Endocytosis
Tags & Description
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