pulmonary tuberculosis-pneumonia pathophysio

Daytonite, BSN, RN · Jan 10, 2008

hi, beautydenia, and welcome to allnurses! :welcome:

here is a website where you can find a little about the pathophysiology of pulmonary tuberculosis and pneumonia:

http://www.emedicine.com/med/topic2324.htm - tuberculosis

the following is from textbooks that i have here at my home:

tuberculosis:

from nurse's 5-minute clinical consult: diseases by lippincott williams & wilkins, page 824, on the pathophysiology of tuberculosis:

"multiplication of the bacillus
mycobacterium tuberculosis
causes an inflammatory process where deposited.
a cell-mediated immune response follows, usually containing the infection within 4 to 6 weeks.
the t-cell response results in the formation of granulomas around the bacilli, making them dormant. this confers immunity to subsequent infection.
bacilli within granulomas may remain viable for many years, resulting in a positive purified protein derivative or other skin test for tb.
active disease develops in 5% to 15% of those infected.
transmission occurs when an infected person coughs or sneezes."

from pathophysiology: the biologic basis for disease in adults and children, third edition, by kathryn l. mccance and sue e. heuther, page 1185, on the pathophysiology of tuberculosis:

"like some types of pneumonia, tuberculosis is transmitted from person to person in airborne droplets. microorganisms lodge in the lung periphery, usually in the upper lobe. once the bacilli are inspired into the lung, they multiply and cause nonspecific pneumonitis (lung inflammation). some bacilli migrate through the lumphatics and become lodged in the lymph nodes, where they encounter lymphocytes and initiate the immune response.

inflammation in the lung causes neutrophils and then alveolar macrophages to migrate to the area. these cells are phagocytes that engulf the bacilli and begin the process by which the body's defense mechanisms isolate the bacilli, preventing their spread. the neutrophils and macrophages seal off the colonies of bacilli, forming a granulomatous lesion called a

tubercle

. infected tissues within the tubercle die, forming cheeselike material called

caseation necrosis

. collagenous scar tissue then grows around the tubercle, completing isolation of the bacilli. the immune response is complete after 10 days or so, preventing further multiplication of the bacilli.

once the bacilli are isolated in tubercles and immunity develops, tuberculosis may remain dormant for life. if the immune system is impaired, however, or if live bacilli escape into the bronchi, active disease occurs and may spread through the blood and lymphatics to other organs. endogenous reactivation of dormant bacilli in elderly persons may be caused by poor nutritional status, insulin-dependent diabetes, long-term corticosteroid therapy and other debilitating diseases."

pneumonia:

from nurse's 5-minute clinical consult: diseases by lippincott williams & wilkins, page 614, on the pathophysiology of pneumonia:

"a gel-like substance forms as micoorganisms and phagocytic cells break down.
this substance consolidates within the lower airway structure.
inflammation involves the alveoli, alveolar ducts, and interstitial spaces surrounding the alveolar walls.
in lobar pneumonia, inflammation starts in one area and may extend to the entire lobe. in bronchopneumonia, it starts simultaneously in several areas, producing patchy, diffuse consolidation. in atypical pneumonia, inflammation is confined to the alveolar ducts and interstitial spaces."

from pathophysiology: the biologic basis for disease in adults and children, third edition, by kathryn l. mccance and sue e. heuther, page 1183 on the pathophysiology of pneumonia:

"pathogenic organisms can reach the lung by the following routes:

when an infected individual coughs, sneezes, or talks, microorganisms are released into the air to be inhaled by other people.
microorganisms can be inspired with aerosols (nebulized gas) from contaminated respiratory therapy equipment.
in illness or poor dental hygiene, normal flora of the oropharynx can become pathogenic.
staphylococcus
and gram-negative bacteria can be spread by the circulation from a systemic infection, sepsis, or contaminated needles of intravenous (iv) drug abusers.

in healthy individuals pathogens that reach the lungs are expelled or held in check by mechanisms of self-defense. the lungs' defense mechanisms--the cough reflex, mucociliary clearance, and phagocytosis by alveolar macrophages--are backed up by the body's immune system and various components of the inflammatory response, including the release of biochemical mediators by alveolar mast cells. in susceptible individuals the invading pathogen is not held in check but multiplies, releasing damaging toxins and stimulating full-scale inflammatory and immune responses, both of which have damaging side effects. the immune response (antigen-antibody reaction) and the endotoxins released by some microorganisms damage bronchial mucous membranes and alveolocapillary membranes. inflammation and edema cause the acini and terminal bronchioles to fill with infectious debris and exudate, leading to ventilation-perfusion abnormalities. if the pneumonia is caused by

staphylococcus

or gram-negative bacteria, necrosis of lung parenchyma also may occur.

"

beautydenia · Jan 11, 2008

THANK YOU so much Daytonite:),

For all the important informations that u have shared to me, for taking the time to impart ur knowledge and very kind enough to help an aspiring nurse someday. The information that u gave me will certainly improve the data in my case presentation. Thank u so much. .IT's really nice to have people share their knowledge to striving student nursing like me. More power., and again thank u

beautydenia · Jan 11, 2008

i have a question, what part of the PTB - Pneumonia pathophysio will the another medical diagnosis "UTI or Urinary tract infection "may fall into. where can i connect it?

Daytonite, BSN, RN · Jan 11, 2008

PTB, pneumonia, and UTI are all infectious processes. The pathophysiology of an infectious process is pretty much the same except the area of the body involved might be different. It usually starts with the inflammation response and proceeds.

beautydenia · Jan 12, 2008

thank u again daytonite:specs:, base from the readings, i come up with diagram form pathophysio, kindly check if the pathophysio for pneumonia is correct, kindly make the appropriate corrections , revisions and please provide explanations in order for me to understand deeper..,then im going to connect it with PTB. thanks:)

----supposedly in Diagram form---

1. to start of infectious organisms entering the respi. system or inhalation of microorganism

2. infection occurs

3. immune reaction follows

4. under the infection and immune response inflammation process proceeded

5. the next thing that happens to inflammation process there will be vasonstriction

6. The release of chemical mediators

7. under the release of chemical mediators vasodilation and increase capillary permeability happens

8. for vasodilation, there will be increase blood pressure then formation of heat and redness to the site

9. under increase in capillary permeability swelling and pain emerges then leds to loss of tissue functions

10. after the release of chemical mediator , there will be an increase in local

capillary leaks

12. still under increase capillary leak , it will eventually lead to spread of infection to other areas of the lungs, two things may happen infection extends into the pleural cavity and organisms move to the bloodstream which causes systemic infection

13. on the other hand, still under increase in capillary leak, theres a decrease in fluid collected around the alveoli, then decrease alveolar-capillary perfusion , which significantly leads to increase spaces between the alveoli and capillary

which therefore decrease gas exchange --then hypoxemia---then hypoxia---that trigers compensatory mechanism form the different systems (respi, CNS, etc)

Under increase in capillary leak-----increased permeability of cell members allowing leukocytes and fibrin to consolidate in involved areas-----ones fibrin and leukocytes stiffen there will be a decrease in lung compliance and decrease lung vital capacity which decreases gas exchange that leads to hypoxemia---hypoxia.--then triggers the compensatory mechanism..

beautydenia · Jan 12, 2008

daytonite , kindly make corrections , comments and improve my pathophysio, thank u:) :specs: :specs: :specs:

Pathophysio (PTB):

----supposedly in diagram form----

infective lung----multiplication of the bacilli occur---two things happen here 1st bacilli migrates or escape towards the lympathic system --lodge in the lymph nodes which it may encounter macrophages: if the immune system is compromised it will goes to the blood stream then to the systemic circulation.

2nd there might be lung inflammatory process that may lead to cell injury --immune response--then the inflammatory process happens (or) the lung inflammatory process leads to ----macrophage and neutrophils phagocytes the Bacilli : in case of IMMUNE COMPROMISE PATIENTS, it will proliferate , (a) bacilli are transported via the lymphatic system --goes to the blood stream--then to the systemic circulation or (b) Bacilli remains in the infective lung --which progresses to PTB into the airway and out into the environment , and this bacilli may also injured the tissues and cells which triggers inflammatory response

But if the patient is IMMUNE EFFECTIVE, it could either make the bacilli dormant or kill the bacilli.

Supposed the patient is immune effective in a dormant state: but some factors arises that suppresses the immune system like for instance pregnancy or prolong used of corticosteroid-- there will be reactivation of bacilli-- leading to ghon tubercle ulceration--then formation of cheesy materials with bacilli released into the bronchi---that causes Secondary PTB formation--then dissemination of mycobacterium into the lungs --then there will be tissue and cellular injury that may occur--what follow is the inflammatory process

In cases of immune effective client---with acquired cellular immunity , the bacilli is contained in the lungs ---then this Bacilli are destroy by the activated macrophages ---which localized the lesions (dissemination of organism via the lymphatic vessels is usually prevented)

Supposing a client is an immune effective client with dormant Bacilli (contained infection)--gets reinfection of another M. Bacilli cause by exogenous factors but with acquired cellular immunity --the bacilli are promptly destroyed by the activated macrophages then lesions remain localized-- it is not disseminated via the lymphatic system

another thing is if the client is immune effective in dormant stage-- with reinfection of M. Bacilli (due to exogenous factors)---there will be reactivation of bacilli-- then formation of ghon tubercle ulcerations-- formation of cheesy material with bacilli release into the bronchi---secondary PTB--then dissemination of M.Bacilli--into the lungs---then bacilli injured the tissues and cells--then leads to inflammatory process which could be connected to inflammation process of pneumonia

Daytonite, BSN, RN · Jan 12, 2008

https://allnurses.com/forums/f50/histamine-effect-244836.html - the pathophysiology of the inflammatory response

pathophysiology of pneumonia with active tuberculosis

pneumonia starts when an infectious microrganism (bacteria, virus) enters the respiratory system
body response (inflammation response): mast cells in the area that the bacteria have nested release histamine, neutrophil chemotactic factor, eosinophil chemotactic factor, prostaglandins and leukotrienes.
histamine causes blood vessels in affected area to dilate and become permeable. physical symptom exhibited by the body: slight increase in blood pressure, elevation of body temperature, the beginning of lung congestion, some chest pain due to swollen lung tissue pressing on surrounding organs
neutrophil chemotactic factor attracts more neutrophils to the site
neutrophils which have antibodies attached to the h1 receptors on them surround the invasive bacteria and begin digesting it
a sac called a phagosome forms and wraps the bacteria and neutrophils in a protective case.
phagocytosis of the bacteria takes place within the phagosome and the bacteria is destroyed
eosinophil chemotactic factor attracts eosinophils to the site to clean up the debris left by the neutrophils resulting in exudates we commonly called pus, or purulence, or suppuration
the exudate is removed and stored in the local lymph nodes for eventual disposal
if bacteria are still present prostaglandins and leukotrienes will attract more white blood cells to the area
as more white blood cells are needed, the white cell count rises.
if the inflammatory response is unable to destroy all the bacteria, the bacteria will begin to multiply and spread due to the permeability of the cells (effect of histamine) while the inflammatory response continues to try to keep the bacterial invasion confined to the local area of the lung
the bacteria release toxins which damage the surrounding bronchial mucous membranes and alveolocapillary membranes
the most distal alveoli (acini) begin to fill with infectious debris and exudate. this can be seen on an x-ray of the lung. the patient may start to have physical symptoms: cough, sputum production, adventitious lung sounds, decreased breath sounds, tachypnea and start to use accessory muscles to breathe.
ventilation-perfusion (ability to breathe) decreases due to decreased gas exchange. this will be noted in arterial blood gas measurements.
hypoxemia develops
then, hypoxia which triggers system wide compensatory mechanisms
if unstopped, necrosis of the lung parenchyma (working parts) occurs
as the infection continues unstopped, death will result from respiratory failure or sepsis
with tuberculosis, invasion into the respiratory track is by airborne droplet when someone coughs or sneezes
the inflammation response, as above, begins.
the specific name given to the phagosome that surrounds the tuberculosis bacteria is a tubercle.
unlike phagosomes in bacterial pneumonia, the bacteria in the tubercles is still alive but remains in the lung tissue while a collagenous scar tissue forms around them isolating the tuberculin bacillus. this takes 10 days for the process to complete.
it takes 4 to 6 weeks from the onset of exposure for the inflammation response of the body to successfully contain a tb infection.
tubercles may remain dormant for the remainder of the person's life.
active tb bacteria can be released from tubercles when a person's health becomes debilitated or immune compromised.

beautydenia · Jan 16, 2008

thank u so much daytonite, the presentation was well presented :) it

could have not done it with out your kind help .. again thank u so

much...more power:specs: :specs: :specs: :specs: :up: :up: :up:

Daytonite, BSN, RN · Jan 17, 2008

You are welcome. I am more concerned that you understand the process of what you need to do in order to get to the information that you needed. This all involved critical thinking as well as knowing where to go to get the information that you needed.

I'm glad it went well for you. And, I hoped you learned a lot from it.