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65 Cards in this Set
- Front
- Back
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Upper resp system includes |
Mouth/nose all the way to trachea |
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Lower resp system includes |
bronchi to alveoli |
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What is Surfactant |
coating on inside layer of alveoli that reduces surface tension and keeps them from collapsing |
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Visveral pleura of lungs is the.... |
inner lung membrane |
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Parietal pleura of the lungs is the... |
outer lung membrane attached to thoracic cavity |
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What happens during inhalation? |
diaphram contracts and descends allowing are to flow in |
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What happens during exhalation? |
Diaphragm rises allowing air to expel from lungs -abs and intercostal muscles help when forced |
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Residual volume |
volume of air remaining in the lungs after max exhalation - allows for continued perfusion of alveoli |
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Vital capacity |
max amount of air that can be moved in and out of lungs |
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Deadspace of respiratory system |
where no gas exchange takes place ex) bronchi, bronchioles, collapsed alveoli |
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What happens to vital capacity if residual volume increases? |
it decreases and accessory muscles may need to be used |
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What parts of brain control ventilation and what is it stimulated by? |
-Pons and Medulla -stimulated by central and peripheral receptors |
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The medulla controls what 3 things in ventilation and stimulates which 2 nerves |
-Rhythm, rate, depth -stimulates phrenic nerves of diphragm and nerves of external intercostal muscles |
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What 3 things can alter the medulla? |
1. CNS depression from meds 2. Hypothalamus stimulation from emotions 3. Hering-Breuer reflex - stretch receptors in lungs that ensure we don't over inflate lungs |
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What are the 3 chemoreceptors? |
CO2, H+ and O2 |
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Primary central chemoreceptors (location and sensitivity) |
-located in medulla -sensitive to elevated H+ (aka low pH aka acidosis) and elevated CO2 |
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Hypercapnia |
Elevated amounts of CO2 in blood common in those with lung dz -this may cause primary central chemoreceptors to "burn out" and cause "secondary peripheral chemoreceptors to take over so don't overoxiginate these patients b/c this can cause respiratory drive to shut off |
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Secondary peripheral chemorecptors (location and stimulation) |
-carotid arteries and aortic body -stimulated by decreased O2 concentration in blood (aka hypoxia) -O2 levels must be VERY low for activation |
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The 4 upper resp disorders |
1. Sinusitis 2. larygotracheobronchitis (croup) 3. Epilottitis 4. Influenza |
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Sinusitis (type, patho, s/sx) |
Type: upper resp disorder Patho: bacterial infection secondary to cold/allergy that impedes sinus draining S/sx: congestion, HA |
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Laryngotracheobronchitis aka Croup (type, patho, s/sx) |
Type: upper resp disorder Patho: viral infection in children 1-2 years old caused by the parainfluenza or adeno virus S/sx: barking cough and inspiratory stridor that gets worse at night or in response to stressor |
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Epiglottitis (type, patho, diagnosis, s/sx, tx) |
Type: upper resp disorder Patho: acute infection by ingluenza B virus in kids ages 3-7 years old with swelling of larynx/epilgottis Diagnosis: round red ball on lateral neck on x-ray S/sx: drooling, dysphagia, jaw forward Tx: O2, antibiotics, possible intubation, DON'T put foreign objects in mouth |
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Influenza (type, patho, s/sx, tx) |
Type: upper resp disorder Patho: viral chest infection S/sx: sudden high fever, body aches, can lead to pneumonia --> leading cause of death from flu Tx: vaccination, antivirals
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The 3 lower resp disorders |
1. Bronchiolitis 2. pneumonia 3. SARS |
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Bronchiolitis (type, patho, transmission, predisposing factors) |
Type: lower resp disorder Patho: caused by RSV in kids 2-12 months Transmission: oral droplets Predisposing factors: winter, 2nd hand smoke |
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Pneumococcal pneumonia aka Lobar (type, patho, s/sx) |
Type: lower resp disorder Patho: strep virus in one lobe causing inflammation and congestion in alveolar wall causing RBC's and WBCS to from mass - interferes with gas exchange S/sx: Rusty colored sputum, fever, chills |
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Severe Acute Resp syndrome aka SARS (type, transmission, incubation, s/sx, mortality) |
Type: lower resp disorder Transmission: fecal-oral Incubation: 2-7 days S/sx: flu like then later dry cough and dyspnea Mortality: 10%, 50% in those over 60 |
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Tuberculosis (patho and primary infection) |
Patho: AFB invades lung tissue Primary : non-contagious time when organism gets englufed by macrophages and there is some inflammation of upper lung lobes ->some of theses bacilli reach lymph nodes causing a type IV delayed hypersensitivity response (TB skin test would recognize) and local infection gets walled off and creates "Ghon Complexes" |
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Tuberculosis (secondary, etiology) |
Secondary: "active infection" causing orgnaism to multiply and cuase necrosis, cavitation and hemoptysis, GI can then become infected due to swallowing Etiology: close quarters, immunocompromised, immigrants, recent travelers |
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Tuberculosis (diagnosis, tx) |
Diagnosis: TB skin test (mantoux) if +, then CXR/culture taken Tx: INH for up to 12 months - compliance very important or else MDR-TB (superbug) can occur |
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Cystic Fibrosis (patho, diagnosis, tx) |
Patho: autosomal recessive disorder in kids where gene defect of chloride ion cell causes exocrine glands to make too thick of secretions leading to obstructions in lungs and pancreas Diagnosis: sweat analysis, stool will have high fat and trypsin Tx: pancreatic enzyme replacement, bile salts, humidifiers, good diet |
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First sign of Cystic Fibrosis in newborn |
Meconium ileus |
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Aspiration (location and effects) |
Right bronchus is most common destination -can cause pneumonia, ARDS, abscess, systemic effects from substance being absorbed into bloodstream |
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Asthma (patho, 2 types, leads to) |
Patho: airway obstruction (5-17 years old) - chronic is a type of COPD Extrinsic: type 1 sensitivity (allergy) in response to inhaled allergen (alleviates after adolesence) Intrinsic: adult onset due to hyper-responseive tissues in airway that can be triggered by stress Can lead to: hypoxia (resp/metabolic acidosis), hypoxemia = vasoconstrict of pulmonary vessels = increased RV afterload = Cor Pulmonale , status asthmatics, thickening membrane, chronic asthma |
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COPD (Patho, 2 types) |
Patho: Emphysema and chronic bronchitis are characterized by tissue degeneration and airway obstruction that is partially irreversible |
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Emphysema aka Pink Puffers (type, patho, etiology) |
Type: COPD Patho: destroyed alveolar walls lead to permanently inflated alveolar airsacs called blebs/bullae that increase deadspace, ruptures of blebs can cause a pheumothorax/hypercapnia = loss of CO2 central resp drive = peripheral resep drive to take over so don't overoxigenate Etiology: smoking decreasing alpha antitrypsin |
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Chronic Bronchitis aka Blue Bloaters (type, patho, s/sx) |
Type: COPD Patho: remodeling in bronchi from constant irritation from smoking/air pollutants S/sx: contant productive cough with thick secretions, cyanosis |
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Pulmonary Edema (patho, etiology, s/sx, tx) |
Patho: collection of fluid in alveoli and intestinal area of lung reducing O2 diffusion into blood Etiology: low plasma proteins due to renal/liver dz, HTN, LV heart failure S/sx: orthopnea, hemoptysis, drowning feeling, rales Tx: O2, elevate HOB, diuretics |
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Pulmonary embolus (patho, 2 types, sizes) |
Patho: blood clot obstructing pulmonary artery typically from DVTs (due to immobility, trauma, surgery, birth) Types: fat = from large bone break, air = from IV or central line Size determines s/sx and damage Small- CP, cough Large- increased SNS Massive- Bad CP, LV heart failure, JVD, shock |
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Atelectasis (patho, etiology, nurse) |
Patho: partial lung collapse = decreased gas exchange in alveoli = necrosis Etiology: obstruction, tumor, pulmonary edema, post-op due to patient failing to take deep breaths because of pain Nurse: elevated HOB, encourage patient to take deep breaths and cough |
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Flail Chest (patho, risk, s/sx) |
Patho: fractures of 3-5 ribs Risk: two places possibly leading to atelectasis S/sx: paradoxical movement, tracheal deviation to affected side |
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ARDS |
Patho: ICP = pulmonary edema, decreased O2 diffusion Etiology: shock, sepsis, inhaled toxins, pnuemonia, lung trauma S/sx: confusion, accessory muscle use, rales, cyanosis, resp acidois leading to resp failure |
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Steathorrhea |
Foul smelling, greasy, fat stools that float |
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Malena |
red tarry stool |
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Occult vs Frank |
-hidden blood in stool -seen blood in stool |
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Risks of Diarrhea |
-Dehydration leading to: Hypovolemia --> ischemia --> anaerobic metabolism --> lactic acidosis Loss of HCO3 from GI leading to further metabolic acidosis |
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Large vs. Small volume Diarrhea |
Large: watery, infection, rapid transit small: containing blood or mucus |
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ELectrolyte imbalances |
Na+: lost by vomiting and diarrhea Cl-: lost by vomiting K+: lost in diarrhea |
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Acid-base imbalance due to Vomiting |
intitally causes alkalosis but then causes dehydration and therefore acidosis |
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Gastritis Acute vs. Chronic |
Acute:inflamed edematous mucosa ulcerated or bleeding due to infection, ASA, ibuprophen, allergy, alcohol, toxin, chemo Chronic: atrophy of mucosa with loss of secretory glands leading to achlorhydria leading to b-12 deficiency (aka pernicious anemia) due to peptic ulcers, alcohol abuse, autoimmune disorder, elderly or spicy food |
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Peptic ulcer dz (patho, etiology, who, s/sx) |
patho: acidic stomach juices creating cavities typically seen in proximal duodenum that can eventually lead to peritonitis Etiology: H-pylori, inadequate blood supply, ASA,, ibuprogen, alcohol, stress, glucocorticoids Who: men, western countries, type O blood S/sx: 2-3 hrs after meal at night, relieved by eating/antacids, melena (black tarry stools) |
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Dumping syndrome (etiology, s/sx) |
Etiology: loss of pyloric sphincter in surgery causing quick dumping of food from stomach into intestine S/sx: N/D, abd distention, hypovolemia, hypoglycemia 2-3 hrs after meal |
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The 3 Types of Gallbladder Disorders |
1. Cholelithiasis - gallstones 2. Cholangitis - inflammation of gallbladder and cyctic duct 3. Choledocholithiasis - obstruction of biliary tract by gallstones |
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Choleyst aka Gallbladder disorders |
Patho: can be caused by E. coli S/sx: after fatty meal, pain in RUQ, rt shoulder/back Can lead to: Pancreatitis caused by an obstruction at the sphincter of Oddi |
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Biliary Colic |
spasm from when stone is actually obstructing bile flow |
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2 Types of Stones |
1. Cholesterol stones - seen in obese women due to high estrogen 2. Chile stones - due to anemia, alcohol cirrhosis, biliary infection |
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Hepatitis (Patho, etiology) |
Patho: virus (HPB) targets hepatocytes causing inflammation/necrosis cells then regenerate but don't function correctly Etiology: fatty liver, infection, toxin (acetaminphen, inhalants, ETOH) |
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Chronic hepatitis (time and 3 stages) |
Lasting longer than 6 months Stage 1: Pre-icteric = fatigue, malaise, RUQ pain Stage 2: icteric = janudice, clay stools, dark urine Stage 3: post-icteric/recovery = development of Liver failure or reduction of symptoms |
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Acute Pancreatitis (patho, s/sx, complications) |
Patho: premature activaction of proenzyme trypiogen into trypsin that activate Amylase (12-24 hrs) and lipase (~1 week) causes autodigestion of pancreatic tissue S/sx: inflammation, bleeding, necrosis, abd pain going into back (worse when laying on back), abd distension, lack of bowel sounds Complications: shock, hemorrhage |
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Appendicitis |
Etiology: obstruction due to infection causing fluid backup inside order resulting in inflammation and necrosis (10% of population, young adults) S/sx: RLQ pain and rebound tenderness Complications: if rupture occurs then peritonitis can happen |
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Mechanical vs Functional Intestinal Obstruction (etiology, s/sx) |
Mechanical: tumor, mass, adhesions, Hirschsprug's dz (aka Megacolon), IBD -s/sx: colicky pain, borborygmi (bad growling) Functional: neurological impairment due to surgery, spinal injury, ischemia, pancreatitis, hypokalemia, toxemia -s/sx: absent bowel sounds, steady pain
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General s/sx of Intestinal Obstructions |
Hypovolemia, shock, peritonitis, electrolyte imbalances , third spacing |
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Peritonitis |
Patho: inflammation of peritoneal membrane due to trauma, chemical, bacterial invasion Can lead to: PID in women which is a chronic STI in uterus and fallopian tubes
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The 2 types of Chronic Inflammatory bowel dz |
1. Crohn's Dz - onset during adolescence characterized by skip lesions in deistal ileium and soft/semi formed stools 2. Ulcerative colitis - onset during young adult years characterized by inflammation of mucosa at base of crypts of lieberkuhn and diarrhea |
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Diverticulosis |
Herniation in sigmoid colon with pain in LLQ |
