Pamantasan ng Cabuyao

Banaybanay, Cabuyao City, Laguna 4025, Philippines

COLLEGE OF HEALTH AND ALLIED SCIENCES

Name: AQUINO, CHELSEA A. Date: August

29, 2022
Year and Section: 4BSN-B Course: NCM118

1. WHAT IS PULMONARY TUBERCULOSIS (PTB)?

Pulmonary tuberculosis (TB) is an infectious disease caused by Mycobacterium tuberculosis. In many patients, M. tuberculosis becomes dormant before it progresses to active TB. TB most
commonly involves the lungs and is communicable in this form, but may affect almost any organ system including the lymph nodes, central nervous system, liver, bones, genitourinary, and
gastrointestinal tract.

PATHOPHYSIOLOGY OF PULMONARY
TUBERCULOSIS (PTB)
PREDISPOSING FACTORS PRECIPITATING FACTORS AGGRAVATING FACTORS
 Age- infants, children, and  Occupation (working in healthcare)  Taking medications that weaken  Cigarette smoking
elderly  Repeated close contact with infected the immune system  Alcohol abuse
 Sex – more common in males persons  Poor hygiene  Substance abuse
than females  People with weakened immune systems  Lack of access to health care  Living in overcrowded areas or
(HIV/AIDS, chemotherapy, diabetes)  Low socio-economic status substandard housing

Etiology
Mycobacterium tuberculosis

Exposed to or inhalation of infected TB avoids the mucus traps Aleveolar macrophages recognize Macrophage fuses the
phagosome with a A protein that inhibits
droplet nuclei from infected clients by and go to the deep airways foreign proteins on their cell surface
Scar tissue present but Mycobacterium
this fusion issurvives,
produced
coughing, sneezing, talking, laughing and
BACTERIA and pulmonary Granuloma
alveoli forms toandattempt to wall
package offinto
them the abacteria and
phagosome 3 weeks after lysosome
primary infection
mycobacteria is killed proliferates, and creates a
CANNOT singing prevent it from spreading (cell-mediated immunity)
off by immune system localized, primary infection
SPREAD
 Tissue in the middle of the granuloma
dies; undergoes caseous necrosis
ACTIVE INFECTION LATENT
Immunocompromised Immunocompetent
individuals
INFECTION
individuals
Extends to nearby
Mycobacteria evades the Ghon focus TB remains viable yet
hilar lymph nodes
immune response dormant; immune system
suppresses the infection

Ghon complex is
SYMPTOMS: formed
 Coughing up blood or sputum LABORATORY:
LABORATORY:
for more than 3 weeks
. Chest pain  X-ray = Cloudy, scar  X-ray = clear
ASYMPTOMAT
tissue present  TB skin test = positive
 Fatigue IC
 Loss of appetite  TB skin test = Positive  Sputum test = negative
 Weight loss  Sputum test = Positive
 Fever
 Chills or night sweats
TREATMENT:
TREATMENT:  Daily dose of antibiotics for 6-9 months:
 Combination of 3 or more  Isoniazid
Ghon complex undergoes fibrosis and calcification antibiotic medications for 6-12
months:
 Isoniazid (INH)
Infection spreads to 1 or both upper lobes of the  Rifampin Immune supprression for months
lungs or vascular system and forms cavities  Pyrazinamide to years and improper treatment
 Ethambutol RECOVER
 Directly observed therapy Y
IMPROPER GHON FOCUS
(DOT)
TREATMENT REACTIVATION;
RECOVER CAN LEAD TO ACTIVE
2. WHAT IS COMMUNITY-ACQUIRED DEAT PNEUMONIA (CAP)? Y OR SECONDARY
H
Community-acquired pneumonia (CAP) is an inflammation of the lung parenchyma caused by various microorganisms, including bacteria, mycobacteria, fungi, and viruses, occuring in the
community or <48 hours after hospital admission or institutionalization of patients who do not meet the criteria for health-care associated pneumonia (HCAP).
 PATHOPHYSIOLOGY OF COMMUNITY-ACQUIRED
PNEUMONIA (CAP)
PREDISPOSING FACTORS PRECIPITATING AGGRAVATING FACTORS
 Age – infants, young children, >60 FACTORS  Smoking
 Sex  Environmental exposures  Malnutrition
 Genetics  Poor dental health
 Immunosuppressive conditions
 Recent antibiotic use
 Respiratory diseases such as
COPD and asthma
 Previous CAP

S. pneumoniae enters the respiratory Bacteria colonization on the mucus and cells of the Respiratory smooth muscle will
tract through inhalation/aspiration nasopharynx; releases endotoxins that produce tissue damage constrict and cause bronchospasm

Normal pulmonary defense mechanisms Endotoxins release inflammatory mediators of Dyspnea and shortness of breath
(cough reflex, mucociliary escalator, inflammation that causes vasodilation and increase
alveolar magcrophages, IgA antibodies) capillary permeability to fight off the bacteria
protect against the bacteria Macrophages fight off bacteria

Edema and
Impaired host defense mechanism inflammation occurs Fever
 FIRST STAGE SECOND STAGE THIRD STAGE FOURTH STAGE
Congestion (Days 1 - Red Hepatization (Days 3 - Gray Hepatization (Days 5 - Resolution (Days 8 to 3 weeks)
2) 4) 7)

Blood vessels and alveoli Pulmonary capillaries get damaged Still firm; color change due to Exudate/consolidation is
fill with excess fuid RBCs in exudate breaking down digested, ingested, or coughed
up
Exudate (RBCs, neutrophils, and
Chest X-ray may show a blotchy, fibrin) fill airspaces making them TYPICAL SYMPTOMS: Sputum from productive cough
white area, where fluid and pud has more solid (consolidation)  Tachycardia
accumulated in the lung’s air sacs  Tachypnea
 Chest Pain ↓ ventilation = ↓ V/Q ratio
 Fever
 Cough with mucopurulent
sputum production Ventilation-perfusion (V/Q)
 Fatigue mismatch occurs in the affected area
 Dyspnea and shortness of of the lung due to hypoventilation
IMPROPER TREATMENT: breath
TREATMENT 1. Pharmacologic Therapy
 Depends on severity for type of
DIAGNOSTIC WORKUP:
antibiotic and route (IV vs. oral) 2. Chest X-ray
1. Physical Examination
COMPLICATIONS:  Antibiotics: PCN sensitive: PCN,
 Inspection  Lobar pneumonia - fluid
 Septic shock amoxicillin, ceftriaxone, cefotaxime,
 ↑ RR (accessory muscle use, localized to a single lobe
 Pleural effusion cefprozil, or a macrolide; PCN
intercostal retraction)
 Superinfections resistant: levoflaxacin, moxifloxacin,
 Pleuritic chest pain 3. Sputum Cytology (Gram-
 Pericarditis vancomycin, linezolid
 Palpation stain/ culture)
 Otitis media  Antitussives
 Respiratory expansion  Rusty, blood-tinged (S.
 Meningitis  Pain medications
 ↓ Unilateral , ↑ tactile vocal fremitus pneumoniae)
 Abcesses 2. Supportive Treatment: hydration,
 Percussion
 Hypoxia bedrest
 Dullness to percussion
3. Oxygen Therapy
 Auscultation
 Bronchial breath sounds
 + Crackles (rales), + egophony,
DEAT RECOVER + bronchophony, + whisper pectoriloquy
H Y