Immunocompromised

PATHOPHYSIOLOGY OF CAP
Typical: Entry of Streptococcus pneumonia, Haemophilus influenza and Staphylococcus species
young and middle-aged adults

Inhalation of microorganism from community

COMMUNITY AQUIRED PNEUMONIA Activation of defense mechanism
Presence of Dse such as lung cancer

Atypical: Mycoplasma pneumonia, Legionella and Chlamydia Species

Smoking and alcoholism

Penetrate the sterile lower respiratoryLoss of (lungs)

tract effectiveness of defense mechanism
Colonization Multiplication alveoli
r/t loss of secondary defense secondary to CAP

Release of damaging toxin Irritation of airways

Infection
Increase goblet cells Increase goblet cells Increase mucus production

Inflammation

Occluded the airway

vasodilation Occluded the airway

↑blood flow Impaired O2 and CO2

Ineffective exchange
airway clearance r/t presence of secretion secondary to CAP
cough crackles
Plasma and CHON rich fluid leakage
Impaired gas exchange r/t occluded airway secondary to CAP
t inflammatory process secondary to CAP

Accumulation of edematous fluid hyperventilation Airway constriction

Increase RR Difficulty of breathing

Inflamed and fluid filled alveolar sac

Decrease CO2 Impaired O2 and CO2 exchange

Lung consolidation
Impaired gas exchange r/t airway constriction secondary t
hypoxia

PATHOPHYSIOLOGY OF HEMOLYTIC ANEMIA

REFERENCE: ROSEMARIE PACHAO’S NOTES

Genetically determined
Amino acid sequence is altered where valine is substituted for glutamic acid in 574 amino acids that make up th
HEMOLYTIC ANEMIA Genetically determined, inherited disease (autosomal recessive
Insufficient beta globulin Sickle cell

sufficient enzyme due to intake of fava beans

Acute pain r/t occlusion of blood vessel

Sickle cell elongares to crescent shaped under low concentration, aci

pain Occlusion of BV Viscous blood

Jaundice Dec HgbRisk for fluid volume deficit r/t decreased hemoglobin

A B
A B

Glucose 6 phosphate dehydrogenase anemia

Thalasemia

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Nursing care plan Submitted by: MEDINA, PATRICK LUIS
 beta globulins allow large amount of unstable chains to accumulate in erythroid cavity as an attempt to copeDecrease g6pd-

Decrease processing of CHO to energyAccumulation of byproducts when in infection

Enormous expansion of bone marrow and thinning of bony cortex

Dec Hgb Destruction of RBC

Skeletal deformities and fractures, growth retardation

Risk for fluid volume deficit r/t decreased hemoglobin

Rapid destruction of RBC
Kernicterus – severe neurologic effect in newborn
Jaundice
uid volume deficit r/t decreased hemoglobin
ecrease hemoglobin and increases iron absorption as an attempt to cope and causes excessive supply

Decrease ability to hold oxygen

PATHOPHYSIOLOGY OF POLYSINUSITIS

URI
ALLERGIES
bacteria such as Streptococcus pneumonia
ALLERGIES Haemophilus influenzae inflammation / swelling and increased production of mucus
ALLERGIES Fullness, purulent material fills the sinus
Moraxella catarrhalis
bacteria such as Streptococcus pneumonia
abnormalities
foreign objects in the noseof the nose POLYSINUSITIS
the structure
stuck
Haemophilus ininfluenzae secretions from the sinuses is blocked
enlarged
ALLERGIESadenoids
Moraxella catarrhalis
bacteria such as
abnormalities inStreptococcus
the structure ofpneumonia
the nose
Bacteria (strep
Haemophilus pneumonia)
influenzae
enlarged adenoids
Streptococcus pneumonia
Moraxella catarrhalis
Haemophilus
abnormalities influenzae
in the structure of the nose Pain/headache
Moraxella
enlarged catarrhalis
adenoids
abnormalities in the
Tooth structure of the nose
infection fever
enlarged adenoids

Acute pain r/t inflammatory process secondary to poly

References: Textbook of therapeutics: drug and disease management By Helms

Pachao’s notes

ry of cancer (Breast, colon, ovary)

Alteration in the oncogene activity and growth factor signals
OVARIAN CANCER
Hereditary

ssant ovulation theory

Mechanisms:
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Lymphatic
Direct extension and peritoneal seeding of the tumor cells drainage spread from ovary Hematogenous spread (rare)
 Spread to lungs

Ovarian cancer cells are carried by peritoneal fluid to peritoneal surfaces wher
r cells invade adjacent tissues and organs (fallopian tubes, cervix)

Inflammation

ck or legs, Diarrhea, gas, nausea, constipation, indigestion, Difficulty eating or feeling full quickly
Increased capillary permeability

Pelvic or abdominal pain, Pain in the back or legs, Diarrhea, gas, nausea, constipation, indigestion,
CTT PLEURAL EFFUSION
o presence of incision secondary to CTT

Accumulation of fluid
Incision on fifth intercostals space Impaired ventilation

Tissue damage Decreased lung expansion

Entry of microbes Imbalanced oxygen supply and demand
presence of incision secondary to CTT
Altered tissue perfusion imbalanced oxygen supply and demand secondary to pleural

Infection (fever, shills) DOB, dyspnea

Ineffective breathing pattern related to decreased

impaired lung expansion
gas exchange secondary
related to to pleural
imbalanced oxygeneffusion
supply and demand secondary to pleural effusion
r Infection related to presence of break on skin integrity secondary to CTT

Activity intolerance related to skeletal muscle weakness secondary to hyperkalemia

CELEBREX) for pain Decrease aldosterone
HYPERKALEMIA Muscle weakness

Activation of D1, D2, D3, D4, D5

CIAL FACTOR, BIOLOGICAL Incoherence of speech, Incongruity Disturbed
of affect,thought process related
stereotypies, to mental
poberty of disorder
speech,secondary
flight ofto ideas
schizophrenia pa
SCHIZOPHRENIA

HYSIOLOGY OF OVARIAN CANCER, PLEURAL EFFUSION AND SCHIZOPHRENIA

By Patrick Luis F. Medina

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Nursing care plan Submitted by: MEDINA, PATRICK LUIS