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First Year Osteopathy > Biomed 3 > Flashcards

Biomed 3 Flashcards

1
Q

Patho

A

suffering/disease

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2
Q

Ology

A

logic/lecture study of

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3
Q

Physiology

A

pertains to functions of organisms

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4
Q

pathophysiology

A

the systematic study of functional changes in cells/tissues

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5
Q

pathology

A

systematic study of structural alterations in cells/tissues

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6
Q

disease

A

a condition in which some functional, biomechanical or genetic abnormality of the body causes a loss of normal health

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7
Q

Aetiology

A

cause of disease

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8
Q

Pathogenesis

A

mechanisms of development of disease

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9
Q

Morphology

A

structural alterations induced in cell and tissues

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10
Q

clinical manifestation

A

obvious effects of the disease as it presents physically

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11
Q

Hypoxia

A

lack of sufficient oxygen to the cell, most common cell injury

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12
Q

chemical agents - causes of cellular injury

A

air pollutants, inhalation, direct contact of the cell with a toxic substance, formation of substances that cause lipids in the cell membrane

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13
Q

nutritional imbalances

A

deficiency or oversupply of certain nutrients in the body, protein deficiency, hyperlipidaemia

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14
Q

Physical agents - causes of cellular injury

A

hypothermic injury, hyperthermic injury, atmospheric pressure, sunlight trauma, musculoskeletal strains and sprains, frostbite

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15
Q

infectious agents - causes cellular injury

A

infectious microorganisms can enter the body - cause widespread or local damage to cells

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16
Q

genetic

A

changes in the DNA of a cell can cause changes in structure, function and metabolism.

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17
Q

atrophy

A
  • 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
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18
Q

Hypertrophy

A
  • 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
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19
Q

Hyperplasia

A

increase in cell numbers, which is resulting from an increased rate of cellular division

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20
Q

Dysplasia

A

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

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21
Q

Metaplasia

A

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.

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22
Q

Apoptosis

A

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

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23
Q

Necrosis

A

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

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24
Q

Chronic inflammation

A

Chronic inflammation is an extended reaction to an inflamed tissue that attempts destruction and repair at once

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25
Q

Cardinal signs of acute inflammation

A

redness, swelling, heat, pain, loss of function

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26
Q

causes of inflammation

A

biological agents, chemical agents, physical agents, immune reaction

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27
Q

muscle strain features

A
  • most likely tear during sudden acceleration/deceleration
  • Grade 1 - 3
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28
Q

Grade 1 muscle strain

A

small number of fibres affected, causes localised pain but no loss of strength

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29
Q

Grade 2 muscle strain

A

greater number of fibres affected, with associated pain and weakness

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30
Q

Grade 3 muscle strain

A

complete tear of the muscle, considerable pain and complete loss of function - most likely to occur at musculotendinous junction

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31
Q

Tendon injury - features

A
  • 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
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32
Q

Ligament sprains

A
  • tearing of a few up to all of the fibres of a ligament
  • Grade 1-3
  • Tendon and ligament repair are similar
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33
Q

Grade 1 Ligament sprain

A

0-50% fibre disruption, but normal ROM on stressing the ligament

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34
Q

Grade 2 Ligament sprain

A

50-80% of fibres disrupted - stressing the ligament will reveal increased laxity but a definite end point

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35
Q

Grade 3 Ligament sprain

A

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

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36
Q

Haemostasis

A

stoppage of blood loss at injury site, requires clotting factors and substances released by platelets and injured tissues, includes 3 steps

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37
Q

Step 1 - Vascular spasm (Haemostasis)

A

smooth muscle contracts, causing vascoconstriction, chemicals released by endothelial cells and platelets, pain reflexes

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38
Q

Step 2 - Platelet Plug Formation (Haemostasis)

A

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

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39
Q

Step 3 - Coagulation (Haemostasis)

A
  • 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
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40
Q

Thrombus

A

formation of presence of blood clot in a blood vessel

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41
Q

Embolus

A

an abnormal particle (e.g. an air bubble or part of a clot) circulating in the blood

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42
Q

Thromboembolus

A

If the clot breaks loose and travels through the bloodstream it is a thromboembolus

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43
Q

the body has several strategies to avoid inappropriate intravascular coagulation. What are they?

A

Platelet repulsion, thrombing, dilution, natural anticoagulants, smooth blood flow

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44
Q

Virchows triad

A

Hypercoagulability of blood, stasis of blood, vessel wall injuries

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45
Q

Arteriosclerosis

A

Thickening and loss of elasticity of arterial walls, can be caused by a range of diseases
- all result in impaired blood circulation

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46
Q

Atherosclerosis

A

build up of fat and fibrin within the arterial walls that hardens over time
leading cause of coronary heart disease and cerebrovascular disease

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47
Q

What are the risk factors of atherosclerosis?

A

modifiable: lifestyle factors, drinking, diet, stress-levels
non-modifiable: age, biological, sex, genetic predisposition

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48
Q

Varicose veins - type

A

superficial

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49
Q

Thrombophlebitis - type

A

both - superficial and deep

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50
Q

Deep vein thrombosis - type

A

deep

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51
Q

Varicose veins - definition

A

Vein in which blood has pooled, producing distended, torturous and palpable vessels. Often due to faulty or incompetent valves within veins

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52
Q

Thrombophlebitis definition

A

Thrombus formation in a vein with the obvious presence of inflammation

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53
Q

Deep vein thrombosis definition

A

Thrombus formation in a vein with the obvious presence of inflammation

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54
Q

deep vein thrombosis - risk factors

A

variscose veins, pregnancy, intravenous injections, anything in virchows triad

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55
Q

thrombophlebitis - risk factors

A

varicose veins, pregnancy, intravenous injections, anything in Virchows triad

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56
Q

Varicose veins risk factors

A

within the veins, standing on your feet, obesity, age, pregnancy, genetics, leg injury

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57
Q

Varicose veins - clinical signs/symptoms

A

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

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58
Q

Thrombophlebitis clinical signs and symptoms

A

Tender, red, cord-like vein that is firm on palpation, potential localised heat and mild swelling

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59
Q

Deep vein thrombosis - clinical signs and symptoms

A

Swelling of affected limb, warmth, change in colour

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60
Q

Prothrombinase

A

converts prothrombin to thrombin

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61
Q

Thrombin

A

converts fibrinigen to fibrin

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62
Q

Fibrin function in coagulation

A

causes plasma to become gel-like; forms basis-structure of clot

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63
Q

Fibrinolysis

A

to loosen or to break down the clot

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64
Q

Why is fibrinolysis an essential process within our bodies?

A

to not block up the blood vessel, if blocked, no oxygen gets to the area which then ends in death of the area

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65
Q

What is a nociceptor?

A

Smallest unmyelinated and lightly myelinated primary afferent nerve fibres that are danger receptors

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66
Q

Allodynia

A

pain due to a stimulus that does not normally provoke pain

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67
Q

Hyperalgesia

A

increased pain from a stimulus that does normally provoke pain

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68
Q

Analgesia

A

absence of pain in response to a stimulation which would normally be painful

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69
Q

Neurapraxia

A

temporary interruption of nerve conduction, due to focal demyelination

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70
Q

Neurapraxia mechanism

A

mild or moderate compression

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71
Q

Neurapraxia - severity

A

mild

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72
Q

Neurapraxia - Wallerian Degeneration?

A

WD does not occur because the axon is not damaged

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73
Q

Neurapraxia - level of sensory and motor deficit

A

begin with paraesthesia & numbness, can progress to muscle weakness and wasting

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74
Q

Neurapraxia - Axon in tact?

A

yes

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75
Q

Neurapraxia - Myelin sheath in tact?

A

yes, however there is damage to the myelin sheath

76
Q

Neurapraxia - neural connective tissue in tact?

A

yes

77
Q

Neurapraxia - regeneration

A

recovery of conduction deficit is typically full (weeks to months)

78
Q

Neurapraxia - surgery?

A

no surgical intervention required

79
Q

Axonotmesis

A

loss of axonal and myelin continuity, however connective tissue framework is preserved

80
Q

Axonotmesis - mechanism

A

result of acute crushing force, stretching/traction injury

81
Q

Axonotmesis - severity

A

moderate

82
Q

Axonotmesis - Wallerian degeneration

A

occurs distal to injury site

83
Q

Axonotmesis - level of sensory and motor deficit

A

dependant on the percentage of axons disrupted

84
Q

Axonotmesis - Axon in tact?

A

no

85
Q

Axonotmesis - myelin sheath in tact?

A

yes however there is damage to the myelin sheath

86
Q

Axonotmesis- neural connective tissue in tact?

A

yes but it may be compressed

87
Q

Axonotmesis- regeneration

A

axonal regeneration occurs and recovery may be possible

88
Q

Axonotmesis - surgery??

A

some surgical intervention may be required due to scar tissue formation

89
Q

Neurotmesis

A

severe or disruption of the entire nerve including the axon and neural connectie tissue

90
Q

Neurotmesis - mechanism

A

nerve may be severed by trauma

91
Q

Neurotmesis - severity

A

severe

92
Q

Neurotmesis - Wallerian degeneration

A

occurs distal to site of injury

93
Q

Neurotmesis - level of sensory and motor deficit

A

completely lost

94
Q

Neurotmesis - axon in tact?

A

no

95
Q

Neurotmesis - myelin sheath in tact?

A

no

96
Q

Neurotmesis - neural connective tissue in tact

A

no

97
Q

Neurotmesis - regeneration

A

connective tissue scarring and poor regeneration tube formation often prohibits nerve repair

98
Q

Neurotmesis - surgery?

A

essential for optimal outcomes, ASAP

99
Q

routes of administration for a drug

A

enteral, topical, parenteral

100
Q

Pharmacodynamics

A

what the drug does to the body, effects of what the drug does to the body

101
Q

Pharmacokinetics

A

What the body does to a drug, how the body processes the drug

102
Q

Pharmacology Agonist

A

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

103
Q

Pharmacology Antagonist

A

binds to a receptor but does not produce an action or reduces the effect of an agonist, block the process

104
Q

Bioavailability of a drug

A

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

105
Q

Half-life of a drug

A

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

106
Q

Adverse drug reaction

A

unintended harm, due to taking a medication a way it should be done

107
Q

Adverse drug event

A

actual potential damage resulting from medical intervention related to medicine

108
Q

therapeutic index

A

ratio between the therapeutic and toxic dose

109
Q

Somites develop within which layer of the embryo?

A

mesoderm

110
Q

What do the following regions of the somite give rise to?

A

Dermatome – dermis of the associated spinal levels
Myotome – muscles of associated spinal levels
Sclerotome – vertebrae, ribs at associated spinal level

111
Q

when do the lower limbs rotate?

A

week 8

112
Q

In which direction do the lower limb rotate?

A

medially/ventrally

113
Q

In which direction do the upper limbs rotate?

A

laterally/dorsally

114
Q

Ossification

A

A process in which new bone is produced - bone formation

115
Q

When does ossification begin?
When does it end?

A

At the end of embryonic period (week 8)
completed by late adolescence (F: 18/M:21)

116
Q

What type of bones form by endochondral ossification?

A

long, short and irregular bones

117
Q

What type of bones form by intramembranous ossification?

A

mostly flat bones

118
Q

Does intramembranous ossification involve a cartilaginous template

A

No, the mesenchyme forms a membranous template for the future bone

119
Q

Flat bones (inner and outer layer)

A

Inner: spongy bone/diploe
Outer: compact bone

120
Q

In endochondral ossification, where does the bone collar form?

A

around the diaphysis of the cartilaginous bone model

121
Q

In what part of a long bone does the primary ossification centre form?

A

diaphysis

122
Q

In what part of a long bone does the secondary ossification centre/s form?

A

Epiphysis

123
Q

In a developing long bone, where will you find the epihyseal plate?

A

Metaphysis

124
Q

Fertilisation

A

Day 1 - the beginning of gestation

Process that combines sperm and ovum together = creates zygote

125
Q

Cleavage

A

Day 2-3

Series of rapid cell divisions that result in formulation of morula

126
Q

Blastocyst

A

Day 4-5

Morula developed fluid filled cavity turning into a hollow ball of cell = blastocyst

127
Q

Implantation

A

Day 7

Blastocyst has formed and implants onto uterine wall

128
Q

Formation of two layer embryo

A

Week 2

Division into two layers:
- Epiblast (upper layer, forms embryo)
- Hypoblast (lower layer, forms supporting tissues, e.g.: placenta)

129
Q

Gastrulation

A

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

130
Q

Primitive streak function

A

establishes all major axes of the embryo

131
Q

Embryonic folding

A

Week 4

Embryo is a trilaminar disc shape, grows rapidly and undergoes folding, end product is roughly a cylindrical 3D shape, vertebrae body shape

132
Q

Tissue formed by ectoderm

A

CNS, PNS, epidermis of the skin, hair follicles and nails

133
Q

Tissue formed by mesoderm

A

Blood vessels, heart walls, reproductive organs, dermis of the skin, muscle and most connective tissue

134
Q

Tissue formed by endoderm

A

Epithelial lining and some glandular tissue of the GI, respiratory and urinary system

135
Q

Neurulation

A

Week 3 and 4 of gestation

responsible for formation of the nervous system

136
Q

What are the end products of neurulation and what will they become?

A

neural tube - brain and spinal cord
neural crest - peripheral nervous system

137
Q

Apical ectodermal ridge

A

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

138
Q

Limb bud

A

Hyaline cartilage models of limb bones are developed

139
Q

Hand plate

A

A hand/foot plate develops at the distal end of each elongating limb bud

140
Q

Digital rays

A

Mesenchymal tissue forms digital rays within the hand/foot plate

141
Q

Notches between digital rays

A

Apoptosis results in removal of cells between digital rays, resulting in seperate digits

142
Q

webbed fingers

A

Apoptosis results in removal of cells between digital rays, resulting in seperate digits

143
Q

Seperate fingers

A

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

144
Q

Limb rotation

A

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.

145
Q

Direct Phosphorylation - Oxygen required?

A

No

146
Q

Direct Phosphorylation - Intensity of activity

A

High

147
Q

Direct Phosphorylation - Duration

A

Seconds

148
Q

Direct Phosphorylation - Speed of production of energy

A

15 seconds

149
Q

Direct Phosphorylation - ATP yield

A

1 ATP per CP

150
Q

Direct Phosphorylation - activity example

A

High jump

151
Q

Anaerobic pathway - oxygen required?

A

no

152
Q

Anaerobic pathway - intensity of activity

A

medium

153
Q

Anaerobic pathway - duration

A

seconds, minutes

154
Q

Anaerobic pathway - Speed of production of energy

A

30-40 seconds

155
Q

Anaerobic pathway - ATP yield

A

2 ATP per glucose

156
Q

Anaerobic pathway - example of activity

A

400m sprint

157
Q

Aerobic pathway - Oxygen required?

A

yes

158
Q

Aerobic pathway - Intensity of activity

A

low

159
Q

Aerobic pathway - Duration

A

hours

160
Q

Aerobic pathway - Speed of production of energy

A

Hours

161
Q

Aerobic pathway - ATP yield

A

32 ATP per glucose

162
Q

Aerobic pathway - example activity

A

marathon

163
Q

What is the role of myoglobin and why is it important for muscle contraction? Which fibre types have the highest number of myoglobin.

A
  • Reservoir for oxygen within the muscle fibres
  • Fast glycotic
164
Q

Type 1 - Slow Oxidative Fibres - speed of contraction

A

slow

165
Q

Type 1 - Slow Oxidative Fibres - primary pathway for ATP synthesis

A

Aerobic

166
Q

Type 1 - Slow Oxidative Fibres - myoglobin content

A

high

167
Q

Type 1 - Slow Oxidative Fibres - rate of fatigue

A

slow (fatigue resistant)

168
Q

Type 1 - Slow Oxidative Fibres - activity type

A

endurance

169
Q

Type 1 - Slow Oxidative Fibres
Mitochondria and Capillaries

A

Mitochondria - many
Capillaries - many

170
Q

Type 2a - Fast oxidative fibres - speed of contraction

A

intermediate to fast

171
Q

Type 2a - Fast oxidative fibres - primary pathway for ATP synthesis

A

aerobic, some anaerobic glycolysis

172
Q

Type 2a - Fast oxidative fibres - myoglobin content

A

high

173
Q

Type 2a - Fast oxidative fibres - rate of fatigue

A

intermediate

174
Q

Type 2a - Fast oxidative fibres - activity type

A

sprinting, walking

175
Q

Type 2a - Fast oxidative fibres - Mitochondria and capillaries

A

Mitochondria - many
Capillaries - many

176
Q

Type 2b - Fast glycolytic fibres - speed of contraction

A

fast

177
Q

Type 2b - Fast glycolytic fibres - Primary pathway for ATP

A

anaerobic

178
Q

Type 2b - Fast glycolytic fibres - myoglobin content

A

low

179
Q

Type 2b - Fast glycolytic fibres - rate of fatigue

A

fast

180
Q

Type 2b - Fast glycolytic fibres - activity type

A

short-term intense or powerful movements, quick dynamical movements

181
Q

Type 2b - Fast glycolytic fibres - Mitochondira and Capillaries

A

Mitochondira - few
Capillaries - few

182
Q

key adaptions to muscle during endurance training

A
  • 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
183
Q

key adaptions to muscle during resistance training

A
  • 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
184
Q

Steps of muscle adaptions to resistance exercise on a cellulary level

A
  • 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
185
Q

neural adaptions that occur to resistance training

A
  • Increased temporal and spatial summation of agonist and synergist motor units
  • Decrease neural inhibitions
  • Increased synchronisation of motor units
186
Q

adaptions during isometric resistance training

A

muscle creates force while shortening
o Increase maximal force production
o Improved tendon structure and function
o Decreased tendon pain

187
Q

adaptions during Isotonic resistance training

A

o Increase maximal force production
o Increased sarcomere length
o Improved tendon structure and function

First Year Osteopathy (8 decks)

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