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Semester 1 > ToB Sessions 7-11 > Flashcards

ToB Sessions 7-11 Flashcards

1
Q

Where is the diaphysis of a long bone?

A

Narrow section in the middle i.e. shaft of humerus

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2
Q

Where is the metaphysis of a long bone?

A

Where the bone widens between the diaphysis and epiphysis

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3
Q

Do bones increase in girth as epiphyseal growth plates move apart?

A

No, only length

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4
Q

What is the first stage in converting the embryonic hyaline cartilage skeleton model into bone?

A

Collar of periosteum bone around diaphysis

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5
Q

As the central cartilage calcifies at the same position as the hyaline cartilage in endochondral ossification, what penetrates the precursor bone?

A

Artery to supply osteogenic cells

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6
Q

Where does the primary ossification centre of a long bone form?

A

At the diaphysis

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7
Q

What forms after the primary ossification centre has formed in endochondral ossification?

A

Growth plates

Secondary centres of ossification

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8
Q

Where are the secondary centres of ossification located in a long bone undergoing endochondral ossification?

A

Epiphyses

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9
Q

What does medulla turn into during endochondral ossification?

A

Cancellous bone

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10
Q

What causes lengthening of the bone in endochondral ossification?

A

Epiphyses ossifying and growth plates moving apart

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11
Q

What are epiphyseal growth plates replaced by?

A

Bone

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12
Q

How is old bone externally remodelled?

A

Epiphysis enlarges by growth of cartilage and replacement of bone
Spicules of bone form
Bone reabsorbed and added to narrow and give shape

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13
Q

How is young bone externally remodelled?

A

Cartilage grows
Columns extend from growth plate
Columns mineralised

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14
Q

What are the zones of bone remodelling?

A 
Bone and calcified cartilage
Zone of reserve cartilage
Zone of proliferation
Zone of hypertrophy
Zone of calcified cartilage
Zone of resorption
Bone, osteoclasts, BV and osteoblasts
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15
Q

What halogens in the zone of reserve cartilage in bone remodelling?

A

Matrix produced

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16
Q

What happens to cells in the zone of proliferation during bone remodelling?

A

Divide
Columns and cells enlarge
Matrix synthesised

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17
Q

What happens in the zone of hypertrophy in bone remodelling?

A

Cells enlarge
Matrix is formed
Cells arrange in linear bands

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18
Q

What happens in the zone of calcified cartilage in bone remodelling?

A

Degeneration

Matrix calcifies

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19
Q

What mixes in the zone of resorption during bone remodelling?

A

Spicules and bone marrow

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20
Q

In which direction does bone grow in bone remodelling?

A

Towards zone of reserve cartilage

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21
Q

What is the calcified matrix in direct contact with in the zone of resorption?

A

Marrow cavity

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22
Q

What invades the dying chondrocyte region in bone growth?

A

Small BV and CT

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23
Q

Where does intramembranous ossification take place?

A

W/in condensations of mesenchymal tissue

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24
Q

What happens in intramembranous ossification?

A

Mesenchyme cells –> osteoblasts –> osteocytes –> osteocytes linked by canaliculi

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25
Q

What bones are formed by intramembranous ossification?

A

Flat bones

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26
Q

Give some examples of flat bones.

A

Skull, maxilla, mandible, pelvis, scapula

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27
Q

What is unique about the formation of the clavicle?

A

Its medial end undergoes endochondral ossification and its lateral end undergoes intramembranous ossification so it is the first to start and last to finish ossifying

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28
Q

Does intramembranous ossification increase girth or length?

A

Girth

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29
Q

What happens to the mineral deposits in intramembranous ossification?

A

Radiate w/in trabeculae from the earlier primary ossification centre

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30
Q

What can be seen in section of intramembranous ossification?

A 
Newly formed woven bone
Osteoblasts, osteocytes, osteoclasts
Bony spicules connected to form trabeculae
Vascularised mesenchymal tissue
Periosteum w/osteoprogenitor cells
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31
Q

What makes the bone formed by intramembranous ossification indistinguishable from that formed by endochondral ossification during postnatal development?

A

Presence of osteocytes, osteons, Haversian and Volkmann’s canals

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32
Q

What is Osteogenesis Imperfecta?

A

Autosomal dominant group of inheritable disorders of CT

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33
Q

What do mutations in the gene for type I collagen as seen in Osteogenesis Imperfecta affect?

A 
Skeleton
Joints
Ears
Ligaments
Teeth
Sclerae
Skin
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34
Q

What can be visible on X-Ray in Osteogenesis Imperfecta?

A

Thin, attenuated long bones

Fracture calluses

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35
Q

Why is type II Osteogenesis Imperfecta a lethal perinatal disease?

A

Almost all bones are fractured during delivery/by uterine contractions

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36
Q

Why does a diagnosis of Osteogenesis Imperfecta have medicolegal importance?

A

Fractures can appear to be caused by deliberate injury

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37
Q

Where is growth hormone synthesised and stored?

A

Anterior pituitary gland

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38
Q

What does high levels of growth hormone before puberty cause?

A

Promoted epiphyseal growth late activity –> gigantism

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39
Q

What does high levels of growth hormone in an adult cause?

A

Increase in bone width –> acromegaly

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40
Q

What is acromegaly usually a result of?

A

Benign tumour of pituitary gland

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41
Q

Why is there no increase in bone length with raised GH in adulthood?

A

Epiphyseal plates have ossified

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42
Q

What feature of bone development do sex hormones influence?

A

Development of ossification centres

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43
Q

Why do sex hormone producing tumour retard bone growth?

A

Premature closing of epiphyseal growth plates

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44
Q

What is seen in the bones when there is a sec hormone deficiency?

A

Epiphyseal plates persist –> tall stature

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45
Q

Are androgens and oestrogens present in both males and females?

A

Yes

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46
Q

What gives rise to the pubertal growth spurt and induces secondary sexual characteristics?

A

Sex hormone

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47
Q

How is neonatal hypothyroidism readily reversed?

A

Prompt administration of thyroxine

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48
Q

What does untreated neonatal hypothyroidism lead to?

A

Cretinism and short stature

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49
Q

What is osteoporosis?

A

Metabolic bone disorder where mineralised bone is creased in mass to the point where it can no longer provide adequate mechanical support

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50
Q

What is osteopenia?

A

Precursor to osteoporosis defined as bone density one standard deviation below that of a 30 y.o. white female

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51
Q

What causes osteoporosis?

A

Osteoclasts outcompete osteoblasts

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52
Q

How does osteoporosis in the cortical nine compare to in the trabecular bone?

A

Cortical bone usually remains thick enough but trabeculae become narrow and prone to #

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53
Q

What is osteoporosis characterised by?

A

Pits in bone dug out by osteoclasts that are not repaired

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54
Q

Why do osteoporosis patients often stoop?

A

Compression #s occur in vertebral bodies and continue down spine to cause wedging of vertebrae

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55
Q

What is type 1 osteoporosis?

A

Increased osteoclast number in post menopausal women caused by oestrogen withdrawal (also decreased osteoblasts stimulation)

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56
Q

What is type 2 osteoporosis?

A

Senile: males and females over 70 have attenuated osteoblasts function

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57
Q

What are the risk factors for osteoporosis?

A 
Lack of exercise - no osteoblasts stimulation
Insufficient calcium absorption 
Insufficient calcium intake
Insufficient vitamin D
Cigarette smoking
Genetics
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58
Q

What is achondroplasia?

A

Most common form of short limb dwarfism

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59
Q

What inheritance pattern does achondroplasia show?

A

Autosomal dominant

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60
Q

What is the mentation and lifespan like in achondroplasia?

A

Normal

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61
Q

What causes achondroplasia?

A

Point mutation in fibroblast growth factor receptor 3 gene (FGFR3) causing decreased endochondral ossification, inhibited proliferation of chondrocytes in growth plate, decreased cellular hypertrophy and decreased cartilage matrix production

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62
Q

What is sealed off in achondroplasia?

A

Epiphyseal growth plate

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63
Q

What is rickets?

A

Childhood deficiency of vitamin D causing insufficient calcium deposition

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64
Q

Where is vitamin D obtained from?

A

Diet

Synthesised in skin by UV light

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65
Q

Where does vitamin D undergo hydroxylation?

A

First in liver

Then in kidney

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66
Q

What does PTH stimulate?

A

Bone degeneration

Calcium absorption by kidney

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67
Q

What is the purpose of hydroxylation get vitamin D twice?

A

To form active D3 to increase calcium absorption by the bowel and promote bone mineralisation

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68
Q

What is osteomalacia?

A

Adult form of vitamin D deficiency which causes insufficient calcium deposition

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69
Q

What changes in bone composition are seen in osteomalacia?

A

Too much non-mineralised bone –> thicker osteoid layer but a normal amount of bone matrix

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70
Q

What can cause osteomalacia?

A

Liver/kidney disease
Intestinal malabsorption
Poor diet
Lack of sunshine

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71
Q

What are the common #s seen in osteomalacia?

A

Femoral neck
Public ramus
Spine
Ribs

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72
Q

What is the consequence of two parents affected by achondroplasia having a homozygous child?

A

Child will not survive

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73
Q

How do most bones in the body develop?

A

Endochondral ossification from hyaline skeleton in foetus

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74
Q

What is myalgia?

A

Muscle pain

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75
Q

What is myasthenia?

A

Weakness of the muscles

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76
Q

What is myoclonus?

A

Sudden muscle spasm

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77
Q

Why is myopathy?

A

Any disease of the muscle

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78
Q

How is muscle tissue classified?

A

Striated or non-striated

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79
Q

Describe the structure of cardiac muscle.

A 
Short, branched cylinders
Single central nuclei in myocytes
Junctions join myocytes end to end
50-100 micrometers in length
10-20 micrometers in diameter
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80
Q

What type of muscle has an involuntary, intrinsic autonomy rhythm which is lifelong and variable?

A

Cardiac

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81
Q

Describe the structure of skeletal muscle.

A 
1 mm-20 cm cell length
10-100 micrometers cell diameter
Long parallel cylinders
Multiple peripheral nuclei
Fascicles bundles and tendons present
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82
Q

What controls skeletal muscle contraction?

A

Somatic motor neurones under voluntary control

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83
Q

What type of contraction can skeletal muscle generate?

A

Rapid and forceful

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84
Q

Describe the structure of smooth muscle.

A 
Spindle shaped myocytes w/tapering ends and single central nucleus
Gap and demosome-type junctions 
5-10 micrometer diameter
20-200 micrometer length
Connective tissue
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85
Q

How is the slow, sustained/rhythmic contraction of smooth muscle cells brought about?

A

Involuntary, autonomic, intrinsic activity or local stimuli

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86
Q

How does skeletal muscle develop?

A

Mesoderm ally derived multipotent myogenic stem cells –> myoblasts –> primary myotube –> newly synthesised actin and myosin filaments

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87
Q

How does development of cardiac and smooth muscle differ to skeletal?

A

Myoblasts do not fuse but develop ago junctions at a very early stage

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88
Q

What is characteristic of the primary myotube in skeletal muscle development?

A

Has multiple central nuclei

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89
Q

How are three types of skeletal muscle fibre identified?

A

Staining for reaction to NADH in mitochondria

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90
Q

What do the proportions of the different types of fibres seen in skeletal muscle depend on?

A

Function

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91
Q

Which type of skeletal muscle fibre has the largest diameter, poor vascularisation and myoglobin levels, few mitochondria and gives a fast and strong contraction?

A

White

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92
Q

What are the three types of skeletal muscle fibre?

A

Red
Intermediate
White

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93
Q

Which type of skeletal muscle fibre has a smaller diameter, is rich in vascularisation and myoglobin, has numerous mitochondria and gives a slow, repetitive, weak contraction?

A

Red

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94
Q

Which type of skeletal muscle fibre fatigues the quickest?

A

White

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95
Q

How do the enzymes in red and white skeletal muscle fibres vary?

A

Red: rich in oxidative, poor in ATPase
White: poor in oxidative, rich in ATPase

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96
Q

Which type of skeletal muscle fibre has more neuromuscular junctions and is found in the extraocular muscles and fingers?

A

White

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97
Q

Where are red skeletal muscle fibres typically found?

A

Limbs

Postural muscles

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98
Q

What is the gross structure of skeletal muscle?

A

Myofibrils –> muscle fibre –> fascicle –> muscle

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99
Q

What surrounds each muscle fibre?

A

Endomysium

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100
Q

What surrounds each fascicle in skeletal muscle?

A

Perimysium

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101
Q

What surrounds the entirety of a skeletal muscle?

A

Epimysium

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102
Q

What is found in the perimysium?

A

Nerves and BV

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103
Q

Where can circular, convergent and parallel structured skeletal muscles be found?

A

Circular: round the mouth
Convergent: pectorais major
Parallel: sartorius

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104
Q

Where can unipennate, bipennate, multipennate and fusiform muscle be found?

A

Unipennate: extensor digitorum longus
Bipennate: rectus femoris
Multipennate: deltoid
Fusiform: biceps brachii

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105
Q

What is the difference between extrinsic and intrinsic skeletal muscle?

A

Extrinsic attach to bones via tendons and allow changes of position. Intrinsic allow change of shape as they are not attached to bone

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106
Q

What allows retraction and side to side movement of the tongue?

A

Protusion of extrinsic muscles

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107
Q

What allows the tongue to changes shape?

A

Intrinsic muscles

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108
Q

How is MHAZI related to myofilament arrangement?

A

M line in H zone which is in the A band

Z disc is in the I band

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109
Q

What is a sarcomere?

A

Length of muscle fibre form Z-line to Z-line

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110
Q

What is the ultra structural appearance of skeletal muscle?

A

In TS enclosures w/dots show myofibrils w/myosin filaments
Abundant mitochondria
Period ally positioned nuclei

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111
Q

How do the bands change in the sliding filament model of muscle contraction?

A

A band is constant

I band shrinks

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112
Q

What forms the thin filaments of skeletal and cardiac muscle?

A

Actin, tropomyosin and troponin molecules in a complex

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113
Q

Which part of the thin filament is useful for assays to investigate chest pain?

A

Troponin - cardiac specific I and T

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114
Q

Which three troponin said form the troponin complex seen in thin filaments?

A

I, C and T

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115
Q

What is the structure of the thin filament of skeletal and cardiac muscle?

A

Actin forms helix
Tropomyosin molecules coil round actin helix
Troponin complex attached to each tropomyosin molecule

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116
Q

What is the structure of thick filaments in skeletal and cardiac muscle?

A

Many myosin filaments whose heads protrude at opposite ends of the filament

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117
Q

Where are the thick filaments devoid of myosin heads?

A

In the centre of the sarcomere

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118
Q

What is rigor configuration?

A

Lack of ATP perpetuates tight binding of myosin head to actin molecule (in death –> rigor mortis)

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119
Q

Describe the myosin-actin interaction in the first stage of contraction?

A

Myosin head in high-energy conformation - ADP and Pi bound

Myosin cross bridge attaches to actin myofilament

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120
Q

What happens in the working stroke of muscle contraction?

A

ADP and Pi released

Myosin head pivots and bends as it pulls on actin filament sliding towards the M line

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121
Q

What happens to the myosin head when it is in the low energy configuration during contraction?

A

New ATP attaches and cross bridge detaches

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122
Q

What happens to ATP when the myosin head is cocked during contraction?

A

Hydrolysed

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123
Q

What is the role of ionic calcium in the contraction mechanism?

A

Bind to TnC of troponin complex to cause a conformational change to move tropomyosin away from the binding site of actin so myosin can bind

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124
Q

What is the neuromuscular junction?

A

Small terminal swelling of the axon containing vesicles of ACh

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125
Q

Why are calcium and sodium ions needed in the neuromuscular junction?

A

Calcium for ACh vesicle fusion and release

Sodium needed in muscle for general depolarisation to release calcium for contraction

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126
Q

What causes depolarisation of the sarcolemma at the NMJ?

A

Nerve impulse along motor neurone axon prompts release of

ACh into synaptic cleft

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127
Q

How does depolarisation spread over the sarcolemma?

A

V-G sodium channels open, general depolarisation spreads over
T-tubules

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128
Q

How does depolarisation over the sarcolemma cause initiation of the contraction cycle?

A

Voltage sensor proteins change conformation so calcium is released from terminal cisternae into sarcoplasm and bind to TnC in troponin

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129
Q

What happens to calcium after it has initiated the contraction cycle?

A

Returned to terminal cisternae of sarcoplasmic terminal

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130
Q

How are T-tubules arranged in skeletal muscle?

A

Triads of 2 terminal cisternae of the SR + tubule itself at every AI junction (so twice in every sarcomere)

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131
Q

What is the function of T-tubules in skeletal muscle?

A

Allow wave of general depolarisation to move across the SR so calcium are released

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132
Q

What features identify cardiac muscle in longitudinal section?

A

Striations
1 or 2 centrally positioned nuclei per cell
Intercalated discs
Branching

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133
Q

What is the function of intercalated discs in cardiac muscle?

A

Substitute Z bands and have gap junctions for electrical coupling and adherens-type junctions to anchor cells and provide anchorage for actin filaments

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134
Q

How does cardiac muscle appear in transverse section?

A

Central nuclei
Capillary rich endomysium
Lobular profiles from emergence of branches

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135
Q

What is the purpose of branching in cardiac muscle?

A

Helps w/synchronised contraction

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136
Q

How does the ultrastructure of cardiac muscle appear in transvers section?

A

Continuous mass of actin and myosin

Mitochondria and SR penetrate b/w myofilaments

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137
Q

How does the position of T tubules in cardiac muscle differ to in skeletal muscle?

A

Lie in register w/ Z bands no AI junction are organised as diads

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138
Q

How are action potentials generated in the SAN spread across the heart?

A

Pass to AVN then ventricles via distal conducting cells of Purkinje fibres

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139
Q

What are Purkinje fibres?

A

Large, modified myocytes w/less actin and myosin, abundant glycogen and extensive gap junction sites that conduct action potentials much more rapidly than cardiac muscle fibres

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140
Q

Why are actin and myosin filaments arranged diagonally and spiralling along longitudinal axis of smooth muscle cells?

A

So smooth muscle contracts in twisting way

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141
Q

What is the function of intermediate filaments in smooth muscle cells?

A

Attach to dense bodies scattered throughout sarcoplasm

Occasionally anchor to the sarcolemma

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142
Q

Is calcium needed for contraction in smooth muscle cells?

A

Yep

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143
Q

How does the contraction of smooth muscle compare to that of skeletal/cardiac?

A

Slower
More sustained - can stay contracted for hours-days
Needs less ATP

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144
Q

What is the relationship between stretch and strength of contraction in smooth muscle cells?

A

More stretched, stronger it contracts

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145
Q

What causes smooth muscle contraction?

A

Nerve signals
Hormones
Drugs
Local blood gas concentrations

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146
Q

What is the clinical significance of smooth muscle?

A

Often form contractile walls of passageways or cavities so their volume can be modified

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147
Q

What are the two types of modified smooth muscle cells?

A

Myofibroblasts

Myoepithelial cells

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148
Q

What is the role of myofibroblasts?

A

Produce collagenous matrix at sites of wound healing - abundant actin and myosin
Pull sides of wound together

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149
Q

What is the role of myoepithelial cells?

A

Stellar cells form basketwork around secretory units of some exocrine glands and assist secretion
Dilate pupil in ocular iris

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150
Q

How is most smooth muscle innervated by the ANS?

A

Releases neurotransmitters from variscoties into a wide synaptic cleft

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151
Q

How does skeletal muscle repair?

A

Satellite cells increase mitotic activity and fuse w/existing muscle cells to cause skeletal muscle hypertrophy

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152
Q

How does cardiac muscle repair?

A

Can’t regenerate so after damage fibroblasts invade, divide and lay down scar tissue

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153
Q

How does smooth muscle repair?

A

Has mitotic activity so can undergo hyperplasia

154
Q

Where can hypertrophy and hyperplasia of cells in combination be seen physiologically?

A

Pregnant uterus

155
Q

Which clinical conditions are associated with smooth muscle?

A 
Hypertension
Dysmenorrhea
Abnormal gut mobility
Atherosclerosis
Asthma
156
Q

What is skeletal muscle needed for?

A

Movement
Posture
Stability of joints
Heat generation

157
Q

Which component of myocytes can increase and decrease in number?

A

Actin and myosin myofilaments

158
Q

What is remodelling in skeletal muscle?

A

Continuous process by which contractile proteins are replaced within two weeks

159
Q

What are the effects of exercise on skeletal muscle?

A 
Metabolic adaptation - increased ATPase
Sarcoplasmic reticulum swells
Increased volume of mitochondria
Increased Z band width
Increased density of T tubules
Increased number of contraction proteins
160
Q

How does endurance exercise such as jogging change muscle?

A

Stimulate synthesis of mitochondrial proteins
Vascular changes for greater oxygen utilisation
Increase endurance w/out hypertrophy

161
Q

Does atrophied muscle have more nuclei than normal?

A

No, just appears so due to less cellular volume meaning more cells in one area

162
Q

How does high resistance exercise change muscle?

A

Stimulates contractile protein synthesis
Fatter muscle fibres and larger muscle
Increases muscle mass and strength
Hypertrophy by satellite cells

163
Q

What happens to muscle in denervation atrophy?

A

Loss of protein
Reduced fibre diameter
Loss of power

164
Q

What is the time scale of nerve repair if a nerve is split?

A

Want to rejoin ends to allow axon to grow done centre w/in 3 months but will not happen 2+ years after injury

165
Q

What are the signs of denervation atrophy?

A

Weakness
Flaccidity
Muscle atrophy

166
Q

What does sustained stretching do to skeletal muscle?

A

Adjusts muscle length and alters CT arrangement

167
Q

How is muscle length adjusted?

A

Unknown - potentially addition of sarcomere a

168
Q

At high motor neurone firing rates what percentage of ACh receptors need to be occupied for the muscle to remain contracted?

A

25

169
Q

What terminates ACh in the NMJ?

A

Acetylcholinesterase

170
Q

What is myasthenia gravis?

A

Autoimmune destruction of ACh receptors and junctional folds at end plate

171
Q

What are the S/S of myasthenia gravis?

A

Drooping of eyelids, double vision, unable to hold arm out for long

172
Q

Why are small muscles affected first in myasthenia gravis?

A

Loss of few muscle fibres is greater proportion so is more noticeable

173
Q

What causes symptoms to fluctuate in myasthenia gravis?

A

General state of health
Fatigue
Emotion

174
Q

How is myasthenia gravis treated?

A

AChE inhibitors
Immune suppressants
Plasmapheresis
Thyrectomy if thymus problems present

175
Q

What in the motor neurone can be affected by toxins that affect the NMJ?

A

Sodium channels
Calcium channels
ACh release
Potassium channels

176
Q

What do tetanus and botulinum toxin interfere with?

A

ACh release

177
Q

What can be affected by toxins acting on muscle in the NMJ?

A

Sodium channels
AChR channel
AChE

178
Q

What is Duchenne-type muscular dystrophy?

A

Complete absence of dystrophin chain in cell allowing muscle fibres to create tearing force on contraction and calcium entry into cell causing necrosis

179
Q

What causes pseudohypertrophy in DMD?

A

Replacement of cells by fat and CT

180
Q

What are the S/S of DMD?

A

Early onset Gower’s sign

Contractures

181
Q

What causes contractures in DMD?

A

Imbalance b/w agonist and antagonist muscles

182
Q

What can be used to measure muscle damage in DMD?

A

Creatine (phospho) kinase

183
Q

What is the treatment for DMD?

A

Short term steroids (they cause muscle damage)

Gene therapy?

184
Q

What is the mutation in the most common and noticeable type of muscular dystrophy?

A

Altered truncated dystrophin in Becker-type muscular dystrophy

185
Q

What are the 7 types of muscular dystrophy?

A 
Duchenne-type
Becker-type
Enary-Dreifuss
Limb girdle
Fascioscapulohumeral
Distal 
Occulopharyngeal
186
Q

Which muscles are particularly affected in DMD?

A

Shoulders
Upper arm
Thigh
Lateral leg

187
Q

What skeletal muscle disorder does hypoparathyroidism cause?

A

Hypocalcaemia –> tetany

188
Q

What skeletal muscle disorder can arise under general anaesthetic?

A

Malignant hyperthermia - high calcium levels

189
Q

What can cause primary muscle disease?

A

Systemic disease
Electrolyte imbalances
Inflammation
Muscular dystrophies

190
Q

How does thyrotoxicosis cause skeletal muscle disorders?

A

Increases protein catabolism and BMR

191
Q

Why are pathogens?

A

Disease causing organisms

192
Q

What are Protozoa, bacteria, viruses, fungi and worms all made of?

A

Proteins, carbohydrates and lipids

193
Q

What causes food poisoning?

A

Campylobacter jejuni

194
Q

How does the immune system detect pathogens?

A

Identifies their different amino acid sequences

195
Q

Why have pathogens evolved to damage the host if it alerts the immune system?

A

Break through barriers to move to more prosperous region so damage and subsequent alert is inevitable

196
Q

What is the first line of defence against infection?

A

Epithelial cells

197
Q

What roles do epithelial cells have in protecting against infection?

A

Block entry of microorganisms
Produce natural antibiotics
Some possess motile cilia and produce mucin
Produce cytokines and chemokines
Transport antibodies from ‘inside’ to ‘outside’

198
Q

What natural antibiotics are produced by epithelial cells?

A

Cationic bacterial peptides - defensins and catheliadins

199
Q

What are cytokines?

A

Proteins that alter the behaviour of other cells

200
Q

What are chemokines?

A

Proteins that attract other cells

201
Q

How are pathogens cleared from epithelial surfaces?

A 
Mucociliary escalator
Sneezing
Coughing
Regular urine flow
Nasal hairs
Ear wax
Flow of tears
Blinking
Peristalsis
Sebum 
Digestive enzymes
Vomiting
202
Q

What are the constituents of sebum?

A

Lactic and fatty acid at a pH of 3-5

203
Q

What do epithelial cells do when activated by pathogen attack?

A

Release cytokines

204
Q

What do inflammatory mediators promote?

A

Increased permeability of the BV

205
Q

What is humoral escape?

A

Cell and fluid migration out of BV that have increased permeability

206
Q

What follows after humoral escape in pathogen attack?

A

Opsonisation and phagocytosis

207
Q

What happens to antibodies and complement at the site of infection?

A

Extravasation of antibodies and complement

208
Q

What happens to the macrophages and neutrophils during cell and fluid migration in response to pathogen attack?

A

Increased microbiocidal activity

209
Q

What are the five cardinal signs of inflammation?

A 
Heat
Redness
Swelling
Pain
Loss of function
210
Q

Which cells are specific to the adaptive immune response?

A

B and T lymphocytes

211
Q

What is the function of antibodies?

A

Block entry
Opsonise
Neutralise
Activate complement

212
Q

What governs the innate immune response?

A

Tissues

Myeloid cells

213
Q

What governs the adaptive immune response?

A

Lymphocytes

214
Q

Is the adaptive immune system cell mediated or humoral immunity?

A

Both

215
Q

What is the innate immune response?

A

Inbuilt immunity to resist infection which is native, natural and present from birth

216
Q

Why is the innate immune response not enhanced by a second exposure?

A

Has no memory so gives same response

217
Q

How are the innate and adaptive immune responses linked?

A

They are poorly effective w/out each other, innate is involved in triggering and amplifying adaptive

218
Q

Which cells are involved in the innate immune system?

A 
Macrophages
Monocytes
Neutrophil
Polymorphonucelar leucocytes
Eosinophils
Basophils
Mast cells
Natural killer cells
219
Q

What is adaptive immunity?

A

Immunity established to adapt to infection which is ‘specific’ or ‘acquired’ and learnt by experience

220
Q

Why is the adaptive immune system enhanced by second exposure?

A

It has memory and confers pathogen-specific immunity

221
Q

Which cells are involved in the adaptive immune system?

A

Lymphocytes

222
Q

What is the role of eosinophils?

A

To attack parasites when activated by IgE presence

Assoc. w/allergy

223
Q

What is the first event of inflammatory response?

A

Arrival of neutrophils

224
Q

How are neutrophils specialised?

A

Can work in the anaerobic conditions found in damaged tissues

225
Q

What happens to neutrophils once they are activated?

A

Can not make more granules so they use the ones they have and die

226
Q

What will patients with neutrophil deficiency suffer from?

A

Recurrent infections, often from microbes of the normal commensal flora

227
Q

How do neutrophils bind to bacteria in order to engulf and digest them?

A

Express lipopolysaccharide receptors for many bacterial constituents

228
Q

Can macrophages continue to generate more lysosomes as needed?

A

Yep

229
Q

Are macrophages short-lived or long-lived?

A

Long-lived

230
Q

What act as professional antigen presenting cells in the development of adaptive immunity to break up pathogen and present parts so it can be recognised by T lymphocytes?

A

Macrophages

231
Q

What is opsonisation?

A

Coating of a microorganism by antibodies or complement to render it recognisable as foreign by phagocytes

232
Q

What does binding of an antibody to a bacteria cause?

A

Activation of complement and bonding of C3b to bacteria

233
Q

What mediates engulfment of a bacterium following opsonisation?

A

Fc and complement receptors

234
Q

How are bacteria killed following opsonisation?

A

Granules fuse w/phagosomes to release toxic oxygen metabolites

235
Q

Which cells are phagocytes?

A

Macrophages and neutrophils

236
Q

What can phagocytes do in the event of parasite infection?

A

Release lysosome contents on the outside of the large pathogen

237
Q

Which cells release chemical mediators that stimulate NK cell activation?

A

Mast

Macrophages

238
Q

Which cells do NK cells closely resemble?

A

T and B lymphocytes - need staining to distinguish

239
Q

What is the function of NK cells?

A

Recognise and kill abnormal cells by directly inducing apoptosis in virus-infected cells

240
Q

How do NK cells kill virus-infected cells?

A

Pump proteases through pores they make in the target cell to directly induce apoptosis

241
Q

What are NK cells an analogue of?

A

Cytotoxic T cells

242
Q

What do NK cell deficient patients suffer from?

A

Persistent viral infection, esp. Herpes which cannot be cleared despite adaptive immune response

243
Q

What do viral infections induce cells to secrete?

A

Burst of cytokines

244
Q

What do cytokines do to NK cells?

A

Induce proliferation and their activation

245
Q

What does the slower cytotoxic T cell response do?

A

Develops to help clear the infection

246
Q

What are the secretory molecules of the innate immune system?

A 
Interferon
Lysozyme
Fibronectin
TNF-alpha
Transferrin/lactoferrin
247
Q

Where are complement proteins ubiquitous?

A

Blood and lymph

248
Q

Where are complement proteins synthesised?

A

Liver and some epithelial tissues

249
Q

What is the role of membrane attack complexes?

A

Assemble to make pore in membrane and punch holes in plasmamlemma

250
Q

Which role of the complement system is most important for host defence against infection?

A

Recruitment of inflammatory cells

251
Q

What enhances complement activation?

A

Antibodies

252
Q

What can be used immediately after infection begins and long before any pathogen specific antibody is made?

A

Complement proteins

253
Q

What is Type III immune complex disease?

A

Inherited complement deficiency of C1, 2 and 4 which results in aggregations of toxins bound by antibodies to not be cleared from the blood

254
Q

What does an inherited deficiency of C3 cause?

A

Recurrent bacterial infection

255
Q

What does an inherited C5-9 deficiency cause?

A

Recurrent Neisserial infections which will only present clinically w/meningitis and gonorrhea

256
Q

What can be said about the activity of T and B lymphocytes?

A

Inactive until exposed to antigens

257
Q

Which type of cell do B cells give rise to?

A

Plasma cells

258
Q

What is the function of plasma cells?

A

Produce antibodies

259
Q

What do plasma cells need to function?

A

Permission from T helper cells

260
Q

Which types of cell can T lymphocytes give rise to?

A

T helper

Cytotoxic T lymphocytes

261
Q

What is the role of T helper cells?

A

Activate B cells and macrophages by releasing cytokines upon activation

262
Q

What do T helper cells need to function?

A

Antigen presenting cells

263
Q

What is the role of cytotoxic T lymphocytes?

A

Present endogenous antigen to major histocompatibility complex which directly kills virus infected cells

264
Q

In which three ways can antibodies protect the host from infection?

A

Neutralisation
Opsonisation
Complement activation

265
Q

Why is the adaptive immune response said to have a clonal nature?

A

Each naive lymphocyte bearing a unique receptor is the potential progenitor of a genetically identical clone of daughter cells

266
Q

What are lymphocytes of a particular specificity too infrequent to mount an effective response in adaptive immunity?

A

Clonal distribution

267
Q

What is the function of clonal selection?

A

Increase clonal frequency of cells w/particular antigen specificity

268
Q

What happens in the process of clonal selection?

A

Antigen interaction
Lymphocyte activation
Daughter cells bear identical specificity
Proliferation induced
Effector cell frequency increases which allows for memory
Secondary response has more antibodies

269
Q

How is memory seeded in the adaptive immune response?

A

Clonal selection and expansion –> differentiation to effector cells –> humoral and cell mediated immunity –> T and B cell apoptosis but lots remain for memory seeding

270
Q

Which cell do cells of the adaptive immune response originate from?

A

Common lymphoid precursor

271
Q

What does the notochord stimulate?

A

Neural tube formation

272
Q

What does the notochord define?

A

Midline

273
Q

What happens to the neural plate during neurulation?

A

Differentiates, thickens and folds to form the neural tube

274
Q

What differentiates to form the brain and spinal cord?

A

Neural tube

275
Q

What limits signalling by the notochord?

A

Diffusion of signal molecules

276
Q

What creates the proud, slipper-shaped neural plate?

A

Notochord releasing signals which cause overlying ectoderm to thicken

277
Q

What happens to the neural plate to form the neural tube?

A

Edges elevate out of the plane of the disc and curl towards each other

278
Q

What does the mesoderm give rise to?

A

Largest number of derivatives in the body

279
Q

What are the three types of mesoderm present in the trilaminar disc?

A

Intermediate
Somatic
Splanchnic

280
Q

What is found between the somatic and splanchnic mesoderm in the trilaminar disc?

A

Intraembryonic coelom

281
Q

What do the different types of mesoderm give rise to?

A

Intermediate: uritogenito tract
Somatic: body
Splanchnic: viscera

282
Q

What forms somites?

A

Organisation of paraxial mesoderm into segments

283
Q

How do somites appear?

A

Sequentially w/first pair at day 20 and subsequently at 3 pairs a day

284
Q

Why can somites be used for aging an embryo?

A

Sequence of presentation is regular

285
Q

Why do some somites disappear?

A

So that 31 are left in total which corresponds to the number of pairs of spinal nerves

286
Q

What is organised degeneration of the somites?

A

Ventral walls break down to form sclerotome

Dorsal wall forms dermomyotome of which the myotome proliferates and migrates and the dermatome disappears

287
Q

What does the dermomyotome give rise to?

A 
Back muscles
Dermis
Myotomes
Ventral body wall muscles
Limb muscles
288
Q

What does the sclerotome give rise to?

A

Proximally: vertebral body
Distally: vertebral arch
Vertebrae
Ribs

289
Q

What is a dermatome?

A

Strip of skin supplied by a single spinal nerve

290
Q

What is a myotome?

A

Single/group of muscles supplied by a single spinal nerve

291
Q

What does the paraxial mesoderm give rise to?

A

Axial skeleton
Dermis
Some limb muscles

292
Q

What is embryonic folding driven by?

A

Neural tube formation

293
Q

What happens in cephalocaudal folding?

A

Head folds first then tail

294
Q

What follows cephalocaudal folding?

A

Lateral folding

295
Q

What drives lateral folding of the embryo?

A

Expansion

296
Q

What is the result of folding of the embryo?

A

Only ectoderm can be seen irrespective of direction of view

297
Q

How does a cavity form in the embryo?

A

Pinched off an incorporated by cephalocaudal folding

298
Q

What happens to the amniotic sac in folding of the embryo?

A

Moves from sitting on top of the embryo to enclosing it

299
Q

What do the lateral edges of the developing embryo do during folding?

A

Push downwards

300
Q

What happens to the somatic and splanchnic mesoderm during embryonic folding?

A

They open further

301
Q

How does embryonic folding draw together the margins of the embryonic disc?

A

Creates a ventral body wall
Pulls amniotic membrane around disc
Pulls connecting stalk ventrally

302
Q

What are the results of embryonic folding?

A

Embryo suspended within amniotic sac
Primordium of gut created from yolk sac
Heart and diaphragm primordium in right place
Forms new cavity within the embryo

303
Q

What are the three main events in week 4 of embryonic development?

A

Neurulation
Organisation of the mesoderm
Segmentation

304
Q

What has happened by the end of the fourth week of development?

A

Nervous system has started to form
Segments have appeared assigning specific tasks to specific cells
Embryo folded so entirely covered by ectoderm and there is a cavity inside
Everything is in the right place

305
Q

What is the lifespan of a RBC?

A

120 days

306
Q

What is the lifespan of a platelet?

A

10 days

307
Q

How do the lifespans of WBC differ?

A

Neutrophils: 2-4 days
Lymphocytes: 1 day - years

308
Q

Where are RBCs, platelets and most WBCs produced?

A

Bone marrow

309
Q

Which system removes RBCs from the circulation?

A

Reticuloendothelial

310
Q

Which organs are involved in the reticuloendothelial system?

A

Spleen mainly but other organs can take over if spleen is compromised

311
Q

How does the bone marrow in the infant compare to in the adult?

A

Extends into periphery but retracts w/age

312
Q

How can cell trails be examined to see if red and white precursors are normal?

A

Take bone from iliac crest and decalcify

313
Q

Where can bone marrow predominantly be found in the adult?

A 
Pelvis
Sternum
Skull
Ribs
Vertebrae
314
Q

How does the production of RBCs, platelets and granulocytes compare?

A

RBCs and platelets produced at 2.5 bn cells/kg/day

1 bn granulocytes produced /kg/day

315
Q

What is haemopoiesis?

A

Process by which all blood cells are derived from progenitor stem cells

316
Q

What drives haemopoiesis?

A

Cytokines such as erythropoietin, thrombopoietin, G-CSF, GMSCF, IL-6 etc

317
Q

What do all blood cells derive from?

A

Haemocytoblasts

318
Q

What precursor do megakaryocytes, erythrocytes, mast cells and myeloblasts all derive from?

A

Common myeloid progenitor

319
Q

What do myeloblasts give rise to?

A

Basophils
Neutrophils
Eosinophils
Monocytes

320
Q

What can a monocytes become within a tissue?

A

Macrophage

321
Q

Where do all myeloblasts derivatives transform?

A

In tissues

322
Q

What does myeloid mean?

A

Generally WBC but anything not lymphoid

323
Q

What stimulates transformation of megakaryocytes into thrombocytes?

A

Thrombopoietin

GM-CSF

324
Q

What do common lymphoid progenitor cells transform into?

A

Small lymphocytes

Natural killer cells

325
Q

What is a B lymphocyte?

A

Transformed small lymphocyte plasma cell not seen in the circulation

326
Q

What name is given to a small lymphocyte which has passed through the thymus?

A

T lymphocyte

327
Q

What plays a major role in the development of lymphoid cells?

A

Interleukins

Tumour necrosis factors

328
Q

How much can one unit of blood raise the haemoglobin levels of an individual?

A

10/L per unit

329
Q

What are RBCs?

A

Bacon cave flexible discs with a diameter of 8 micrometers which carry oxygen in its reduced (ferrous) state to tissues

330
Q

What must enzymes in the RBCs do?

A

Maintain osmotic equilibrium so that they can move through the microcirculation

331
Q

How do RBCs generate ATP?

A

Anaerobic glycolytic pathway

332
Q

What makes up the membrane of an RBC?

A

Actin and spectrin structure with glycophorins, glycoproteins and antigens

333
Q

What maintains elasticity of the RBCs?

A

Actin and spectrin structure

334
Q

Which pathways are used in RBC metabolism?

A

Embolen Meyerhof which metabolises glucose to lactate

Hexose monophosphate pathway to metabolise G6P

335
Q

What do the globin chains in haemoglobin protect the haem molecule from?

A

Oxidation

336
Q

When does beta-haemoglobin chain production start?

A

~3-6 months

337
Q

What transition occurs in early life which causes a shift of the oxygen dissociation curve to the left?

A

Switch from HbF –> HbA

338
Q

What are delta-haemoglobin chains good for?

A

Thalassaemia diagnosis but nothing else

339
Q

Where are primitive oxygen carriers formed in the developing embryo?

A

Yolk sac

340
Q

Is oxyhaemoglobin the R or T state of haemoglobin?

A

Relaxed R state

341
Q

How are RBCs broken down?

A

RBCs –> haemoglobin –> heam –> bilirubin

342
Q

Where can bilirubin go from the liver?

A

Straight to kidney

Stored in gall bladder –> small intestine then large and into kidneys

343
Q

What is bilirubin that passes to the kidneys called?

A

Urobilinogen

344
Q

What is sterobilin?

A

Bilirubin excreted from the GI tract

345
Q

What happens in erythropoiesis?

A

Kidney senses hypoxia
Increases endogenous erythropoietin production
Erythropoietin acts on E-progenitor cells in BM
RBCs maturation and release
Hb and p(oxygen) increase detected by kidney and decreases erythropoietin production

346
Q

Where is hypoxia sensed in the kidneys?

A

Interstitial peritubular cells

347
Q

How are platelets formed?

A

Magakaryocytes increase in size and replicate DNA

TPO causes platelets to bud off from the cytoplasm

348
Q

What are platelets?

A

2-3 micrometer diameter cell fragments w/no nuclei, mostly stored in the spleen

349
Q

What is the structure of a platelet?

A

Phospholipid membrane
Glycoprotein receptors
Glycoprotein alpha granules
Dense bodies of 5HT, ADP, catecholamines and calcium

350
Q

What is the function of the dense bodies present in platelets?

A

ADP release for aggregation

351
Q

What is the function of the glycoprotein receptors in the membrane of platelets?

A

Platelet adhesion

352
Q

What does primary platelet aggregation cause?

A

Activation of the clotting cascade

353
Q

What does secondary aggregation of platelets cause?

A

Fibrin mesh to form in clot formation

354
Q

What is the purpose of the fibrin mesh in clot formation?

A

Trap platelets and RBCs

355
Q

How does platelet aggregation occur?

A

Damage to vessel wall exposes underlying tissue and platelets can bind to blood glycoprotein von Willebrand factor

356
Q

Why must platelets be kept moving in clinical practice?

A

Keep them agitated so they will work

357
Q

What are the stages of neutrophil maturation?

A

Myeloblast –> promyelocyte –> myelocyte –> metamyelocyte –> bond –> neutrophil

358
Q

How can neutrophils be identified on histological examination?

A

Multiplied nucleus w/granular cytoplasm

359
Q

What is the effect of GCSF on neutrophils?

A

Increase production
Decreases time for release from BM
Enhances chemotaxis
Enhances phagocytosis and killing of pathogens

360
Q

What do neutrophils use to destroy pathogens?

A

Hypochlorous acid and lysozymes

361
Q

What is the role of monocytes?

A

Migrate to tissues and become macrophages
Respond to inflammation and antigenic stimuli
Phagocytosis and pinocytosis

362
Q

What do lysosomes w/in monocytes contain to stimulate production of more monocytes?

A 
Lysozyme
Complement
Interleukins
Arachidonic acid
CSF
363
Q

How do monocytes enter tissues?

A

Diapedesis (roll)

364
Q

What is the function of eosinophils?

A

Spend 3-8 hrs in circulation to migrate to epithelial tissues to phagocytise antigen-antibody complexes and mediate hypersensitivity reactions such as asthma and skin inflammation

365
Q

What do the granules in eosinophils contain?

A

Arginine
Phospholipid
Enzymes

366
Q

What is the lifespan of an eosinophil?

A

8-12 days

367
Q

What do basophils resemble on histological examination?

A

Blackberries

368
Q

What is the function of basophils?

A

Active in allergic reactions

369
Q

Which are the least common of the circulating leucocytes which have a half life of 2.5 days?

A

Basophils

370
Q

What do the dense granules in basophils contain?

A

Histine
Heparin
Hyaluronic acid
Serotonin

371
Q

Are lymphocytes active in the circulation?

A

Nope

372
Q

Which type of cells use the same mechanism of using peroxide to kill cells by cytotoxic activity?

A

T cells and natural killer cells

373
Q

What do CD4+ helper cells do?

A

Induce proliferation and differentiation of T and B cells as well as activate macrophages

374
Q

What do CD8+ suppressor cells do?

A

Induce apoptosis in infected cells

375
Q

What happens when T lymphocytes migrate to the thymus?

A

Undergo receptor gene rearrangement

376
Q

Can B lymphocytes recirculate?

A

Yes

377
Q

Which lymphocytes are part of humoral immunity?

A

B lymphocytes

378
Q

What do B lymphocytes do when they interact with T lymphocytes?

A

Transform to plasmablasts or memory cells within lymph nodes

379
Q

What do plasmablasts do?

A

Migrate from lymph nodes to BM to form plasma cells which produce antigen specific antibodies

380
Q

Which type of lymphocytes are involved in cellular immunity?

A

T

381
Q

What do NK cells carry?

A

Membrane receptors for functional end of Ig

Semester 1 (7 decks)

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