohol toxicity. This is
BRONCHIAL ASTHMA discontinued and only available in the
→ Bronchospasm manifested by wheezes/ stridor black market 👀
• Wheezes and stridor are both heard during • SE: oral and nasal dryness
inhalation and exhalation o Oral dryness: Increase fluid intake, oral care
o WhEEzEs- more heard in Exhalation than o Nasal dryness: Nasal saline spray (contains
inhalation sodium that attracts water)
o StrIdor- more heard in Inhalation than 3. Leukotriene Receptor Antagonist- prevent
exhalation bronchospasm
→ Affects males, onset before 12 years old • Montelukast- can cause mental retardation (long
→ Intrinsic- autoimmune disorder (genetic, from an term)
asthmatic mother) • Zafirlukast
• Mother is the carrier, manifested by males
• A pregnant woman can have asthma CHRONIC OBSTRUCTIVE PULMONARY DISORDER
→ Extrinsic- allergens (COPD)
• Anaphylaxis can occur d/t airway obstruction
caused by severe allergy

Pathophysiology
→ Autoimmune/allergens→ trigger mast cells→
precursor:
A. Histamine
o urticaria
o inflammation of the airways→ inflammation of
goblet cells→ increased cough production→
DOB/accessory muscle use→ increase
→ ↓oxygen, ↑carbon dioxide
oxygen consumption→ fatigue→ hypoxia
→ No cure, only symptomatic management
→ Smoking 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
• 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
• Main problem: hypercapnia→ DOB, ineffective
cough
→ Puffer
• Pursed-lip breathing
o Exhalation is longer than inhalation
o Goal: remove carbon dioxide
• Hyperresonance on percussion
• Exertional dyspnea
• Short jerky sentences (hinihingal)

→ Chronic inflammation of the bronchus d/t smoking, Management

environment pollutants→ injury to the bronchioles→ 1. Avoid:
inflammation of airways→ inflammation of the goblet • Suctioning (further increase hypoxia)
cells: • Chest physiotherapy (bleb rupture)
• Increased cough production→ accessory muscle • Nebulization (not needed)
use/DOB→ fatigue→ hypoxia 2. Low flow oxygen via venturi mask
• Increased mucus production→ ineffective airway 3. Promote rest
clearance→ obstruction→ decreased gas 4. Prevent complication: closed pneumothorax
exchange→ hypoxia and hypercapnia
→ Clinical symptom: chronic productive cough for 3 HEMATOLOGY
months in 2 consecutive years
Red Blood Cells (RBC)
Symptoms (BLUE BLOATER) → Male- 4.7-6.2 x 1012/L
→ Blue d/t dusky cyanosis → Female- 4.2-5.4 x 1012/L
• Main problem: hypoxia
• Clubbing of fingernails (chronic hypoxia) Hemoglobin
→ Bloater → Oxygen carrying capacity of the blood
• Overweight → Male- 14-18 g/dl (140-180 mmol/L)
• Edematous → Female- 12-16 g/dl (120-160 mmol/L)
• Diaphragmatic breather (inhalation is longer than
exhalation) Hematocrit
o Goal: get oxygen → Concentration of RBC in the blood
o Lumalaki ang tiyan during inhalation = • ↑HCT- concentrated blood→ dehydrated
bloated • ↓HCT- diluted blood→ overhydrated
→ Male- 42-52% (0.42-0.52 volume fraction)
Diagnosis → Female- 37-47% (0.37-0.47 volume fraction)
→ ABGs- respiratory acidosis

Management ↓RBC, HGB- the problem is oxygen

1. Maintain patent airway (CPT, suctioning, nebulization) ↓HCT- fluid imbalances
2. Low flow oxygen via venturi mask (inhibit hypoxic drive
if too much O2) Mean Corpuscular Volume (MCV)
3. Promote rest → Determines the size of RBC
4. WOF complication: Bronchiectasis- permanent • ↑MCV→ megaloblastic RBCs (pernicious anemia/
dilatation and necrosis of the bronchus folic acid deficiency anemia)
• Halitosis • ↓MCV→ microcytic RBCs (iron deficiency anemia,
• Foul-smelling sputum sickle cell anemia, thalassemia)
→ Male- 79-103 fl
EMPHYSEMA → Female- 78-102 fl

White Blood Cells (WBC)

→ Overdistended, over inflated alveoli (bleb) d/t short
expiratory phase→ air trapping→ over inflated alveoli:
→ 5000-10000/mm3 (5-10 x 109/L)
• ↓WBC- risk for infection
→ Segmented neutrophils: 62-68% (3.5-7.5 x 109/L)
• Kills bacteria and viruses
→ Band neutrophils: 0.9% (0-1 x 109/L)
→ Lymphocytes: 1000-4000/mm3 - 20-40% (0.1-0.4 x
109/L)
• Kills bacteria and viruses
→ Monocytes: 100-700/mm3 - 2-8% (0.1-0.7 x 109/L)
• First responders
→ Eosinophils: 50-100/mm3 - 1-4% (0.00-0.5 x 109/L)
• Kills parasites
→ Basophils: 15-50/mm3 - 0.5-1% (0.0200.05 x 109/L)
 • For allergic reaction • Cannot be donated

Platelets TYPES OF ANEMIA

→ 150,000-400,000/mm3 (150-400 x 109/L)
• ↓platelet- risk for bleeding Microcytic Anemia- small RBCs→ ↓MCV levels
→ Iron Deficiency Anemia
APLASTIC ANEMIA → Thalassemia
→ Pancytopenia- decreased RBC, WBC, platelet d/t bone → Sickle Cell Anemia
marrow suppression/myelosuppression related to
chemo drugs, cancer Macrocytic Anemia- large RBCs (obstructs blood flow)→
• Pan means all ↑MCV levels→ paresthesia- numbness and tingling
sensation & claudication- painful walking
Symptoms of decreased RBC → Pernicious Anemia
→ Weakness → Folic Acid Deficiency Anemia
→ Easy fatigability
→ Dizziness
→ Pallor IRON DEFICIENCY ANEMIA
→ Activity intolerance → Microcytic and hypochromic (maputla) RBCs
→ Management for anemia • Iron gives color to the RBCs
• Blood transfusion for severe cases → D/t severe bleeding
• Promote rest → Clinical symptoms
• Oxygen • Angular cheilitis
• Epogen/erythropoietin (SQ route)- increases RBC
production (Php 4,500 per tusok) 😩

Symptoms of decreased WBC • Spoon shaped nails (koilonychia)

→ Body malaise
→ Weakness
→ Management for neutropenia
• Avoid crowds
• Limit visitors • Smooth sore tongue
• Avoid fresh flowers and potted plants (opportunistic
infection)
• Avoid raw/fresh foods
• Promote hand washing
• Use PPEs
Management:
→ Iron supplement
Symptoms of decreased Platelets (bleeding tendencies)
• Absorbed at acidic environment (given before
→ Bruises
meals)
→ Petechiae
• Can be given with Vitamin C/citrus juice
→ Hematoma
• Not taken with milk, cereal (removes acidity of the
→ Management for thrombocytopenia
stomach)
• Use electric razors
• Oral SE: constipation. black tarry stool
• Use soft bristle toothbrush
• Liquid SE:teeth staining (use straw)
• Avoid IM route, vaginal, rectal
• IM SE: skin staining (Z track method)
• Avoid contact sports
o Retract the skin first→ wait for 10 seconds after
• Raise and pad side rails
injection→ remove the hand after withdrawing
• Avoid dark colored foods in the diet
the needle→ seals the medicine in the
• Minimize infection- use smallest gauge possible muscular layer for it not to stain the skin
Diagnostic
→ Complete blood count
→ MRI/CT scan- to determine problem in the bone
marrow

Medical Treatment
→ Stem cell therapy
→ Bone marrow transplant

POLYCYTHEMIA VERA THALASSEMIA

→ Increased RBC, WBC, platelet→ viscous blood flow→ → Microcytic RBCs with short RBC lifespan (10-12 days)
decreased perfusion status • N: 90-120 days
→ D/t overreacted bone marrow functioning → Thalassea means near the sea (mediterraneans: Greek,
→ Idiopathic/ autoimmune disorder Italian, Syrian)

Symptoms (RED) Management: Thalassemia Minor

→ Ruddy complexion (clinical symptom)
→ Elevated RBC., WBC, platelet; enlarged liver
→ Decreased blood flow (viscous)
Diagnostic
→ CBC- elevated RBC, WBC, platelet
→ Asymptomatic, carrier- no management
Management: Thalassemia Minor
→ Symptomatic- lifetime blood transfusion as often as
every week

Management
→ Avoid iron
→ Phlebotomy- withdraw blood
SICKLE CELL ANEMIA • Grains
→ Sickle cells can obstruct the blood flow→ problems with
oxygenation→ necrosis can occur→ amputation HEMOPHILIA

→ Vaso-occlusive crisis→ obstruct blood flow→

decreased O2→ necrosis→ organ death/extremity → Generalized bleeding d/t absent clotting factors
death→ amputation → X-linked disorder
→ Management
• Clotting factor
• Cryoprecipitate (contains clotting factor)

Types
A B C

It is the most common It is the second most Is is a mild

type of hemophilia common type of form of
(severe) hemophilia hemophilia
(moderate)

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
→ Priority nursing diagnosis: pain (crisis is already deficiency
present; sign of vaso-occlusive crisis) X-linked gene
→ Priority nursing management: Prevent/manage triggers X-linked gene Autosomal
of the crisis
1. Dehydration- fluids ➢ X-linked ➢ X-linked
2. Hypoxia recessive recessive
3. Infection ➢ Decreased ➢ Decreased
→ DOC: hydroxyurea/hydrea- decreases HGB S levels synthesis of synthesis of
factor VIII (8) factor IX (9)
• HGB S causes the sickling of cells
➢ Treat with ➢ Treat with
recombinant recombinant
PERNICIOUS ANEMIA factor VIII factor IX
→ Vitamin B12 deficiency ➢ Christmas
→ Clinical symptom: red beefy tongue disease
→ Affects vegetarians (no meat/dairy sources)
• Meat and dairy are the highest source of vitamin
B12
• Management: oral vitamin B12
o Vegetarians have intrinsic factor
→ People with absent/decreased intrinsic factor
(requirement of vitamin B12 to be absorbed in the small
intestine)
• Intrinsic factor is produced in the stomach via
parietal cells
• Peptic ulcer, gastrectomy, antrectomy (removal of
lower part of stomach)→ less stomach tissue→
less intrinsic factor→ less vitamin B12 absorption
• Management: injectable vitamin B12 (monthly,
lifetime)- directly to the blood
o Oral route would not be absorbed since
intrinsic factor is absent/decreased
o Water soluble (no toxic reaction)

FOLIC ACID DEFICIENCY ANEMIA

→ D/t alcoholism, jejunum (vitamin B9 absorption site)
resection
→ Management: Vitamin B9 Supplements (injectable),
Vitamin B9-rich foods
• Oats
• Wheat
• Rice