Chapter 4 Altered Cellular & Tissue Biology Flashcards
Why do cells adapt
To escape and protect themselves from injury
What is atrophy
Decrease in cellular sizeWh
What are the mechancicsm of atrophy
Decrease protein synthesis and increase protein metabolism
What is hypetrophy
Increase in cellular size
What are the mecahncims of atropjy
Increase in protein synthesisWh
What is hyperplasia
Increase in number of cells due to cell divisions
What is the mechanics of hyperplasia
Release of growth hormones
What is dysplasia (Atypical hyperplasia)
Abnormal size, shape, or organization of the cells
What is metaplasia
Reversable replacement of one mature cell type by another
Affects of ATP depletion
Reduces cells ability to maintain essential functions.
Leads to failure of energy dependent functions resulting in cellular dysfunction and death
Mitochondrial Damage
Affects ATP production and triggers apoptosis
Release cytochrome C which activates cell death pathways
Oxygen and free radical damage
Free radicals cause lipid per oxidation, protein modification, and DNA damage
Result from hypoxia and reperfusion injury
Protein folding mechanisms
Misfiling proteins accumulate disrupting cellular function and disrupting triggering cellular death
DNA Damage defects
Mutations or breaks in DNA can lead to malfunction cells or cancer
Calcium level alterations
Disrupts cell signalling, leading to activation of enzymes that damage cell components
What is ischemia reperfusion injury
This occurs when blood flow and oxygen is restored causing further injury
Mechanisms include increased oxidative stress
Increased intracellular calcium
Inflammation
Complment activation
What is the affect of prolonged hypoxia
Valculoation, lysomal swelling
Oxidative stress
Occurs when ROS overwhelms the bodies antioxidant defences leading to cellular damage
Free Radicals
Unstable molecules with unpaired electrons making them highly reactive and capable of injuring key cellular components
They stabilize by donating or accepting electrons which can turn other molecules into free radicals causing a chain reaction
Sources of free radicals
Redox reactions (Normal respirations(
Absorption of extreme energy (Uv light and radiation)
Enzymatic metabolism of chemicals
Transition metals
Nitric oxide
Lipid per oxidation
Destruction of polyunsaturated lipids damaging cells and increasing permeability
Protein alterations
Causes fragmentation and misfiling proteins impacting cell function
DNA Damage
Leads to mutations contributing to cellular function and disease
Implications of oxidative stress
plays a role in many pathological conditions including chemical and radiation injuries aging immune responses and schema reperfusion injury
ROS can alter intracellular signalling pathways modulating enzymes and transcription factors involved in cell regulation
What are xenobotics
Foreign compounds including toxic mutagenic and carcinogenic chemical
What organ is the most susceptible to xenobiotic induced injury
Liver
How does liver process the injected chemicals
The liver metabolizes xenobiotics through biotransformation converting lipophilic compounds into hydrophilic forms for excretion
This process can produce toxiphores though which can damage proteins and DNA through concealment binding forming adducts
Electrophiles
Attract to electrons, acce[t electrons creating charged centres that can disrupt cellular structures
Nucleophiles
Donate electron pairs and can be oxidized to free radicals causing further dmage
Adduct formation
Leads to protein dysfunction fibrogeneis and immune activation
Defence mechanisms against xenobiotics
Cytochrome p-450 causes oxidation reduction and hydrolysis Conjugation enzymes like glutathione detoxify reactive intermediates making them water soluble, efflux transporter enzymes remove xenobiotics from cells
What does antioxidant systems do against xenobiotics
Counteract the effects of rot and other active species
Refer to box 4.1 on page 83 for more info on free radicals
Mechancims of chemical injurt
Direct damage: Chemicals interact with critical molecular substances such as cyandie inhibiting mitochondrial function
Exaggerated response: Overdose such as birth defects from thalidomide or tumours from industrial chemical
Toxic metabolites: Many chemicals are biologivcally inactive until metabolized by enzymes like cytochrome p45- leading to toxic intermediates that damage cell membranes through free radicals
Hypersensitivity reactions
Carmon toxic agents
Lead and carbon monoxide which binds to o2 more effectively than o2
What are asphyxial injuries
a failure of cells to receive oxygen
what is the pathogenicity (virulence) of an organizm
The ability to survive and proliferate in the human body
What does the disease producing potential of a microorganism depend on i
It depends on its ability to invade and destroy cells, produce toxins and produce damaging hypersensitivity reactions
What happens when a membrane is damaged
There is rapid leakage of potassium out of the cell and an influx of water
Antibodies bind to membrane receptors blocking their function and destroying cellular junctions (cell communicators)
What are infiltrations
Acculations result from sustained injury or inefficient normal cell functions and can be toxic or harmless
Mechanicsms of abnormal intracellular acccumulaton
Insufficient removal (altered packaging and transport)
Abnormal substance accumulation (Defective protein folding or degradation)
Inadequate metabolism
lack of vital lyxsomal enzymes
Accumulation of heavy metal dust or microorganisms
What are the signs and symptoms of accumulation
Causes tissues to swell as well ad phagocytes try to remove excess substances
hemoproteins
Include hug and cytochromes responsible for oxygen transport and cellular respiration
Accumulation of iron due to breakdown of hemoprotesin can lead to hemosiderosis
What is dystrophic calculations
Occurs in dying or dead tissue despite normal calcium levels
What is metastatic calciufication
Occurs in normal tissues due to hyperglycemia
What is urate crystals
Result from disorders in purine. metabolism
what is oncosis
Cellular swelling due to shift of water into cells it is reversible
Causes oncosis
Hypoic injury
Atp depletion
Ion imbalance (NA in cell K out of cell)
What pathophysiological changes occurs with oncosis
Sweeping or ER cistern, rupture and formaition of large values
Clinical manifestations of oncosis
Increase weight pale and distended organ
Refer to slide 21 and 22 for manifestations of cellular injury
What is necrosis
Leathal cell injury or accidental cell death and the process of cellular autodigestion
Characteristics of necrosis
Rapid loss of the plasma membrane structure
Swelling
mitochondrial dysfunction
Coagulative necrosis
Associated with ischemia or hypoxia commonly seen in solid organs
Liquefactive nectosis
Usually associated with infections and brain injuries commonly observed in brain due to its high water cnotent
Causes necrosis
Associated with tuberculosis
Programmed necorisis
Is a term for regulated or programmed necrosisW
What is apoptosis
Programmed cellular death (physiological not pathological)
Apoptosis process
Cells death that involves orderly dismantling of cell components and packing the remainder in vesicles there is no loss of mitochondrial function
Aging characteristics
Increased damage to cells and reduced repair capacity
accumulation of damage accumulation of Falange in in dividing cells
Somatic death
Death of the person not cellular death
Signs of death
No respiration and circulation becomes pale algor mortis (Temp decrease to room temperature)
Occular changes decreased bp in retinal festal cause pupil dilation
Liver mortis blood settles in dependent tissues creating a purple discolouration skin becomes less elasticc and transparent
Purtefecation
Apparent 24-48 hours after death
Signs and symptoms of purtefecation
green skin, loosening skin enzymatic breakdown and tissue dissolution
What is rigor mortis
Muscle stiffening after death
What is liquefactive necrosis
When cells are digested by their own enzymes and become soft and runny
What is autophagy
When cells digests its own components
What is Caseous necrosis
Dead cells disintegrate but debris is not digested completely
Coagulative necrosis
Cell death in which denatured proteins appear firm and opaqu
Liver mortis
blood settles in dependent tissues creating a purple discolouration
Which cell death causes inflammation
Necrosis
Dysplasia
Refers to abnormal change
During schema what ion is involved and what does it do
Calcium damages the membrane
How does ROS damage cells
They attack the membranes of a cell
True or false postmortem changes involve the inflammatory response
False
Gangeren occurs when cells dies of
Hypoxia
