TUBERCULOSIS

B. Disease Process
Tuberculosis has three stages: (1) primary (initial) infection; (2) latent
(dormant) infection; and (3) recrudescent (post primary) disease. During the
first stage, the mycobacteria invade the tissues at the port of entry (usually
the lungs) and multiply over a period of approximately 3 weeks. They form a
small inflammatory lesion in the lungs before traveling to the regional lymph
nodes and throughout the body, forming additional lesions. The number of
lesions formed depends on the number of invading bacteria and the general
resistance of the host. This stage is generally asymptomatic. Lymphocytes
and antibodies mount a fibroblastic response to the invasion that encases
the lesions, forming noncaseating granulomas. This marks the latent stage,
and the individual may remain in this stage for weeks to years, depending on
the bodys ability to maintain specific and nonspecific resistance. Stage three
occurs when the body is unable to contain the infection, and a necrotic and
cavitation process begins in the lesion at the entry port or in other body
lesions. Caseation occurs and the lesions may rupture, spreading necrotic
residue and bacilli throughout the surrounding tissue. Disseminated bacteria
form new lesions, which in turn become inflamed and form noncaseating
granulomas and then caseating necrotic cavities. The lungs are the most
common site for recrudescent disease, but it may occur anywhere in the
body. Untreated disease has many remissions and exacerbations.
 VIRAL HEPATITIS

A. Pathophysiology

Risk Factors:
- Poor sanitation and hygiene
- Contaminated food and water
- Multiple sexual partners
- Immunosuppressed
- Injecting drug users
- Blood transfusion
- Health care workers
- Infants born to HBV-infected
mother

Etiology:
Hepatitis A, B, C, D, E

Acute liver inflammation

Cytotoxic cytokines and Induction of immune

Pre - icteric phase
natural killer cells cause lysis response
of infected hepatocytes

Sign &
Antigen-antibody complexes
Symptoms:
Kupffer cells proliferate
- Anorexia
- RUQ pain,
- Nausea Activation of complement
Cell injury - Malaise system
- Weight loss (1
21 days)
Fibrous scars *maximum Immune complex formation
infectivity for in circulation

Obstruction of
blood and bile flow Immune complex deposition
in vascular

Ischemia
Vasculitis (inflammation of
blood vessels)
Necrosis

Impairs blood supply

Ischemia
 Liver damage Icteric phase Liver

If managed: Same GI s/s as Pre Icteric Virus is not killed

- Adequate rest phase, dark urine, jaundice,
- Avoid alcohol and hepatomegaly (2 -4 weeks
drugs detoxified by duration) Viral antigens persists
the liver
in the liver
- Vitamin
supplements
- High in calorie and
protein Viral infection
carbohydrates and
low in fat diet.

Carrier of state B, C,
Promotes liver cells for D, (asymptomatic)
regeneration

Transmit disease
Liver resume to normal
appearance and function

Malaise, Fatigue,
Hepatomegaly may
remain (2 4 months
duration)
May progress to:
- Hepatocellular
Post - icteric phase carcinoma
- Liver cirrhosis
- Liver failure

Death
 VIRAL HEPATITIS

B. Disease Process
The cause is a variety of hepatotropic viruses. To date, five viral types
that cause primary hepatitis have been positively identified; these viruses
are known as hepatitis A (HAV), hepatitis B (HBV), hepatitis C (HCV), hepatitis
D (HDV), and hepatitis E (HEV). Viruses F and G have been discovered and
may also cause primary hepatitis. Other viruses tentatively labeled as GB-A,
GB-B, and GB-C are being tested to see if they differ from F and G and if they
also cause hepatitis. HAV is transmitted by contaminated food and water and
by the fecal-oral route; HBV and HDV are transmitted by contact with bodily
fluids, HCV by percutaneous exposure to blood, and HEV by contaminated
water and the fecal-oral route. Note: Hepatitis may also occur as a secondary
infection and is associated with viruses from other primary diseases,
including cytomegalovirus, Epstein-Barr, herpes simplex, varicella-zoster,
coxsackie B, and rubella viruses.

The etiologic agent, mode of transmission, and clinical course vary

according to the hepatitis type. However, the pathophysiology is the same.
The causative agent invades the mononuclear cells in the liver, replicates,
and sets up an inflammatory process in the parenchyma and portal ducts,
causing hepatic cell necrosis, cellular collapse, and accumulation of necrotic
tissue in the lobules and portal ducts. This results in interference with
bilirubin excretion. Cellular regeneration and mitosis occur simultaneously
with cellular necrosis, and the liver regenerates within 2 to 3 months.
Continuation of the inflammatory response sets up a chronic disease process.
 RABIES

A. Pathophysiology

Rabies virus

Entry into break in Incubation period (4

skin (bites, abrasions, days 2 years)
mucosa)

Invasion phase - Pain

- Fever
- Headache
- Malaise
- Sore throat
- Imminent thoracic- - Anorexia
lumbar - Increased
involvement(PNS): sensitivity
Pupillary dilation,
lacrimation,
- increased thick saliva
production / foaming - Gradual weakness of muscle
of mouth, excessive groups: muscle spasms cease,
perspiration Excitement phase ocular palsy, vertigo, facial
- Anxiety & fear &masseter palsy, weakness of
- Hydrophobia muscles of phonation, loss of
- Pronounced tendon reflexes, neck stiffness
muscular stimulation - (+)Babinski [lesions at pyramidal
Paralytic phase tract], (-) Kernigs, (-)
& general tremor (Depression phase) Brudzinskis
- Mania
&hallucinations with - HR shifting from tachycardia
lucid intervals (100-120) to bradycardia (40-60)
- Convulsions - Cheyne stokes respiration
Coma - Local sensation diminished (pain,
heat, cold)
- Incoordination
- General arousal
- Bladder & intestinal retention
Death (damage to the innervation of the
musculature of intestine
&bladder)
- Hydrophobia disappear but
with slight difficulty swallowing
In some cases, patient
shows period of recovery,
this apparent remission is
followed by
rapid progressive paralysis
- Ascending paralysis, flaccid
paralysis of extremities until it
reaches the respiratory muscle
 RABIES

B. Disease Process

The causative agent is a neurotropic rhabdovirus that is often present

in the saliva of infected animals and is usually transmitted to humans
through the bite of a rabid animal. Dogs are the most common source of
infection, but bats, raccoons, skunks, foxes, cats, and cattle are all known to
carry rabies.

The virus travels from the site of entry via the peripheral nerves to the
spinal cord and brain, where it incubates for 10 days to 1 year. It then
multiplies and travels from the CNS through the efferent nerves to many
body tissues, including the salivary glands, saliva, urine, cerebrospinal fluid,
corneal cells, and skin. It causes vessel engorgement, edema, and punctate
hemorrhages in the meninges and the brain, and diffuse degenerative
changes occur in the neurons of the brain and spinal cord. Negri bodies may
be formed in the hippocampus or neurons in the cerebellum, cortex, and
spinal cord.
 PERTUSSIS
(Whooping Cough)

A. Pathophysiology

Bortella Pertussis
attaches to and multiplies
on the respiratory
epithelium

Spread in the
nasopharynx and end
primarily in the bronchi
and bronchioles

Bacteria attacks the cillia

Damage ciliated
respiratory epithelium

Causes inflammation of
the respiratory tract

Mucus production

Narrowing of the
respiratory tract

Breathing
Difficulties Air moves to narrowed
spaces

Whooping sound
 PERTUSSIS
(Whooping Cough)

B. Disease Process

Whooping cough is caused by Bordetella pertussis, a nonmotile, gram-

negative cocco - bacillus. It is usually transmitted through aspiration of
droplet spray produced by an infected individual during paroxysms. Pertussis
is endemic throughout the world and becomes epidemic in 2- to 4-year
cycles. It occurs in all age groups, but infants and toddlers are the most
susceptible.

When inhaled, B. pertussis attaches itself to the cilia of the respiratory

epithelial cells and incubates for about 7 to 10 days before producing
symptoms. The pertussis toxin is absorbed from the respiratory tract into the
lymph system, causing a lymphocytosis. The pathogenesis of the paroxysmal
cough is unknown.
 MENINGITIS

A. Pathophysiology

Predisposing Factors: Direct/indirect Precipitating

- Age contact with an Factors:
infected person - Environment
- Poor Hygiene

Acquire Infectious Agents like

parasite, virus, bacteria, and
fungus.

Initially, the infectious agent

colonizes or establishes a localized
infection in the host.

- Fever
- Through infecting
Irritability
- Poor Sucking Reflex

Skin, nasopharynx, respiratory tract,

gastrointestinal tract, or
genitourinary tract.

From this site, the organism invades

the submucosa by circumventing host defenses,
like physical barriers, local immunity,
phagocytes/macrophages by:

Invasion of the A retrograde neuronal Direct contiguous

bloodstream like pathway like olfactory spread like
bacteremia, viremia, and peripheral nerves. sinusitis, and otitis
fungemia, parasitemia media

Meningitis
 MENINGITIS

B. Disease Process

Bacterial meningitis can be caused by any number of bacteria, but

80% of cases are caused by one of three strains: Neisseria meningitides,
Haemophilus influenzae, and Streptococcus pneumoniae. Spread is through
droplet contact, and the disease can be transmitted as long as the
respiratory tract contains the causative bacteria. Children under 5 years of
age are at greatest risk. Pneumococcal meningitis is the most common form
of adult meningitis.

The bacteria invade the respiratory passages and are disseminated by

the bloodstream to the cerebrospinal fluid (CSF) space and the meninges of
the brain and spinal cord. A growing exudate damages cranial nerves,
obliterates CSF pathways, and induces vasculitis and thrombophlebitis. The
exudate also generates metabolites and cytokines, which damage cell
membranes, disrupt the blood-brain barrier, and cause cerebral edema and
ischemic brain damage.