Acute Bacterial Conjunctivis (Pathogenesis) Haemophilus Influenzae enters in the eye by direct contact with infected secretions l series

of defense mechanisms prevent bacterial invasion l bacteria adheres to overwhelm normal defense mechanisms l external flora is contaminated very quickly and spreads to the adjacent sites of the eye through the medium of blood l pathogenic bacteria occurs l produce clinical symptoms of eye redness, discharges, irritation, itching, and possibly photophobia l ACUTE BACTERIAL CONJUNCTIVITIS Acute Rhinitis (Pathogenesis) infected person release droplet through sneezing or coughing l susceptible host inhales Rhinovirus – becomes infected l invasion of virus in the nasal mucous membrane l acute inflammation occurs l promoting redness, swelling, nasal discharges & sneezing l ACUTE RHINITIS Acute Rhinitis (Pathophysiology) Acute Rhinitis l nasal discharges clogs passage way of air to nose l mouth breather l DYSPNEA

Acute Gastroenteritis (Pathogenesis) ingestion of fecally contaminated food and water (Escherichia coli) l invasion of gastric mucosa l penetration of bacterium in gastric mucosa l toxin producing pathogens cause watery, large volume diarrhea l AGE Acute Gastroenteritis (Pathophysiology) Acute Gastroenteritis l irritation of gastric lining – cause vomiting l fluid & electrolyte imbalance too much Na+ and H2O are expelled from the body l increased fluid loss – decrease skin turgor, sunken eyes l DEHYDRATION Amebiasis (Pathogenesis) ingestion of cyst of Entamoeba histolytica through contaminated water l cyst travels & survives in gastric juice l metacyst begins to move within cyst wall in the intestinal area l quadrenucleate amebas emerge and divide into amebulas l invades the cecum and multiply in mucosa l promoting abdominal cramps/pain and diarrhea l AMEBIASIS Amebiasis (Pathophysiology) Amebiasis l Trophozoite (active form of protozoan) l cause thinning of mucous layers, shortening of microvilli, separation of apical epithelial cells, and degradation of extracellular matrix l ulcerations may occur l alteration of peristalsis l LOSS OF APPETITE & WEIGHT

l epistaxis. epistaxis. and frequently tiny spots on the skin (petechia) l DENGUE DENGUE (Pathophysiology) Dengue virus goes into blood circulation l infects cells & generate cellular response l initiates destruction of platelets l increase potential of hemorrhage (petechial hemorrhage) l stimulates intense inflammatory response 1 2 release of release of exogenous anti-inflammatory pyrogen mediators l l increase vascular response WBC count l l redness & heat release of throughout the body endogenous l pyrogens headache. abdominal reset of pain hypothalamic l thermostat circulatory l collapse shock FEVER l DEATH FEVER(1) muscles contract to produce additional heat l SHIVERING FEVER(2) blood vessels contract to prevent loss of body heat l CHILLS .Dengue (Pathogenesis) aedes aegypti mosquito bites infected person having dengue l mosquito gets infected & carries dengue virus l mosquito bites & infect susceptible host l virus circulates in the blood l causing fever. vomiting.

NSAID’s & stress l ulcer worsens l burning sensation on the left upper abdomen . increased vaginal discharge(female). pelvic pain white. yellow or green discharge from the penis(male). frequency of urination. painful & swollen testicles l Gonorrhea Urinary Tract Infection (Pathogenesis) Staphylococcus saprophyticus gains access to the bladder through urethra l bacterium attach and colonize the epithelium of urinary tract l evade host defense mechanisms & initiate inflammation l symptomatic cystitis occur l dysuria. & frequently hematuria l URINARY TRACT INFECTION Urinary Tract Infection (Pathophysiology) UTI l loss integrity of the bladder’s mucosal lining l decreased resistance to invading microorganisms l inflammatory changes occur l clumps of bacteria ascend to the ureter up to kidneys l inflammatory changes occur in the renal pelvis and throughout the kidney l scarring of the kidney parenchyma l KIDNEY DYSFUNCTION Peptic Ulcer Disease (Pathogenesis) impaired stomach lining defenses l Helicobacter Pylori’s destructive role l breach in the mucosa of the alimentary tract l ulcer gets worse because of acidic. spicy food.Gonorrhea (Pathogenesis) Neisseria gonorrhoeae enters external genitalia through sexual contact goes internally through surface pili l attachment of pili containing IgA protease which digest IgA(responsible for mucosal immunity) from the surface of the urethra l adherence to the surface of spermatozoa l allows transmission of the organism to the fallopian tube and into the peritoneal cavity l occurrence of inflammatory response l resulting dysuria.

. DOB. Tuberculosis gains entry via respiratory tract through airborne route l proliferation of bacteria in the alveoli l transported in other areas of the lungs l immune system responds by phagocytosis l after phagocytosis. active disease may develop when: Immune system is weakened l reinfection and activation of dormant bacteri l Ghon tubercle ulcerates releasing the cheesy material into the bronchi l ulcerated tubercle heals forming scar tissue again l development of bronchopneumonia and tubercle formation l resulting to symptoms of productive cough. lymphocytes lyse (destroy) the bacilli and normal tissue l resulting to the accumulation of exudate in the alveoli l formation new masses of live and dead bacilli (granulomas) surrounded by macrophages l formation of fibrous tissue mass composed of Ghon tubercle and macrophages l becomes necrotic forming a cheesy mass l becomes calcified (harden) forming a collagenous scar l bacteria either becomes DORMANT or progess to PTB Pulmonary Tuberculosis (Pathophysiology) After initial exposure and infection. hemoptysis. & chest pain.Pulmonary Tuberculosis (Pathogenesis) M.

producing IL-1 l IL-1 stimulates the hypothalamus to produce prostaglandins l once metabolized. hypothalamic thermostat is set to higher level l nerves causes the vessels to contract.Chicken pox (Pathogenesis) Varicella Zoster Virus gains entry via the respiratory tract through airborne route. the skin (malpighian layer) l intracellular edema occurs l resulting to these vesicles l SECONDARY VIREMIA Chicken pox (Pathophysiology) VZV infects the blood stream l macrophages defend our body (phagocytosis). conserving heat l increased body temperature Otitis Media (Pathophysiology) Upper respiratory infection l obstructed eustachian tube l Haemophilus influenzae enter middle ear l causes infection l inflamed middle ear l presence of purulent exudate l conductive hearing loss . droplets or contact with these vesicles l proliferates in the upper respiratory tract l incubates for 14 days l PRIMARY VIREMIA l viral invasion of the capillary endothelial cells and the epidermis l targeting the main organ.

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