Biomed 3 Flashcards
Patho
suffering/disease
Ology
logic/lecture study of
Physiology
pertains to functions of organisms
pathophysiology
the systematic study of functional changes in cells/tissues
pathology
systematic study of structural alterations in cells/tissues
disease
a condition in which some functional, biomechanical or genetic abnormality of the body causes a loss of normal health
Aetiology
cause of disease
Pathogenesis
mechanisms of development of disease
Morphology
structural alterations induced in cell and tissues
clinical manifestation
obvious effects of the disease as it presents physically
Hypoxia
lack of sufficient oxygen to the cell, most common cell injury
chemical agents - causes of cellular injury
air pollutants, inhalation, direct contact of the cell with a toxic substance, formation of substances that cause lipids in the cell membrane
nutritional imbalances
deficiency or oversupply of certain nutrients in the body, protein deficiency, hyperlipidaemia
Physical agents - causes of cellular injury
hypothermic injury, hyperthermic injury, atmospheric pressure, sunlight trauma, musculoskeletal strains and sprains, frostbite
infectious agents - causes cellular injury
infectious microorganisms can enter the body - cause widespread or local damage to cells
genetic
changes in the DNA of a cell can cause changes in structure, function and metabolism.
atrophy
- decrease or shrinkage in cell size
- physiological occurs with early development
- pathological occurs as a result of decrease in workload, pressure, use, blood supply, nutrition and hormonal and nervous system stimulation
Hypertrophy
- increase in cell size and size of affected organ
- Mammary cells during pregnancy, increase in cardiac cells due to faulty valves
- It occurs due to mechanical signals, such as stretch
Hyperplasia
increase in cell numbers, which is resulting from an increased rate of cellular division
Dysplasia
Dysplasia describes the adaption of a cell that
changed their size and shape abnormally due to a stimulus over an extended period. If a cell is adapted into an abnormal shape/size this cell cannot reverse back to the original cell unless the damaging stimulus is removed immediately. The cells are often linked with cancer
Metaplasia
Cells change their shape and size to another cell type due to a certain stimulus such as smoking, for a short period of time. If the stimulus is affecting the cells for a short period only, then these cells are able to reverse to the original shape/size.
Apoptosis
o Programmed cell death
o Physiological: bone growth - osteoblast/osteoclast regeneration over the lifetime
o Pathological: result of intracellular events or advere external stimulus such as liver cells infected with hepatitis C
Necrosis
o Premature death of cells and living tissue
o Associated with inflammation
o Four types:
§ Coagulative - occurs in almost all tissues
§ Liquefactive - occurs primarily in the brain
§ Caseous - occurs in the lung due to tuberculosis
§ Fatty - occurs primarily in the pancreas and abdominal structures
o Gangrenous: refers to death of tissue from severe hypoxic injury
Chronic inflammation
Chronic inflammation is an extended reaction to an inflamed tissue that attempts destruction and repair at once
Cardinal signs of acute inflammation
redness, swelling, heat, pain, loss of function
causes of inflammation
biological agents, chemical agents, physical agents, immune reaction
muscle strain features
- most likely tear during sudden acceleration/deceleration
- Grade 1 - 3
Grade 1 muscle strain
small number of fibres affected, causes localised pain but no loss of strength
Grade 2 muscle strain
greater number of fibres affected, with associated pain and weakness
Grade 3 muscle strain
complete tear of the muscle, considerable pain and complete loss of function - most likely to occur at musculotendinous junction
Tendon injury - features
- acute overload
- may become chronically injured due to repeptitive movement/overload
- usually occur at points of poor blood supply
- Tendon and ligament repair are similar
Ligament sprains
- tearing of a few up to all of the fibres of a ligament
- Grade 1-3
- Tendon and ligament repair are similar
Grade 1 Ligament sprain
0-50% fibre disruption, but normal ROM on stressing the ligament
Grade 2 Ligament sprain
50-80% of fibres disrupted - stressing the ligament will reveal increased laxity but a definite end point
Grade 3 Ligament sprain
complete tear of a ligament, excessive joint laxity with no firm end point, can be pain free if sensory fibres are significantly damaged by the injury
Haemostasis
stoppage of blood loss at injury site, requires clotting factors and substances released by platelets and injured tissues, includes 3 steps
Step 1 - Vascular spasm (Haemostasis)
smooth muscle contracts, causing vascoconstriction, chemicals released by endothelial cells and platelets, pain reflexes
Step 2 - Platelet Plug Formation (Haemostasis)
injury to lining of vessel exposes collagen fibers, platelets adhere - platelets release chemicals that make nearby platelets sticky; platelet plug forms
platelets stick to collagen fibers that are exposed when a vessel is damaged
Step 3 - Coagulation (Haemostasis)
- Intrinsic (damaged vessel wall, Injury of vessel wall)
o Turbular blood flow in the blood vessel - Extrinsic (trauma to extravascular cells, Tissue injury)
o Damage that has occurred outside the vessel, such as a cut, injury to external tissues - prothrombin to thrombin
- common pathway to fibrin mesh
Thrombus
formation of presence of blood clot in a blood vessel
Embolus
an abnormal particle (e.g. an air bubble or part of a clot) circulating in the blood
Thromboembolus
If the clot breaks loose and travels through the bloodstream it is a thromboembolus
the body has several strategies to avoid inappropriate intravascular coagulation. What are they?
Platelet repulsion, thrombing, dilution, natural anticoagulants, smooth blood flow
Virchows triad
Hypercoagulability of blood, stasis of blood, vessel wall injuries
Arteriosclerosis
Thickening and loss of elasticity of arterial walls, can be caused by a range of diseases
- all result in impaired blood circulation
Atherosclerosis
build up of fat and fibrin within the arterial walls that hardens over time
leading cause of coronary heart disease and cerebrovascular disease
What are the risk factors of atherosclerosis?
modifiable: lifestyle factors, drinking, diet, stress-levels
non-modifiable: age, biological, sex, genetic predisposition
Varicose veins - type
superficial
Thrombophlebitis - type
both - superficial and deep
Deep vein thrombosis - type
deep
Varicose veins - definition
Vein in which blood has pooled, producing distended, torturous and palpable vessels. Often due to faulty or incompetent valves within veins
Thrombophlebitis definition
Thrombus formation in a vein with the obvious presence of inflammation
Deep vein thrombosis definition
Thrombus formation in a vein with the obvious presence of inflammation
deep vein thrombosis - risk factors
variscose veins, pregnancy, intravenous injections, anything in virchows triad
thrombophlebitis - risk factors
varicose veins, pregnancy, intravenous injections, anything in Virchows triad
Varicose veins risk factors
within the veins, standing on your feet, obesity, age, pregnancy, genetics, leg injury
Varicose veins - clinical signs/symptoms
visibly dark purple/blue in colour, appear twisted and bulging, may be palpable
achy/heavy feeling legs, burning, throbbing, muscle cramping and swelling in the legs
increase pain/swelling after sitting or standing for a long time
Thrombophlebitis clinical signs and symptoms
Tender, red, cord-like vein that is firm on palpation, potential localised heat and mild swelling
Deep vein thrombosis - clinical signs and symptoms
Swelling of affected limb, warmth, change in colour
Prothrombinase
converts prothrombin to thrombin
Thrombin
converts fibrinigen to fibrin
Fibrin function in coagulation
causes plasma to become gel-like; forms basis-structure of clot
Fibrinolysis
to loosen or to break down the clot
Why is fibrinolysis an essential process within our bodies?
to not block up the blood vessel, if blocked, no oxygen gets to the area which then ends in death of the area
What is a nociceptor?
Smallest unmyelinated and lightly myelinated primary afferent nerve fibres that are danger receptors
Allodynia
pain due to a stimulus that does not normally provoke pain
Hyperalgesia
increased pain from a stimulus that does normally provoke pain
Analgesia
absence of pain in response to a stimulation which would normally be painful
Neurapraxia
temporary interruption of nerve conduction, due to focal demyelination
Neurapraxia mechanism
mild or moderate compression
Neurapraxia - severity
mild
Neurapraxia - Wallerian Degeneration?
WD does not occur because the axon is not damaged
Neurapraxia - level of sensory and motor deficit
begin with paraesthesia & numbness, can progress to muscle weakness and wasting
Neurapraxia - Axon in tact?
yes
Neurapraxia - Myelin sheath in tact?
yes, however there is damage to the myelin sheath
Neurapraxia - neural connective tissue in tact?
yes
Neurapraxia - regeneration
recovery of conduction deficit is typically full (weeks to months)
Neurapraxia - surgery?
no surgical intervention required
Axonotmesis
loss of axonal and myelin continuity, however connective tissue framework is preserved
Axonotmesis - mechanism
result of acute crushing force, stretching/traction injury
Axonotmesis - severity
moderate
Axonotmesis - Wallerian degeneration
occurs distal to injury site
Axonotmesis - level of sensory and motor deficit
dependant on the percentage of axons disrupted
Axonotmesis - Axon in tact?
no
Axonotmesis - myelin sheath in tact?
yes however there is damage to the myelin sheath
Axonotmesis- neural connective tissue in tact?
yes but it may be compressed
Axonotmesis- regeneration
axonal regeneration occurs and recovery may be possible
Axonotmesis - surgery??
some surgical intervention may be required due to scar tissue formation
Neurotmesis
severe or disruption of the entire nerve including the axon and neural connectie tissue
Neurotmesis - mechanism
nerve may be severed by trauma
Neurotmesis - severity
severe
Neurotmesis - Wallerian degeneration
occurs distal to site of injury
Neurotmesis - level of sensory and motor deficit
completely lost
Neurotmesis - axon in tact?
no
Neurotmesis - myelin sheath in tact?
no
Neurotmesis - neural connective tissue in tact
no
Neurotmesis - regeneration
connective tissue scarring and poor regeneration tube formation often prohibits nerve repair
Neurotmesis - surgery?
essential for optimal outcomes, ASAP
routes of administration for a drug
enteral, topical, parenteral
Pharmacodynamics
what the drug does to the body, effects of what the drug does to the body
Pharmacokinetics
What the body does to a drug, how the body processes the drug
Pharmacology Agonist
a molecule that binds to specific receptors to cause a process in the cell to become more active
it will cause specific physiological response in the cell and can be natural or artificial
Pharmacology Antagonist
binds to a receptor but does not produce an action or reduces the effect of an agonist, block the process
Bioavailability of a drug
used to describe the percentage of administered dose of a medication that reaches the circulation in the unchanged form
how much of the drug can enter the bloodstream
Half-life of a drug
time that takes for the plasma concentration to reduce by 50%
Patient specific: age, sex, diet, kidney, liver function
drug specific: how the drug is administered, how the drug is cleared from the body, size of the drug
Adverse drug reaction
unintended harm, due to taking a medication a way it should be done
Adverse drug event
actual potential damage resulting from medical intervention related to medicine
therapeutic index
ratio between the therapeutic and toxic dose
Somites develop within which layer of the embryo?
mesoderm
What do the following regions of the somite give rise to?
Dermatome – dermis of the associated spinal levels
Myotome – muscles of associated spinal levels
Sclerotome – vertebrae, ribs at associated spinal level
when do the lower limbs rotate?
week 8
In which direction do the lower limb rotate?
medially/ventrally
In which direction do the upper limbs rotate?
laterally/dorsally
Ossification
A process in which new bone is produced - bone formation
When does ossification begin?
When does it end?
At the end of embryonic period (week 8)
completed by late adolescence (F: 18/M:21)
What type of bones form by endochondral ossification?
long, short and irregular bones
What type of bones form by intramembranous ossification?
mostly flat bones
Does intramembranous ossification involve a cartilaginous template
No, the mesenchyme forms a membranous template for the future bone
Flat bones (inner and outer layer)
Inner: spongy bone/diploe
Outer: compact bone
In endochondral ossification, where does the bone collar form?
around the diaphysis of the cartilaginous bone model
In what part of a long bone does the primary ossification centre form?
diaphysis
In what part of a long bone does the secondary ossification centre/s form?
Epiphysis
In a developing long bone, where will you find the epihyseal plate?
Metaphysis
Fertilisation
Day 1 - the beginning of gestation
Process that combines sperm and ovum together = creates zygote
Cleavage
Day 2-3
Series of rapid cell divisions that result in formulation of morula
Blastocyst
Day 4-5
Morula developed fluid filled cavity turning into a hollow ball of cell = blastocyst
Implantation
Day 7
Blastocyst has formed and implants onto uterine wall
Formation of two layer embryo
Week 2
Division into two layers:
- Epiblast (upper layer, forms embryo)
- Hypoblast (lower layer, forms supporting tissues, e.g.: placenta)
Gastrulation
Week 3
Transformed intro three layers on day 15 - ectoderm, mesoderm and endoderm
Primitive streak starts the process of grastrulation, process forms bilaminar into trilaminar embryo
Primitive streak function
establishes all major axes of the embryo
Embryonic folding
Week 4
Embryo is a trilaminar disc shape, grows rapidly and undergoes folding, end product is roughly a cylindrical 3D shape, vertebrae body shape
Tissue formed by ectoderm
CNS, PNS, epidermis of the skin, hair follicles and nails
Tissue formed by mesoderm
Blood vessels, heart walls, reproductive organs, dermis of the skin, muscle and most connective tissue
Tissue formed by endoderm
Epithelial lining and some glandular tissue of the GI, respiratory and urinary system
Neurulation
Week 3 and 4 of gestation
responsible for formation of the nervous system
What are the end products of neurulation and what will they become?
neural tube - brain and spinal cord
neural crest - peripheral nervous system
Apical ectodermal ridge
Structure called AER induce mesoderm and ectoderm to proliferate (grow) and create limb buds
- AER is a layer of cells which forms the cap of the limb bud and induces growth
Limb bud
Hyaline cartilage models of limb bones are developed
Hand plate
A hand/foot plate develops at the distal end of each elongating limb bud
Digital rays
Mesenchymal tissue forms digital rays within the hand/foot plate
Notches between digital rays
Apoptosis results in removal of cells between digital rays, resulting in seperate digits
webbed fingers
Apoptosis results in removal of cells between digital rays, resulting in seperate digits
Seperate fingers
Week 8 - all components of the upper and lower limb are distinct.
Bones will now undergo endochondral ossification - structure of the upper limb has now been formed, now it needs to get bigger and ossify
Limb rotation
In the 8th week the limbs rotate in opposite directions to reach the anatomical position.
The upper limb rotate laterally/dorsally. This is a relatively minor rotation which does not tend to change the alignment of the dermatomes.
The lower limbs rotate medially/ventrally. This is a more dramatic rotation which results in the dermatomes spiraling around the lower limb.
Direct Phosphorylation - Oxygen required?
No
Direct Phosphorylation - Intensity of activity
High
Direct Phosphorylation - Duration
Seconds
Direct Phosphorylation - Speed of production of energy
15 seconds
Direct Phosphorylation - ATP yield
1 ATP per CP
Direct Phosphorylation - activity example
High jump
Anaerobic pathway - oxygen required?
no
Anaerobic pathway - intensity of activity
medium
Anaerobic pathway - duration
seconds, minutes
Anaerobic pathway - Speed of production of energy
30-40 seconds
Anaerobic pathway - ATP yield
2 ATP per glucose
Anaerobic pathway - example of activity
400m sprint
Aerobic pathway - Oxygen required?
yes
Aerobic pathway - Intensity of activity
low
Aerobic pathway - Duration
hours
Aerobic pathway - Speed of production of energy
Hours
Aerobic pathway - ATP yield
32 ATP per glucose
Aerobic pathway - example activity
marathon
What is the role of myoglobin and why is it important for muscle contraction? Which fibre types have the highest number of myoglobin.
- Reservoir for oxygen within the muscle fibres
- Fast glycotic
Type 1 - Slow Oxidative Fibres - speed of contraction
slow
Type 1 - Slow Oxidative Fibres - primary pathway for ATP synthesis
Aerobic
Type 1 - Slow Oxidative Fibres - myoglobin content
high
Type 1 - Slow Oxidative Fibres - rate of fatigue
slow (fatigue resistant)
Type 1 - Slow Oxidative Fibres - activity type
endurance
Type 1 - Slow Oxidative Fibres
Mitochondria and Capillaries
Mitochondria - many
Capillaries - many
Type 2a - Fast oxidative fibres - speed of contraction
intermediate to fast
Type 2a - Fast oxidative fibres - primary pathway for ATP synthesis
aerobic, some anaerobic glycolysis
Type 2a - Fast oxidative fibres - myoglobin content
high
Type 2a - Fast oxidative fibres - rate of fatigue
intermediate
Type 2a - Fast oxidative fibres - activity type
sprinting, walking
Type 2a - Fast oxidative fibres - Mitochondria and capillaries
Mitochondria - many
Capillaries - many
Type 2b - Fast glycolytic fibres - speed of contraction
fast
Type 2b - Fast glycolytic fibres - Primary pathway for ATP
anaerobic
Type 2b - Fast glycolytic fibres - myoglobin content
low
Type 2b - Fast glycolytic fibres - rate of fatigue
fast
Type 2b - Fast glycolytic fibres - activity type
short-term intense or powerful movements, quick dynamical movements
Type 2b - Fast glycolytic fibres - Mitochondira and Capillaries
Mitochondira - few
Capillaries - few
key adaptions to muscle during endurance training
- Muscles need more ATP, number of mitochondria increase
- Increasing capillaries, for better oxygen and nutrients tranfer
- Most evident in the slow oxidative fibres
- Chronic endurance exercise will convert some fast glycolytic fibres into fast oxidative fibres
key adaptions to muscle during resistance training
- Increase in the number of mitochondria, myofilaments and myofibrils and glycogen storage – for power
- Promotes hypertrophy of the muscle cells
- Some fast oxidative fibres will convert to fast glycolytic fibres
Steps of muscle adaptions to resistance exercise on a cellulary level
- Exercise facilitates muscle cellular changes
- These are caused by ‘micro-traumas’ and metabolic muscle fatigue
- Myofibrils split and sub-divides
- Z-Lines split and divides
- Oblique pulling breaks the Z-disc, which constitutes a mechanical process
- The number of sarcomeres increases with increased function
neural adaptions that occur to resistance training
- Increased temporal and spatial summation of agonist and synergist motor units
- Decrease neural inhibitions
- Increased synchronisation of motor units
adaptions during isometric resistance training
muscle creates force while shortening
o Increase maximal force production
o Improved tendon structure and function
o Decreased tendon pain
adaptions during Isotonic resistance training
o Increase maximal force production
o Increased sarcomere length
o Improved tendon structure and function
