Patho Exam 1 Flashcards
What happens to a stressed cell
It adapts It heals- reversible injury It dies-irreversible injury Apoptosis Necrosis Autolysis
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____ is programmed, internal or external triggers. It kills cell off.
Apoptosis
___ is sudden death, due to severe injury- cell explodes or dissolves
Necrosis
____ is self eating, cell cannibalizes itself for the nutrients
Autolysis
___ response to pathological (normal) and pathologic (adverse) changes
Adaptive changes: Atrophy Hypertrophy Hyperplasia Dysplasia Metaplasia
Reversible
____ - cells get smaller
If you don’t use it you lose it
Atrophy
___ cells get bigger
Ex: hypertrophic cardiomyopathy
Hypertrophy
___ is more cells.
Example: endometrial hyperplasia & benign prostatic hyperplasia
Hyperplasia
___ is abnormal type of growth of cells
Dysplasia
____ is chronic irritation that leads to change in cell type to less functional, less mature type:
Example: bronchial cell type changes
Metaplasia
Pathogenesis
Normal-Barrett’s esophagus-dysplasia-cancer
The progression: metaplasia, then goes to dysplasia, and then cancer.
Know
____ (not really adaptive) cells irregular sizes and shapes. Another name is atypical hyperplasia, pre-cancerous
Dysplasia
___ ___ in infants due to respiratory distress requiring increased oxygen flow, tissue gets thicker, with poor gas exchange.
Bronchopulmonary dysplasia
Mechanisms of cellular injury. How is cell actually hurt?
Cell membrane damage- cell explodes or can’t transport over the membrane anymore
Mitochondrial damage, no ATP, so no energy, can’t maintain cell membrane
Unstable calcium- may accumulate in cells (calcification of cancer cells or instance)
Oncotic pressure changes- water drawn into cell, it blows up.
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4 types of cellular injury
___ is lack of oxygen in cells common reason is ischemia. The single most common cause of cellular injury
Hypoxic
4 main types of cellular injury
___ is return of oxygen to hypoxic cells
Reperfusion
___ ___- formation of ROS (reactive oxygen species)
Oxidative stress
___ ___ many chemicals toxic to cells
Chemical injury
Cellular response to hypoxia- cell swells up.
ATP production is decreased.
Sodium and water move into cell. Potassium moves out of cell.
Osmotic pressure increases
More water moves into cell
Cisternae of endoplasmic reticulum distention, rupture and form vacuoles
Extensive vacuolation
Hypertropic degeneration
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____ ___:
Additional injury is caused by restoration of blood flow and oxygen.
4 mechanisms** Oxidative dress** Increased intracellular calcium Inflammation Complement activation
Ischemia reperfusion
Cellular injury: free radicals and reactive oxygen species (ROS)
These do damage to cells.
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Chemical or toxic injury
Environmental toxins especially air pollution is the main one.
Heavy metals will cause toxic injury to cells
Alcohol exposure will lead to cellular death
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Blunt force injuries
Contusions
Lacerations
Fractures
Sharp force injury: Incised wound Stab wounds Puncture wound Chopping wound
Gunshot wounds
Asphyxial injuries Suffocation Strangulation Chemical asphyxiants Drowning
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___ injury is disease producing potential
Invasion and destruction
Toxin production.
Production of hypersensitivity reactions
Infectious
___/___ injury
From substances generated during inflammatory response
Phagocytes
Biochemical substances
Membrane alterations
Immunologic/inflammatory
Other types of injury:
Excessive or deficient cell nutrients- sugar
Environmental factors- temperature, radiation, noise
Genetic abnormalities
Asphyxia
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Manifestations of cellular injury
Abnormal metabolism can cause fatty liver
Lack of enzyme can cause lysosomal storage disease: accumulation of endogenous materials
Defect in protein folding transport can cause accumulation of abnormal proteins
Ingestion of indigestible materials can cause accumulation of exogenous materials
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Manifestations of cellular injury: accumulations of endogenous materials.
Bruising> extravasated red cells> phagocytosis of red cells by macrophages> hemosiderin and iron free pigments
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Example of manifestations of injury
___ ___ water blows up cell
Oncotic damage
Example of manifestations of injury
___ ___ seen in cancer
Calcium accumulation
Example of manifestations of injury
___ Uric acid crystals accumulate
Gout
Example of manifestations of injury
___ is bruises, bilirubin
Pigmentation
Systemic (whole body) manifestations of cell injury
Fever Malaise (sore tired sick) Fatigue Pain Stress response- heart rate up Enzymes in the blood (blood tests for tissue damage, like heart and liver enzymes) Increased wbc Much due to the inflammatory response How you know your sick
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Cellular death:
Due to necrosis or apoptosis
Know
___ is rapid loss of plasma membrane organelle swelling, mitochondrial dysfunction, lacks typical features of apoptosis
May be regulated or programmed
Autolysis (auto digestion) one type
Necrosis
___ necrosis is from protein denaturation
Albumin is transformed from a gelatinous, transparent state to a FIRM OPAQUE substance
Example is infarct
Most common
Coagulative necrosis
___ necrosis
Example: neurons and glial cells of the brain
Cells digested by own enzymes
Tissues become soft and liquefied
Triggered by bacterial infection.
Staphylococci, streptococci, and E. coli.
Liquefactive necrosis
___ necrosis- from tuberculosis infection.
Combination of coagulative and liquefactive necrosis
Caseous
___ necrosis affects the breast and abdominal organs.
Action of lipases (fat digesting enzymes)
Fatty acids combine with elements to create soaps
Tissue appears opaque and chalky white
Fatty necrosis
Gangrenous necrosis
___ is worse and spreads fast
Wet
Gangrenous necrosis ___ is slow and red rim
Dry
___ is a programmed death, active processed cells targeted.
Physiologic vs pathologic- no inflammation & normal part of aging
Apoptosis
___ is self destructive & a survival mechanism
Cytoplasmic contents degraded by lysosomes
May be die to lack of nutrients
Autophagy
___ ___ is death of an entire person.
Somatic death
___ ___ is pale skin
Pallor Mortis
___ ___ is cold
Algor mortis
___ ___ is stiffness
Rigor mortis
___ ___ blood sinks to low areas
Livor mortis
___ is dissolving tissue
Putrefaction
___ absorb into environment
Decomposition
Total body water= 60% of body weight in adults.
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___ ___ pushes water out of capillaries (filtration)
Hydrostatic pressure
___ ___ pulls water into capillaries (reabsorption)
Osmotic/oncotic pressure
Water movement- balance of push and pull
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Capillary fluid movement by net filtration pressures
Cell- fluid movement by passive and active forces
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___ is fluid movement OUT of the capillary and into the interstitial space
Filtration
___ is fluid movement INTO the capillary from the interstitial space.
Reabsorption
What causes edema??
Excessive accumulation of fluid that’s within the interstitial spaces
(Renal failure generalized edema)
(Congestive HF lower extremity edema)
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Albumin is a protein that attracts and holds water in the blood vessels
If albumin is low then your edema will be worse
What causes this? Kidney disease Open wounds Hemorrhage Burns
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Severe generalized edema
Anasarca
___ ___ gravity dependent edema; will see in legs and feet with standing and sacrum and buttocks when supine
Dependent edema
___ is fluid gathered in body cavity or space (pulmonary and cardiac is common)
Effusion
___ edema is edema more widespread
Generalized
___ edema is limited to a single body region, maybe with trauma (sprained ankle) or could be organ related (cerebral pulmonary or laryngeal)
Localized edema
___ ___ is an area where edematous fluid gathers/process of edema formation
This fluid is NOT available for perfusion (trapped)
Third spacing
Antidiuretic hormone secretion ADH
Made in posterior pituitary.
Increases water reabsorption into the blood from urine; in the kidney.
Secreted if blood volume of patient decreases or drop in BP
Thirst perception- (osmoreceptors cause thirst)
Two types:
volume sensitive receptors- right and left atria of heart and found in thoracic vessels of chest
Baroreceptors- pressure sensitive receptors. Found in aorta, pulmonary arteries, and carotid sinus
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Sodium and chloride travel together.
Sodium- accounts for 90% of positive charged ions.
Primary extra cellular fluid cation +
Regulates osmotic forces, thus regulates water
Roles: nerve impulse conduction, acid base balance and cellular biochemistry, and membrane transport
Chloride:
Primary ECF anion -
Provides electroneutrality (keeping the pulses and minuses equal)
Levels vary inversely (opposite) with those of biocarbonate
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Renin angiotensin aldosterone system (RAAS)- keep water IN.
When the blood pressure drops the kidney will secrete renin and released if there is low sodium or potassium.
Renin stimulates the formation of angiotensin 1. Made from angiotensinogen (secreted by liver)
Angiotensin converting enzyme (ACE) converts angiotensin 1 to angiotensin 2.
Angiotensin 2 narrows vessels to rise blood pressure and get kidney perfusion restored and you won’t need renin anymore. It also stimulates secretion of aldosterone which helps the body reabsorption of sodium and water and secrete potassium.
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RAAS keeps water IN.
Balanced with
Natriuretic peptides keeps water OUT.
BNP shows patient is in HF.
ANH produced by atria.
Natriuretic peptide go against RAAS and makes BP lower.
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Total body water volume changes, with proportional electrolyte and water change (no change in concentration)
Isotonic fluid loss: hypovolemia
Isotonic fluid excess- hypervolemia
Isotonic
___ is increased osmolality (concentration)
Hypernatremia
Water deficit in extra cellular fluid (dehydration)
Hypertonic
___ is decreased osmolality
Hyponatremia
Water excess in ECF (water intoxication)
Hypotonic
Hypokalemia:
Alkalosis
Shallow respiration’s
Irritability
Confusion, drowsiness
Weakness, fatigue, lethargy
Arrhythmias: tachycardia, irregular rhythm and or bradycardia
Threads pulse
Intestinal motility- nausea vomiting lieus
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Hyperkalemia: muscle twitches, cramps, parenthesia,
Irritability and anxiety
Low BP
EKG changes
Dysrhythmia-irregular rhythm
Abdominal cramping
Diarrhea
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Hypocalcemia:
Chvosteks sign: a light tap over the facial nerve in front of the ear will cause contraction of facial muscles
Trousseaus sign- client thumb and index finger will draw together when a blood pressure cuff is inflated above systolic pressure for 3 mins
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Hypercalcemia-
Bone pain
Arrhythmia
Cardiac arrest
Kidney stones
Muscle weakness
Excessive urinarion
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Hypo phosphatemia
S/s
Anemia, bruising
Seizure, coma
Constipation
Muscle weakness
Hypoactive bowel sounds
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Hyper phosphate
No dairy
Increase fluids
Phosphate restricted diet.
Lower level by correcting calcium deficiency, monitor for cardiac, neuro and GI activity. Watch for changes in calcium levels
(Kidney failure, long term laxitives, chemo cause this)
May have tingling and muscle spasms in hands feet and face, convulsions and cardiac arrest)
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Hypo magnesium
Confusion
Increased DTR
Neuromuscular irritability
Seizure
Muscle cramps
Tremors
Insomnia
Tachycardia
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Calcium is good for teeth, bones, transmission of nerve impulses.
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If calcium is up phosphate is down and vice versa
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Hyper magnesium
Flushing
Decreased DTR
Muscle weakness
Lethargy
Decrease respiration
Bradycardia
Hypotension
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Ph 7.40 is neutral for biological fluid
If hydrogen is high- ph Is low (acidic)
If hydrogen is low- ph is high (alkaline)
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Ph:
Acids are formed as end products of protein, carbs, and fat metabolism, acids are substances that donate H+
To maintain the body’s normal PH, the acids must be balanced by base substances, bases are substances that accept H+
The bones, lungs and kidneys are the major organs involved in the regulation of the acid base balance
Know
Body acids exist in two forms:
Volatile(lungs)
Can be eliminated as CO2, gas blown off by LUNGS.
Carbonic acid only exists for a second until it changes into a mix of HCO3 and H+ ions
HCO3 biocarbonate ion is the major ph buffer in the body fluids
Non volatile acid (kidneys) (take longer but a better system)
Can only be eliminated by the kidneys
Takes hours to days to correct
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Control of serum pH
Buffer pairs in the blood respond to ph changes IMMEDIATELY
respiratory system can alter carbonic acid levels/co2 to change ph quickly
Kidneys can modify the excretion rate of acids and absorption of biocarbonate ions to regulate ph
Most significant control mechanism but slowest mechanism
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Sodium biocarbonate carbonic acid system
Major ECF buffer
Controlled by the respiratory system and kidneys
Other buffering systems:
Phosphate
Hemoglobin
Protein
Know
Normal PH 7.35-7.45
Acidosis: ph falls below 7.35
Systemic increase in Hydrogen (acid) concentration or loss of base (decrease in biocarbonate)
Alkalosis above 7.45
Systemic decrease in Hydrogen (acid) concentration or excess of base (increase in biocarbonate)
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Respiratory acidosis
Low ph, high paco2
Result of alveolar hypoventilation
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Respiratory alkalosis
High Ph low paco2
Result in alveolar hyperventilation
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Respiratory acidosis occurs when there is hypoventilation, not getting rid of carbon dioxide CO2 or acid in the blood (high pco2)
Low ph/high paco2
Causes: depression of the respiratory centers (opioids) impaired alveolar ventilation, impaired respiratory movements (chest pain) head injury, broken ribs.
Symptoms: headache/blurred vision, lethargy, confusion, convulsions, coma, restlessness
Compensation: kidneys conserve HCO3 (base) and excrete H (acid) in acidic urine- takes 3-4 days
Know
Respiratory alkalosis:
Occurs when there is hyperventilation (deep rapid respiration’s) “blows off” carbon dioxide, getting rid of too much CO2 or acid (low pco2)
High ph/ low paco2
Causes: hyperventilation (anxiety) hypoxemia, early salicylate intoxication, fever, anemia
Symptoms: dizzy, confusion, tingling of extremities, convolsions, coma
Compensation: kidneys conserve H+ (acid) and excrete HCO3- in alkaline urine
Know
Metabolic from body acids-
Metabolic acidosis- low ph, normal or low paco2, low HCO3
Example is diabetic ketoacidosis
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Metabolic alkalosis- high Ph, high HCO3
Result of excessive loss of metabolic acids in urine
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Metabolic acidosis:
There is not enough base or there is too much acid in the blood (low HCO3 and I’m high h2co3
Low ph/ low HCO3
Causes DKA, diarrhea, late stages of aspirin poisoning, renal failure
Symptoms: headache, lethargy, coma, anorexia, nausea, vomiting, diarrhea, abdominal discomfort, flushing skin
Compensation: kussmaul respiration (deep and rapid) to blow off CO2 and get rid of acid. Kidneys conserve HCO3- base and excrete h+ in acidic urine
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Metabolic acidosis- too much base HCO3 or excessive loss of acid H+ (increase of HCO3- usually caused by decrease of metabolic acids)
High ph/high HCO3
Causes: vomiting, suction of stomach, excessive intake of base, loop diuretic.
Symptoms: weakness, muscle cramps, hyperactive reflexes, tetany, confusion, convulsions, and atrial tachycardia.
Compensation: suppress breathing to retain CO2 (acid) conserve H+ (acid) and excrete HCO3 in alkaline urine
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Cellular adaptation:
Reversible response to physiologic normal and pathologic (adverse) changes
Adaptive changes:
Atrophy, hypertrophy, hyperplasia, dysplasia, metaplasia
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Atrophy- smaller
Hypertrophy- bigger cells
Hyperplasia- more cells
Know
___ is a chronic irritation leads to change in the cell type to less functional, less mature type.
Example: bronchial cell type changes
Metaplasia
Cellular adaption:
Metaplasia then dysplasia.
This progression: metaplasia, then goes to dysplasia, then cancer.
Know
__ (not really adaptive) cells irregular sizes and shapes:
Another name: atypical hyperplasia pre cancerous
Dysplasia
Bronco pulmonary dysplasia
In infants due to respiratory distress requiring oxygen flow, tissues get thicker, with poor oxygen exchange
Know
4 main types of cellular injury
Hypoxic- lack of oxygen in cell, common reason is ischemia (lack of blood flow)
Reperfusion: return of oxygen to hypoxic cells
Oxidative stress- formation of ROS (reactive oxygen species)
Chemical injury- many chemicals toxic to cells
Know
Hypoxic injury- single most common cause of cellular injury
Most common cause of hypoxia is ischemia
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Cellular response to hypoxia- cells swell up.
Know
Ischemia reperfusion injury
Additional injury caused by restoration of blood flow and oxygen
Four mechanism: oxidative stress**, increased Intracelluar calcium, inflammation, complement activation
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Free radicals and reactive oxygen species (ROS)
Causes: oxidative stress
Free radicals are atoms with an unpaired electron makes the atom react with other atoms causing damage.
Lipid peroxidation
Protein alteration
Dna damage
Mitochondrial effects
Know
Chemical or toxic injury
Chemical agents/ drugs
Environmental toxins- air pollution
Heavy metals
Alcohol
Know
Infectious injury: disease producing potential
Invasion and destruction
Toxin production
Production of hypersensitivity reactions
Know
Immunologic/inflammatory injury
From substances generated during inflammatory response
Phagocytes
Biochemical substances
Membrane alterations
Know
Other types of injury:
Excessive or deficient cell nutrients- sugar
Environmental factors- temperature, radiation; noise
Genetic abnormalities
Asphyxia
Know
Manifestations of cell injury: abnormal metabolism, lack of enzyme, deficit protein folding transport, ingestion of indigestible materials
Know
Manifestations of cellular injury: accumulation of endogenous material
Bruising- extravasated red cells- phagocytosis of red cells by macrophages- hemosiderin- iron free pigments
Know
Oncotic damage- water blows up cell
Calcium accumulation- seen in cancer
Gout- Uric acid crystals accumulate
Pigmentation- bruises; bilirubin
Know
Systemic (whole body)
Fever Malaise (sore tired sick) Fatigue Pain Stress response-increased HR Enzymes in the blood (blood tests for tissue damage like heart and liver enzymes Increase WBC Much due to inflammatory response How you know your sick
Know
Cellular death-
Due to necrosis or apoptosis
Necrosis- rapid loss of plasma membrane, organelle swelling, mitochondrial dysfunction, lacks typical features of apoptosis
May be regulated or programmed
Autolysis (auto digestion) one type
Know
Coagulative necrosis
From protein denaturation
Albumin is transformed from gelatinous, transparent state to a firm opaque substance:
Example: infarction
Know
Liquidfactive necrosis
Example: neurons and glial cells of the brain
Cells digested by own enzymes
Tissues become soft and liquidfied
Triggered by bacterial infection
Staphylococci, streptococci, and E. coli.
Know
Caseous necrosis: from tuberculosis infection
Combination of coagulative and liquidfactive necrosis
Know
Fatty necrosis
Affects breast and abdominal organs
Action of lipases (fat digesting enzymes)
Fatty acids combine w elements to create soaps
Tissue appears opaque and chalky white
Know
Gangrenous necrosis
Wet- worse, fast spread
Dry- slow, red rim
Know
Apoptosis- programmed cell death, active process, cells targeted
Physiologic vs pathologic- no inflammation
Normal part of aging
Know
Autophagy
Self destruction & survival mechanism
Cytoplasmic contents degraded by lysosomes
May be due to lack of nutrients
Know
Somatic death
Death of an entire person
Postmortem stages:
Pallor mortis: pale skin Algor mortis: cold Rigor mortis: stiffness Livor mortis: blood sinks to low areas Putrefaction: dissolving tissue Decomposition: absorb into environment Skeletonization
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First line: innate immunity (natural)
Second line; inflammation
Third line: adaptive (acquired) immunity
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Cell derived chemical barriers:
Secrete saliva tears, earwax, sweat, and mucus
Lysozymes attack bacteria
Antimicrobial peptide kill bacteria, fungi, viruses
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Normal micro biome:
Produces enzymes for digestion
Synthesizes metabolites
Releases antibacterial substances
Competes with pathogens for nutrients
Fosters adaptive immunity
Helps with communication between brain and GI
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Inflammation is emergency response to injury
First- hemostasis, stop bleeding to survive- clots and vasoconstriction
- Vasodilation- bring flow of blood, oxygen and resources
- Increased vascular permeability and leakage to deliver cells and chemicals to injury site
- WBC stick to the inner walls of the vessels and migrate through the vessels to the injury
Response causes the 5 classic local signs:
- Heat
- Redness,
- Swelling
- Pain
- Loss of function
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Inflammation is a VASCULAR response to injury
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Inflammations protective functions:
Prevent/ limit infection and further damage
Limit the inflammatory process
Prepare injury for healing
Facilitate starting adaptive immune response
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3 plasma protein systems
Essential for effective inflammatory response
- Complement
- Clotting
- Kinin
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- Complement system- produces biologically active fragments that are most potent defenses
Activation of C3 & C5
Pathways
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- Clotting system- forms mesh work of fibrin strands and platelets at injured site which
Prevents spread of infection
Localizes micro organisms and foreign bodies
Forms a clot that stops bleeding
Provides a framework for repair and healing
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- Kinin system- activates and assists inflammatory cells
Primary kinin for Bradykinin
Kinin causes: dilation of blood vessels, pain, smooth muscle contraction, increased vascular permeability
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Cytokines- activate cell and regulate inflammatory response
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Chemokines
Chemotaxic- attract leukocytes to sites of inflammation
Made by many cells (macrophages, fibroblasts, endothelial cells.)
More than 50 chemokines have been described
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Pro inflammatory cytokines:
Tumor necrosis factor alpha TNF-A
Interleukin-1
Interleukin-6
Anti inflammatory cytokines
Interleukin 10
Transforming growth factor beta TGF
Very high levels can be lethal
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Cytokines interleukin
Produced primarily by macrophages and lymphocytes responding to PRRs or other cytokine
Alter behavior of cells
Functions
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Interleukin 1- secreted by macrophages- triggers chemokines production and causes fever
Interleukin 2- secreted by t helper- triggers the growth of t helpers and cytotoxic T cells
Interleukin 3- secreted by T cells- stimulates bone marrow
Interleukin 4- secreted by t helper 2- class switching to ige
Interleukin 5- t helper 2- class switching to IGA and promotes the activation of eosinophils
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Cytokines- interferons IFNs- protect against viral infections
Type 1: released by virally infected host cells, induce anti viral proteins and protect neighboring healthy cells
Type 2: produced by lymphocytes and activate macrophages and increase capacity to detect and process abnormal cells
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Cellular components of inflammation
These cells respond to molecules at site of damage and rush there chemotaxis
Cell surface receptors activate cell and Intracellular signaling pathways
Functions: confine extent of damage, kill micro organisms, remove cellular debris, activate healing
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Cells of inflammation
Neutrophils Eosinophils Macrophages Lymphocytes Mast cells Endothelial cells Platelets
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Cells of inflammation
Pattern recognition receptors (PRRs)
Monitor for cellular damage and micro organisms
Recognize two patterns:
Pathogen- associated molecular patterns (PAMPs)
Damage- associated molecular patterns (DAMPs)
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Mast cells:
Potent activators of inflammatory response >
Contain granules with biochemical mediators that are released with tissue injury
Chemical release in two ways: 1. Degranulation 2. Synthesis
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Mast cell degranulation
Chemotaxic factors
Forms a chemical gradient leading to directional movement of neutrophils and eosinophils
Neutrophil chemotaxic factor
Eosinophil chemotaxic factor of anaphylaxis ECF-A
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Mast cell degranulation- histamine release
H1 receptor - pro inflammatory response
H2 receptor- anti inflammatory
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Histamine- vasoactive amine, causes temporary, rapid constriction of large blood vessels and dilation of post capillary venules
Retraction of endothelial cells lining the capillaries, leaving gaps between cells for rescue cells to pass out of capillaries
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Mast cell synthesis of 3 mediators
Leukotrienes- similar effects to histamine but in later stages
Prostaglandins- similar effects to leukotrienes; they also induce pain
Platelet activating factor- similar effect to leukotrienes and platelet activation
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Endothelial cells- regular circulation through micro vessels
Control movement of water and solutes
Maintain normal blood flow
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Platelets- activated by tissue destruction and inflammation
Activation leads to interaction with coagulation cascade
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Neutrophils:
Also referred to as polymorphonuclear neutrophil (PMNs)
Predominate phagocytes In early inflammation
Ingest bacteria, dead cells and cellular debris
Cells are short lived and become a component of purulent exudate
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Eosinophils- mildly phagocytic, defense against parasites, regulation of vascular mediators
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Basophils- least prevalent granulocyte, basophilic granules, release histamine, important source of cytokines, like mast cells
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Monocytes:
Produced in the bone marrow and enter the circulation
Migrate to the inflammatory site, develop into macrophages
Monocytes derived macrophages arrive at the inflammatory site 24 hour or later after neutrophils
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Dendritic cells- in peripheral organs and skin
Migrate through lymph vessels to lymph tissue and interact w t lymphocytes to generate an adaptive immune response
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Lymphocytes activate macrophages, initiate immune responses
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Natural killer cells- type of lymphocyte, eliminate cells infected with viruses and cancer
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Phagocytosis
Steps: recognition and adherence
Engulfment and phagosome formation
Fusion of phagosome with Lysosomal granules
Destruction of target
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Local manifestations
Result from cellular and vascular changes and corresponding leakage of circulating components into the tissue
Heat, swelling, redness, pain, loss of function
Exudative fluids
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Systemic manifestations
Fever, leukocytosis, increased plasma protein synthesis
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Acute inflammation
Self limiting
Lasts 8-10 days
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Chronic inflammation
Initiated if acute proves inadequate
Lasts weeks to months
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Chronic inflammation lasts two weeks or longer, unsuccessful acute inflammation, high lipid and wax content of micro organisms, ability to survive inside macrophage, toxins, chemicals, particulate matter, or physical irritants
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Chronic inflammation characteristics
Dense infiltration of lymphocytes and macrophages
Granuloma formation
Epithelioid cell formation
Giant cell formation
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Wound healing
Resolution (regeneration) back to original called “healing by primary intention”
Possible if; not much tissue missing/ distorted and cells are able to regenerate
Repair: formation of a scar, called healing by secondary intention. Occurs if: big loss of tissue or cells can’t regenerate
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Phases of wound healing
Phase 1: hemostasis
Phase 2: inflammation
Phase 3: proliferation
Phase 4: remodeling and maturation
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Dysfunctional wound healing
May occur during any phase of wound healing due to
Ischemia Excessive bleeding Excessive fibrin deposition Altered collagen deposition Pre disposing disorders-DM inadequate nutrition Infection NSAID or steroids
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Dysfunctional wound healing
Dysfunction collagen synthesis
Keloid, hypertrophic scar
Wound disruption: dehiscence- wound pulls apart at suture line. Increased risk of infection
Contracture- excessive contraction causes an atomic deformity
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Older adults: impaired function of innate immune cells (phagocytes)
Impaired inflammation is likely a result of chronic illness
Chronic medication intake decreases the inflammatory response
Healing response is diminished because of skins loss of regenerative ability
Infections and chronic inflammation are more common in older adults
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Allergy
Harmful effects of hypersensitivity to environmental (exogenous) antigens
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Autoimmunity
Immune response against cells or tissues
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Alloimmunity
Immune reaction to tissues of another individual
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Immunodeficiency
Immune response is not adequate to protect the body
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Type 1 hypersensitivity
Mediated by IGE and production of mast cells
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Type 2 hypersensitivity
Tissue specific reactions
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Type III hypersensitivity
Immune antigen antibody complex mediated
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Type IV hypersensitivity
Cell mediated Tc or cytokine producing Th1
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Allergy
Allergens- environmental antigens that cause atypical immune responses
Pollens, molds, and fungi, foods, animals, cigarettes smoke, house dust
Most common hypersensitivity and usually type 1
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Anaphylaxis- most rapid and severe immediate hypersensitivity reaction
Occurs within minutes of re exposure to antigen
Systemic of cutaneous
Most severe reactions can lead to death
Most common: bee stings, peanuts, shellfish, or eggs
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Desensitization- may reduce the severity of the allergic reaction but could also cause anaphylaxis
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Type 1 hypersensitivity:
IgE mediated
Against environmental antigens (allergens)
IgE binds to receptors on surface of mast cells (cytotrophic antibody “sensitized”)
Histamine release- h1 and h2 receptors, antihistamine
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Type II hypersensitivity
IgG mediated
Tissue specific
Specific cell or tissue (tissue specific antigens) is the target of an immune response
Five mechanism: cell is destroyed by antibodies and complement
Soluable antigen may enter the circulation and deposit on tissues and tissues destroy by complement and neutrophil granules
Antibody dependent cell mediated cytotoxicity ADCC
Causes target cell malfunction (Graves’ disease and hyperthyroidism)
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