Pathophysiology

Front 1

Pneumonia

Back 1

PROBABLY ONE OF THEMOST COMMON

Can be primarydisorder or secondary (due to something else) like flu.The bacteria of thepneumonia will enter through inhalation, and then spreads along through themucosa. Will see a widing of the alveoli because of a lot of gunk.Asperation pneumonia=when you breathe fluid or food into the lungs, setting up an infection there inthe lung. Occurs at all ages, and is one of the leading causes of death (#6) SOit can be very serious in those who have a demised immune system. Causative agent maybe a virus, bacterium, or fungus. INCREASE^^ inalveolar capillary membrane widthàDiminishing air flow & gas exchange Can be hospital (nosocomial)klbesiella pneuomiae acquired or community (viral or bacterial) acquired. Different typesLobar, Atypical, or Bronchopneumonia

Front 2

Pneumonia Types: Lobar

Back 2

Lobar is bacterial

and is the most common agent is streptococcus pneumococcus (pneumoniae)Infection localizedin one or more lobes àcausing inflammation and vascular congestion – exudate forms in the alveoliforming a consolidated mass. **** Inflamation of alveolar wall and leakage ofcell, fibrin, and fluid into alveoli causing consolidation*** Pleura may beinflamed1st stagecongestion which is inflammation of alveolar wall, 2nd stage then wehave consolidation (formation of solid mass by the neutrophils, RBCs, andfibrin. 3rd stage Because of the presence of RBC and so much gunkstart to cough (exudate) we have the rusty sputum à because of this we have areduced diffusion of gases (mostly oxygen) and also in blood flow through theaffected lobe causing HYPOXIA and metabolic acidosis! 4th stage bodybegins to rid the pneumoniaIf infection is notresolved it may spread to pleural cavity (known as empyema)

Front 3

Pneumonia Types: Bronchopneumonia

Back 3

pattern of infection in both lungs (often in lower lobes) many differentmicrogrmuns can cause infection beginning in the bronchial mucosa and spreadinginto the local alveoli. Inflammation and purulent exudate in alveoli oftenarising from prior pooled secretions or irritation INSIDIOUS*** Have fever,cough, rales (can also be treated with antibodtics SAME PROCESSES OUCCRS LIKELOBAR

Front 4

Interstitial Pneumonia (Primary AtypicalPneumonia) PAP

Back 4

DIFFERS IN BOTH THE CAUSATIVE ORGANISMS can be both viral or mycoplasma AND the pathophysiology which involvesinterstitial inflammation. Cause= Influenza virus Mycoplasma, scattered smallpatches. Interstitial inflammation around alveoli, necrosis of bronchialepithelium

Front 5

Extra on Pneumonia

Back 5

Common in olderchildren and young adults Transmitted byaerosol- not highly contagious / frequent cough, can be treated withantibiotics.VIRAL Caused by influenza Aor B, adenoviruses, and RSV. Unproductive cough, hoarseness, sore throat,headache, mild fever, malaiseInfection variesgreatly in severity. Infection is usually self-limiting (don’t last very long)/ x-ray-diffuse poorly defined patches. MAIN THING TO REMEMBER IS THAT IT IS AN OBSTRUCTED DISORDERthat gets in the way of gas exchange so it decreases because of an increase ofEXUDATE (GUNK)

Front 6

SARS (Severe AcuteRespiratory Syndrome)

Back 6

SARS (Severe AcuteRespiratory Syndrome)RNA VIRUS that’stransmitted by respiratory droplets during close contact causative microbe:SARS- associated coronavirus***Frist stage presents flu-like symptoms last 3-7days effects on lungs are evident several days later, with a dry cough andmarked dyspnea. Radiographs by day 7 indicate spreading patchy areas ofinterstitial congestion and hypoxia increases rapidly, with mechanical ventilationoften required. à AND a number of patients continue on to the third stage withsevere, sometimes fatal, respiratory distress.

Front 7

TUBERCULOSIS

Back 7

Risk Factors: arepeople living in crowded conditions, immunodeficiency (people with weak immune systems,malnutrition, alcoholism, conditions of war, chronic disease, HIV infection(highestdeath rate).Thought it was under control but its increasing globally** particularlyin AIDS patients in Africa. RESISTANT DISEASE so complicated to controlMany people go undiagnosedbecause of a large number of latent cases. When someone has it treatment forthe entire household is necessary, high risk of contracting it. LONGTERMtreatment

Front 8

TUBERCULOSIS (2)

Back 8

Mycobacterium is anacid-fast, aerobic, slow-growing aerobic bacillus that is somewhat resistant todrying and many disinfectants, can survive in dried sputum for weeks. Destroyedby ultra violet light, heat, alcohol, glutaraldehyde, and formaldehyde. THE CELL WALL APPEARSTO PROTECT THE ORGANISM FROM DESTRUCTION BY NORMAL BODY DEFENSES. Normalneutrophil response DOES NOT OCCUR!TRANSMISSION:DROPLET, can stay dormant for a long time so it goes through different stages

Front 9

There are two stagesin the pathogenesis; primary or latent infection (TB infection) and secondaryinfection or reinfection (TB disease)

Back 9

Primary infection occurswhen microorganisms first enter thelungs may invadeother organs, are engulfed by macrophages, and cause a local inflammatory reaction, usuallyon the periphery of the upper lobe. Granuloma formation (tubercle) is a clusterof alive stuff that has bacillus living in the middle. Some bacilli migrate tothe lymph nodes, activating a type IV or cell-mediated hypersensitivityresponse with the t-cells. So they are dormant inside the tubercle, they getcasious necrosis (cheesy looking) with dead macrophages. So these bacilli orlegions are walled off in the lung becoming like a classification/see it onx-ray but not an active infection yet. STAYS dormant if patients’ immune systemremains high. AT THIS POINT THEY HAVE BEEN EXPOSED BUT DO NOT HAVE THEDISEASE

Front 10

Secondary or reinfection tuberculosis

Back 10

Secondary or reinfection tuberculosis isthe stage of active infection. Often arises years after primaryinfection, when bacilli, hidden in the tubercles, are reactivated, usuallybecause of decreased host resistance. When the client’s cell mediated immunityis impaired due to stress, malnutrition, HIV infection, age. As organismsmultiply, tissue destruction occurs, forming large area of necrosis.CAVITATION occurs with formationof a large open area in the lung and erosion into the bronchi and bloodvessels. Hemoptysis (bloody sputum) is common as blood vessels are eroded. Cavitationpromotes the spread to other parts of the lung and bacilli are present insputum where they can be passed on to others. Airborne so they are verycontagious. JE]S;

Front 11

Testfor active infections:

Treatment:

Back 11

Test for primaryinfection: indicated by positive tuberculin (skin) testTest for activeinfections: acid-fast sputum test, chest radiograph, sputum culture andsensitivity, GOLD blood test (standard test).Treatment: Long-termtreatment with a combination of drugs – length of treatment varies from 6months to 1 year.

Front 12

ASTHMA

Back 12

Type 1hypersensitivitySEVERE BUT CAN BE AREVERSIBLE CONDITION, they experience periodical attacks of bronicalobstruction, can be due to anything (triggers) weather, ageriges, exercise ect.End game you have lots of inflammation and bronchi construction. Inflammatoryresponse comes in with a lot of histamineàcapillarypermeability à^^ in fluids/mucous that will obstruct the airwayàbronchi constrictionàso air will not flow and gas exchange will be diminished or not take placeà leading to partial ortotal/complete obstruction of airway. Two types: Extrinsic and Intrinsic Extrinsic involves actue episodestriggered by type 1 hypersensitivity

Front 13

**CHRONIC OBSTRUCTIVE PULMONARYDISEASE**

Back 13

Three Examples Of These Disorders areEMPHYSEMA, CHRONIC BRONCHITIS, CHRONIC ASTHMA

Chronic obstructive pulmonary diseasecauses irreversible and progressive damage to the lungs. Eventually,respiratory failure may result because of severe hypoxia or hypercapnia. INmany cases it can lead to cor pulmonale (right-sided congestive heart failure)due to lung disease. Early stages symptoms are minimal ormasked by the primary problem so many people are unaware they have it so it isprobably underestimated.

Front 14

Emphysema:

Back 14

The significant change in emphysemais the destruction of the alveolar walls and septate, which leads to large,permanently inflated alveolar air spaces. Several factors contribute to thedestruction of tissue in the alveoli*** some might be genetic deficiency, aprotein normally present in tissues and body fluids that inhibits the activityof proteases (destructive enzymes released by neutrophils during an inflammatoryresponse) Cigarette smoking increasesboth number of neutrophils in the alveoli and the release and activity ofelastase, but decreases the effect of alpha antitrypsin, thus greatlycontributing to the breakdown of alveolar structures. Changes have effect on lung function:1. Breakdown of alveolar wall =loss ofsurface area or gas exchange, loss of pulmonary capillaries=affecting perfusionand diffusion of gases. Loss of elastic fibers, affecting the ability of thelung to recoil on expiration. 2 --> On the next card!!

Front 15

Emphysema (2)

Back 15

2. Fibrosis and thickening of the bronchial wallshave resulted from chronic irritation and the frequent infections associatedwith smoking and increased mucus production leading to = narrowed airways,weakened walls 3. Progressive difficulty with expiration leads to = airtrapping ^residual volume, over inflation of lungs, fixation of the ribs in aninspiratory position (barrel chest) 4.Hypercapnia and hypoxic drive^^, moreinfections, and pulmonary hypertension^^ pressure in pulmonary circulation ^^resistance to right ventricle eventually the ventricle fails, many patientswith respiratory disease manifest signs of heart failure.Causes:Cigarette smoking, however geneticfactor can play a role early in development of disease in nonsmokers. Andexposure to air pollutants.Its Insidious!

Front 16

CHRONIC BRONCHITIS “BlueBloaters”

Back 16

Chronic bronchitis is differentiatedby significant changes in the bronchi resulting from constant irritation fromsmoking or exposure to industrial pollution. Effects are irreversible and progressive. Mucosais inflamed and swollen hypertrophy and hyperplasia of the mucous glands, and increased secretions areproduced. ^goblet cells decreased ciliated epithelium. à chronic irritation andinflammation lead to fibrosis and thickening of the bronchial wall and furtherobstruction. Oxygen levels are low, during coughingcyanosis may be seen, and edema, the “blue bloater” of bronchitis. à Severe dyspnea andfatigue interfere with nutrition, communication, and daily activities, leadingto general debilitation. Pulmonary hypertension and cor pulmonal arecommon.

Front 17

Pulmonary Edema

Back 17

Refers to fluid collecting in thealveoli and interstitial area. Accumulation of fluid reduces the amount ofoxygen diffusing into the blood and interferes with lung expansion, alsoreducing oxygenation of the blood. Fluid develops when à inflammation is present in lungs, increasing capillary permeability orwhen ** Plasma protein levels are low, decreasing plasma osmotic pressure or*** Pulmonary hypertension develops. (type of high blood pressure affecting the arteries of thelungs and in the heart)

Front 18

Pulmonary Edema (2)

Back 18

Normally pressure in the pulmonary capillariesis very low, and there is just a little fluid in air passages and alveoli. BUTwhen hydrostatic pressure in PC (pulmonary capillaries) becomes high (like in congestiveright heart failure) à leading to a shift of fluid OUT of the capillaries into thealveoli…. SO excessive amounts of fluid in the interstitial areas and alveoliinterfere with diffusion of oxygen, causing severe hypoxemia leading to adifficulty in expanding the lungsà which will ultimately collapseà capillaries may rupture causingblood-streaked sputum.

Front 19

Pulmonary Edema: Causes And Symptoms

Back 19

CAN BE CAUSED BY:Left-sided congestive heart failure (back-up of blood from left ventricle)or Hypoproteinemia (serum albumin levels are low), Inflammation in lungs withincreased capillary permeability (due to inhalation of toxic gases or tumors), Symptoms:Cough, orthopnea, and rales. Sputumis frothy owing, blood tinged, individual feels as if he or she is drowning!

Front 20

Pulmonaryembolus

Back 20

A BLOOD CLOT or a mass of other material obstructs pulmonary artery or abranch of it, blocking the flow of blood through the lung tissue.MOST ORIGINATE FROM DEEP LEG VEINSIt will lodge itself as soon as itreaches a smaller artery in the lungs which it cannot pass, due to deep veinthrombosis (DVT). Effects seen depend on the size and thereforelocation of obstruction in the pulmonary circulation. Infarction usuallyinvolves a segment of the lung and the pleural membrane in the area. SMALLpulmonary emboli are “silent” or asymptomatic. However many small ones can havean effect equal to that of a larger embolus. Emboli that block moderate sizedarteries usually cause respiratory impairment because fluid and blood fillalveoli of the involved area. LARGE emboli (involving more than 60%of lung tissue) affect the cardiovascular system, causing right-sided heartfailure and deceased cardiac output (shock). Sudden death results in most cases.

Front 21

RISK FACTORS:

Back 21

Immobility,trauma or surgery to the legs, childbirth, congestive heart failure,dehydration, increased coagulability of the blood, and cancer. Sitting in aplane or car for a long time period can predispose to thromboembolus.

Front 22

Pneumothorax

Back 22

Refers to air in the pleural cavity.Prevent the expansion of the lung,leading to atelectasis (nonaeration or collapse of a lung or part of a lung)When caused by malignant tumor or trauma, fluid or blood may also be present inthe cavity.

Front 23

Different Types:

Back 23

Closed pneumothorax= when air enters the pleural cavitythrough an opening directly from the internal airways. No opening in chestwall.Simple or Spontaneous pneumothorax= occurs when a tear on the surfaceof the lung allows air to escape from the inside the lung through a bronchusand the visceral pleura into the pleural cavity. Following collapse, themediastinum can shift toward the affected lung, allowing the other lung toexpand more

Front 24

Secondarypneumothorax

Open

Back 24

Secondary pneumothorax = underlying respiratory diseaseresulting of an emphysematous bled on the surface of the lung or erosion bytumor through the visceral pleura. Again this condition lets inspired air passinto the pleural cavity.Open = atmospheric air entering thepleural cavity through an opening in the chest wall. This could result fromtrauma or surgery. A sucking wound is alarge opening in the chest wall, the air moving in and out make a suckingsound. on the gA]z��M

Front 25

Tension pneumothorax

Back 25

Tensionpneumothorax= isa serious form, that can result of either open (puncture through thorax) orclosed (tear in lung surface) pneumothorax, both with flap or one-way valve

Front 26

FailChest

Back 26

Falls and car accidents cause most chest injuries, fail chest resultsfrom factures of the thorax, usually from factures of three to six ribs in twoplaces OR fracture of the sternum and a number of consecutive ribs. Often seen is a contusion with edema and some bleeding lung tissueadjacent to the flail section. ATELECTASIS will only take place of ribpunctures the pleura!Chest wall rigidity is lost à results in paradoxical (opposite)movement during inspiration and expiration/ both of these are effected. y

Front 27

Inspiration with Fail Chest

Back 27

·

Brokenor flail section of ribs moves inward rather than out (intrathoracic pressureis decreased)·

Inwardmovement prevents expansion of affected lung.·

Largeflail section compresses the other lung tissueà pushing air out of that section andback to the bronchusà because of the downward flow of air being breathed the “stale”air from the damaged lung crosses over to the good lung with new air.

Front 28

With Expiration:

Back 28

With Expiration: The unstable flailsection is pushed outward by the increasing intrathoracic pressure.

TheFlail section is large, the paradoxical (contradictory) movement of ribs altersairflow during expiration.

Airfrom the UNAFFECTED lung moves into the AFFECTED lung due to movement of ribsthus decreasing the pressure in the affected lung.

Front 29

Adult or Acute Respiratory DistressSyndrome

Back 29

Also known as shock lung, wet lung,stiff lung, and post perfusion lung. Names related to specific causes. Considered to be a restrictive lung disorder.Multitude of predisposing conditionslike; systemic sepsis, prolonged shock, burns, aspiration, and smoke inhalationmay cause ARDS. Onsetoccurs 1-2 days after injury or other precipitating event. Associated withmultiple organ dysfunction or failure to secondary to a severe insult to thebody.

Front 30

Patho: For ARDS

Back 30

Patho: Basic changes result from injury to the alveolar wall andcapillary membrane, leading to release of chemical mediators, ^ permeability ofalveolar capillary membranes, ^fluid and protein in the interstitial area andalveoli, and damage to the surfactant-producing cells.

Front 31

Cause:

Back 31

These events result in decreased diffusion of oxygen, reduced blood flowto the lungs, difficulty in expanding the lungs, and diffuse atelectasis. Reductionsin tidal volume and vital capacity occur. Excess fluid in the lungs predisposes to pneumonia asa complication. Congestive heart failure may develop.Cause: = Severeor prolonged shock because ischemic damage to the lung tissue.

Front 32

Gas Exchange

Back 32

Pressure gradients (partial pressure gradient movement ofgas takes place from high-pressure area to low pressure area)Proximity= WANT ALVEOIL AND CAPILLARIES TO BE AS CLOSE ASPOSSIBLE FOR ADUQUATE GAS EXCHANGE. Alveoil has two types of cells, type 1provides structure, type 2 secretes surfactant (helping it stay open) andreducing surface tension. Surface Area= helps out with the surfactant and diffuses ondown into that capillary. Takes place because of that pressure gradient.Other major factors in gas exchange are totalsurface area available for diffusion and the thickness of the alveolarmembranes.

Front 33

Gas Exchange (2)

Back 33

Widening of alveoli will lessen the amount of gas exchangethat will take place.Flow of gases betweenthe alveolar air and the blood (external respiration)Gas exchange dependson the relative concentrations (partial pressures) of the gases. à PO2 –Partial pressureof oxygen. àPCO2 –partial pressure of carbon dioxideEach gas in a mixturemoves along its partial pressure gradient, independent of other gases (Dalton’slaw).

Front 34

More Information:

Back 34

The alveoli are the only structures that provide such a surfacearea, and both ventilation and perfusion must be adequate for diffusion tooccur. If part of the alveolar wall is destroyed, as in emphysema, or fibrosisoccurs in the lungs, the surface area is greatly reduced. If airflow into the alveoli is obstructed or the capillaries aredamaged, the involved surface area becomes nonfunctional.