presence of air in the pleural spacecaused 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.

Spontaneous/Bleb = weakened, when opened air is released into chest instead of going out

One-way valve, lung collapses as air escapes

Secondary/Trauma- ex GSW where open pneumothorax occurs, chest tube needed to reinflate lung

Tension- area can leave lung but not chest capacity causing increased pressure that collapses the lung then eventually collapse the other; both lungs at risk

characterized by decreased compliance of lung tissue -more self effort to expand the lungs during inspiration, which increases the work of breathing -complaints of dyspnea and they have increased RR and decreased TV

PFT reveal decreases in FVC - can cause venitlation and perfusion mismatch or can affect the alveolocapilary membrane, therefore decreased diffusion of oxygen from the alveoli into the blood, resulting in hypoxemia

characterized by airway obstruction that is worse with expiration -either more force or more time is required to expire a given volume of air, or both - unifying Sx: dyspnea; unifying Sign: wheezing

increased work of breathing, ventilation/perfusion mismatch, and decreased forced expiratory volume

Seen more frequently than restrictive

Exert more force to expel air

Increased effort to push the air out of the lungs

DONT smoke!

- Figure 33-8 p1280 - massive pulmonary inflammation - alveolar capillary membrane injury - severe pulmonary edema (noncardiogenic pulmonary edema) and shunting (mismatching of vent. To perfusion ratios, specifically inadequate ventilation to a well perfused area of the lung ) causing hypoxemia

- neutrophils are central to development of ARDS - increased capillary permeability is hallmark of ARDS - lung compliance reduces drastically can lead to SIRS then MODS then Death

- progressive dyspnea; initially tachypnea, gradually increasing inspiratory crackles - 24-48hrs after injury, interstitial and alveolar infiltrates appear on chest radiographs; hypoxemia and respiratory alkalosis usually occur here - as it progresses: hypoxemia becomes refractory to oxygen therapy and hypoventilation develop w/ increased carbon dioxide - worsening hypoxemia and hypercapnia lead to resp. failure - metabolic acidosis and organ dysfunction (decreased urine output and decline in cognitive functioning) - decreased cardiac output and hypotension lead to death

shallow breathing, inspiratory crackles, resp alkalosis, decreased lung compliance

- highly contagious and transmitted from person to person in airborne droplets - influenced by genetic polymorphisms that affect macrophages, TNF, and interleukins - bacteria lodge in lung periphery - multiple-cause pneumonitis- neutrophils and macrophages migrate to area - engulf and isolate bacteria to prevent spread- bacteria survives and multiplies within - interferon released to attract more macrophages - tubercle forms around bacilli - caseation necrosis occurs - scar tissue forms around the tubercle - immune response complete after 10 days - once isolated and immunity develops, - TB may remain dormant for life or if immune impaired or poor nutrition or aging then the bacilli will escape and secondary form will happen

- Infection with HIV is greatest risk factor for reactivation of TB infection; others include cancer, immunosuppresive medications, antirejection meds, renal failure - reactivation in elderly: poor nutritional status, insulin-dependent diabetes, long-term corticosteroid therapy

-Latent TB is asymptomatic - fatigue, weight loss, lethargy, anorexia, low grade fever in the afternoon/evening (diurnal) - cough producing purulent sputum develops slowly and becomes more frequent over weeks to months - night sweats and general anxiety seen - dyspnea, chest pain, hemoptysis - amenorrhea if they loose a lot of weight

in HIV pts: neuro deficits, meningitis sx, bone pain, urinary sx

acute infection or inflammation of the airways or bronchi; mainly caused from viruses; self-limiting - CM: similar to pneumonia (fever, cough, chills, malaise) - exam does not reveal signs of pulmonary consolidation and chest radiographs do not show infiltrates - nonproductive cough that occurs in paroxysms and aggravated by cold, dry, or dusty air - purulent sputum and chest pain may occur - BActerial: productive cough, fever, and pain behind sternum aggravated by coughing; more common in COPD pts

Very uncomfortable but will go away on its on

Startswith bad cold and pt will say “its gone to my chest” – nonproductive cough with chest pain

*(info from mayo clinic site) -inflammation of the lung, loss of ciliary action, and bronchospasm

-difficulty breathing and cough; fatigue, weight loss -caused by pneumonia, some cancers, and other environmental irritants (molds, birds, drugs)

- Can be from bad gases like a soldier would inhale

- Person debilitated may aspirate acidic fluids -OJ or stomach juices

- effect of embolism depends on the extent of pulmonary blood flow obstruction, size of affected vessels, nature of embolus, and secondary effects - embolus w/ infarction - embolus w/o infarction - massive occlusion - multiple pulmonary emboli - neurohumoral substances released cause widespread vasoconstriction impeding blood flow to lungs which can lead to RSHF - increased dead-space and decreased surfactant production - resulting atelectasis of affected lung segment contributes to hypoexmia - thrombus large: infarction - dysrhythmias - decreased CO - shock - death - if infarction does not occur, clot is dissolved

Different from pulmonary edema like in LSHF – fluid not pumped out to periphery by left ventricle backflows into capillary bed and settles in the alveoli

secondary to pulmonary artery HTN and consists of Right ventricular enlargement (hypertrophy, dilation, or both)

RVF secondary to lung diseases like pulmonary HTN or severe COPD or emphysema 

- prodrome of rhinorrea, sore throat, low grade fever for a few days - harsh (seal-like) barking cough, hoarse voice, inspiratory stridor - Spasmodic croup: similar hoarseness, barking cough, and stridor but is sudden, usually at night and without viral prodrome - inflammation and edema - UAO - increased resistance to airflow - increased intrathoracic negative pressure - collapse of upper airway - resp failure

Croup resolves spontaneously.

- severe life threatening rapidly progressive infection of the structures above the insertion point of the glottis, which include epiglottis, aryepiglottic folds, arytenoid soft tissue, and uvula - decreased incidence since we have flu vaccine - caused by strep, pneumonia, candidiasis, s. aureus; most commonly by Hib - thermal injuries, trauma, and posttransplant lymphoproliferative disorder also cause acute epiglottitis

age 2-7yo

- tachypnea, expiratory wheezing, cough, rhinorrhea, mild fever, varying grades of resp. distress - mild conjunctivitis and otitis media may occur - infants may have apnea - chest x ray: hyperexpanded lungs, patchy or peribronchial infiltrates, and atelectasis - anxious; thoracic cage overexpanded (flat diaphragm and displacement of spleen and liver); rapid short breaths with wheezing and rales heard; abdominal distention - increased risk for asthma

others mentioned: tight cough, poor feeding, lethargy

- Figure 34-14 p1331 and Fig35-15 p1332 - obstructive airway disease characterized by reversible airflow obstructions, bronchial hyperactivity, and inflammation - most prevalent chronic disease in childhood - prepubertal years, more boys than girls - populations most affected urban areas, ethnic minorities, and low-socioeconomic status - inner city blacks and hispanics have higher morbidity and mortality than whites - genetics and environment: allergens, smoke, air pollutants, and viral infections; long list of polymorphisms for asthma genes and chromosomes - “hygiene hypothesis”

theory that asthma occurs in kids who havent been exposed to agents aka mothers kept them too clean therefore never built immune system to counteract inflammation of asthma

p1330 Th2 predominant phenotype and viral infection interact to cause asthma

Over 20 genes that play a role in susceptibility or pathogenesis of asthma

Other causes: Recurrent upper resp viral infections; atopic disoreders like allergic dermatitis, hay fever (rhinitis)

fig34-15

inflammation – hyper responsiveness of airways – exposure to allergen – mast cell degranulation – release histamine, interleukins, prostaglandins, leukortrienes, nitric oxiode  – vasodilation, increased capillary permeability

  also increase in chemotactic factors that draw neutrophils, eosinophils (release toxic chemicals that increase inflammation and tissue damage), and lymphocytes to the area

  bronchiole smooth muscle spasm, vascular congestion, edema, impaired ciliary action (damaged from smoke and air pollution), thickened mucous, increased bronchiole responsiveness and spasms

- attack = cough, wheezing, SOB, signs of previous upper resp. infection like rhinorrhea and low fever (RSV in younger than 2 and rhinovirus in other kids) - expiratory wheeze with high pitch musical sound, prolongation of the expiratory phase of the resp. cycle; hyperinflation may be visible, elevated RR and HR - nasal flaring and accessory muscle use - infants may head bob - pulsus paradoxus may be seen; anxiety, diaphoresis

CM: between attacks there are no symptoms; during attack chests restriction, expiratory wheezing, nonproductive coughing, prolonged expiration, tachycardia and tachypnea

If not treated then bronchiospasm and then statisasthmatica which is life threatening

- unknown cause and most common cause of unexplained infant death in Western countries - sudden death of infant under 1 which remains unexplained after thorough examination, complete autopsy, exam of death scene, and review of clinical hx - low during first month of life but markedly increases in 3-4mo and unusual after 6mo - more in male than female; almost always during nighttime sleep; higher during winter months - Risks: babies who were preterm or LBW, multiple births, siblings prior SIDS victims, - occurs more in low-socioecoonminc groups and large families - maternal risks: smoking, young maternal age (under 20), unmarried mother, less prenatal care, poverty, illicit drug use or binge-drinking - prone positioning, sleeping on soft bedding, overheating; loose bedding and sleeping on top of any soft surface, bed sharing - Etiology unknown p1339 - avoid all controllable risk factors, particularly unsafe sleeping practices and maternal smoking

¾ of deaths have actually no risk factors

Decrease in numbers of SIDS since “back to sleep” campaign

Exclusive Bfing!!!

- alkaline urine increases risk of calcium/phosphate stones - supersaturation of one or more of the salts in urine - precipitation of the salts from liquid to a solid state - growth through crystallization or agglomeration - presence or absence of stone inhibitors that most of us have in our urinary system but if there is problem in inhibitors or alkaline pH overrides those inhibitors than risk for stone formation increases

moderate to severe pain often originating in the flank and radiating to the groin; n&v may occur; hematuria may be present

PAIN, colicky pain (comes and goes)

aka painful bladder syndrome: condition that includes nonbacterial infectious cystitis usually in immunocompromised and noninfectious cystitis associated with pelvic or urogenital cancers(radiation, chemical, autoimmune, hypersensitivity - mostly in women 20-30 with cystitis sx but neg urine cultures - cause unknown, but mast cell activation, altered epithelial permeability, and increased sensory nerve sensitivity noted - antiproliferative factor (APF) is a protein expressed by those with IC, it blocks normal growth of cells that line the inside of the bladder and indirectly increase bladder sensation

PIGN usually involves an immunologic mechanism that activates inflammation with damage to the glomerular basement membrane, capillary endothelium, and mesangium - most often caused by strep infections abrupt and occurs 7-10 days after strep infection of the skin or throat and more common in children - immune mediated with strep antibody-antigen complexes either depositing in the GBM or forming in situ against planted antigens - altered permeability and proliferation

-Immune responses, metabolic disorders, or circulatory problems

-Most due to type II and III hypersensitivity

- Other types of glomerulonephritis: lupus nephritis, IgA, nephropathy, and others

- Chronic: progression leads to renal failure; associated with hypercholesterolemia and proteinuria seen in SLE and DM

disturbances in GBM and podocyte injury lead to increased permeability to protein and loss of electrical negative charge - Figure 36-11 p1385

Severe loss of serum protein

Primary-idiopathic

Secondary- caused by systemic disease, drugs, toxins

- r/t loss of serum proteins and sodium retention - edema (ascites and periorbital edema), hyperlipidemia, lipiduria, vitamin D deficiency, and hypothyroidsim - thromboembolic events may occur in young adults due to hypercoagulability

embryonal tumor of the kidney arising from the epigenetic and genetic changes that lead to abnormal proliferation of renal stem cells (metanephric blastema) - arising from the mesoderm; aka nephroblastoma; most common solid tumor in kids - diagnosed between age 1-5yo, peak age 2-3yo; more common in girls and in blacks - composed of stromal, epithelial, and blastemic cells

- colonization of a pathogen anywhere along the urinary tract - greater in boys up to 1yr, particulary those not circumcised; girls have greater incidence after 1yr with increased incidence in adolescence - perineal bacteria, espec. E.Coli, ascending the urethra

whos at risk: Premature infants, girls, sexually active women, women who are pregnant, estrogen deficient women, use of spermicides, women who used antibiotics recently, persons with indwelling cath, or comorbidity like DM

Most common UTI-bladder infection

nonspecific - infants- nausea, vomiting, diarrhea, jaundice - fever; urinary freq & urgency; enuresis or incontinence; abdominal, flank or back pain; foul urine; sometimes hematuria

- voluntary or involuntary passage of urine by a child who is beyond the age when voluntary bladder control should have been acquired (by age 4yr) - functional incontinence: no cause identified; underlying mechanism may include disorders of both the storage and voiding phase of bladder cycle - boys more often affected 

-familial link noted

- organic: 2-10%; ex: UTI, neuro, congenital, or allergies, increased UO during DM; disease or infection r/t due to increased output or inability of kidney to concentrate urine - MAturational lag: smaller functional bladder capacity - genetic links noted on chrom: 8,12,13, 22 - link between enuresis and sleep-disordered breathing and prolonged non-REM sleep and sleep arousal difficulty - temper tantrums, fear, excitabilty, LBW, minimal brain dysfunction

Infection of lower resp. trac- 6th leading cause of death in US

Mostcommon form is streptococcus pneumonia (have vaccination for)

Caused by bacterial, viral (influenza), fungal, protozoan, or parasites, and atypical forms (more in dorms)

RF for bacterial type: advanced age, immunocompromised, underlying lung disease, smoking, alcoholic

Patho: pathogens inhaled into lung or in oralpharyngeal secretions and aspirated, or in very debilitated pts it can be blood borne

CM: URI, fever, chills, productive, or dry cough, malaise, pleural pain, dyspnea, rust colored sputum or hemoptysis (bacterial), inspiratory crackles, dull percussion, and increased tacho crepitus,

Emphysema