Pathophysiology of Koch’s Disease

(Tuberculosis)
Predisposing Factors:
Precipitating Factors:
•
Age
- Occupation (e.g Health Workers)
•
Immunosuppression
- Repeated close contact w/ infected
persons
o

Prolonged corticosteroid therapy

- Indefinite substance abuse via IV
•
Systemic Infection:
- recurrence of infection
o

Diabetes Mellitus
o

End-stage Renal Disease

o

HIV or AIDS infection

Exposure or inhalation of infected

Aerosol through droplet nuclei

(exposure to infected clients by coughing,

sneezing, talking)

Tubercle bacilli invasion in the apices of the

Lungs or near the pleurae of the lower lobes
Bronchopneumonia develops in the lung tissue
(Phagocytosed tubercle bacilli are ingested by macrophages)


bacterial cell wall binds with macrophages



arrest of a phagosome which results to bacilli replication

Necrotic Degeneration occurs

(production of cavities filled with cheese-like

mass of tubercle bacilli, dead WBCs, necrotic lung tissue)

drainage of necrotic materials into the

tracheobronchial tree

(eruption of coughing, formation of lesions)

PRIMARY INFECTION
Lesions may calcify (Ghon’s Complex)
and form scars and may heal
over a period of time
Tubercle bacilli immunity develops
(2 to 6 weeks after infection)
(maintains in the body as long as living
bacilli remains in the body)
Acquired immunity leads to further growth
Of bacilli and development of ACTIVE INFECTION
SIGNS AND SYMPTOMS
Pulmonary Symptoms:
General Symptoms:
•
Dyspnea
- Fatigue
•
Non-productive or productive cough
- anorexia
•
Hemoptysis (blood tinge sputum)
- Weight loss
•
Chest pain that may be pleuritic or dull
- low grade fever with
chills and
•
Chest tightness
sweats (often at night)
•
Crackles may be present on auscultation
With Medical Intervention
Without Medical intervention
•
Early detection/ diagnosis of the dse
Reactivation of the tubercle bacilli
•
Multi-antibacterial therapy
(Due to repeated exposure to infected
•
Fixed- dose therapy
Individuals, Immunosuppression)
•
TB DOTS (Direct Observed Therapy)
SECONDARY INFECTION
•
BCG vaccination
Severe occurrence of lesions in the lungs
No Recurrence
Recurrence
Cavitation in the lungs occurs
Good Prognosis
Bad Prognosis
Active infection is spread throughout
the body systems
(infiltration of tubercle bacilli in other organs)


TB of the Bones

Pott’s Disease


Renal TB
SEVERE OCCURRENCE OF
INFECTION
Client becomes clinically ill
BAD PROGNOSIS
DEATH
The Pathophysiology of Cancer

When you are healthy, your body has over a trillion cells that divide at standard rate
and pace. When you develop cancer your normal cells turn into cancer cells.
Cancer cells have different DNA that healthy cells.

One of the first steps in a healthy cell becoming a cancer cell is the change of the
proto-oncogens to oncogenes. Proto-oncogenes are genes that are coded to
maintain normal cell growth. An oncogenes is a gene that has changed to make the
cells grow and divide faster. In cancer cells the cell grows and divides very quickly.

The second step to becoming a cancer cell is the tumor suppressor genes get
turned off. Tumor suppressor genes are a part of a healthy cells DNA that help stop
cancer from forming in healthy cells. Tumor suppressor genes help slow down cell
growth, when these genes are turned off the cell with grow and divide very quickly.

The last step to becoming a Cancer cell is the DNA repair genes gets turned off.
DNA repair genes help your healthy cells know if something is wrong with its DNA
and how to fix it. When these genes get turned off the cell doesn’t know if it is sick,
and it can’t fix any problems with its DNA.

PATHOPHYSIOLOGY
(Chronic Renal Failure)
Predisposing
Factors:
■ Ages 55 and
above
■ Family History
(Diabetes Mellitus,
Hypertension)
Precipitating
Factors:
■ Lifestyle
- smoking
- alcohol drinking
■ Certain Diseases
(Hypertension,

Diabetes Mellitus,
Recurrent
infections

Thickening and/or an
in the amount of collagen in
the basement membranes
of the small vessels
Impaired/sluggish blood flow
GFR
(Glomerular Filtration Rate)
Glomerulosclerosis
proteinuria
Renal blood

Stage I
DIMINISHED RENAL
RESERVE

GFR 50%
Normal BUN,
creatinine
More than 75%
damage
BUN, creatinine
levels begin to rise
Stage II
RENAL INSUFFICIENCY
GFR 20-50%

Remaining nephrons undergo

changes to compensate for
those damaged nephrons

Filtration of more concentrated

blood by the remaining
nephrons

Hypertrophy of
nephrons
Intolerance and exhaustion
of the remaining nephrons
Further damage of
the nephrons
80-90% damage
Stage III
RENAL FAILURE
GFR 10-20%

Impaired kidney
function and
Uremia