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Pulmonary Disorders

Pathophysiology
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Definition: Restrictive Pulmonary Disorders
Decreased compliance of the lungs causing dyspnea, increased respiratory rate and decreased tidal volume
Pulmonary function test seen with restrictive pulmonary disorders
Decreased forced vital capacity
How does restrictive pulmonary disorders affect the alveolocapillary membrane
causes decreased diffusion of O2 from alveoli to blood
Examples of restrictive pulmonary disorders
Pulmonary Fibrosis, pneumoconiosis, ARDS
Pneumothorax
Presence of air in the pleural space caused by an opening in the pleura or chest wall. This destroys the negative pressure that helps the lung recoil after expiration so the lung collapses.
Types of pneumothorax
Spontaneous (bleb), Secondary (trauma), open, tension
Spontaneous pneumothorax
bleb - bubble develops in lungs and ruptures spontaneously sending direct air into lung cavity if left untreated can result in death
Trauma pneumothorax
caused by crushing injury, ie MVA
Open pneumothorax
air from lung seeps into space
Tension pneumothorax
rupture is one-way valve - air in - collapsing lung and eventually compromising the other lung - air is out of the lung and cannot get back in
Obstructive pulmonary disorders
airway obstruction that is worse on expiration, needs more force to expel than inhale
examples of obstructive pulmonary disorders
asthma, chronic bronchitis, emphysema
All obstructive pulmonary disorders cause
dyspnea and wheezing, increased WOB, V/Q mismatch and decreased forced expiratory volume
Primary cause of COPD
smoking, second hand smoke
Classic sign of emphysema
barrel chest
Pathophysiology of emphysema
mucus in bronchioles, enlarged alveoli, fewer capillaries (ballooned substantially)
Pneumonitis
inflammation of the lower respiratory tract
Causes of pneumonitis
aspiration of acidic fluids, orange juice or stomach juices p/ vomiting
Bronchial damage 2ndary to pneumonitis
includes inflammation, loss of ciliary action, and bronchospasm caused by acidic fluids
Alveoli damage 2ndary to pneumonitis
if acidic substance enters alveoli, damages to the membrane occur resulting in hemorragic pneumonitis
Is pneumonitis life threatening?
yes, the lungs become stiff and surfactant production is decreased, if severe enough, can be life threatening
Where might you see TB on Xray?
Listen to Apex anteriorly and posteriorly
Acute bronchitis
acute infection or inflammation, usually viral of airways and bronchi, self-limiting - needs time to get better
clinical manifestations of acute bronchitis
starts with bad cold and goes to chest; non productive cough or small amt of clear sputum; chest pain with cough, muscular and burning bronchius
Pulmonary Embolism
Occlusion of portion of pulmonary vascular bed with an embolism, usually from clots formed in the veins of the legs and pelvis; may or may not cause lung infarction and necrosis
Clinical manifestations of PE
usually non-specific, clinician must look closely at history and suspect DVT. Chest pain, dyspnea, tachypnea, anxiety, etc, sudden onset chest pain
Possible cause of SIDS
immature ventilatory and arousal response to hypoxia - cause is unkown
Incidence of SIDS
most common cause of unexplained death under 1 year old, boys 3-4 mos, night, winter, maybe URI related
Risks of SIDS
LBW, preemie, multiple, sibling w/ SIDS, maternal smoking; 3/4 cases showed no risk factors
Back to Sleep campaign
has reduced the incidence of SIDS
Painful Bladder Syndrome AKA Interstitial Cystitis
more common in women 20-30 years old who have usual UTI symptoms but negative cultures - non-bacterial cystitis
Interstitial cystitis caused by
no known cause; may be autoimmune derangement of bladder mucosa - ulcers (Hunner) may be present and fibrosis related will decrease bladder volume
Interstitial cystitis pathophysiology
antiproliferative factor blocks normal growth of cells of the wall of the blader and increase bladder sensation (pain)
Clinical manifestations of interstitial cystitis
feeling of fullness, frequency, nocturia, pelvic pain, small urine volume
Nephrotic syndrome excretes
3.5 grams or more of protein in the urine/day - loss of lipids, severe loss of serum proteins
Clinical manifestations of Nephrotic Syndrome
edema, hyerlipidemia, lipiduria, Vit D deficiency, hypercoagulability
Difference between Nephritic and Nephrotic Syndromes
Nephritic has blood loos and is not as sever as nephrotic
Polycystic Kidney dz
an inherited d.o. - autosomal dominant (may not manifest until 40 years old) or autosomal recessive (manifests at birth)
Clinical manifestation of polycystic kidney
affected kidney has large fluid filled cyst - other organs may also have cysts; aneurysms may develop in adulthood
Potter syndrome
Bilateral renal agenesis (no kidneys) - more common in males
Clinical Manifestations of Potter Syndrome
more common in males, facial anomolies - wide eyes, low ears, receding chin
Prognosis with Potter Syndrome
fatal, may only live a few hours
IgA Nephropathy
most common form of glomerulonephritis worldwide, occurs more often in males
Pathophysiology of IgA Nephropathy
Deposits of IgA, IgM and complement proteins in glomerular capillaries; no systemic immunologic disease is evident, usually reversible
Clinical Manifestations of IgA Nephropathy
gross hematuria, mild proteinuria, post URI
Wilm's Tumor (Nephroblastoma)
Rare embryonal tumor of the kidney arising from the epigenetic and genetic changes of renal stem cells
Genetic disposition of Wilm's Tumor
most are sporadic, no known genetic predisposition; looks like there may be some autosomal dominant gene involved
Clinical Manifestations of Wilm's Tumor
enlarging asymptomatic abdominal mass before age 5
Primary Enuresis
never continent (nocturnal - never dry at night), matter of development maturity - most will outgrow by age 6; familial tendency
Secondary Enuresis
period of dryness for 3-6 months after toilet training, more likely from UTI (ecoli), neuro changes, disorders that cause increased output like diabetes, new sibling
ARDS
Acute lung inflammation with diffuse alveolarcapillary injury
Causes of ARDS
extensive burns, CABG, pancreatitis, DIC, severe trauma, sepsis (primary predisposing factor), fat emboli, shock, pancreatitis, pneumonia
Pathophysiology of ARDS
massive pulmonary inflammation that injures the alveolar capiliary membrane and produces pulmonary edema
Clinical Manifestations of ARDS
pink tinged frothy sputum, lungs with rales (earliest symptom); shunting/mismatched V/Q ratio; inadequate ventilation of the well-perfused areas of the lung; good blood flow, but inadequate ventilation; pt will develop hypoxemia; marked dyspnea, rapid, shallow breathing, inspiratory crackles (called rales); resp alkalosis, decreased lung compliance, hypoxemia unresponsive to O2 therapy, diffuse alveolar infiltration on Xray,
Pulmonary Edema
collection of fluid within the lung. other than ARDS, the most common cause of pulmonary edema is Left Sided Heart Failure
Blood volume flow between lungs and heart
left ventricle goes out to the periphery, if LV is not contracting well, the volume builds up and back flows into L atrium and into the lungs
Asthma
inflammatory disorder of airways, reversible, familial disorder that occurs in all ages
Risk Factors for Asthma
family history, allergen exposure, urban living, air pollution, cigarette smoke, other atopic disorders, recurrent URI (viral)
Asthma Patho
inflammation, leads to hyperresponsiveness of the airways; can begin when exposure to allergen occurs, causes mast cell degranulation and the release of inflammatory mediators including hystamine, interlukens, prostaglandins, leukotryines, and nitric oxide; these inflammatory mediators cause a vasodilation and increase in capillary permeability; and an increase chemotactic response that draws neutrophils, eosinophils and lymphocytes to the inflammed areas
Asthma clinical manifestations
during attack: chest constrictiction, dyspnea, expiratory wheezing, non-prod cough, some are cough-variant where only symptom is cough; prolonged expiration, tachycardia and tachypnea
Urban Living and Asthma
kids that are clean and haven't played in dirt, more susceptible to asthma; very poor families have more exposure to coachroaches and increase asthma
Eosinophils in asthma
release toxic chemicals that increase the inflammation further and tissue damage occurs; the inflammation causes bronchial smooth muscle spasm; vascular congestion, edema, a thickening of the mucus and impaired ciliary function, increased bronchial hyperresponsiveness
ciliary
little hairlike projections on epithelial cells that line the airways trachea, bronchioles and alveoli have cilliary; move mucus, dirt and bacteria up and out of the lungs; destroyed by smoking and air pollution
status asthmaticus
bronchospasms that are not reversed and become more and more severe; can be deadly
Chronic Bronchitis
Caused by smoking, the change in the lung produces hypersecretion of mucous and chronic productive cough for at least 3 months of each year x 2 years
Patho of Chronic Bronchitis
airway inflammation with infiltration of neutrophils, macrophages and lymphocytes into bronchial walls and more bronchial edema, an increase in mucus cells and thick tenatious mucus, poor ciliary action, increased susceptibility to infection; expiratory airway obstruction and air trapping
Clinical Manifestations of Chronic Bronchitis
chronic bronchitis is more mucus related
Emphysema
Abnormal permanent enlargement of gas exchange airways with destruction of alveolar walls without fibrosis due to loss of elastic recoil of alveioli
Causes of Emphysema
primary cause is smoking, childhood URI, air pollution
Primary Emphysema
few rare cases, inherited, autosomal recessive; alpha 1 anti-tripson
Clinical Manifestations of emphysema
barrel chest
pathophysiology of emphysema
cig smoking inhibits the antiproteases and stimulates inflammation with an increase in the proteases; these proteases digest/destroy the inner layer of the alveoli and the ability to elastic recoil is lost, the alveoli grow
Pneumonia
infection of the lower respiratory tract - 6th leading cause of death in US
Pneumonia causative agents
bacteria, virus, fungi, protazoa, parasits, most common is community aquired pneumonia is streptococcos pneumonia, can make polysaccahride covering to protect from body defenses, but there is a vaccine available to protect against;
Pneumonia risk factors
advanced age, compromised immune system, underlying lung dz, COPD, emphysema, ETOH, smoking
Pneumonia pathophysiology
pathogens are inhaled or in oralpharengeal secretions aspirated or lungs seeded from sepsis
Pneumonia clinical manifestations
starts with URI, then develops fever quite high, chills, productive or dry cough - strep-> rust colored or blood tinged sputum, pleural pain, mailase, dyspnea, physical exam shows inspiratory crackles, dullness to percusion, increase in egophany (voice changes)
Micoplasma pneumonia
less virulent type of pneumonia found among military and groups, less severe, walking pneumonia, continue to go to school while running fever
Tuberculosis
infection with mycobacterium tuberculosis, rod shaped bacteria, affects lungs during dz, in other countries in joints, kidneys
Pathophysiology of tuberculosis
mycobacterium tb spread via airborne droplett, rod shapped, lodge in lung, discovered in upper lobes of the lung when the bacteria enter lung, cause pneumonitis which leads to baccili migrating to lymph system and the lymphocytes initiate an immune response, because of being in lymph system that's how they lodge in upper lobes; cell mediated immune response - macrophages and neutrophils engulf the bacilli, the engulfed baccili produce a terburcal - creating caseation necrosis and then scar tissue around tubercal. Then the bacilli remains isolated and dormant for life, which then shows on CXR or skin test. poor immune system can result in TB dz. most risky time is 2 years p exposure, then old age.
Clinical manifestations of tuberculosis
fatigue, wt loss, lethargy, evening low grade fever, night sweats, purulent sputum, anxiety ; primary exposure has no symptoms
Cor Pulmonale
right ventricular failure d/t lung dz right ventricle is trying to push blood into the lung and the lung is resisting causing a back flow of volume and the r ventricle gets larger with a back flow into the periphery
Croup
acute laryngeotracheobronchitis; little boys 6mos-5yrs, 85% caused by parainfluenza virus
Croup clinical manifestations
rhinorria, sore throat, LGF, seal cough, viral - resolves spontaneously
Acute epiglotits
caused by HIB, reduced d/t vaccine, strep throat can also cause, children 2-7yo,
Acute Epiglotitis clinical manifestations
fever, inspiratory stridor, drooling, dysphagia, resp distress, can die; drooling child - do not use tongue blade, can spasm/airway obstruction
Bronchiolitis
viral, lower respiratory tract infection in infants and young toddlers
Usual cause of bronchiolitis
viral nov-april, RSV, healthy infants fair well
Pathophysiology of bronchiolitis
causes necrosis of bronchial epitheliam and destruction of the ciliated epithelial cells causing a cell mediated hypersensitivity causing inflammation, edema, bronchialspasm which causes narrow airways and airtrapping/atelectasis
Clinical manifestations of bronchiolitis
running nose, tight cough over several days, then fever, poor feeding, lethargy, rapid respirations and acute RDS, wheezing, rales, rhonchi
Nephrolithiasis
kidney stones, masses of material that occur in the kidney and obstruct urine flow can be crystals or proteins
Most common type of neprholithiasis
calcium oxalate or calcium phosphate - calcium primary type
Pathophysiology of kidney stones
stone formation based on supersaturation of salts in the urine, precipitation of salts from liquid to solid and growth from crystalizations and presense or absense of stone inhibitors, alkaline PH increases risk of stone formation. Chips, soda, and phosphorus increase alkalinity
clinical manifestations of kidney stones
mod to severe pain in flank and radiating to groin, colicky, comes and goes with paristalsis, may cause bleeding as it moves,
Urinary tract infection
inflammation or infection of the urinary epithelium, caused by colon germs like ecoli
Who is at risk for UTI
premature infants, pre-pubertal children, sexually active women, pregnant, abx, spermicide users, estrogen deficient women and indewlling catheters, DM
Protects against UTI
increased fluids, low PH (acidic), presence of Tamm-Horsfall protein, and secretions from the euroepithelium (bactericidal)
Most common UTI
bladder infection (cystitis), Ecoli, klebsiella, proteus, pseudomonas
Clinical manifestations of UTI
asymptomatic (esp preg, elderly), sometimes first clue is that they are confused, frequency, urgency, dysuria, suprapubic, low back pain
Acute pyelonephritis
infection of the renal pelvis and interstitium
Risk factors for acute pyelonephritis
urinary obstruction, urinary reflux, women, blood infection may seed kidney
Organisms associated with acute pyelonephritis
ascends from bladder to kidney, ecoli, can also see proteus or psudomonas if iatrogenic
Pathophysiology of acute pyelonephritis
bacteria ascend from bladder and infection causes inflammation of renal pelvis, calcis and medulla, medulary infiltration of WBC, and renal edema an purulent urine, may see absess of kidney
Clinical manifestations of acute pyelonephritis
very sick, high fever, chills, flank or groin pain, costal vertibral angle tenderness, will have UTI symptoms
Glomerulonephritis
inflammation of the glomerulus; related to inflammatory process by immune responses
Acute glomerulonephritis
associated with streptococcal infection - impetigo or pharygitis; immune disregulation response; 7-10 days post infection glomerular injury occurs as a result of the immune mediated response
Immune mediated response to glomerulonephritis
Type II and Type III hypersensitivity
Clinical manifestations of glomerulonephritis
10-21 days after infection, hematuria, protenuria, edema around eyes, feet, ankles
Clinical manifestations of nephrotic syndrome
frothy, foamy urine, edema, poor appetite, diarrhea, protein deficiency, more susceptible to infection (lots of protein and fat being lost)
Wilm's Tumor
occurs on the kidney - rare embryonal tumor, most common solid tumor in children, sporadic, no genetic disposition, possibly autosomal dominant may have lack of iris of eye, mother often finds mass before age of 5 years old - abd pain, fever, blood in urine
Types of adult incontinence
Urge (detrusor muscle not working), stress, overflow (BPH), mixed (stress and urge mixed), functional (dementia and immobility)
PND is a symptom of
left ventricular heart failure. Individuals wake up in the middle of the night gasping for air and have to sit or stand up to relieve the dyspnea. This dyspnea results from redistribution of body water into the lungs while the individual is recombent.
empyema
pus in the pleural space
bronchiolitis
inflammatory obstruction of the small bronchioles occurring most often in children
hypoxemia
reduced oxygenation of arterial blood
dead space
area where alveoli are ventilated but not perfused
cough
explosive respiration to clear the lower airways
hemoptysis
coughing up blood
cavitation
process of abcess emptying into a bronchus and cavity formation
hypoxia
reduced oxygenation of cells in tissue
pulmonary fibrosis
excessive amount of fibrous or connective tissue into lungs
pleural effusion
presense of fluid in the pleural space
aspiration
passage of fluid and solid particles into lungs
pulmonary edema
excess water in the lung
atelectasis
collapse of lung tissue
cyanosis
bluish coloration of skin and mucous membranes caused by desaturation or reduced hemoglobin
dyspnea
sensation of uncomfortable breathing
pneumothorax
presense of air in the pleural space
pneumoconiosis
change in lung caused by inhalation of inorganic dust particles
clubbing
bulbous enlargement of the end of finger or toe
flail chest
from fracture of several ribs, making the chest wall unstable
bronchiectasis
persistant abnormal dilation of the bronchi
restrictive lung disorders are characterized by
decreased compliance of lung tissue, takes more effort to expand lungs, c/o dyspnea, increased resp rate and decreased tidal volume
Obstructive lung disorders are characterized by
airway obstruction which is worse with expiration, either more force or more time (or both) are required to expire a given volume of air. c/o dyspnea and wheezing, a decreased forced-expiratory volume (FEV1) will be noted.
exstrophy of bladder
rare anomaly where the bladder opens directly onto abdominal wall
renal agenesis
absence of one or both kidneys
hypospadias
birth defect where urethral opening is on the lower portion of the shaft of the penis
hypoplastic kidney
very small normal kidney
chordae
skin tethering and shortening of tissue causing penis to bow ventrally
renal dysplasia
abnormal differentiation of renal tissue
polycystic kidney
autosomal dominant and auto recessive inherited disorder where cysts form on the kidneys and other organs
renal aplasia
growth of the kidney does not occur
epispadias
male urethral opening is on the dorsal surface of the penis
TB infection rate
declined in US to 4.8 cases per 100,000; hispanics, blacks an asians had TB rates 7.3, 8.3 and 19.6 times higher than whites in US in 2005
Seven states with highest TB incidence
California, Florida, Georgia, Illinois, New Jersey, New York and Texas
Rates of COPD
underlying cause of 1 in 20 deaths in US in 2005, death rates have decreased amount men but increased among women keeping the death rate of COPD the same overall. Deaths are higher among whites than backs or people of other races, smoking is the most important cause of COPD.