URINARY TRACT

INFECTION, APPENDICITIS
and PULMONARY
TUBERCULOSIS
EXTENSIVE with
PNEUMONIA
PATHOPHYSIOLOGY

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 URINARY TRACT INFECTION (UTI)
PATHOPHYSIOLOGY

Loss of integrity of the mucosal lining

Decrease resistance to invading organism

Pathogen colonizes the periuretheral area and ascends through the

urethra upwards towards the bladder

Fimbria allow bladder epithelial cell attachment and penetration

Following penetration, bacteria continue to replicate and may form biofilms

Once sufficient colonization occurs, bacteria may ascend ascend

towards the ureter to Kidney
Fimbria may aid in the ascension process
Bacterila toxins may also play a role by inhibiting peristalsis (reducing
the flow of the urine)

Infection in the renal parenchyma causes an inflammatory

response called pyelonephritis
While infection of the renal parenchyma is usually the result of
bacterial ascension, it can also occur from hematogenous spread

Upper back pain

Side (flank) pain
High fever
Shaking and chills
Nausea
Vomiting
Pelvic Pressure
Lower abdomen discomfort
Frequent and painful urination
Blood in urine
Burning sensation upon urination

Manifested by the patient:

 Side (flank) pain

 High fever

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  Lower abdomen discomfort

APPENDICITIS

Episodes of constipation Low Fiber diet

Occlusion of foreign the appendex

Increase intra luminal presssure

Vasocongestion

Decrease bloos supply in the appendix

Decrease oxygen supply in the appendix

Disrupt of cell membrane of appendix

Start inflammatory process Right lower abdominal

pain

Rupture of the appendix Vomiting

Release of fecal materials in the abdominal cavity

Decrease peristalsis Hypoactive

bowel sounds
Secondary peritonitis

Increase inmmune response Hyperthermia Increase WBC

Release chemical mediators (macrophages, fibrin, blood cells)

NOT MANIFESTED BY THE PATIENT Adhesions

Intestinal obstruction

Ischemia of the bowel wall

Necrosis of the intestine Page 23

 Exploratomy Laparotomy
PULMONARY TUBERCULOSIS EXTENSIVE with PNEUMONIA

Immune system compromised

Etiologic Agent: Mycobacterium Tuberculosis

Mode of Transmission: Droplets Nuclie

Invades to nasal passages

Activation of immune response

Inflammatory response

Passes through the larynx, pharynx to trachea

Bacteria extends to brochus

Abscess become encapsulated

Bacteria then become airborne resulting in

Tissues necrotize further spread of infection

Ghon tubercle ulcerates and releasing cheesy Hemoptysis

material into the bronchi
Impaired Oxygenation and Carbon Dioxide
exchange
Macrophages and leukocytes mucus and phlegm
production
Increase
RR
Ulcerated tubercle heals and become scar tissue Low RBC

Infected lung become inflamed Productive coughing

Further development of pneumonia and tubercle formation

Patient manifested: Productive coughing

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