PATHOPHYSIOLOGY EXAM 1

Endocytosis

process by which a cell takes material into the cell by infolding of the cell membrane

Exocytosis

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

bacteria

produce endocrine/exo toxins that can damage cell tissue and activate the arachidonic acid cascade

endotoxins

produced by gram negative cells upon death (liposaccharide A)

Viruses

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

atrophy

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

Hypertrophy

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)

hyperplasia

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

metaplasia

increase in the conversion of one differentiated cell type to another (ex. smoking can turn columnar epithelial cells in lungs to squamous epithelial cells)

Dysplasia

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

necrosis

-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

apoptosis

programmed cell death

normal pH

7.35-7.45

PaO2

80-100 mmHg

PaCO2

35-45 mmHg

HCO3

22-26 mEq/L

O2 sats

95-100%

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

cilia

filters debris; affected by smoking and tracheostomy

lower respiratory tract

trachea, bronchi, lungs

trachea

-the last cartilage (carina) is very sensitive

bronchi and bronchioles

Smaller airways leading into the lungs

alveoli

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

hypoxemia

deficient amount of oxygen in the blood

hypoxia

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

Bronchiolitis

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

asthma

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)

COPD

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

Emphysema

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)

Pneumothorax

-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

Hemopneumothorax

-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

Pneumonia

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

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)

Gastritis

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