Immunocompromised young and middle-aged adults

PATHOPHYSIOLOGY OF CAP

Typical: Entry of Streptococcus pneumonia, Haemophilus influenza and Staphylococcus species

Inhalation of COMMUNITY AQUIRED PNEUMONIA microorganism from community Presence of Dse such as lung cancer

Activation of defense mechanism

Atypical: Mycoplasma pneumonia, Legionella and Chlamydia Species Smoking and alcoholism

Colonization

Multiplication

Loss of effectiveness of defense mechanism Penetrate the sterile lower respiratory tract (lungs) alveoli

r/t loss of secondary defense secondary to CAP Release of damaging toxin Irritation of airways

Infection Inflammation vasodilation

Increase goblet cells

Increase goblet cells

Increase mucus production

Occluded the airway

Occluded the airway

blood flow

Impaired O2 and CO2 exchange Ineffective 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 hyperventilation Airway constriction

t inflammatory process secondary to CAP

Accumulation of edematous fluid

Inflamed and fluid filled alveolar sac

Increase RR

Difficulty of breathing

Decrease CO2 Lung consolidation hypoxia

Impaired O2 and CO2 exchange

Impaired gas exchange r/t airway constriction secondary t

PATHOPHYSIOLOGY OF HEMOLYTIC ANEMIA

REFERENCE: ROSEMARIE PACHAOS NOTES Genetically determined Insufficient beta globulin HEMOLYTIC ANEMIA

Amino acid sequence is altered where valine is substituted for glutamic acid in 574 amino acids that make up th Genetically determined, inherited disease (autosomal recessive 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 Hgb Risk for fluid volume deficit r/t decreased hemoglobin

A A
Thalasemia

B
Glucose 6 phosphate dehydrogenase anemia

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Nursing care plan Submitted by: MEDINA, PATRICK LUIS

Decrease g6pdbeta globulins allow large amount of unstable chains to accumulate in erythroid cavity as an attempt to cope

Decrease processing of CHO to energyAccumulation of byproducts when in infection Enormous expansion of bone marrow and thinning of bony cortex

Skeletal deformities and fractures, growth retardation

Dec Hgb

Destruction of RBC

Rapid destruction of RBC

Risk for fluid volume deficit r/t decreased hemoglobin 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 ALLERGIES Moraxella catarrhalis bacteria such as Streptococcus of the nose POLYSINUSITIS abnormalities in the structure pneumonia foreign objects stuck ininfluenzae Haemophilus the nose enlarged adenoids ALLERGIES Moraxella catarrhalis bacteria such as Streptococcus of the nose abnormalities in the structure pneumonia Bacteria (strep influenzae Haemophilus pneumonia) enlarged adenoids Streptococcus pneumonia Moraxella catarrhalis Haemophilus influenzae abnormalities in the structure of the nose Moraxella catarrhalis enlarged adenoids abnormalities in the structure of the nose Tooth infection enlarged adenoids

inflammation / swelling and increased production of mucus Fullness, purulent material fills the sinus secretions from the sinuses is blocked

Pain/headache fever

Acute pain r/t inflammatory process secondary to poly

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

ry of cancer (Breast, colon, ovary)

OVARIAN CANCER
Hereditary

Alteration in the oncogene activity and growth factor signals

ssant ovulation theory

Mechanisms:

uma w/c breaks the epithelium

Nursing care plan

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Submitted by: MEDINA, PATRICK LUIS

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

presence of incision secondary to CTT

Decreased lung expansion Imbalanced oxygen supply and demand Tissue damage of microbes Entry
Altered tissue perfusion imbalanced oxygen supply and demand secondary to pleural

Infection (fever, shills)

DOB, dyspnea

Ineffective breathing pattern related to decreased lung expansion to imbalancedpleural effusion and demand secondary to pleural effusion impaired gas exchange related secondary to oxygen supply

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 Incoherence CIAL FACTOR, BIOLOGICAL

of speech, Incongruity Disturbed thought process related to mental disorder secondary to ideas of affect, stereotypies, poberty of speech, flight of 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