exam 5 2016

CROUP know pathophysiology, etiology, inheritary,prevention clinical manifestations, treatment and complicatoins of croup

*Acute laryngotracheobronchitis* -Common in children from 6 months to 3 years of age -Commonly caused by a virus -Parainfluenza, influenza A, or respiratory syncytial virus (RSV) -Highest incidence in late autumn and winter *Pathophysiology*: Causes subglottic edema *Clinical manifestations* -Usually occurs after an episode of rhinorrhea, sore throat, fever -Seal-like barking cough -Hoarse voice, inspiratory stridor -Self-limiting condition *Westley croup score* -Estimates severity *Treatment* -Most cases No treatment -Glucocorticoids, either injected or oral (dexamethasone) or nebulized (budesonide) -Corticosteroids -Severe cases -Nebulized epinephrine -Oxygen *Spasmodic croup* -Hoarseness, barking cough, and stridor similar to croup -Sudden onset, usually at night and without viral prodrome -Usually in older children -Resolves quickly

PYELONEPHRITIS know patho, etiology, prevention, clinical manifestation, treatment, complication of pyelonephritis

*Acute pyelonephritis* -Acute infection of the ureter, renal pelvis, and/or renal parenchyma *Clinical manifestations* Flank pain Fever, chills Costovertebral tenderness Purulent urine *Evaluation* White blood cell casts, indicating pyelonephritis *Treatment* Antibiotic administration *Chronic pyelonephritis* Persistent or recurrent infection of the kidneys, leading to scarring of the kidneys Inflammation and fibrosis, located in the interstitial spaces between the tubules, leading to chronic kidney failure *Treatment* Antibiotic administration Prolonged antibiotics with recurrent infections

ASTHMA- ADULT-CHILD know asthma in adult in child patho, etiology, prevention, inflammatory mediators, clinical manifestations, treatment (acute and chronic), complication. slide 57ch 35

*Clinical Manifestations* - asymtptomatic between attacks - chest constriction, expiration, wheezing, dyspnea, nonproductive coughing, prolonged expiration, tachycardia, tachypnea - pulsus paradoxus - status asthmaticus -- bronchospasm not reversed by usual measures -- life threatening *ominous signs of impending death* -silent chest (no audible movement of air) and a Pac02 greater than 70

CYSTITIS know patho, etiology, prevention, clinical manifestation, treatment, complication of cystitis

*Cystitis* -Inflammation of the bladder -Acute or chronic *Clinical manifestations* -Asymptomatic -Frequency, dysuria, urgency, and low back and/or --suprapubic pain *Evaluation* Urine culture of specific microorganisms with counts of 10,000/ml or more *Treatment* Antimicrobial therapy *Nonbacterial infectious cystitis,* noninfectious cystitis (radiation, chemical), and interstitial cystitis (autoimmune, hypersensitivity) Symptoms of cystitis for longer than 6 weeks' duration but with negative urine cultures and no other known cause *Treatment* Oral and intravesical therapies, sacral nerve stimulation, onabotulinumtoxinA; surgery

ASTHMA- ADULT-CHILD know asthma in adult in child etiology, slides 49-ch 35

*Etiology* - chronic inflammatory disorder of the bronchial mucosa - causes bronchial hyperresponsiveness, constriction of the airways and variable airflow obstruction that is reversible. - one half of all cases develop during childhood - is a familial disorder over 100 genes have been identified.. - Hygiene hypothesis is suggested.

BRONCHITIS/ACUTE

CHAP 35 SLIDE 92

PULMONARY HYPERTENSION know pulmonary hypertension: pathophysiology, etiology, prevention, clinical manifestations, pressures, treatment and alterations of complications. slides 96-98 ch 35

*Etiology* Mean pulmonary artery pressure above 25 mm Hg at rest Idiopathic, familial, or associated Causes Elevated left ventricular pressure Increased blood flow through the pulmonary circulation Obliteration or obstruction of the vascular bed Active constriction of the vascular bed produced by hypoxia or acidosis *Pathophysiology* Overproduction of vasoconstrictors and decreased production of vasodilators Remodeling Resistance to pulmonary artery blood flow, thus increasing the pressure in the pulmonary arteries Workload of the right ventricle increases and subsequent right ventricular hypertrophy, may be followed by failure and eventually death *Clinical manifestations* Masked by primary pulmonary or cardiovascular disease First indication: Chest radiograph (enlarged pulmonary arteries and right heart border) or an electrocardiogram that shows right ventricular hypertrophy *Treatment* Oxygen, diuretics, anticoagulants Avoidance of contributing factors such as air travel, decongestant medications, nonsteroidal antiinflammatory medications, pregnancy, and tobacco use Prostacyclin analogs (epoprostenol, beraprost, iloprost) Endothelin receptor antagonists (bosentan, ambrisentan) Phosphodiesterase-5 inhibitors Lung transplantation Secondary pulmonary artery hypertension Treat the primary disorder. Once pulmonary hypertension has persisted long enough for hypertrophy to develop, it is no longer reversible. Supplemental oxygen reverses hypoxic vasoconstriction.

BERGER NEPHROPATHY what is the patho, etiology, clinical manifestation, treatment, complication of berger nephropathy

*Immunoglobulin A (IgA) nephropathy (Berger disease): Most common form Binding of abnormal IgA to mesangial cells in the glomerulus, resulting in injury and mesangial proliferation* Pathophysiology Formation of immune complexes (antigen/antibody) in the circulation with subsequent deposition in glomerulus Antibodies produced against the organism that cross-react with the glomerular endothelial cells Activation of complement Recruitment and activation of immune cells and mediators Decreased glomerular filtration rate (GFR) Decreased glomerular perfusion (glomerular blood flow) as a result of inflammation Glomerulosclerosis (scarring) Thickening of the glomerular basement membrane, but increased permeability to proteins and red blood cells *Clinical manifestations* Hematuria with red blood cell casts Smoky, brown-tinged urine Proteinuria exceeding 3 to 5 g/day with albumin Low serum albumin Edema Severe or progressive glomerular disease: Eventual oliguria Oliguria: Urine output <30 ml/hr or <400 ml/day *Clinical manifestations* *Nephrotic Sediment* Contains massive amounts of protein and lipids and either a microscopic amount of blood or no blood. *Clinical manifestations Nephritic Sediment* Blood is present in the urine with red cell casts, white cell casts, and varying degrees of protein, which is not usually severe. *Treatment* Antibiotics Corticosteroids Cytotoxic agents Anticoagulants

KIDNEY HORMONES ANP BNP understand ANP AND BNP hormones

*Natriuretic peptides * --Atrial natriuretic peptide (ANP) is secreted from myocardial cells in the atria. --Brain natriuretic peptide (BNP) is secreted from myocardial cells in the ventricles. *ANP and BNP* --Inhibit sodium and water absorption by kidney tubules. --Inhibit secretion of renin and aldosterone. --Vasodilate the afferent arterioles; constrict the efferent arterioles. --Increase urine formation, leading to decreased blood volume and blood pressure; promote sodium and water loss.

ASTHMA- ADULT-CHILD know asthma in adult in child patho slides 49-ch 35

*Pathophysiology* - episodic attacks of bronchospasms, bronchial inflammation, mucosal edema, and increased mucous production - early asthmatic response --- immunoglobulin E (IgE) causes the mast cells to degranulate, releasing a large number of inflammatory mediators ---- vasodilation ----increased capillary permeability ---- mucosal edema ---- bronchial smooth muscle contractions (spasm) ---- tenacious mucous secretion ----antigen exposure to the bronchial mucosa activates dendritic cells (antigen-presenting cells) to present the antigen to CD4* T cells ---- interleukin 4 (IL-4) stimulates B-cells activation and the production of antigen-specific IgE ----IL-5 stimulates the activation of eosinophils, which contributes to increased bronchial hyperresponsiveness fibroblast proliferation epithelial injury and airway scarring ---- IL-8 activates neutrophils that cause a more exaggerated inflammatory response. ----IL-13 impairs mucociliary clearance, enhances fibroblast secretion and contributes to bronchoconstriction. ----IL-17 increases neutrophilic inflammation ----IL- 22 stimulates airway epithelial cells, causing further innate and adaptive immune responses.

PNEUMOCOCCAL PNEUMONIA

*Pneumococcal pneumonia* -ALI, resulting in inflammatory cytokines and cells, -causes alveolar edema. -Edema creates a medium for the multiplication of -bacteria and aids in the spread of infection into -adjacent portions of the lung. -Involved lobe undergoes consolidation. *Four phases* -Consolidation -Red hepatization -Gray hepatization -Resolution

RESPIRATORY DISTRESS SYNDROME (RDS) NEWBORN know patho, etiology, prevention, clinical manifestation, treatment, complication

*RDS* -Progressive respiratory distress, severe hypoxemia refractory to treatment with supplemental oxygen, decreased pulmonary compliance *Patho* -AKA HMD - Is primarily a disease of preterm infant - immature lung has not yet developed adequate surfactant production and secretion - causes widespread atelectasis and hypoventilation, --- shunting --- hypoxemia --- hypercapnia *clinical manifestation* - tachypnea - grunting -intercostal subcostal retraction - nasal flaring - dusky skin *Treatment* -Oxygen administration with mechanical ventilation and relatively high levels of positive end-expiratory pressure (PEEP) ventilation -Lung protective strategies such as low tidal volumes, PEEP ventilation, prone position - surfactante - inositol administration - glucocorticoid to women in preterm labor.

UTI know patho, etiology, prevention, clinical manifestation, treatment, complication of UTI

*Urinary tract infection (UTI)* -Inflammation of the urinary epithelium after invasion and colonization by some pathogen in the urinary tract -Retrograde movement of bacteria into the urethra and bladder Classification: Location or complicating factors Complicated UTI versus uncomplicated UTI Cystitis: Bladder inflammation Pyelonephritis: Inflammation of upper urinary tract *Most common pathogens* Escherichia coli Staphylococcus saprophyticus Virulence of uropathogens Ability to evade or overwhelm the host defense mechanisms and cause disease in a host Adherence to the uroepithelium Have pili or fimbriae or both Ability to resist the host's defense mechanisms Biofilms *Protective urinary mechanisms* Washed out of the urethra during micturition Low pH and high osmolality of urea Presence of Tamm-Horsfall protein Secretions from the uroepithelium: Bactericidal effect Ureterovesical junction: Closes to prevent reflux of urine to the ureters and kidneys Women: Mucus-secreting glands Men: Length of the male urethra Lewis blood group

PNEUMONIA/VIRAL

*Viral pneumonia* -Is seasonal; usually mild and self-limiting. -Can set the stage for a secondary bacterial infection. -Provides an ideal environment for bacterial growth and -by damaging ciliated epithelial cells, which normally -prevent pathogens from reaching the lower airways. *Most common form: Influenza*

CHRONIC BRONCHITIS Chronic bronchitis, patho, etiology, prevention, clinical manifestation, treatment, complications. chap 35 slide 65-69

*definition*- hypersecretion of mucus and chronic productive cough that lasts at least 3 months of the year and for at least 2 consecutive years. *patho* -- inspired irritants increase mucous production, size and number of mucous glands, and bronchial edema; mucus is thicker than normal --hypertrophied bronchial smooth muscle --hypoxemia and hypercapnia -- airways collapse early in expiration, trapping gas in the lung *clinical manifestation* -- decreased exercise tolerance -- wheezing and shortness of breath -- productive cough become copious -- polycythemia -- decreased FEV1 *treatment* -- smoking cessation -- bronchodilators -- expectorants -- chest physical therapy -- antibiotics -- steroids -- mechanical ventilation prn -- oxygen therapy *teaching* -- nutritional counseling -- respiratory hygiene -- recognition of the early signs of infections -- techniques that relieve dyspnea such as pursed lip breathing.

PULMONARY EDEMA know pulmonary edema patho, etiology, prevention, clinical manifestation, treatment and complications

*patho* -excess water in the lung from disturbances of capillary hydrostatic pressure capillary oncotic pressure or capillary permeability *etiology* - most common cause is left sided heart failure *complication* -postobstructive pulmonary edema: negative pressure pulmonary edema --- is a rare life threatening complication that can occr after relief of upper airway obstruction *clinical manifestation* -dyspnea - orthopnea - hypoxemia - and increased work of breathing *treatment* - increased hydrostatic pressure caused by heart failure --- improve cardiac output and volume status with diuretics,vasodilators and drugs that improve the contraction of the heart muscle - increased capillary permeability resulting from injury --- remove offending agent and supportive therapy to maintain adequate oxygenation, ventilation, and circulation. -POPE ---provide PEEP ventilation - any type of pulmonary edema --- provide supplemental oxygen and or mechanical ventilation.

EMPYEMAS know empyemas: pathophysiology, etiology, prevention, clinical manifestations, treatment, complication

*patho* Infected pleural effusion *etiology* Pus in the pleural space *Clinical manifestations* Cyanosis, fever, tachycardia (rapid heart rate), cough, and pleural pain *Treatment* Administration of antimicrobial medications Drainage of the pleural space with a chest tube Severe cases: Ultrasound-guided pleural drainage, instillation of fibrinolytic agents, or deoxyribonuclease (DNase) injected into the pleural space

ARDS know ARDS pathophysiology, etiology, description, prevention, prevention, clinical manifestations, treatment, complication

*patho/etiology* Acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) Forms of respiratory failure characterized by acute lung inflammation and diffuse alveolocapillary injury Injury to the pulmonary capillary endothelium Increased capillary permeability Inflammation Surfactant inactivation Edema and atelectasis *Clinical manifestations* Dyspnea and hypoxemia with poor response to oxygen supplementation LEADS TO Hyperventilation and respiratory alkalosis LEADS TO Decreased tissue perfusion, metabolic acidosis, and organ dysfunction LEADS TO Increased work of breathing, decreased tidal volume, and hypoventilation LEADS TO Hypercapnia, respiratory acidosis, and worsening hypoxemia LEADS TO Decreased cardiac output, hypotension, death *Treatment* Mechanical ventilation with PEEP and high oxygen concentrations Low-volume ventilation, noninvasive positive pressure ventilation, permissive hypercapnia, prone positioning, extracorporeal gas exchange, and partial liquid ventilation Low-dose steroid administration

PULMONARY FIBROSIS know pulmonary fibrosis: pathophysiology, etiology, prevention, clinical manifestion, treatment, complications

*pathophysiology* Pulmonary fibrosis Excessive amount of fibrous or connective tissue in the lung *etiology* Exposure to toxic gases Ammonia, hydrogen chloride, sulfur dioxide, chlorine, phosgene, and nitrogen dioxide Idiopathic pulmonary fibrosis: No specific cause *Clinical manifestations:& Increasing dyspnea on exertion Burning of the eyes, nose, and throat; coughing; chest tightness; dyspnea; hypoxemia *Treatment:* Corticosteroids; combined treatment with cytotoxic drugs; antifibrotic drugs (such as N-acetylcysteine and pirfenidone), interferon, and anticoagulant agents; lung transplantation Supplemental oxygen, mechanical ventilation with PEEP, and support of the cardiovascular system Steroid administration; effectiveness has not been well documented

ASTHMA- ADULT-CHILD know asthma in adult in child patho, etiology, prevention, inflammatory mediators, clinical manifestations, treatment (acute and chronic), complication. slide 58 ch 35

*treatment* - immediate administration of oxygen and inhaled beta agonist brinciduaktirs - oral corticosteroids administration early in the course of management -careful monitoring of gas exchange and airway obstruction in response to therapy -antibiotics are not indicated for acute asthma unless a bacterial infection is documented -education over allergens and irritants and peak flow meters. -*pharmacological* -mildest form is short acting beta agonist inhalers used intermittently - Persistent asthma: anti inflammatory medications and inhaled corticosteroids the mainstay of therapy -no adequately controlled on inhaled corticosteroids: leukotriene antagonists. - severe asthma: long acting beta agonists can actually worsen asthma in some individuals -reduction of asthma exacerbations: immunotherapy - monoclononal antibodies to IgE

AGING AND PULMONARY SYSTEM What happens in the pulmonary system with aging slide 48 ch 34

- loss of elastic recoil - stiffening of the chest wall - alterations in gas exchange - increases in flow resistance - alveoli tend to lose alveolar wall tissue and capillaries - decrease in respiratory muscle strength and endurance

NASAL CONGESTION understand the danger of nasal congestion in infants

--Airways are smaller in diameter and increase in size -throughout childhood. --Infants up to 2 to 3 months of age are "obligatory nose breathers." --Lower airways and lung parenchyma ----Infants and young children continue to form new alveoli for several years after birth. --Airways are narrower than those of adults, thus making them more prone to obstruction.

GOODPASTURE SYNDROME know patho, etiology, prevention, clinical manifestation, treatment, complication of goodpasture syndrome

-Goodpasture syndrome is a pulmonary-renal syndrome, which is a group of acute illnesses involving the kidneys and lungs. Goodpasture syndrome includes all of the following conditions: -glomerulonephritis—inflammation of the glomeruli, which are tiny clusters of looping blood vessels in the kidneys that help filter wastes and extra water from the blood -the presence of anti-glomerular basement membrane (GBM) antibodies; the GBM is part of the glomeruli and is composed of collagen and other proteins -bleeding in the lungs -In Goodpasture syndrome, immune cells produce antibodies against a specific region of collagen. The antibodies attack the collagen in the lungs and kidneys. *fatal unless treated quickly* *Clinical manifestations* - fatigue, - nausea, - vomiting, - weakness, -foamy urine -hypertension *treatment* -immunosuppressive medications, such as cyclophosphamide, to keep the immune system from making antibodies -corticosteroid medications to suppress the body's autoimmune response -plasmapheresis *prevention* -Eating, diet, and nutrition have not been shown to play a role in causing or preventing Goodpasture syndrome.

CYSTIC FIBROSIS know pathophysiology, etiology, inheritary pattern prevention clinical manifestations, treatment and complicatoins of cystic fibrosis.

-Is an autosomal recessive multisystem disease. -Abnormal secretions cause obstructive problems within the respiratory, digestive, and reproductive tracts. -Chloride transport is a fundamental abnormality. -Respiratory failure is almost always the cause of death. -Typical features: Mucus plugging, chronic inflammation, and infection of the small airways -Exocrine or mucus-producing glands secrete -abnormally thick mucus as a result of defective -epithelial ion transport. -In the lungs, thick secretions obstruct the bronchioles -and predispose the lungs to chronic infections. -Chronic inflammation leads to hyperplasia of goblet -cells, bronchiectasis, pneumonia, hypoxia, and fibrosis, among other conditions -Mucus plugging: Is a combination of increased -production of mucus, altered physicochemical -properties of mucus, and reduced mucociliary -clearance. -Mucus becomes even more viscous because of -deoxyribonucleic acid (DNA) and filamentous (F) actin -released from the high number of degraded -neutrophils present in the airways of a child with cystic -fibrosis. -Abnormal cytokines promote inflammation. *Clinical manifestations* -Persistent cough or wheeze, sputum production, --recurrent or severe pneumonia, and clubbing *Evaluation* -Immunoreactive trypsinogen (IRT) blood test -Sweat test -Universal newborn screening in the United States *Treatment* -Chest physical therapy and related equipment, such as the high-frequency chest wall oscillation vest -Assortment of handheld positive-expiratory pressure (PEP) devices -Aerosol therapy: Antibiotics, bronchodilators, and nebulized deoxyribonuclease -Inhaled hypertonic saline -Azithromycin, ibuprofen, and corticosteroids -IV administration of antibiotics -Nutritional support --Meticulous monitoring of growth parameters --Controlling fat malabsorption --Ensuring adequate caloric intake --Keeping overall health stable --Including exogenous pancreatic enzymes with meals and snacks --Providing supplemental fat-soluble vitamins

PNEUMONIA CHILDREN

-infection and inflammation in the terminal airways and alveoli - community acquired pneumonia (CAP) is one of the most common global infections in the pediatric age group and the leading cause of morbidity and mortality in infants. *BACTERIAL* -streptococcal and staphylococcal microorganisms are the two most common causes of infection. -*clinical manifestations* -increased temperature - increased absolute neutrophil -increased bands -preceding viral illness, followed by fever, chills, rigor, SOB, and increasingly productive cough all higher than found in viral pneumonia. -usually begins with one's own nasopharyngeal bacteria into the trachea *VIRAL* - two to three times more likely in children than in adults - MCC is RSV - acquired by direct contact, aerosol, or droplet. - destruction of ciliated epithelium of the distal airway and sloughing of cellular material. *TREATMENT* -outpatient -02 - hydration -nutrition - supportive pulmonary therapy -if pneumococcal tx with vaccine antigens, antibiotic combinations, and immunoadjuvant tx. *PREVENTION* -influenza vaccine - pneumococcal vaccine *ATYPICAL PNEUMONIA* - mycoplasma, pneumoniae, chlamydophila pneumoniae - most common cause of CAP of children 5 and older and young adults *PATHO* -local sloughing of cells - peribronchial lymphocytic infiltration develops along with neutrophil recruitment to the airway lumen

ASTHMA a child has asthma which pathophysiologic process occurs in this disease.

Chronic inflammatory disorder causing mucosal edema and reversible airflow obstruction. asthma is a chronic inflammatory disorder of the bronchial mucosa that causes bronchial hyperresponsiveness, constric tion of the airways and variable airflow obstruction that is reversible episodic attacks of bronchospasm bronchial inflammation mucosal edema and increased mucus production occur in asthma.

KIDNEY HORMONES ADH understand ADH

ADH Controls the concentration of final urine. Increases water permeability in the last segment of the distal tubule and along the entire length of the collecting ducts. In the presence of ADH, water reabsorption is high, causing less urine volume.

ACINUS what is the acinus chap 34 slide 6-9

AKA: Acinus Includes the: Respiratory bronchioles Alveolar ducts Alveoli : primary gas exchange units. Alveoli: primary gas exchange units, O2 enters the blood and CO2 is removed. Pores of Kohn: allow air movement between alveoli epithelial cells: Alveolar type I: structure Alveolar type II: produce surfactant prevent lung collapse contain alveolar macrophages ingest foreign material and remove it through the lymphatic system.

COPD

Airflow limitation that is not fully reversible Usually progressive and associated with an abnormal inflammatory response of the lung to noxious particles or gases Third leading cause of death in the United States and the sixth leading cause of death worldwide COPD: Chronic bronchitis plus emphysema

COPD

Airway obstruction is worse with expiration. More force or more time is required to expirea given volume of air; emptying the lungs is slowed. Unifying signs and symptoms Wheezing and dyspnea. *Clinical manifestations* Increased work of breathing, ventilation-perfusion mismatching, decreased forced expiratory volume in one second (FEV1). Asthma Chronic bronchitis Emphysema Chronic bronchitis plus emphysema equals chronic obstructive pulmonary disease (COPD)

ACINUS QUESTION A nurse recalls that the acinus contains 1. cliliated cells 2. goblet cells 3. alveolar ducts 4. striated muscles.

ANSWER/RATIONALE CHAP 34 3. alveolar ducts slide 9

VENTILATION QUESTION J-receptors are: 1. sensitive to noxious aerosois 2. located in the smooth muscle of airways 3. stimulted by incrases in volume 4. sensitive to alterations in the pulmnary capilary pressure.

ANSWER/RATIONALE CHAP 34 SLIDE 25 4. sensitive to alterations in the pulmonary capillary pressure.

ACUTE TUBULAR NECROSIS-ETIOLOGY what is the patho, etiology, clinical manifestation, treatment, complication of acute tubular necrosis

ATN is generally caused by an acute event, either ischemic or toxic. *Causes of ischemic acute tubular necrosis* -Ischemic ATN may be considered part of the spectrum of prerenal azotemia, and indeed, ischemic ATN and prerenal azotemia have the same causes and risk factors. Specifically, these include the following: *Hypovolemic states:* hemorrhage, volume depletion from gastrointestinal (GI) or renal losses, burns, fluid sequestration *Low cardiac output states*: heart failure and other diseases of myocardium, valvulopathy, arrhythmia, pericardial diseases, tamponade *Systemic vasodilation*: sepsis, anaphylaxis Disseminated intravascular coagulation *Renal vasoconstriction*: cyclosporine, amphotericin B, norepinephrine, epinephrine, hypercalcemia Impaired renal autoregulatory responses: cyclooxygenase (COX) inhibitors, angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs) *Causes of nephrotoxic acute tubular necrosis* The kidney is a particularly vulnerable target for toxins, both exogenous and endogenous. Not only does it have a rich blood supply, receiving 25% of cardiac output, but it also helps in the excretion of these toxins by glomerular filtration and tubular secretion. *Exogenous nephrotoxins that cause ATN include the following:* *Aminoglycoside*-related toxicity occurs in 10-30% of patients receiving aminoglycosides, even when blood levels are in apparently therapeutic ranges (risk factors for ATN include preexisting liver disease, preexisting renal disease, concomitant use of other nephrotoxins [eg, amphotericin B, radiocontrast media, cisplatin], advanced age, shock, female sex, and a higher aminoglycoside level 1 hour after dose; a high trough level has not been shown to be an independent risk factor) *Amphotericin B* nephrotoxicity risk factors include male sex, maximum daily dose (nephrotoxicity is more likely to occur if >3 g is administered) and duration of therapy, hospitalization in the critical care unit at the initiation of therapy, and concomitant use of *cyclosporine* *Radiographic contrast media* can cause contrast-induced nephropathy (CIN) or radiocontrast nephropathy (RCN) (commonly occurs in patients with several risk factors, such as elevated baseline serum creatinine, preexisting renal insufficiency, underlying diabetic nephropathy, congestive heart failure [CHF], or high or repetitive doses of contrast media, as well as volume depletion and concomitant use of diuretics, ACE inhibitors, or ARBs). The 2011 UKRA guidelines recommend that patients at risk of CIN should have a careful evaluation of volume status and receive volume expansion with 0.9% sodium chloride or isotonic sodium bicarbonate before the procedure. [3] *OTHER* Cyclosporine and tacrolimus (calcineurin inhibitors) Cisplatin Ifosfamide Foscarnet Pentamidine, which is used to treat Pneumocystis jiroveci infection in individuals who are immunocompromised (risk factors for nephrotoxicity include volume depletion and concomitant use of other nephrotoxic antibiotic agents, such as aminoglycosides, which is common practice in the immunosuppressed) Sulfa drugs Acyclovir and indinavir Mammalian target of rapamycin (mTOR) inhibitors (eg, everolimus, temsirolimus) [4]

EMPHYSEMA

Abnormal permanent enlargement of thegas-exchange airways accompanied by the destruction of the alveolar walls without obvious fibrosis Loss of elastic recoil *Primary emphysema* Inherited deficiency of the enzyme α1-antitrypsin *Secondary emphysema* Cigarette smoke: Main cause Air pollution, occupational exposures, and childhood respiratory infections: Possible contributors *Centriacinar(Centrilobular) * Septal destruction occurs in the respiratory bronchioles and alveolar ducts, usually in the upper lobes. Alveolar sac (alveoli distal to the respiratory bronchiole) remains intact. *Tends to occur in smokers with chronic bronchitis.* *Panacinar (Panlobular)* Involves the entire acinus. Damage is more randomly distributed. Involves lower lobesof the lung. *Pathophysiology* Destruction of the alveoli occurs through the breakdown of elastin in the septa as a result of an imbalance between proteases and antiproteases, oxidative stress, and apoptosis of the lung's structural cells. Alveolar destruction also produces large air spaces within the lung parenchyma (bullae) and air spaces adjacent to pleurae (blebs). *Clinical manifestations* Dyspnea on exertion Later progresses to marked dyspnea, even at rest Little coughing and very little sputum Thin Tachypnea with prolonged expiration; use of accessory muscles for ventilation; pursed lips Increased anteroposterior diameter of the chest (barrel chest) To increase lung capacity: Leans forward with arms extended and braced on knees when sitting *Treatment* Oxygen; may require noninvasive positive pressure ventilation or mechanical ventilation Inhaled bronchodilators by either an inhaler or a nebulizer Immediate administration of oral corticosteroids and antibiotics Inhaled anticholinergic agents and beta agonists Inhaled corticosteroids can be added Smoking cessation Pulmonary rehabilitation Improved nutrition Breathing techniqueP

ACUTE TUBULAR NECROSIS what is the patho, etiology, clinical manifestation, treatment, complication of acute tubular necrosis

Acute tubular necrosis (ATN) is the most common cause of acute kidney injury (AKI) in the renal category (that is, AKI in which the pathology lies within the kidney itself). ATN follows a well-defined three-part sequence of initiation, maintenance, and recovery (see Pathophysiology). The initiation phase is characterized by an acute decrease in glomerular filtration rate (GFR) to very low levels, with a sudden increase in serum creatinine and blood urea nitrogen (BUN) concentrations. The maintenance phase is characterized by a sustained severe reduction in GFR that persists for a variable length of time, most commonly 1-2 weeks. Because the filtration rate is so low during the maintenance phase, the creatinine and BUN levels continue to rise. The recovery phase, in which tubular function is restored, is characterized by an increase in urine volume (if oliguria was present during the maintenance phase) and by a gradual decrease in BUN and serum creatinine to their preinjury levels. The tubule cell damage and cell death that characterize ATN usually result from an acute ischemic or toxic event. Nephrotoxic mechanisms of ATN include direct drug toxicity, intrarenal vasoconstriction, and intratubular obstruction (see Pathophysiology and Etiology). Most of the pathophysiologic features of ischemic ATN are shared by the nephrotoxic forms.[1]

TREATMENT HYPERKALEMIA how does insulin and glucose treat hyperkalemia

Administer glucose and insulin or sodium bicarbonate to drive potassium into the cells.

RENAL CALCULI=KIDNEY STONE know renal calculi (all types) patho, etiology, prevention, clinical manifestation, treatment, complication

Are also called renal calculi or urolithiasis. Masses of crystals, protein, or mineral salts form in the urinary tract and may obstruct the urinary tract. *Risk factors* -Male -Most develop before 50 years of age -Inadequate fluid intake: Most prevalent -Geographic location -Temperature, humidity, rain fall, fluid, and dietary -patterns *Composition of mineral salts* -Calcium oxalate and calcium phosphate: 70% to 80% -Struvite (magnesium, ammonium, phosphate): 15% -Uric acid: 7% -Genetic disorders of amino acid metabolism -Excess urine can cause cystinuria, or xanthine, stone -formation in the presence of a low urine pH. *Staghorn calculi* -Are large and fill the minor and major calyces -Kidney stone formation -Supersaturation of one or more salts -Presence of a salt in a higher concentration than the -volume is able to dissolve the salt -Precipitation of a salt from a liquid to a solid state -Temperature and pH -Growth into a stone via crystallization or aggregation -Process by which crystals grow from a small nidus or -nucleus to larger stones -Embedded in matrix -Presence or absence of stone inhibitors -Alkaline urinary pH: Increases the risk of calcium *phosphate stone formation.* -Acidic urine: Increases the risk of a uric acid stone. -Potassium citrate, pyrophosphate, and magnesium: --Prevent stone formation. *Clinical manifestation* -Renal colic (pain) *Treatment* -Parenteral and/or oral analgesics for pain -Medical therapy that promotes stone passage (alpha--antagonists or calcium channel blockers) -High fluid intake -Alteration in urine pH -Removal of stones using percutaneous -nephrolithotomy, ureteroscopy, or ultrasonic or laser -lithotripsy to fragment stones for excretion

ASPIRATION what is the most likely site of aspiration in the pulmonary system.

Aspiration Passage of fluid and solid particles into the lungs Right lower lobe: Is the most frequent site.

ASTHMA ADULT CHILD PATHO Chap 35 fig 35-10

Bronchial asthma thick mucus, mucosal edema and smooth muscle spasm cause obstruction of small airways. breathing becomes labored and expiration becomes difficult.

PNEUMONIA QUESTION a person has pneumococcal pneumonia which pathophysiologic process has occurred. 1. progressive airflow limitation is associated with an abnormal inflammatory response and is not fully reversible. 2. continue bronchial inflammation causes bronchial edema and increases the size and number of mucous glands and goblet cells 3. abnormal permanent enlargement of the acini is accompanied by the destruction of alveolar walls without obvious fibrosis 4. inflammatory cytokines cause alveolar edema which creates a medium for microorganisms that leads to consolidation.

Chapter 35 slide 84 answer rationale 4.

KIDNEY HORMONE C-TYPE NATRIURETIC HORMONE Understand C-type natriuretic hormone

C-type natriuretic peptide Is secreted from vascular endothelium and in the nephron. Causes vasodilation.

BREATHING MECHANICS CHAP 34

CHAP 34 Major accessory muscle slide 29 alveolar surface tension slike 32 elastic properties of lung and chest slide 32-33 airway resistance slide 34 work of breathing slide 35

CHEST WALL/PLEURA

CHAP 34 chest wall slide 17 pleura slide 18-19

GAS TRANSPORT

CHAP 34 four steps slide 38 effective gas exchange slide 39 distriution of vent/perf slide 39 diffusion across alveo/membrane slide 40 oxy/hem association dissociation slide 41-42

PULMONARY/BRONCHIAL CIRCULATION

CHAP 34 pulmonary circulation functions slides 10-15

VENTILATION NEUROCHEMICAL CONTROL

CHAP 34 respiratory center slides 22-23 lung receptors 24-28

PULMONARY FUNCTION TEST

CHAP 34 spirometry slide 46 diffusion capacity slide 46 residual volume slide 46 functional reserve capacity slide 47 total lung capacity slide 47 ABG slide 47 Chest x-ray slide 47

STRUCTURES OF THE PULMONARY SYSTEM CHAP 34

CHAP 34 structures slides 3-8

FUNCTIONS OF PULMONARY SYSTEM CHAP 34 definition slide 20

CHAP 34 ventilation slide 21

CARBON DIOXIDE TRANSPORT

CHAP 34 SLIDE 45

LUNG CANCER

CHAP 35 laryngeal slide 102 lung cancer slide bronchogenic carcinoma slide 103 non small cell slide 104 neuroendocrine slide 105 other cancer slide 106-107 patho/clinical/class/tx slides 108-109

PULMONARY VASCULAR DISEASE

CHAP 35 pulmonary embolism slides 91-94 pulmonary artery hypertension slides 95-98 cor pulmonale slides 100-101

PNEUMONIA know viral and bacterial pneumonia in adults. Infection of the lower respiratory tract

CHAP 35 SLIDES 77-84 *Responsible for more disease and death than any other infection* *TYPES* -Community-acquired pneumonia ----Streptococcus pneumoniae -Health care-associated pneumonia -Hospital-acquired (nosocomial) pneumonia -Ventilator-associated pneumonia *Routes of infection* Aspiration Inhalation Endotracheal tubes and suctioning Respiratory defenses cannot destroy the microorganism *Clinical manifestations* -Preceded by an upper respiratory infection -Cough, dyspnea, and fever -Chills, malaise, and pleuritic chest pain *Treatment* -Prevention -Prevention of aspiration -Respiratory isolation of immunocompromised -individuals -Vaccination for appropriate populations -Reduction of ventilator-associated pulmonary -infections through a variety of dental and endotracheal -tube interventions -Establishment of adequate ventilation and oxygenation -May require mechanical ventilation -Adequate hydration -Good pulmonary hygiene (e.g., deep breathing, -coughing, chest physical therapy) -Bacterial pneumonia: Antibiotics -Viral pneumonia: Supportive therapy alone, unless -secondary bacterial infection is present -Severe cases: Antiviral medications and/or antifungal, --multiple drugs

ABSCESS FORMATION/CAVITATION

CHAP 35 SLIDES 88-89

TRACHEOMALCIA/TRACHEOBRONCHOMALACIA CHAP 36

CHAP 36 TRACHEOMALACIA SLIDE 33

VOCAL CORD PARALYSIS CHAP 36

CHAP 36 vocal cord paralysis- slide 35

ANGIOEDEMA CHAP 36

CHAP 36 angioedema- slide 30

ASPIRATION OF FOREIGN BODIES CHILDREN CHAP 36

CHAP 36 aspiration of foriegn body- slide 29

CONGENITAL MALFORMATIONS AIRWAY CHAP 36

CHAP 36 coanal atresia slide 36 laryngeal atresias and webs slide 36 tracheal stenosis slide 36

INFECTION UPPER AIRWAY CHILDREN CHAP 36

CHAP 36 croup- slides 17-20 question slide 21 acute epiglottities- slide 22 tonsillar infections - slide 23-25 bacterial tracheitis- slide 26-27 retropharyngeal abcess- slide 28

LARYNGOMALACIA CHAP 36

CHAP 36 laryngomalacia slides-31-32

OBSTRUCTIVE SLEEP APNEA CHAP 36

CHAP 36 obstructive sleep apnea - slide 37

UPPER AIRWAY DISORDERS CHILDREN CHAP 36

CHAP 36 signs of ARF- slide 11 upper airway obstruction-slide 12 breathing sounds - slide 13-15

SUBGLOTTIC STENOSIS CHAP 36

CHAP 36 subglottic stenosis - slide 35

PULMONARY/CHILDREN/STRUCTURE/FUNCTION

CHAP 36 upper airway slide 2 lower airways slide 2 surfactant slides 4-5 chest wall dynamics slide 6 metabolic characteristics slide 6 immunologic incompetence slide 8 physiologic control of breathing slide 9

OBSTRUCTIVE PULMONARY DISEASES Definition: slide 47

CHAPTER 35 Asthma slides 49-60 chronic bronchitis slides 65-69 emphysema slides 70-76 COPD slides 61-64

CONDITIONS CAUSED BY PULMONARY DX OR INJURY

CHAPTER 35 SLIDES 11-14

S/S PULMONARY DISEASE

CHAPTER 35 SLIDES 2-10

CO2 TRANSPORT QUESTIONS how is carbon dioxide carried in the blood

Carbon dioxide - transported from the body cells back to the lungs as: 1 - bicarbonate (HCO3) - 60% formed when CO2 (released by cells making ATP) combines with H2O (due to the enzyme in red blood cells called carbonic anhydrase) as shown in the diagram below 2 - carbaminohemoglobin - 30% formed when CO2 combines with hemoglobin (hemoglobin molecules that have given up their oxygen) 3 - dissolved in the plasma - 10%

PULMONARY CIRCULATION CONTROL definition chap 34 slide 16

Chap 34 slide 16

RESTRICTIVE LUNG DISORDERS

Chapter 35 aspiration slide 24 atelectasis slide 25-26 bronchiectasis slide 27-28 bronchiolitis slide 29 bronchiolitis obliterans slide 30 pulmonary fibrosis slide 31-32 oxygen toxicity slide 33 pneumoconiosis slide 34-35 allergic alveolitis slide 37 systemic disorders slide 38 pulmonary edema slide 39-41 acute lung injury (ARDS/ALL) slides 42-46

ROLE OF SURFACTANT ADULT chap 34 pg 1229

Contributes to to control of lung inflammation and innate and adaptive immunity. alveoli contain cellular components of inflammation and immunity particularly the mononuclear phagocytes the mononuclear phagocytes of the lungs are called alveolar macrophages these cells ingest foreign material that reaches the alveoli and prepare it for removal through the lymphatics.

NEPHROTIC SYNDROME know patho, etiology, clinical manifestation, treatment, complication of nephritic syndrome

Group of symptoms characterized by proteinuria, hypoalbuminemia, hyperlipidemia, and edema -Minimal change nephropathy (MCN) -Fusion of epithelial cell podocyte foot processes -Focal segmental glomerulosclerosis (FSGS) -Effacement (thinning or deletion) of epithelial -podocytes, with a significant increase in pore size -Primary (idiopathic) versus secondary -Congenital, or infantile, nephrotic syndrome (Finnish type) Is caused by an autosomal recessive mutation of the NPHS1 gene that encodes an immunoglobulin-like protein, nephrin, at the podocyte slit membrane. *Lack of nephrin:* - Proteinuria -Is expressed within the first 3 to 12 months of life. -Infants do not respond to steroidal treatment *Clinical manifestations* -Edema -Develops from hypoalbuminemia (decreased plasma oncotic pressure) and sodium retention. -Also develops from increased activity of aldosterone and ADH (vasopressin). -Is caused by a decrease in atrial natriuretic peptide. *First clinical manifestation:* -Periorbital edema -During the day, the edema shifts to the abdomen and -lower extremities. -Hyperlipidemia -In inverse proportion to the decrease in plasma -proteins -High concentrations of triglycerides, low-density -lipoprotein (LDL), and very low-density lipoprotein -(VLDL) cholesterol -Decreased high-density lipoprotein (HDL) cholesterol -Hypercoagulation -Risk for arterial or venous thrombosis -Results from abnormalities in the coagulation -pathways -Diminished, frothy, or foamy urine output -Diarrhea, anorexia, and poor absorption *Treatment* -Reduce the excretion of protein, and maintain a --protein-free urine. -Prevent or treat infection. -Administer glucocorticosteroids (prednisone). -Maintain a low-sodium, well-balanced diet. -Provide skin care. -If edema becomes problematic: Administer diuretic -agents (furosemide, metolazone). -Administer angiotensin-converting enzyme (ACE) -inhibitors. -Administer non-corticosteroidal immunosuppressive agents.

RENAL BLOOD FLOW NEUROREGULATION how does exercise and body position affect renal blood flow.

Exercise and change of body position Activate renal sympathetic neurons, causes mild vasoconstriction.

EXUDATIVE EFFUSION QUESTION what is exudative

Exudative effusion Is less watery and contains high concentrations of white blood cells and plasma proteins. "PUS"

KIDNEY FUNCTION what is the best indicator of kidney function

GFR: Is the best estimate for the functioning of renal tissue Uses inulin. Creatinine: Provides a good estimate of GFR; only one blood sample is required in addition to a 24-hour volume of urine.

GAS EXCHANGE what is gas exchange

Delivery of oxygen to the cells of the body and the removal of CO2 Four steps 1. Ventilation of the lungs 2. Diffusion of oxygen from the alveoli into the capillary blood 3. Perfusion of systemic capillaries with oxygenated blood 4. Diffusion of oxygen from systemic capillaries into the cells --Diffusion of CO2 occurs in the reverse order. Effective gas exchange: Needs approximately even distribution of gas (ventilation) and blood (perfusion) in all portions of the lungs. Distribution of ventilation and perfusion Gravity and alveolar pressure Ventilation and perfusion depend on body position. If a standing individual assumes a supine or side-lying position, the areas of the lungs that are then most dependent become the best ventilated and perfused. *Ventilation-perfusion ratio* Perfusion exceeds ventilation in the bases of the lungs. Ventilation exceeds perfusion in the apices of the lungs Diffusion across alveolocapillary membrane Ideal medium for oxygen diffusion Large total surface area Very thin Partial pressure of oxygen molecules (Po2) is much greater in alveolar gas than it is in capillary blood: Promotes rapid diffusion from the alveolus into the capillary Determinants of arterial oxygenation

ANEMIA/RENAL FAILURE know patho, etiology, clinical manifestation, treatment, complication of anemia in renal failure

Erythropoietin Is produced in the adult kidney; is essential for erythropoiesis. Chronic renal failure: Causes anemia from reduced erythropoietin secretion.

KIDNEY HORMONES ERYTHROPOIETIN understand erythropoietin role in the kidney.

Erythropoietin Is produced in the adult kidney; is essential for erythropoiesis. Chronic renal failure: Causes anemia from reduced erythropoietin secretion.

HEMOLYTIC UREMIC SYNDROME what is the patho, etiology, clinical manifestation, treatment, complication of HUS

Hemolytic-uremic syndrome (HUS) Is the most common cause of acute renal failure in children; most occur in those younger than 4 years of age. -Is associated with bacterial and viral agents. -Escherichia coli O157:H7 -Bacterial toxin from E. coli damages red cells and -endothelial cells. -Arterioles of the glomerulus become swollen and -occluded with fibrin clots. -Causes a decreased glomerular filtration rate with -hematuria and proteinuria. -Swollen vessels damage red cells as they pass. -Spleen removes the damaged red cells from the -circulation, causing acute hemolytic anemia. -Microcirculation develops numerous thrombi. *Clinical manifestations* -Are preceded by a prodromal gastrointestinal illness -with diarrhea. -Sudden onset of pallor, bruising or purpura, irritability, -and oliguria; can lead to renal failure. *Treatment* -Maintain nutrition and hydration (to dilute toxins). -Control hypertension, hyperkalemia, and seizures. -When renal failure occurs: Treat with dialysis. -Blood transfusions with packed red blood cells are -needed to maintain reasonable hemoglobin levels. -Most children recover.

LEFT SHIFT CAUSE what condition will cause a shift to the left in the oxyhemoglobin dissociation curve?

High pH and hypocapnia. The curve is shifted to the left by alkalosis (high pH) and hypocapnia (decreased PaC02). A shift to the left depicts hemoglobins increased affinity for oxygen which promotes association in the lungs and inhibits dissociation in the tissues

RAAS what is the RAAS system

Hormones Renin-angiotensin-aldosterone system (RAAS) -Increases systemic arterial pressure, and increases sodium reabsorption. *Renin:* - Enzyme is formed and stored in afferent arterioles of the juxtaglomerular apparatus. -Renin helps form angiotensin I (physiologically inactive). -In the presence of angiotensin-converting enzyme (ACE), angiotensin I is converted to angiotensin II. *Angiotensin II * -Stimulates the secretion of aldosterone by the adrenal cortex. -Is a potent vasoconstrictor. -Stimulates antidiuretic hormone (ADH) secretion and thirst.

O2 TRANSPORT IN BLOOD how is oxygen carried in the blood

How are oxygen & carbon dioxide transported in the blood? Oxygen is carried in blood: 1 - bound to hemoglobin (98.5% of all oxygen in the blood) 2 - dissolved in the plasma (1.5%) Because almost all oxygen in the blood is transported by hemoglobin, the relationship between the concentration (partial pressure) of oxygen and hemoglobin saturation (the % of hemoglobin molecules carrying oxygen) is an important one. Hemoglobin saturation: extent to which the hemoglobin in blood is combined with O2 depends on PO2 of the blood: The relationship between oxygen levels and hemoglobin saturation is indicated by the oxygen-hemoglobin dissociation (saturation) curve (in the graph above). You can see that at high partial pressures of O2 (above about 40 mm Hg), hemoglobin saturation remains rather high (typically about 75 - 80%). This rather flat section of the oxygen-hemoglobin dissociation curve is called the 'plateau.' Recall that 40 mm Hg is the typical partial pressure of oxygen in the cells of the body. Examination of the oxygen-hemoglobin dissociation curve reveals that, under resting conditions, only about 20 - 25% of hemoglobin molecules give up oxygen in the systemic capillaries. This is significant (in other words, the 'plateau' is significant) because it means that you have a substantial reserve of oxygen. In other words, if you become more active, & your cells need more oxygen, the blood (hemoglobin molecules) has lots of oxygen to provide When you do become more active, partial pressures of oxygen in your (active) cells may drop well below 40 mm Hg. A look at the oxygen-hemoglobin dissociation curve reveals that as oxygen levels decline, hemoglobin saturation also declines - and declines precipitously. This means that the blood (hemoglobin) 'unloads' lots of oxygen to active cells - cells that, of course, need more oxygen.

TUBERCULOSIS what is the patho etiology prevention clinical manifestations treatment complications of TB

Infection caused by Mycobacterium tuberculosis, an acid-fast bacillus Leading cause of death from a curable infectious disease throughout the world *Pathophysiology* -Airborne droplet transmission -Tubercle formation: Granulomatous lesion -Caseous necrosis: Cheeselike material -May remain dormant for life or cause active disease -Isolation of bacilli by enclosing them in tubercles and --surrounding the tubercles with scar tissue *Clinical manifestations* -Latent tuberculosis infection: Asymptomatic -Fatigue, weight loss, lethargy, anorexia (loss of appetite), a low-grade fever that usually occurs in the afternoon, and night sweats; purulent cough *Diagnosis* -Positive tuberculin skin test (TST) a purified protein -derivative (PPD): Does not differentiate past, latent, or -active disease -Sputum culture, immunoassays -Chest radiographs *Treatment* -Isoniazid, rifampin, pyrazinamide, and ethambutol -Drug-resistant bacilli: Combination of at least four drugs to which the microorganism is susceptible, administering for 18 months -Review drug effectiveness at 6 months.

SQUAMOUS CANCER CELL LUNG what is the patho etiology prevention clinical manifestations treatment complications of squamous cell cancer of the lung.

Is also known as bronchogenic carcinomas. *Is the most frequent cause of cancer death in the United States*. -Most common cause: Cigarette smoking -Smoking is related to cancers of the larynx, oral cavity, esophagus, and urinary bladder. -Genetic, environmental, or occupational risk factors are also associated with lung cancer *Non-small-cell lung cancer* Approximately 85% of all lung cancers Squamous cell carcinoma clinical manifestations -Nonproductive cough or hemoptysis *Adenocarcinoma* -Tumor arising from glands -Asymptomatic or pleuritic chest pain and shortness of breath *Treatment* -Surgical resection Large cell carcinoma (undifferentiated) *Treatment* -Surgical therapy limited to palliative procedures -Radiation and chemotherapy not helpful *Neuroendocrine* -Approximately 14% of all lung cancers *Small cell carcinoma: Most common* -Worst prognosis -Limited versus extensive disease -First manifestations: Paraneoplastic syndrome -Large cell neuroendocrine carcinoma: Typical carcinoid -tumors -Atypical carcinoid tumors

WILMS TUMOR what is wilms tumor patho, etiology, clinical manifestation, treatment, complication

Is an embryonal tumor of the kidney. Most common between birth and 5 years of age Is also called nephroblastoma. -Arises from the proliferation of abnormal renal stem cells (metanephric blastema). -Is the most common solid tumor of childhood. -Is composed of three cellular components -Stromal, epithelial, blastemic -Inherited and sporadic forms -Is staged I through V -Two-hit" hypothesis --Children who inherit a mutation in one allele of a -tumor-suppression gene require just one more somatic --mutation for a tumor to form. --Wilms tumor-suppressor genes WT1 andWT 2 are -located on chromosome 11. *Clinical manifestations* --Enlarging asymptomatic upper abdominal mass in a -healthy, thriving child --Vague abdominal pain, hematuria, fever, and hypertension *Treatment* --Surgical exploration and resection Chemotherapy, followed by surgical resection *Bilateral disease* --Heminephrectomy of the less involved kidney and nephrectomy of the other --Radiation therapy: Most effective if begun 1 to 3 days after surgery for stages III and IV disease and *metastases* Chemotherapy: -Specific to histologic structure and stage of disease

ASTHMA- ADULT-CHILD know asthma in adult in child patho LATE chap 35 slide 54-55

Late asthmatic response - begins 4-8 hours after the early response -chemotatdctic recruitment of lymhocytes, eosinophils, and neutrophils occurs. -- jprologed smooth muscle contraction -- airway scarring -- increased bronchial hyperresponsiveness -- impaired mucociliary function with accumulation of mucous and cellur debris forming plugs in the airways -- leads to airway7 remodeling if left untreated. -- air trapping --hyperinflation distal to obstructions -- increased work of breathing -- hypoxemia

OXYHEMOGLOBIN ASSOCIATION what is oxyhemoglobin association and dissociation

Oxyhemoglobin association and dissociation Hemoglobin molecules bind with oxygen: Oxyhemoglobin. When hemoglobin saturation and desaturation are plotted on a graph, the result is a distinctive S-shaped curve known as the *oxyhemoglobin dissociation curve.* *Shift to the right* depicts the hemoglobin's decreased affinity for oxygen or an increase in the ease with which oxyhemoglobin dissociates and oxygen moves into the cells. Acidosis (low pH) and hypercapnia and hyperthermia *Shift to the left* depicts the hemoglobin's increased affinity for oxygen, which promotes association in the lungs and inhibits dissociation in the tissues. Alkalosis (high pH) and hypocapnia and hypothermia *Bohr effect: * Shift in the oxyhemoglobin dissociation curve caused by changes in CO2 and H+ concentration in the blood.

KIDNEY what is the anatomy of the kidney how much cardiac output does it get.

Paired organs located in the posterior region of the abdominal cavity behind the peritoneum (retroperitoneal) *Renal capsule* Tightly adhering capsule surrounds each kidney; each kidney then is embedded in a mass of fat. *Renal fascia* Fibrous tissue attaches each kidney to the posterior abdominal wall. *Hilum* Is where the renal blood vessels, nerves, lymphatic vessels, and ureter enter and exit the kidneys. *Renal cortex* Is the outer layer of each kidney. Contains all of the glomeruli, most of the proximal tubules, and some segments of the distal tubule. Renal medulla Is the inner part of each kidney that contains tubules and the collecting duct. Consists of regions called the pyramids. *Renal columns* Extend from the cortex down between the renal pyramids. *Minor calyx* Apexes of the pyramids project into a cup-shaped cavity that join together to form a major calyx. Receives urine from the collecting ducts through the renal papilla. *Major calyx* Joins to form the renal pelvis. *Renal pelvis* Joins the proximal end of the ureter Each kidney contains 1.2 million nephrons. Is the functional unit of the kidney. Superficial cortical nephrons: Make up 85% of all nephrons, which extend partially into the medulla. *Midcortical nephrons* Have short or long loops. *Juxtamedullary nephrons:* Lie close to and extend deep into the medulla and are important for the process of concentrating urine; secrete renin. Kidneys receive 1000 to 1200 ml/min of blood. 600 to 700 ml as plasma (renal plasma flow [RPF])

PLEURAL EFFUSIONS what is the patho etiology prevention clinical manifestations treatment complication of pleural effusions.

Pleural effusion Presence of fluid in the pleural space Transudative effusion Is watery and diffuses out of the capillaries. Exudative effusion Is less watery and contains high concentrations of white blood cells and plasma proteins. Chylothorax: Chyle exudate Hemothorax: Blood exudate *Clinical manifestations:* Dyspnea and pleural pain *Treatment:* Thoracentesis, chest tube, and surgery

POSTSTREPTOCOCCAL GLOMERULONEPHRITIS what is the patho, etiology, clinical manifestation, treatment, complication of poststreptococcal glomerulonephritis in children

Poststreptococcal glomerulonephritis (PSGN) Occurs after a throat or skin infection with certain strains of group A α-hemolytic streptococci. Antigen-antibody complexes and complement are deposited in the glomerulus. Immune complexes initiate inflammation and glomerular injury. Mainly occurs in children, 5 to 15 years of age. *Clinical manifestations* Sudden onset of hematuria, edema, hypertension *Treatment* Restrict fluid, sodium, potassium intakes Administer an antihypertensive medication and diuretic agents

KIDNEYS PROTIEN understand protein metabolism in the kidney.

Protein The kidneys uses urea a metabolite from proteins to concentrate urine.

PULMONARY COMPLIANCE understand pulmonary compliance in adults, children/infants and alterations of compliance

Pulmonary compliance is: Measures lung and chest wall distensibility. -Represents the relative ease with which these structures can be stretched -Reciprocal of elasticity ---Low: Increased work of inspiration Stiff lungs ---High: Increased work of expiration ---Easy to inflate; has lost some elastic recoil -Compliance is high in infants, particularly premature infants. -*ARDS* Progressive respiratory distress, severe hypoxemia refractory to treatment with supplemental oxygen, decreased pulmonary compliance

PURULENT what does purulent mean

Purulent effusion 1. pertaining to or consisting of pus. 2. containing pus.

RESPIRATION CONTROL QUESTION what part of the brain controls respiration

Respiratory center Is located in the brainstem. --Dorsal respiratory group: Sets the basic automatic rhythm. --Receives impulses from peripheral chemoreceptors in the carotid and aortic bodies: Detects the Paco2 and the amount of oxygen in the arterial blood. ---Ventral respiratory group: Contains inspiratory and expiratory neurons. ---Becomes active when increased ventilatory effort is required. ---Pneumotaxic and apneustic centers: Are located in the pons. ---Modifiers of the inspiratory depth and rate are established by the medullary centers.

SPECIFIC GRAVITY what is specific gravity

Specific gravity Estimated measure of the solute concentration of urine Normal value: 1.016 to 1.022

VENTILATION MEASUREMENT how is the patient's alveolar ventilation measured. slides 46-47 ch 34

Spirometry-measures volume and flow rate during forced expiration diffusion capacity- measures the gas diffusion rate at the alveolocapillary membrane residual volume function reserve capacity total lung capacity *arterial blood gas analysis- determines pH and oxygen and CO2 concentrations* Chest radiograph-evaluates air trapping, consolidation, cavity formulation or presence of tumors.

ACUTE RENAL FAILURE know patho, etiology, clinical manifestation, treatment, complication of Acute renal failure

Sudden decline in kidney function with a decrease in glomerular filtration and accumulation of nitrogenous waste products in the blood -Increase in serum creatinine and blood urea nitrogen *Oliguria processes* -Less than 400 ml of urine output per day -Alterations in renal blood flow -Efferent arteriolar vasoconstriction -Impaired autoregulation -Tubular obstruction -Necrosis of the tubules causes sloughing of cells, cast formation, or ischemic edema, which results in obstruction. -Backleak Glomerular filtration remains normal, but tubular reabsorption or a "leak" of filtrate is accelerated from permeability. *Prevention* Maintenance of fluid volume before and after surgery or diagnostic procedures or when nephrotoxic drugs or contrast agents are used. *Treatment* -Correct fluid and electrolyte disturbances. -Manage blood pressure. -Prevent and treat infections. -Maintain nutrition. -Remember certain drugs can be toxic. -Hyperkalemia -Restrict dietary sources of potassium. -Use non-potassium-sparing diuretic agents, or use -cation-ion exchange resins. -Administer glucose and insulin or sodium bicarbonate -to drive potassium into the cells. -Administer calcium. -May need dialysis. -Azotemia -Adopt a low-protein, high-carbohydrate diet. -Recovery May take up to a year. *Classification* RIFLE: Risk; Injury; Failure; Loss; End-stage disease Criteria to guide the diagnosis of renal injury

BLADDER FULLNESS How much urine in the bladder causes a person to feel fullness.

The adult human bladder has a maximum capacity of about 500 ml (1 pint) but the average full bladder sensation peeks when the urine levels reach about 350 mL (three quarters of a pint). The bladder fullness sensation becomes intense as the bladder fills to capacity.

TRANSUDATIVE what is transudative

Transudative effusion Is watery and diffuses out of the capillaries.

ALVEOLAR CELL TYPE II What is an alveolar cell type II ch 34 pg 1229

Type II alveolar cells secrete surfactant a lipoprotein that coats the inner surface of the alveolus and facilitates its expansion during inspiration lowers alveolar surface tension at end expiration and thereby prevents lung collapse. Surfactant also contributes to control of lung inflammation and innate and adaptive immunity.

FETAL KIDNEY DEVELOPMENT know kidney formation and urine production in the fetus

The kidneys are formed by three separate, but interrelated, structures: the ureteric bud, the metanephric blastema and the cloaca. By 20 weeks of pregnancy, the excretory system is already completely formed, including the ureter, renal pelvis, calyxes, and papillary and collecting ducts. However, by this time, when the collecting system has finished its formation, only a third of the total number of nephrons is present; nephrogenesis continues until 36 weeks of gestation.[1] Fetal urine contributes to the quantity and quality of the amniotic fluid depending on the gestational time. At the beginning of pregnancy, the amniotic liquid is a transudate of maternal plasma, and as the fetus grows, the amniotic liquid becomes similar to the fetal plasma, which is thought to be due to diffusion through the fetal skin. Production of fetal urine begins after the ninth week of pregnancy, and the kidneys are capable of excreting sodium and concentrating urea between 12 and 14 weeks of gestation. After 18 weeks, and especially after 20 or 22 weeks, all the amniotic liquid is constituted by fetal urine.

ACUTE TUBULAR NECROSIS TREATMENT what is the treatment of acute tubular necrosis

The main goal of treatment of acute tubular necrosis (ATN) is to prevent further injury to the kidney. Extracellular fluid (ECF) volume should be assessed promptly, either on clinical grounds or by invasive means (Swan-Ganz catheter), and repletion of any deficit should be initiated promptly. The 2011 UKRA guidelines recommend optimizing hemodynamic status by appropriate fluid therapy, giving vasopressors and/or inotropes and treating any underlying sepsis.[3] All possible nephrotoxic drugs should be stopped. In addition, doses of all medications that are eliminated by the kidney should be adjusted. Medications have only an ancillary role in the treatment of acute tubular necrosis (ATN). Antioxidants and diuretics may be helpful in specific circumstances. Therapeutic mainstays are prevention, avoidance of further kidney damage, treatment of underlying conditions, and aggressive treatment of complications. Any complications that develop must be aggressively treated.

RENAL OBSTRUCTION QUESTION why does unilateral renal obstruction predispose patients to HTN

The reduced perfusion of the affected kidney activates the renin-angiotensin-aldosterone system, which causes constriction of peripheral arterioles.

KIDNEY HORMONE URODILATIN understand urodilatin

Urodilatin Is secreted by distal convoluted tubules and the collecting ducts. Causes vasodilation, natriuretic, and diuretic effects

BLADDER CANCER what is the patho, etiology, clinical manifestation, treatment, complication of bladder cancer

Urothelial (transitional cell) carcinoma: Most common *Risk factors* -Smoking -Exposure to metabolites of aniline dyes or other --aromatic amines or chemicals -High arsenic in drinking water -Heavy consumption of phenacetin -Oncogenes of the ras gene family and tumor--suppressor genes including TP53 mutations -Inactivation of retinoblastoma gene (pRb) -Loss of heterozygosity at Chromosome 9 *Clinical manifestation* -Painless microscopic hematuria *Treatment* -Transurethral resection or laser ablation, combined -with intravesical chemotherapy or immunotherapy -Radical cystectomy with urinary diversion -Adjuvant chemotherapy -Radiation therapy

VESICOURETERAL REFLUX know patho, etiology, clinical manifestation, treatment, complication of vesicoureteral reflux

Vesicoureteral reflux is the abnormal flow of urine from your bladder back up the tubes (ureters) that connect your kidneys to your bladder. Normally, urine flows only down from your kidneys to your bladder. Vesicoureteral reflux is usually diagnosed in infants and children. The disorder increases the risk of urinary tract infections, which, if left untreated, can lead to kidney damage. Vesicoureteral reflux can be primary or secondary. Children with primary vesicoureteral reflux are born with a defect in the valve that normally prevents urine from flowing backward from the bladder into the ureters. Secondary vesicoureteral reflux is due to a urinary tract malfunction, often caused by infection. Children may outgrow primary vesicoureteral reflux. Treatment, which includes medication or surgery, aims at preventing kidney damage.

KIDNEY HORMONES VIT D understand vit D role in the kidney

Vitamin D Calcitriol (1,25-dihydroxyvitamin D3 or vitamin D3) Is necessary for the absorption of calcium and phosphate by the small intestine. Can be obtained in the diet or synthesized by action of ultraviolet radiation on cholesterol in the skin. Decreased phosphate levels stimulate calcitriol

GLUCOSURIA know BG level necessary to cause glucosuria

When the blood glucose level exceeds about 160 - 180 mg/dl, the proximal tubule becomes overwhelmed and begins to excrete glucose in the urine.This point is called the renal threshold of glucose (RTG).[3] Some people, especially children and pregnant women, may have a low RTG (less than ~7 mmol/L[3] glucose in blood to have glucosuria). If the RTG is so low that even normal blood glucose levels produce the condition, it is referred to as renal glycosuria. Glucose in urine can be identified by Benedict's qualitative test.

ASTHMA A child has asthma which pathophysiologic process occurs in this disease? 1. acute injury to alveolocapillary membrane, producing severe pulmonary edema and shunting 2. chronic inflammatory disorder causing mucosal edema and reversible airflow obstruction 3. airway obstruction increasing resistance to airflow and decreasing flow rates especially inspiratory flow 4. IL-17 impairs mucociliary clearance and contributes to bronchoconstriction.

answer rationale chap 35 2. slide 60

PNEUMOCONIOSIS QUESTION a person has pneumoconiosis which information would the nurse find in the hx. 1. inhaled inorganic dust particles resulting in a change in the lungs 2. fractured ribs causing paradoxical movement of the chest with breathing 3. ruptured visceral pleura which allows air or gas into the pleural space 4. bronchial inflammation with persistent abnormal dilation of the bronchi.

answer/rational chapter 35 1. inhaled inorganic dust particles resulting in a change in the lungs slide 36

PULMONARY DISEASE/INJURY The most common cause of hypoxemia is 1. reduced diffusion distance 2. hyperventilation with hypocapnia 3. ventilation perfusion mismatch 4. traveling to a low altitude

answer/rationale 3. V/Q mismatch chaper 35 SEE SLIDE 14

BLUNTED VENTILATORY RESPONSE QUESTION A newborn has a blunted ventilatory response to hypoxia. what process causes this to occur 1. increased responsiveness in the respiratory center in the cerebral cortex 2. reduced activity of the peripheral chemorecetptors 3. cell mediated immunity not fully developed 4. nonadaptive responses from inspiratory intercostal muscles.

answer/rationale CHAP 36 2. Reduced activity of the peripheral chemoreceptors slide 10

CROUP QUESTION A child has laryngottacheobronchitis. which information should the nurse remembert when planning care of rthis child? 1. is usually caused by parainfluenza 2. usually occurs in the spring and fall 3. produces supraglottic edema and airway obstruction 4. requires antibiotic therapy

answer/rationale CHAP 36 SLIDE 21 1. is usually caused by parainfluenza.

OBSTRUCTIVE SLEEP APNEA QUESTION OSA, is most commonly associated with. 1. seal like barking cough 2. epiglottis folding inward, covering the glottis 3. adenotonsillar hypertrophy 4. allergy

answer/rationale CHAP 36 SLIDE 38 3. adenotonsillar hypertrophy

BREATHING MECHANICS QUESTION Which statement indicates the nurse has a correct understanding of surfactant 1. found in the bronchi 2. is produced by type 1 alveolar cells 3. reduces surface tension 4. promotes phagocytosis.

answer/rationale 3. reduces surface tension slide 36

HYPOXEMIA what are the causes of hypoxemia

hypoxemia is a reduced Pa02 caused by: 1. decreased oxygen content of inspired gas 2. hypoventilation 3. diffusion abnormality 4. ventilation perfusion mismatch 5. shunting

PNEUMOCOCCAL PNEUMONIA QUESTION a person has pneumococcal pneumonia, which pathophysiological process has occurred.

inflammatory cytokines cause alveolar edema which creates a medium for microorganisms that leads to consolidation. in pneumococcal pneumonia inflammatory cytokines and cells are released that cause alveolar edema. edema creates a medium for the multiplication of bacteria and aids in the spread of infection into adjacent portions of the lung the involved lobe undergoes consolidation.

PNEUMOCONIOSIS what information would the nurse find in the hx of a person with pneumoconiosis

inhaled inorganic dust particles resulting in a change in the lungs. pneumoconiosis represents any change in the lung caused by inhalation of inorganic dust particles which usually occurs in the workplace. pneumoconiosis is caused by long term inhalation of dust particles dust particles that produce this disorder include coal asbestos silica talc fiberglass and mica.

PLEURAL ABNORMALITIES.

pneumothorax chapter 35 slides 17-20 pleural effusion chapter 35 slides 21 empyema chapter 35 slide 22

BLUNTED VENTILATORY RESPONSE a newborn has a blunted ventilatory response to hypoxia what process has caused this to occur.

reduced activity of the peripheral chemoreceptors. for up to 3 wks of age the newborn has a blunted ventilatory response to hypoxia compared with older children and adults. the mechanisms for this are not well understood but may reflect reduced activity of the peripheral chemoreceptors (in the carotid body) and nonadaptive responses in the respiratory center ( in the brainstem)

EMBOLISM ASSESSMENT QUESTION a person has an embolism what will the nurse find upon assessment

sudden pleuritic chest pain, dyspnea, unexplained anxiety, an individual with pulmonary embolism usually presents with the sudden onset of pleuritic chest pain, dyspnea tachypnea, tachycardia, and unexplained chest pain.

ALVEOLAR CELL TYPE I what is an alveolar cell type I ch 34 pg 1229

the primary gas exchange units of the lung where oxygen enters the blood and CO2 is removed. thiny passages called pores of Kohn permit some air to pass through the septa from alveolus to alveolus promoting collateral ventilation and even distribution of air among the alveoli. the lungs contain approximately 50 million alveoli at birth and 480 million in adulthood., Type I cells provide structure.

J-RECEPTORS What are J-receptors (juxtapulmonary)

they are sensitive to increased pulmonary capillary pressure

HYPOXEMIA MCC what is the most common cause of hyoxemia

ventilation perfusion mismatch an abnormal ventilation perfusion ratio is the most common cause of hypoxemia. hypoxemia can be be caused by inadequate ventilation of well perfused areas of the lung low v/q, by poor perfusion of well ventilated portions of the lung high v/q resulting in wasted ventilation

ROLE OF SURFACTANT INFANT what is the role of surfactant in infants. chap 35 pg 1292

without surfactant the alveoli tend to stay closed demanding greater inspiratory force and work of breathing to re expand on the next breath deficiency of surfactant is often seen in premature infants and causes respiratory distress syndrome also known as hyaline membrane disease. surfactant is produced by 20-24 wks of gestation

COPD ACUTE EXACERBATION QUESTION discuss how cigarette smoking causes/exacerbates pulmonary disease processes.

• irritating effect of the smoke causes hyperplasia of cells, including goblet cells, which subsequently results in increased production of mucus. • Hyperplasia reduces airway diameter and increases the difficulty in clearing secretions. • Smoking reduces the ciliary activity and may cause actual loss of cilia. • Produces abnormal dilation of the distal air space with destruction of alveolar walls. • Many cells develop large, atypical nuclei, which are considered a precancerous condition. • Early stage changes are mostly inflammatory with mucosal edema and an influx of inflammatory cells. • Later stage changes involve thickening of the airway wall from a remodeling process related to tissue repair and the inability of cilia to clear mucus, thus resulting in accumulation of inflammatory exudates in the airway lumen.