PATHO EXAM 4- REZ STUFF

- Restrictive Lung diseases and lung volumes HELP

-increased rez rate (why)

-decreased tidal volume (huh)

-decreased lung compliance

-decreased vital capacity (huh)

t or f: in kids u can see barrel chest with chronic asthma

ye

true

this breathing pattern occur from decreased drive to breathe (neuro cause) or bad at responding to ventilatory stimulation (pul)

hypovent

this breath pattern caused by anx, head injure or v bad hypoxemia

hypervent

hyperventilation

-co2 levels? leading to blank

hypocapnia leading to rez alkalosis

-     Chronic bronchitis pathophysiology

you breathe in the irritants. now you get airway inflammation. this I leads to infiltration of neutrophils, macrophages and lymphos.then you get bronchial edema and increase in size/number of mucous glands/goblet cells. the so much mucus cant be cleared because of impaired cilary function.

this breath type will show wheezing sound cuz of two factors: narrowed airways due to constriction/fluid accumulation and cuz pt needs more force to provide good ventilation

dyspnea

in chronic bronchitis: to get diaged you must have the cough for at least (insert timeline)

lasts for 3 months out of the year and for at least 2 consecutive years

this breath type is usually caused by diffuse and extensive pul disease

hyperpnea

hypoventilation

hypervent

dyspnea

dyspnea

s and s of chronic bron (10)

bronchospasm

infection

prolonged expiration

cyanosis

dyspnea

cough

hypoxemia

hypercapnia

cor pulmonale

hypoventilation

chron bronchitis air obstruction causes (hypo or hyper co2) and (hypo and hyper o2) due to (hypo or hyper vent)

hyper co2, hypo o2, hypovent

Breathing patterns: Hyperpnea.

-aka?

-whats going on?

-talk about rez factors like tidal vol, vent rate and expiratory pause

known as kussmual rez. deep breathing so we inhale more o2 which helps get rid of more o2.

slightly increased ventilatory rate and v large tidal volume w no expiratory pause

Breathing patterns: Orthopnea (two reasons it can happen)

one: lying flat causing abdom contents exert pressure on diaphragm during when indiv lies flat

two: lying flat where fluid shift from lower body to lungs

Hypoventilation: wut going on

minulate ventilation ?

causes (low or high) co2 which leads to (acid or alka)

t or f: this is a very noticable clinical manifestation

s and s: name 3

--minute ventilation (rez rate x tidal vol) v low

-causing end result of a lot of co2 in arterial blood leading to rez acidosis cuz decrease in blood ph

-can initally go unnoticed

-s and s: mental change, weird HR, rez arrest

this breath pattern happen when indiv with pul/heart D awake at night and gasp for air. (WHAT SHUD THEY DO TO RELIEVE THE DYSPNEA)

Paroxysmal nocturnal dyspnea

-sit or stand

this breathing pattern has alternating periods of apnea (no breathing) and deep rapid breathing. basically being shallow- increase to deep and rapid- and then back to shallow- repeat

Cheyne-Stokes respirations

this breathing pattern is the subjective experience of breathing discomfort (even at rest) and may be result from pul disease or other conditions like pain heart issue or anx

dyspnea

result from any condition that reduces blood flow to the brainstem, which in turn slows impulses sending information to the respiratory centers of the brainstem.

cheyne stokes

wheezing sound heard during dyspnea due to:

air being forced thru narrow airways cuz of constriction or so much fluid

in dyspnea this will be seen

flaring nostrils

retraction of intercoastal spaces

increased compliance

non use of acessory muscles

truth: flaring nostrils, retraction of inter/supra coastal spaces

lie: compliance will be decreased and access muscles used

-        Accessory Muscles used in dyspnea? who is more likely to use it

kids.

sternocleidomastoid and scalene muscles

visible neck contraction and intercoastal/supracoastal retractions

Tuberculosis: which germ? trans how

mycobacterium TB

airbone

TB: patho? what type of lesions seen

bac are inhaled, lodged in lung. can also become lodged in lymph nodes. in either case- the bac encounters macrophages and neutrophils and lymphos. granulomatous lesions form. then (only with imparied imm sys) they can get active and slip thru- traveling on blood or lymph to other places

granulomatous lesions seen in blank. why does this happen? which necrosis type is seen?

imm sys is alerted to bac presecne. get a bunch of imm cells coming and form around the bac, in order to contain it. caseous necrosis- infected tissues within the tubercle die showing a cheeselike material

pleural effusion vs pulmonary edema
def vs s and s vs diseases connected

pleural effusion

DEF: buildup of fluid in the pleural cavity. many diff fluid types seen.

s and s: dyspnea and pleural pain.

diseases connected to: cancer, cirrhosis or monia

pul edema

def: water within the lung tissue itself

connected to: left heart disease, llung/H fail, toxic gas inhale, ARDS, lymph sys going bad

s and s: dyspnea, hypoxemia, increased work of breathing, rales/inspiratory crackles, dullness with percussion. severe cases show pink froth sputum, awful hypoxemia, hypercapnia and hypovent

Pleural effusion types:

transudative,

exudative/pneumothorax,

hemothorax,

empyema,

chylothorax

-another word for transudative is blank

bloody

Watery fluid that diffuses out of capillaries

Chyle (milky fluid containing lymph and fat droplets) that moves from lymphatic vessels into pleural space instead of passing from gastrointestinal tract to thoracic duct

Microorganisms and debris of infection (leukocytes, cellular debris) accumulate in pleural space

Fluid rich in cells and proteins (leukocytes, plasma proteins of all kinds

hydrothorax/transudative - watery fluid

exudate- lotta teins and leukos

hemo- bloody

emp- pussy. debris of infection and microorgs in pleural cav

chylo= milky fluid with lymph and fat that goes from lymph vez to lung cav

s and s of ARDS in kids

7 days of blank, blank and blank.

(hyper or hypo) vent can be seen at start but then (hyper or hypo) occurs too in later stages because of non functioning lungs leading to co2 retention

7 days of dyspnea, hypoxemia, pulmonary infiltrates

hypervent can be seen at start but co2 retention can happen cuz of bad func air space and rez muscle fatigue

-        ARDS 3 steps of increasing gravity (list in gen)

exudative

proliferative

fibrotic

what will be seen with ards

unilateral infiltrates

or

low ratio of pao2 to fio2

low ratio. bilateral infiltrates seeen

ARDS is a clincal syndrome in which there is blank that is not the result of cardiac disease. this is a blank response that causes blank injury

pul edema. I response. aleveolocapillary

pathophys of ards in general

I and injury to alveolocapp membrane. damage causes pul edema.

exudative phase of ARDS what happens ? pathophys steps

what are the stats of lung factors

lung injury hurt endo cells of the pul caps/alveolar cells. now u get neutrophils, macros, platelets and cytokines that inflame and increase cap mem permeability. fluid, teins and blood cells leak from cap and into the alveoli. now u see v reduced surfactant production- leading to atele.

factors: low lung compliance, low tidal volume, high co2

s and s of ARDS list progressively

Dyspnea and hypoxemia (bad o2 supplementation)

hypervent lead to rez alka

low perfusion and organ dysfunction lead to meta acid

hard breathing and low tidal volume lead to hypoventilation

worse hypoxemia and co2 retention lead to rez acidosis

low co and low bp. rez failure then death

proliferative

-whats going on

in order to resolve the damage, fibroblasts and myofibros begin to be made. the bloody exudate becomes a cellular granulation tissue, appearing as hyaline mems that are a barrier for oxyen exchange. slowly but surely hypoxemia seen

fibrotic phase

-what going on

remodeling and fibrosis of lung.

fibrosis may be seen to destory alveoli, rez bronchioles and intersittium

asthma is the blank of the air ways which causes these bron (hyper or hypo) responsiveness, (dilation or constrict) of airways and reversible blank as well as (more or less) mucus

chronic I.

hyper, constriction, airflow obstruction, more mucus

s and s of asthma

wheezing

cyanosis

pursed lip breathing

coughing

rapid breathing

nasal lfare

use accs muscles

blank is most prev chronic D of kids

asthma

in kids asthma result from complex interaction tween blank and blank

genetic susceptibility and enviro factors

pulsus paradoxus is connected to blank. def is

asthma. def= very low systolic bp seen everytime u inhale

status asthmaticus is connected to blank. def

asthma. u just have a very bad continous asthma attack that wont stop and is getting worse and needs intervention

-        Asthma attack treatment

-beta agnoist bronchodilator like albuterol using neb or inhaler

-oral corticosteroids like prednisolone. do IV cort if that not work

-anti I drugs

-peak flow meters

atele types and match: compressed or obstructive or adhesive

seen w mucus plugs or foreign object causing blockage. hypovent is gradually absorbed out of the alveoli into the blood. An obstruction triggers a partial or complete lack of ventilation to the impacted area, though gas uptake into the blood still occurs.. When all of the gas is absorbed, the air sacs eventually collapse as the obstruction prevents more gas from entering.

external P on lung

v low prody or not making an surfactant

obstructive/absorp

compressed

adhesvie

atelectasis

collapse of lung tissue where alveoli became deflated now there is lack of gas exchange and impaired breathing

bronchiolitis

what

s and s

more common in kids or adults

how is is it different that chron bron

I obstruction of small airways and bronchioles (think of how the term includes bronchiol (itis) , common viral rez tract infection (DIFF THAN CHRONIC BRONCHITIS BECAUSE BRONCHITIS AFFECTS LARGE AIRWAYS AND HAS NOTHING TO DO ABOUT INFECTIONS)

common in kids

Clinical manifestations include a rapid ventilatory rate, use of accessory muscles, low-grade fever, and a nonproductive cough. A decrease in the V̇/Q̇ results in hypoxemia.

monia in kids show symps of blank and blank with (abnormal or norma) wbc count. the most common viral monia is blanik

cough, no fever, norm wbc

rsv

most common assc pathogen with bronchiolitis

RSV

bac monia most common is connected to this bac.

strepto.

s and s of bronchiolitis in kids

6 symps

runny nose

low app

v tired

fever

wheezing

tachypnea

which one: bronchiolitis, pulmonary fibrosis, bronchiectasis, pulmonary edema

connected to adults with chronic bronchitis or cuz viral infection or cuz toxic gases

bronchiolitis

bronchiectasis is connected to which disease

coronary artery disease

stomach cancer

AIDS

HIV

AIDS

bronchiectasis

what

s and s- four

persistent abnormal dilation of the bronchi leading to mucus buildup and a lot of infections

s and s: productive cough, lower rez tract infections, foul smelling purulent sputum, clubbing fingers and hemoptysis

ARDS symps in kids: whats true (from slide)

orthopnea

sputum

cyanosis

tachypnea

expiratory grunts

muffled breaths

nasal flares

retractions

productive cough

tachypnea

expiratory grunts

nasal flare

retractions

cyanosis

pleurisy

what

s and s

I of plerua membrane

sharp chest pain, short of breath, cough, grating/creak sound during inhalation

majority of acute bron is caused by blank

virus

-        Acute bronchitis vs pneumonia

differences vs same

the definition is different. bron is infection/I of bronchial tubes while monia is infection/I of alveoli itself. plus monia is more serious

a few symps are different. monia has dullness to percussion, crackles, ehophony (pul consolidation) and chest radiographs show infiltrates.

both have= fever cough chills malaise chest pain. both can have a viral or bac cause

ppl w/ acute bron have a blank cough that occurs as blank and is aggravtared by cold or dry dusty air. blank type of sputum is seen in bacterial bron.

nonprod. paroxysm. purulent

-        Cor Pulmonale def. the organ involved in blank and what happens is blank cuz of these 3 common diseases.

name 4 s and s

Cor pulmonale is a condition where the right side of the heart becomes enlarged and weakened due to increased pressure in the lungs' arteries, which is typically caused by a chronic lung disease.

happens from copd, pul fibrosis or pul hypertension.

s and s: R heart fail, short breath, swelling in legs and abds, big spleen

in cor pul, the H appears abnormal at rest and at working out t or f

f. it is norm at rest but during excersice cardiac output fails

u will see paradoxical mvmt of chest wall during breathing. ALSO WHAT DOEES PARADOXICAL BREATHING MEAN

cor pulmonale

pleurisy

flail chest

ARDS

flail chest . so when u inhale ur chest movves inward

-        Flail chest

def

will u see hyper or hypo capnic rez fail

instability of a portion of the chest wall cuz of rib/sternal fractures.

hypercapnic rez fail

-        Small cell carcinoma and ADH?

SSC can lead to prody of ADH cuz it is being made ectopically by the tumor. now u get siadh causing water retention and hyponatremia

-        Pulmonary embolism and V/Q ratio

-what does v vs q mean? whats going on? why?

-will it be high or low

v/q or vent/perfusion mismatch. ventilation is normal but perfusion sucks due to how pulmonary artery is obstructed which restricts blood flow to a part of the lungs.

now u have areas in lung that are ventilated but not perfused so VQ ratio is high in that area.

-        Blue bloater vs pink puffer

basically answer which disease it connects to ONLY

blue bloater= someone with chronic bron

pink puffer= someone with emphysema

pt comes in with dyspnea, wheezing, barrel chest, prolonged expiration, hunched over, breathing thru pursed lips. there is permenant enlargement of gas-exchange airways aka acini plus destruction of alveoli walls. thiis person also shows inheritied deficiency of enzyme a-antitrypsin. is this a blue bloated or pink puffer

pink puffer aka emphysema girl

this disease shows elastin breakdown cuz of a lot of protease activity

pink puffer or blue bloated

pink puffer

this D shows I cells and release of cytokines from these I cells

pink puffer or blue bloater

haha both

this pt shows cough, dyspnea on exertion, hypercapnia, hypoxemia and mild cyanosis

pink puffer or blue bloater

blue bloater

air trapping and loss of elastic recoil highly seen

pink puffer or blue bloater

emphysema aka pink puffer

this pt comes in with a hypersecretion of mucus and chronic prod cough. there has been continous bronchial irritation and I.

chronic bron