Endometrial Polyp

Risk factors: advanced age, history of smoking,

Risk factors: Family history of
asthma and/or allergies,
exposure to smoke, stress,
exercise, changes in
temperature & strong odors
smoking, upper respiratory
infection, tracheal intubations, prolonged immobility, immunosuppressive
therapy, nonfunctional immune system, malnutrition, altered
consciousness, aspiration of food, liquid or gastric material.
Etiologic Agent: allergens & irritants. (dust,
+ pollen,
pollen, smokes,
smokes, mold, medications, foods, +
respiratory infections)
Etiologic Agent: Bacteria, viruses, mycoplasma, fungi,
parasites & chemicals
Exposure to allergens
& irritants.
Sputum Examination: Muco-salivary Inhalation/aspiration of
Negative microorganisms

Production of Immunoglobulin E (IgE) Increase mucus Stasis of secretions in

by B lymphocytes Microorganisms reach
secretion large airways (medium the alveoli
for bacterial growth)

Medical Diagnosis: Bronchial asthma Invasion of microorganisms in the

anterior exacerbation IgE antibodies attach to Mast cells & spaces between cells & between
basophils in the bronchial walls Cefdinir m300mg BID alveoli through connecting pores
Clindamycin 30mg q 8hr
IVTT
Ceftriaxone sodium 1 gm q 8
hr IVTT Organisms multiply in the serous fluid
Zithromax 500mg 1 tab P.O. & spread of infection
Budesonide neb Mats cells degranulate
Hydrocortisone 200mg IVTT
Release of bacterial endotoxin
Early phase response (30-60 mins.): Release of
chemical mediator of inflammation Late phase response (4-8 hrs)
(histamine, prostaglandin, bradykinins, SRS-A Release of chemotactic mediators Damage on bronchial & alveolar
mucous membranes

Salbutamol neb q 4 Cellular infiltrations (neutrophils,

PNSS 1l+ 2 amp Aminophylline lymphocytes, eosinophil) and Transient vasoconstriction
Vasodilation and Increase airway smooth muscle accumulation in the airways
Increase capillary contraction (bronchospams) Increase mucus
permeability secretion Release of chemical mediator of inflammation
S/S:
S/S: shortness of breath S/S: Tissue damage (histamine, prostaglandin, bradykinins, SRS-A
Chest tightness  Coughing
Capillary leaks fluid protein Wheezing  sachet in ½
into tissue spaces Fluimucil
glass water TID Damaged cells are Vascular changes: massive vasodilation and
Ambroxol Hcl 2 tsp TID shed into the airways
Edema of the airway increase permeability of capillaries &
P.O.
P.O.
(mucosal edema) increase blood flow
 Microorganisms travel from the
infected lung into the bloodstream

Sepsis Microorganisms Microorganisms Microorganisms Microorganisms

enters pleural cavity enters the brain enters peritoneum enters endocardium

Septic shock Builds up of Meningitis Peritonitis Endocarditis

Blood pressure fluid in the
pleural cavity
(empyema)
Death
Med. Mgt:
Thoracentesis/surgery

Pleuritis
 O2 inhalation Airway obstructions
Lab results: Attraction of neutrophils, accumulation
@ 2L/min & narrowing WBC= 11,2 T/cumm
Neutrophil 86% of fibrinous exudates, RBC & bacteria
Lymphocyte 10% in the alveoli (congestion/hyperemia)
Monocyte 2%
Eosinophil 2%
Increase resistance to air S/S: Basophil 0%
flow & decrease flow rates  Wheezing
upon S/S:
S/S: dullness to percussion, Red hepatization (lungs appears red &
(expiratory flow) expiration increase fremitus, bronchial granular) & consolidation of lung
breath sounds, crackles parenchyma
Impaired
expiration S/S:
S/S: cough productive of
S/S: Patchy consolidation Consolidation of purulent, rust colored/blood-
colored/blood-
 Dyspnea S/S: low-grade fever, cough, involving several a large portion streaked sputum; hemoptysis
 Prolonged Air trapping scattered cackles, minimal lobes of an entire lung pleuritic or aching chest pain;
expiration dyspnea & respiratory distress (Bronchopneumonia) lobe (lobar  breath sounds & crackles
pneumonia) over affected area;
area; possible
Blood flow & RBC in the dyspnea & cyanosis
Hyperinflation distal to Increase intrapleural
exudates; leukocytes
exudates
obstruction alveolar gas pressure (neutrophils & macrophages) Tissue become solid grayish (Gray
infiltrate the alveoli hepatization) & deposition of fibrin on
Absorption of pleural surface; phagocytosis in alveoli
air trapped in CO2 retention Decrease perfusion
the alveoli of alveoli

Resolution of infection: Resolution does not occur

Uneven ventilation- Polymophonuclear leukocytes are
Alveolar sacs perfusion
collapsed Respiratory  Lung replaced by macrophages that
acidosis relationship within engulf & destroy the organisms
(atelectasis) volume
(if severe) different lung
Conversion of exudates
segment
to fibrous tissue
Perfusion Exudates liquefies
without Respiratory Respond of the
ventilation shunt failure lung receptor Hypoxemia
Affected alveoli
(ventilation- triggering becomes functionless
perfusion hyperventilation
mismatch) Cough out Exudates reabsorbed
Increases the work of by macrophages
breathing
Hypoxemia Lymphocytes carry
S/S:
exudates away from site of
 Tachypnea
infection
 Blood loss

↓ Iron (iron deficient)

Alveoli becomes
airless
CBC: ↓ Hgb concentration in
Sustained perfusion with Hgb- 11.5 %. RBC
poor ventilation in the Hct- 35.5 vol% (Anemic condition)
consolidated area

↓ oxygen-carrying
Hypoxemia capacity of blood
(hypoxemia)

Tissue hypoxia

Ischemia Weakness,  Pallor Respiratory Central nervous system Liver

fatigue (skin/
(skin/mucous ( respiratory rate,
rate, depth, (dizziness,
dizziness, fainting, (fatty changes; fatty
membrane)
membrane) exertional dyspnea) lethargy) changes can also
Claudication occur in heart and
(Muscle) Respiration: 35 cpm
irregular, and shallow kidneys)
 Restoration of both
structure & function of
lung

Gas-exchange returns to
normal
 Compensatory
Mechanism

 heart rate Cardiovascular Capillary Renal

Heart (angina)  O2 demands dilation
for work of heart

 Renin-aldosterone
(diphosphoglycerate)
response
DPG cells
 stroke volume  Salt and H2O
 erythropoietin retention
 Intracellular fluid

Stimulates bone Hyperdynamic  Extracellular

marrow to circulation fluid
produce RBC

 Release of oxygen
from hemoglobin in
Increase Cardiac murmurs High-output tissues
production of cardiac failure
RBC