Quiz 1 Flashcards
What is meant by altered cellular tissue
not normal or abnormal but changed
Disease
Anything outside of normal (the failure to maintain homeostatic conditions)
What is meant by idea conditions?
An average of the normal range
Homeostasis
maintenance of a relatively constant range of environment within the body
If homeostatic mechanisms cannot cope with a particular stress what happens?
physiologic values will drift outside the normal range
Stress
non-specific response of the body to any demand placed on it
Stressor
agent responsible for producing stress
Distress
harmful or unpleasant stress
Eustress
positive events that stimulate growth
Stress forms
may come in small, chronic doses; single, sudden large doses; or somewhere in between
Responses to stress
- specific homeostatic adjustments
- General Adaptation Syndrome
General Adaptation Syndrome
- Alarm phase
- Resistance phase
- Exhaustion phase
Alarm phase
- immediate response
- directed by SNS
- energy reserves are mobilized
- “fight or flight” responses
Dominant hormone in alarm phase
epinephrine (o adrenaline)
Supporting hormones in alarm phase
renin & ADH, glucocorticoids (control glucose in the brain levels)
Resistance phase
- either from emergency or build up of things in life
- occurs when stress lasts longer than a few hours
- mobilize lipid and protein reserves to conserve glucose for neural tissues
Resistance phase dominant hormone
glucocorticoids
Supporting hormones in resistance phase
Thyroid, ADH, renin, GH, epinephrine (supporting hormones control metabolism, retain H2O, and synthesize proteins (GH))
Goals of resistance phase
- mobilize lipid and protein reserves
- conservation of glucose for neural tissues
- elevation of blood glucose concentrations
- conservation of salts and water
Problems with resistance phase
- glucocorticoids: anti-inflammatory; suppresses healing & immune system
- conservation of fluid: -> high BP -> stress for L heart, gain of Na+ leads to loss of K+
- depletion of lipid reserves: tear down structural proteins
Exhaustion Phase
- collapse of vital systems
- causes: exhaust of lipid reserves, inability to produce glucocorticoids, failure of electrolyte balance, cumulative structural or functional damage to vital organs
- unless corrective actions are taken almost immediately, the failure of one or more systems will prove fatal
Stress related disorders
- Hypertension (renin/ADH)
- Ulcers (prostaglandins)
- skin disorders
- cardiovascular disease
- migrane headaches
- eating disorders
- anxiety
- arrhythmias
- asthma
- cancer (immunosurveillance)
- alcoholism
- drug abuse
- endocrine disorders
- GI disorders
- muscular tension
- sleep difficulty
Etiology
the initial cause of disease (what started everything)
Pathogenesis
Sequence of events in the development of disease (the story)
Pathophysiology
Study of functional and structural changes caused by disease
Types of etiologies
- inherited
- congenital
- acquired
- multifactorial
- idiopathic
- iatrogenic
Inherited
Due to a genetic defect
Congenital
present at birth
acquired
developed during lifetime
multifactorial
more than one factor
idiopathic
no understood cause
iatrogenic
treatment-induced
Intrinsic Etiologies
From within the body itself
- degenerative
- immunologic
- metabolic
- nutritional
- psychogenic
degenerative
progressive loss of normal structure and function
immunologic
abnormal immune response (allergies)
metabolic
abnormal body chemistry
nutritional
abnormal dietary intake or nutrient use (something inside of the body differs from one person to another)
psychogenic
related to psychological state
Extrinsic Etiologies
From the environment
- Infectious
- trauma
- hypoxia
- chemicals, drugs, toxins
- environmental agents
Infectious
due to a microorganism (bacterial, viral, fungal) or parasite (internal-tapeworm or external-lice, ticks)
hypoxia
insufficient oxygen
environmental agents
- temperature or atmospheric pressure
- radiation
- electrical
Cellular Adaptations
- adapted cells are neither normal or abnormal, they are stressed
- reversibile is stressor is removed
- often only temporarily successful
- may lead to cell injury or death
Cellular injury
- reversible (may recover)
- irreversible (will die)
- the cell is unable to maintain homeostasis above or below normal range
- macromolecules, enzymes, and organelles within the cell are closely interdependent
- difficult to distinguish between the primary target of injury from any secondary or ripple effect
- the precise cut-off point between reversible and irreversible is often difficult to determine.
Dysplasia
- is not an adaptation it is ALWAYS abnormal = pre-cancerous
- an abnormal change in the size shape, and arrangement of mature cells in response to a stimulus
- often called atypical hyperplasia
- dysplasia may be reversible if the stimulus is discontinued
- if the stimulus persists, it may progress to neoplasia (benign or malignant growth)
- examples: cervix, breast
Atrophy
shrinkage in cell size by loss of cell substance
-these cells have diminished function
Causes of cell atrophy:
- decreased workload
- loss of innervation
- diminished blood supply
- inadequate nutrition
- loss of endocrine stimulation
- aging
- brain can atrophy
Hypertrophy
Increase in the size of individual cells
- no new cells, just larger ones
- not swollen by fluid, but by increased synthesis of structural proteins and organelles
- these cells have improved function
- a limit is reached beyond which more enlargement is no longer helpful
Hypertrophy caused by?
- increased functional demand
- specific hormonal stimulation
Hypertrophy examples
-skeletal muscle and cardiac muscle
Hyperplasia
An increase in the number of individual cells in an organ or tissue
-process remains controlled
3 cell types that are unable to undergo hyperplasia
neural, skeletal m., and cardiac m.
Types of hyperplasia
- compensatory hyperplasia: one kidney example
- hormonal hyperplasia: breasts enlarge with hormones
- pathogenic hyperplasia: problem
Metaplasia
the reversible replacement of one cell type by another in response to a particular stress or stimuli
- an orderly arrangement of the new cell type is found
- example: cigarette smokers
- if stressor continues, may progress to dysplasia
cellular response to injury depends on?
- type of injury
- duration of the injury (makes a difference)
- severity of the injury
Consequences of injury depend on?
- type of cell injured (different cells have different abilities to heal)
- the cell’s current health status
- the cell’s adaptability (regenerative ability)
Descriptions of disease for how bad it is
- peracute (super-fast onset)
- acute (today)
- subacute (a little longer)
- chronic (over a longer time period)
Descriptions of disease for where it is
- focal or localized (one area)
- multifocal (several areas)
- systemic or generalized (over whole body or in entire system)
General mechanisms of cell injury
- hypoxia injury ( cells don’t have enough O2)
- Free radicals and reactive oxygen species
- chemical injury
- tissue trauma
Reperfusion injury
oxygen restored to ischemic tissue -> generation of free radicals
Free radicals
- unstable unpaired electrons: “activated oxygen species”
- they come from UV light, X-rays, oxidative rxns, normal metabolism
- they cause injury by lipid peroxidation, fragmentation of polypeptide chains and alteration of DNA
- we can decrease damage of this by using antioxidants (vitamin C, E)
Chemical injury
- toxic chemical agents can injure cell membranes and cell structures, clock enzymic pathways, coagulate cell proteins, and disrupt osmotic and ionic balance
- carbon tetrachloride (can cause liver damage)
- carbon monoxide (it loves hemoglobin, no O2 carried)
- alcohol (ethanol -> aldehydes cause damage)
Traumatic tissue injury
- blunt force
- contusion (bruise)
- hematoma (blood clot)
- abrasion (scrape)
- laceration (cut)
- stab wound - deeper than it is long
- incision- longer than it is deep
- Avulsion (degloving inj.)
- gunshot wound (speed)
- Asphyxiation (air not going to lungs)
- suffocation (nose and mouth)
- strangulation (trachea)
- drowning (lungs fill with H2O)
Anoxia
a complete lack of oxygen
Hypoxia
a lack of sufficient oxygen supply to the tissues
ischemia
inadequate blood flow in the tissues
Hypoxia can result from
- decreased amount of oxygen in air
- diseases of lungs or heart
- lack of RBCs/anemia (decreased production of RBCs or increased loss of RBCs)
- inadequate or dysfunctional hemoglobin
- ischemia
Effects of hypoxia
- decreased ATP production
- mitochondria needs O2 to make ATP
- lactic acid and is less efficient
ATP depletion leads to
- increased anaerobic glycolysis: problem is that it’s much less efficient (36 ATP vs. 2 ATP), lactic acid -> acidosis
- leads to myocardial infarction
- failure of the potassium pump: sodium accumulates in the cell, potassium diffuses out of the cell, and the net gain in sodium results in an osmotic gain of H2O
- acute cellular swelling results (not the same as hypertrophy)
Acute cellular swelling
- cellular swelling causes:
- dilation of the endoplasmic reticulum (ribosomes pop off/detach)
- lysosomal swelling leads to leakage of lysosomal enzymes
- if severe, can cause mitochondria to swell. Can’t do Kreb’s cycle
Reversible cell inury
- if injury is mild or short-lived
- ATP production must be restored to reestablish O2
- cell recovers by pumping out the water
- cell reverts from state of acute cellular swelling to the original steady state
- must take place before mitochondrial and membrane damage occurs
Mechanisms of irreversible injury
- inability to reverse mitochondrial dysfunction
- cell membrane damage: increased permeability of membrane, loss of volume regulation, massive calcium influx (activated proteases, phospholipases, ATPases, Ca++ goes to mitochondria), and loss of proteins, essential coenzymes, and ribonucleic acids
- clinical: liver cells die and liver enzymes get into blood and same with any enzyme not normally found in the blood
Necrosis
changes that follow cell death in living tissue (often due to hypoxia)
Apoptosis
programmed cell death that occurs normally in developing and adult tissues
Autolysis
postmortem dissolution and disintegration of cells or tissues by the enzymes present in those tissues
Types of necrosis
- coagulative
- liquefactive
- caseous
- fat
coagulative necrosis
- protein denaturation (coagulation)
- kidneys, heart
- often due to hypoxia
Liquefactive necrosis
- solid tissue is dissolved into fluid by hydrolyses
- brain: neural and glial cells
- often due to hypoxia
caseous necrosis
- combination of coagulative and liquefactive
- dead cells disintegrate, but the debris is not complete digested (tuberculosis)
fat necrosis
- lipases degrade triglycerides
- free fatty acids combine with calcium ions to form soaps (pancreas, and breast tissue)
Gangrene
necrosis + bacterial infection
- wet gangrene
- dry gangrene
- gas gangrene
wet gangrene
-neutrophils invade necrotic site causing secondary liquefaction
dry gangrene
area of coagulative necrosis becomes dried out, wrinkled, and dark black (likely diabetics since they have poor circulation)
gas gangrene
infection of necrotic tissue by clostridium species
pathologic calcification
- dystrophic calcification
- metastatic calcification
dystrophic calcification
- deposition of calcium in dead or dying tissues
- advanced arteriosclerosis
- evidence of previous cell injury
- often a cause of organ dysfunction
- for example: damaged heart valves
- normal blood levers but high number of injured cells
metastatic calcification
- occurs in normal tissues whenever there is hypercalcemia
- high blood levers and normal cells
