PATHOPHYSIOLOGY EXAM 1

Endocytosis

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