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Atrophy
Cells decrease in size because demand decreases
Reversible
Etiologies of Atrophy
Disuse
Ischemia
Endocrine dysfunction
Persistent cell injury
Aging
Hypertrophy
Cells increase in size because of increased demand
Physiologic Etiologies of Hypertrophy
Normal
Weightlifting
Pathologic Etiologies of Hypertrophy
Abnormal
Enlarged Organs
Hyperplasia
Increase in number of cells
Physiologic Etiologies of Hyperplasia
Breast and uterine enlargement during pregnancy
Pathologic Etiologies of Hyperplasia
Enlargement of the prostate gland.
Metaplasia
Replacement of one differentiated cell type with another
Cell retains same basic tissue type
Reversible
Etiologies of Metaplasia
Occurs in response to chronic irritation and inflammation
Dysplasia
Deranged cellular growth, cells mutate with abnormal variations in size, shape, and arrangement
Can be reversible if you remove the trigger
Dysplasia is a strong precursor to what?
Cancer
Most common cause of cellular injury is?
Hypoxia
Hypoxia
Lack of oxygen inside the cells
Hypoxia results from…
Reduced amount of oxygen in the air
Loss of hemoglobin or decreased efficacy of hemoglobin
Decreased production of red blood cells
Diseases of the respiratory and cardiovascular systems
Poisoning of the oxidative enzymes within the cells (carbon monoxide)
Most common cause of Hypoxia is?
Ischemia
Can be progressive or acute
The progressive cause of ischemia which causes hypoxic injury is?
Arteriosclerosis
The acute cause of ischemia which causes hypoxic injury is?
Thrombosis
Ischemia-Reperfusion Injury
Free radicals and reactive oxygen species
Additional injury can be caused by the restoration of blood flow and oxygen
Chemical Injury
Direct toxicity to the cell membrane or formation of free radicals.
Necrosis
Cell injury which results in the premature death of cells in living tissues by autolysis
Caused by factors external to the cell or tissue such as infection, toxins, and trauma
Apoptosis
The process of eliminating unwanted cells, called programmed cell death
Coagulative Necrosis
Interruption of blood flow
Etiologies of Coagulative Necrosis
Ischemia
Location of Coagulative Necrosis
Kidneys, heart, and adrenal glands
Liquefactive Necrosis
Ischemia of neurons and glial cells of the brain
Etiologies of Liquefactive Necrosis
Bacterial Infection
Staphylococci
Streptococci
Escherichia Coli
Location of Liquefactive Necrosis
Neurons and glial cells of the brain
Caseous Necrosis
Combination of liquefactive and coagulative necrosis
Etiologies of Caseous Necrosis
TB infection
Location of Caseous Necrosis
Lungs
Etiologies of Fat Necrosis
Action of lipases
Location of Fat Necrosis
Breast, pancreas, and other abdominal organs
Gangrenous Necrosis
Death of tissue from severe hypoxic injury
Etiologies of Gangrenous Necrosis
Severe hypoxic injury
Location of Gangrenous Necrosis
Wet: Feet and toes
Dry: Toes
Gas (Clostridium): Thigh
Somatic Death
Systemic death of an entire person
Algor Mortis
Postmortem reduction of body temperature
Livor Mortis
Purple discoloration from settling of blood in the most dependent tissues
Rigor Mortis
Stiffening develops within 12-14 hours and usually affects entire body
Gradually diminishes as the body becomes flaccid between 36-62 hours
GAS
General Adaptation Syndrome
Three stages: Alarm, Resistance, and Exhaustion
Alarm Stage
“Fight or Flight”
Stressors trigger hypothalamic-pituitary-adrenal (HPA) axis which activates sympathetic nervous system
Epinephrine, Norepinephrine, and Cortisol are released
Resistance Stage
Body attempts to restore homeostasis
Actions of adrenal hormones
Continued mobilization of the body’s resources to cope and overcome a sustained challenge
Exhaustion/Allosteric Overload Stage
Body can no longer produce hormones, Marks the onset of disease
Occurs only if the stress continues and adaptation is not successful
Body’s physiologic and immune systems no longer effectively cope with the stressor
Osmotic Pressure
Pulling pressure
Hydrostatic Pressure
Pushing pressure
Edema
Excessive accumulation of fluid within the interstitial spaces
Etiologies of Edema: Increased capillary hydrostatic pressure
Venous obstruction, salt and water retention, heart failure
Etiologies of Edema: Decrease in plasma oncotic pressure
Decreased synthesis of plasma proteins (cirrhosis, malnutrition)
Increased loss of plasma proteins (nephrotic syndrome)
Increased plasma Na+ and H2O retention (dilution of plasma proteins)
Etiologies of Edema: Increase in capillary permeability
Burns and inflammation
ADH
Tap water hormone
Causes kidneys to reabsorb water
Aldosterone
Saltwater hormone
Causes kidneys to reabsorb sodium and water
Etiologies of Fluid Volume Excess
Excessive sodium or water intake
Inadequate sodium or water elimination
Clinical Manifestations of Fluid Volume Excess
Generalized edema
Localized edema
Dyspnea
Bounding pulse
Tachycardia
Polyuria
Rapid weight gain
JVD
Crackles
Etiologies of Fluid Volume Deficit
Inadequate fluid intake
Excessive fluid or sodium loss
Clinical Manifestations of Fluid Volume Deficit
Thirst
Altered level of consciousness
Hypotension
Tachycardia
Weak, thready pulse
Flat jugular veins
Dry mucous membranes
Decreased skin turgor
Oliguria
Weight loss
Normal Sodium Values
136 - 145
Etiologies of Hyponatremia
Loss of sodium
Inadequate sodium intake
Sodium dilution from too much water
Clinical Manifestations of Hyponatremia
Lethargy
Confusion
Decreased reflexes
Muscle cramps and fatigue
Complications of Hyponatremia
Cerebral edema
Increased intracranial pressure
Seizures
Coma
Etiologies of Hypernatremia
Inadequate water intake
Loss of water in ECF
Increased concentration of sodium in ECF
Clinical Manifestations of Hypernatremia
Thrist
Weight loss
Increased blood pressure
Muscle twitching
Increased reflexes
Complications of Hypernatremia
Coma
Convulsions
Cerebral Hemorrhage
Seizures
Normal Potassium Values
3.5 - 5
Etiologies of Hypokalemia
Decreased intake
Increased entry of potassium into cell
Acid base balance
Increase in aldosterone
Insulin overuse
Increased loss of potassium
NG suctioning
Burns
Vomiting and diarrhea
Use of non potassium sparing diuretics
Clinical Manifestations of Hypokalemia
Neuromuscular excitability decreases
Skeletal muscle weakness
Loss of smooth muscle tone
Cardiac dysrhythmias
Prolonged PR interval
Flat T wave
Prominent U wave
Etiologies of Hyperkalemia
Increased intake
Potassium leaves the cells and goes into the blood
Decreased renal excretion of potassium
Insulin deficiency
Large infusion of stored blood
Cell trauma
Clinical Manifestations of Hyperkalemia
Neuromuscular excitability increases THEN decreases
Mild Attacks:
Tingling of the lips and fingers
Restlessness
Tall, peaked T waves
Severe Attacks:
Muscle weakness
Loss of muscle tone
Flaccid paralysis
Cardiac dysrhythmias
Normal Calcium Values
9 - 10.5
Etiologies of Hypocalcemia
Insufficient dietary intake
Inadequate intestinal absorption
Blood administration
Renal Disease
Vitamin D Deficiency
Decreased in PTH
Clinical Manifestations of Hypocalcemia
Neuromuscular irritability (spasms, cramps)
Hyperactive reflexes
Tetany
Positive Trousseau sign
Positive Chvostek sign
Cardiac dysrhythmias
Etiologies of Hypercalcemia
Vitamin D overdose
Prolonged immobilization
Some cancers
Hyperparathyroidism
Clinical Manifestations of Hypercalcemia
Muscle weakness
Cardiac dysrhythmias (bradycardia, cardiac arrest)
Bone pain, osteoporosis
Pathological fractures
Impaired renal function
Kidney stones
Fatigue, weakness, lethargy, nausea, constipation
Normal Phosphate Values
3 - 4.5
Normal Magnesium Values
1.3 - 2.1
Neutrophils
Predominate in early inflammatory responses, around 6-12 hours after initial injury
Ingest bacteria, dead cells, and cellular debris
Short lived and become a component of the purulent exudate
Eosinophils
Mildly phagocytic
Defense against parasites and regulation of vascular mediators
Basophils
Least prevelant
Primary role is unknown
Act like mast cells
Monocytes
Produced in the bone marrow, enter circulation, and migrate to the inflammatory site where they develop into macrophages
Macrophages
Typically arrive at the inflammatory site 24 hours or later after the neutrophils
Can live for months to years because they are capable of cellular division
Dendritic Cells
In peripheral organs and skin
Migrate through lymph vessels to lymph tissue and interact with T lymphocytes to generate an acquired immune response
Primary Intention Wound Healing
Wounds that heal under conditions of minimal tissue loss
Secondary Intention Wound Healing
Wounds that require a great deal more tissue replacement.
Ex: open wounds
Naturally Acquired Active Immunity
Exposure to antigen
Antigens enter the body naturally; body induces antibodies and specialized lymphocytes
Naturally Acquired Passive Immunity
Maternal antibodies in the mother’s breast milk (IgA) or antibodies that cross the placenta (IgG)
Artificially Acquired Active Immunity
Antigens introduced by vaccines
Antigens enter the body through vaccines; body produces antibodies and specialized lymphocytes
Artificially Acquired Passive Immunity
Preformed antibodies or T-cells are injected
Antibodies
Protect the individual from infection
Produced by B cells
IgG, IgA, IgM, IgE, and IgD
IgG
Most abundant (80-85%)
Accounts for most of the protective activity against infections
Transported across the placenta
Major antibacterial and antiviral antibody
IgA
IgA found predominately in the blood
IgA-2 found predominately in bodily secretions (most important)
Defends against pathogens on body surfaces, especially those that enter the respiratory and GI tracts
IgM
First antibody produced during the primary response to an antigen
Eliminates pathogens in the early stages of B-cell mediated immunity before there is sufficient IgG
IgD
Low concentration in the blood
Function as one type of B cell antigen receptor
Activates basophils and mast cells to produce antimicrobial factors
IgE
Mediator of many common allergic reactions
Defender against parasites
Stimulates the release of mast cell granules, which contain histamine and heparin
Hypersensitivity Type 1
IgE mediated
Genetic/hereditary in origin
Ex: Allergies, Hay Fever
Hypersensitivity Type 2
Tissue-specific reactions
Cell destruction by antibody and complement (ex blood transfusion)
Cell destruction through phagocytosis
Hypersensitivity Type 3
Immune complex mediated
Antibodies bind to soluble antigen that was released into the body or fluids, and then complex is deposited into tissues (ex gluten allergy, lupus)
Hypersensitivity Type 4
Does not involve antibodies at all
Cell mediated
Mediated by T lymphocytes (ex poison ivy, TB skin test)
Shunting
Perfusion without ventilation
Dead Space
Ventilation without perfusion
Hypoxemia
Abnormal low amount of O2 in the blood