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process by which a cell takes material into the cell by infolding of the cell membrane
a process by which the contents of a cell vacuole are released to the exterior through fusion of the vacuole membrane with the cell membrane.
Hypoxic Injury
rise in the need for glucose in the cells to maintain ATP production due to a lack of O2 damaging the cell membrane -ischemia is the most common cause
hypoxia etiology
-loss of hemoglobin (carries O2) -decreased O2 in the air (altitude) -Decreased oxygen delivery due to low cardiac output (circulation) -poisoning of cytochromes (cyanide poisoning)
Hypoxia manifestations
-increasing membrane permeability because the Na/K pump is not maintained (lack of ATP) -cell death due to the influx of calcium causing membrane potentials to not be maintained -water follows Na+, so if Na is stuck in the cell, water will follow and the cell will swell and lyse
Reperfusion injury
More damage than hypoxic injury due to the production of reactive O2 species that bind with nucleic acids, proteins, and membrane lipids -causes myocytes to become necrotic, so the goal is to restore blood flow, but fresh blood pushes the reactive O2 species through the heart causing irritation of the myocardium (irritation usually manifests as V.tach or V.fib)
Reactive Oxygen Species
oxygen free radicals, hydrogen peroxide, superoxide, and hydroxyl radicals
Reactive Oxygen etiology
-inflammatory cells -hypoxia -oxygen toxicity -reperfusion -exogenous oxidants (environmental pollutants, cigarette smoke, chemotherapeutic agents, hyperoxia, radiation exposure)
Reactive oxygen mechanism of injury
bind with nucleic acids, proteins, and membrane lipids that can cause mitochondrial injury
antioxidant therapies
vitamin E, mannitol, surfactant, methylene blue, beta keratin, etc gather reactive oxygen species from the body and eliminate them
produce endocrine/exo toxins that can damage cell tissue and activate the arachidonic acid cascade
produced by gram negative cells upon death (liposaccharide A)
require a permissive host, can be RNA or DNA, have an envelope or not
Direct Chemical injury
injures by breaking down the cell wall (ex. heavy metals like mercury, lead, iron)
Indirect chemical injury
injury caused by a metabolite
Blunt force injury
initial trauma causes swelling and increased intracranial pressure but secondary inflammation causes the primary damage 48-72 hours later
Temperature Extremes
Cells die due to hypothermia, vasoconstriction causes perfusion injury and ischemia
decrease in size and function of a cell (most common in brain, heart, skeletal muscle, and secondary sex organs) due to reduced functional demand, inadequate O2 supply, insufficient nutrients, persistent cell injury, and/or aging
An increase in the cell size accompanied by augmented functional capacity (physiologic or increased functional demand) can be adaptive (athletes) or maladaptive (left ventricle increase during heart failure)
increase in the number of cells in an organ or tissue due to increased functional demand (BPH), perisistent cell injury atypical form can be precancerous
increase in the conversion of one differentiated cell type to another (ex. smoking can turn columnar epithelial cells in lungs to squamous epithelial cells)
Alteration in the size, shape, and organization of the cellular components of a tissue strong indicator of cancer most often seen in lungs and cervix
Hydropic Swelling etiology
chemical, biotoxins, ischemia, physical injury
hydropic swelling mechanism
injurious agents cause swelling by increasing the permeability of the plasma membrane to sodium, exceeding the capacity of the pump, damaging the sodium pump directly interfering with the synthesis of ATP organelles become swollen and decrease function which decreases the output of ATP from mitochondria due to swelling
-irreversible injury (cells swell and die) -the sum of cellular changes after local death -necrosis appears the same no matter how the cell has been killed -usually related to the loss of plasma membrane
programmed cell death
normal pH
80-100 mmHg
35-45 mmHg
22-26 mEq/L
O2 sats
metabolic acidosis
pH less than 7.35 HCO3 less than 22
metabolic acidosis etiology
increased production of metabolic acids, decreased acid secretion by kidney, excessive loss of bicarbonate
metabolic acidosis manifestations
(neuro) weakness, lethargy, confusion, coma (cardiovascular) cardiac arrhythmias, decreased HR (gastrointestinal) anorexia, nausea and vomiting, abdominal pain
metabolic alkalosis
pH greater than 7.45 HCO3 greater than 26
metabolic alkalosis etiology
loss of hydrogen ions (vomiting, removal of gastric secretion, hyperaldosteronism) and increased retention of bicarbonate
metabolic alkalosis manifestations
(neuro) hyperexcitability of tissues including seizures, mental confusion, hyperactive reflexes, tetany (cardiovascular) hypotension, dysrhythmias
Respiratory Acidosis
pH less than 7.35 and PaCO2 greater than 45mmHg
Respiratory Acidosis etiology
impaired function of medullary respiratory center in the medulla, chest injury, weakness of respiratory muscles (ALS), chronic obstructive pulmonary disease, kyphoscoliosis, extreme obesity, pneumonia, anesthetics, opioids and sedatives, 3rd trimester pregnancy
respiratory acidosis manifestations
impaired consciousness, headache, irritability, muscle twitching, weakness
Respiratory alkalosis
pH greater than 7.45 PaCO2 less than 35 mmHg
respiratory alkalosis etiology
hyperventilation syndrome, hyperventilation due to fever, O2 deficiency, encephalitis, anxiety
respiratory alkalosis manifestations
(neuro) hyper excitability of the nervous system-tingling in toes, fingers- , dizziness, positive Chvostek's and Trousseau's sign because calcium levels drop, tetany, seizure (cardiovascular) cardiac dysrhythmias
oxygenation factors
cardiac output (SVxHR), hemoglobin, oxygenation
upper airways and nasal cavity
warm, filter and humidify air
filters debris; affected by smoking and tracheostomy
lower respiratory tract
trachea, bronchi, lungs
-the last cartilage (carina) is very sensitive
bronchi and bronchioles
Smaller airways leading into the lungs
gas exchange occurs in the capillaries here
dead air space
air that occupies the space between the mouth and alveoli but that does not actually reach the area of gas exchange
tidal volume
Amount of air that moves in and out of the lungs during a normal breath (usually 400-500)
inspiratory reserve volume
Amount of air that can be forcefully inhaled after a normal tidal volume inhalation -IRV + TV= Inspiratory lung capacity
Vital capacity
The total volume of air that can be exhaled after maximal inhalation.
expiratory reserve volume
Amount of air that can be forcefully exhaled after a normal tidal volume exhalation
residual volume
Amount of air remaining in the lungs after a forced exhalation, prevents lung collapse
functional residual capacity
expiratory reserve volume + residual volume
deficient amount of oxygen in the blood
deficiency in the amount of oxygen reaching the tissues
ventilation-perfusion ratio
the ratio of the amount of air reaching the alveoli to the amount of blood reaching the alveoli -apex is 3 -zone 2 is 1 -zone 3 is .63
patient positioning
GRAVITY -good lung should always be down because in impaired lung there is poor gas exchange
Obstructive Pulmonary Disorders
decreased FEV1/FVC asthma, COPD, bronchiolitis, cystic fibrosis, acute bronchitis
inflammation of the bronchioles
bronchiolitis etiology
-RSV (respiratory syncytial virus) is most common -influenza (mostly small children)
bronchiolotis manifestations
-exudate in airways -increased lymphocytes in airways -increased inflammatory response causes the airway to narrow -dyspnea causes wheezing -course crackles -retractions (mainly in kids) -nasal flaring -elevated WBC count -atelectasis
recurring attacks of diffuse wheezing, dyspnea, and cough resulting from spasmodic contractions of the bronchi and inflammation
asthma etiology
constriction of the airway due to inflammation and muscular contraction of the bronchioles, known as "bronchospasm" -extrinsic (allergic asthma usually occurring in children and young adults) -intrinsic (caused by respiratory infections, usually occurring in middle age) -exercise induced asthma -occupationsal asthma (fumes, formaldehyde, NSAIDs)
asthma manifestations
-wheezing -tightness in chest -dyspnea -productive (has sputum, assess color and consistency) -decreased peak expiratory flow rate -Decreased FEV1
Status Asthmaticus
severs attack, unresponsive to therapy -in constant bronchospasm, no wheezing -all air is trapped (silent chest indicates no movement)
chronic obstructive pulmonary disorder; developed by serious smokers; emphysema and chronic bronchitis
chronic bronchitis population characteristics
-40 year old make, incidence in women is increasing -overweight -smokers -acute bronchitis can become chronic
chronic bronchitis etiology
-smoking -repeated viral or bacterial respiratory infections -physical or chemical irritants -normal aging process (causes airway thickening)
chronic bronchitis pathogenesis
-chronic inflammation -scarring and swelling of the bronchial mucosa -impaired mucociliary elevator function due to metaplasia -increased thickness of mucosal wall (increased chance of infection)
chronic bronchitis manifestations
-shortness of breath -excessive sputum production -chronic cough -fatigue, hypoxia, CO2 retention -loss of libido -insomnia -decreased FEV1 -Elevated PaCO2, decreased PaO2
hypoxic drive
A condition in which chronically low levels of oxygen in the blood stimulate the respiratory drive; seen in patients with chronic lung diseases (COPD)
Acute Bronchitis
an inflammation of the lower respiratory tract that is usually due to infection.
acute bronchitis etiology
bacterial infection
acute bronchitis pathogenesis
Airways become inflamed/narrowed from capillary dilation Swelling from exudative fluid Infiltration with inflammatory cells Increased mucous production Decreased function of cilia
acute bronchitis manifestations
-fever -productive cough -increased mucous production
destructive changes in the alveolar wall without fibrosis and abnormal enlargement of the distal air sacs
emphysema population
thin males mid 50s
emphysema etiology
-cigarette smoking -air pollution -occupational conditions (asbestos) -normal aging (alpha 1 antitrypsin decreases with age)
emphysema pathogenesis
-inflammation of lung tissue -loss of alveolar walls (decrease in surface area limits gas exchange) -loss of elastic tissue in the lungs -air trapping (barrel chests)
emphysema bronchitis manifestations
-progressive exertional dyspnea -use of accessory muscle to breathe -pursed lip breathing -decreased FEV1 -increased residual volume because of alveolar wall collapse -slight decrease in in PaO2, normal PaCO2 -lungs are too compliant
Restrictive Pulmonary Disorders
pulmonary fibrosis, neuromuscular, kyphoscoliosis
Pulmonary Fibrosis
thickening of the alveolar interstitium (scarring inside the lungs)
pulmonary fibrosis etiology
-related to immune reaction (lymphocytes, plasma cells, macrophages flood the lungs)
pulmonary fibrosis pathogenesis
-infiltration of lung tissue with lymphocytes, macrophages, and plasma cells -vital capacity is significantly less -FEV1 test is normal but total lung volume is less
pulmonary fibrosis manifestations
-rapid, shallow breathing -dyspnea -non productive cough -clubbing -decreased lung volumes (FVC drop)
-disruption of the parietal or visceral pleura; injury to the pleura -air in the pleural space -hear nothing -symptom: O2 drops, tachypnea, dyspnea
Open pneumothorax
-hole in chest wall causes lung collapse (penetrative injury) -can become infected -pressure on wound (gauze) can only be applied on 3 sides or it can become a tension pneumothorax -same symptoms as regular pneumothorax
Tension Pneumothorax
-medical emergency that can result from regular from a regular or open pneumothoarx -shifting/compresses the side the injury is not on; since the heart is in between, as pressure shifts, the heart is crushed -symptoms include pneumothorax symptoms and decreased BP, mediastinal shifting and tracheal deviation -dropped HR/weak pulse, bad cap refill, cold limbs, hypoxemic, short of breath
-blod buildup in pleural space -usually results from another trauma -hematocrit and CO drop
Pleural Effusion
-fluid in the pleural space -cancer patient, renal failure, shock (septic) patients, older adults -can cause lungs to collapse -muffled, waterlogged sound
Acute respiratory failure etiology
ANYTHING THAT DROPS THE PaO2 BELOW 60 AND ELEVATES THE PaCO2 ABOVE 50 -CNS causes like seizure tumors -Neuromuscular diseases like ALS, muscular dystrophy, virus that causes paralysis -chest wall problems (flail chest, scoliosis) -airway problem like trauma to the trachea -pulmonary parenchymal diseases like ARDS, pneumonia -vascular diseases (pulmonary embolus)
acute respiratory failure pathogenesis
-ventilation perfusion mismatch --Ventilation: leaking fluid into alveoli, shunting results in dropped O2, interstitial fluid leaking out of lungs --Perfusion: alveolar hyperventilation caused by choking or overdose, blood clot, decreased CO
Acute respiratory failure manifestations
-hypoxemia (SOB, dyspnea) -hypercapnia (tachypnea)
Acute respiratory distress syndrome
damage to the alveolar-capillary membrane causing intrapulmonary shunting -inflammation response (protein rich fluid, WBC count increase, surfactant decrease causes alveolar collapse) -40% mortality rate; most common and worst kind of respiratory failure
ARDS etiology
-trauma -sepsis -aspiration -fat emboli -shock
ARDS pathogenesis
-shunting (oxygenated blood goes back to the heart) -decreased lung compliance (decreased surfactant) -decreased functional residual capacity -infiltrates -atelectasis due to decreased surfactant
ARDS manifestations
-tachycardia -shallow, rapid respirations -hypotension -restlessness -decreased mental status -hypoxemia -hypercapnia
refractory hypoxemia
as O2 (cannula) increases, blood oxygen remains the same because of decreased gas exchange from decreased alveolar surface area
Infant respiratory distress syndrome
-often in babies whose lungs are not developed (no surfactant)
IRDS etiology
-occurs in neonates delivered before 25 weeks gestation -poorly controlled diabetes mellitus in mother -Rh incompatibility
IRDS pathogenesis
lack of production of surfactant causes alveolar collapse
IRDS manifestations
-rapid, shallow respirations -intercostal, subcostal, sternal retractions -nasal flaring, hypoxemia, respiratory distress
pulmonary embolism
clot or other material lodges in vessels of the lung (usually from lower limb)
PE etiology
-venous stasis (most common- sluggish blood that most likely starts in lower limbs) -injury to vascular endothelium -hypercoagulability (genetic)
PE pathogenesis
-ventilation perfusion mismatch (perfusion issues cause too much dead space) -bronchoconstriction -compensatory shunting -hemodynamic consequences
PE manifestations
-dyspnea, tachypnea -chest pain -cough -tachycardia -apprehension -diaphoresis -hypoxemia -low grade fever
inflammatory reaction in the alveoli and interstitium in the lungs -disease of lung tissue often seen in the elderly, cancer patients, transplant patients, immunocompromised patients
pneumonia etiology
-aspiration (causes coughing) -inhalation of a bacteria or virus (airborne) -contamination of systemic circulation (translocation from gut bacteria- sepsis travels through lungs)
pneumonia pathogenesis
bacterial- exudate in alveoli made of dead neutrophils; no air, hear crackling or no breathing sounds, percussion sounds are dull viral- no exudate, generally less sick
pneumonia manifestations
-rales (coarse crackles) -fever -chills -cough -purulent sputum
Gastrointestinal bleeding
-10% mortality rate -can be upper or lower tract
Upper GI bleed
esophagus, stomach, duodenum
Lower GI bleed
Jejunum, ileum, large intestine
GI bleed etiology
-Ulcers (peptic ulcer disease) -Esophageal Varices (liver cirrhosis) -hemorrhoids (lower GI, varicies in anus, rectum) -Ulcerative Colitis, Chrone's Disease (lower GI)
GI bleed manifestations
-hematemesis (blood in vomitus) --> more common for upper GI bleed (bright red, coffee) -Melena (blood in stool) --> more common for lower GI (bright red, black tarry) -Occult Blood (hidden in stool) --> seen in colorectal cancer (guiac's test)
active bleed
bright red, no clots
inactive bleed
8 hrs post, clots, dark red
port wine
dark, burgundy color, 8 hrs, may clot
coffee grounds
indicates a stomach bleed (not active)
Gastroesophageal Reflux disease
lack of pressure causes the relaxation of the cardiac (gastroesophageal) sphincter, so chyme moves back up into esophagus
GERD risk factors
smoking, ETOH, chocolate, caffeine, fatty foods, medications (birth control), obesity, pregnancy, diabetes mellitus
GERD manifestations
heartburn, chest pain, dysphagia, esophageal ulcerations, strictures
scar tissue that causes narrowing and vomiting
Hiatal Hernia
movement of the stomach through the opening for the esophagus into the diaphragm (sliding hernia is most common) -present to some degree in 50% of the population
hiatal hernia manifestations
-heartburn -dysphagia -GERD -Epigastric Pain
Esophageal Varicies
complication of potal vein hypertension usually due to cirrhosis (common cause of upper GI bleed) -walls of bulged vessel are fragile and burst (bulged from portal vein pressure)
inflammation of gastric mucosa (ranges from mild to severe)
Gastritis Etiology
-bacterial endotoxin -caffeine -alcohol -Aspirin, NSAIDs (cease prostaglandin activity)
mild gastritis
gastric discomfort
severe gastritis
vomiting, bleeding
Peptic Ulcer Disease
can be gastric or duodenal
Peptic Ulcer Disease Etiology
-alcohol -aspirin (NSAIDs) -bile acids -stress -Helicobacter pylori (most common)
Peptic Ulcer Disease Mechanism
-decreased mucous production and prostaglandin deficiency
Peptic Ulcer disease manifestations
-vague abdominal pain to life threatening discomfort -pain usually burning or cramping -pain when stomach is empty between meals -pain in mid-esophageal region -perforation can lead to peritonitis -decreased hematocrit