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Y1 Medicine > L&B + CV&R - Non-Anatomy Lectures > Flashcards

L&B + CV&R - Non-Anatomy Lectures Flashcards

1
Q

What are the 2 types of bone ?

A

Cortical (compact) and trabecular (spongy)

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2
Q

What type of bone makes up diaphyses (shafts) ?

A

Cortical

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3
Q

What type of bone makes up epiphyses (ends of bone) and vertebral bodies ?

A

Trabecular

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4
Q

Which bone type is more susceptible to conditions associated with increased bone turnover ?

A

Trabecular

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5
Q

What percentage of the human skeleton is comprised of trabecular bone ?

A

20%

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6
Q

What percentage of bone is inorganic ?

A

70%

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7
Q

What percentage of bone is organic ?

A

22%

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8
Q

What percentage of bone is water ?

A

5-8%

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9
Q

What is inorganic bone comprised of ?

A

95% calcium hydroxyapatite (the rest is impurities)

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10
Q

What is organic bone composed of ?

A

85% collagen type 1, 15% other collagens, proteins, glycoproteins and cells

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11
Q

What are the 3 types of bone cell ?

A

Osteoblasts
Osteoclasts
Osteocytes
(+ osteogenic)

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12
Q

What is the function of osteoblasts ?

A

Bone formation, regulation of bone turnover

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13
Q

What is the function of osteocytes ?

A

Sense mechanical strain and release signals (prostaglandins, nitric oxide) that modulate the function of neighbouring cells

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14
Q

Where are osteocytes found ?

A

Embedded in the bone matrix, each within their own lacuna

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15
Q

What is the function of osteoclasts ?

A

Bone removal (resorption)

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16
Q

What are osteoblasts and osteocytes derived from ?

A

mesenchymal stem cell precursor

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17
Q

What are osteoclasts derived from ?

A

hemopoietic mononuclear cells

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18
Q

What are the 4 stages of the bone remodelling cycle ?

A

Quiescence
Resorption
Reversal
Formation

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19
Q

What are osteoclasts rich in ?

A

Enzyme TRAP

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20
Q

What does the RANK-RANKL interaction do ?

A

Responsible for osteoclasts maturation, Stimulates bone resorptive activity of mature osteoclasts

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21
Q

What does osetoprotegerin (OPG) do ?

A

It bins to RANKL and prevents RANK activation, inhibiting osteoclasts formation

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22
Q

What do osteoclasts secrete ?

A

Hydrochloride acid and proteolytic enzymes

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23
Q

What can mesenchymal stem cells differentiate into ?

A

Osteoblasts, myocytes and chondrocytes

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24
Q

What molecule causes osteoblasts differentiation ?

A

Cbfa1

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25
Q

What do osteoblasts secrete ?

A

Cytokines/GF, enzymes and proteins

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26
Q

What are the 2 eventual forms of osteoblasts ?

A

Osteocytes or lining cells

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27
Q

What secretes RANKL?

A

Osteoblasts

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28
Q

What do osteoblasts secrete that creates new bone ?

A

Osteoid

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29
Q

What stimulates bone remodelling ?

A

IL-1,tumour necrosis factor, PTH, Vit D

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30
Q

What inhibits bone remodelling ?

A

Oestrogens, androgens and calcitonin

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31
Q

What changes to the spine occur during adolescence ?

A

Increase in size and trabecular thickness

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32
Q

What changes to the long bones occur during adolescence?

A

Increased length and diameter

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33
Q

What age is peak bone mass obtained ?

A

~30 yrs

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34
Q

What happens to bone mass post-menopause?

A

Accelerated bone loss

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35
Q

What do oestrogens and androgens do to bone ?

A

Oestrogen = bone maturation and mineralisation
Androgen = proliferate chondrocytes

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36
Q

Define osteoporosis

A

A decrease in bone mass causing compromised bone strength and an increased risk of fracture

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37
Q

What happens to trabecular bone in osteoporosis?

A

The trabecular thins and it’s continuity is disrupted

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38
Q

What causes post-menopausal osteoporosis (PMO)?

A

decided oestrogen levels, resulting in an excess of RANK-L

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39
Q

What percentage of BMD variability is caused by genetic factors ?

A

60-80%

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40
Q

What is Colles fracture ?

A

Falling onto outstretched hand , radius fractures and displaces dorsally

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41
Q

At what age does the risk of hip fractures massively increase ?

A

70 yrs

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42
Q

Name 3 risk factors for osteoporotic fractures

A

Older than 65, family history, malabsorption syndrome

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43
Q

Outline percentages detailing the complications of osteoporotic fractures

A

30% permanent disabled, 50% can’t return to full independence, 12-20% die within 1 year

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44
Q

What scanning method is used in the diagnosis of osteoporosis ?

A

DXA Scan

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45
Q

What are the T-score ranges for diagnosis ?

A

Greater or equal to -1 = normal
-1 to -2.5 = osteopenia
Less than -2.5 = osteoporosis
More than -2.5 + prescience of 1 or more fractures = established osteoporosis

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46
Q

What is the aim in managing osteoporosis?

A

Reducing Fx risk

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47
Q

What is absolute fracture risk ?

A

Age + past history + BMD

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48
Q

What is the calcium intake recommended for post-menopausal women ?

A

1000-1500 mg/day (vit D = 800 IU/day)

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49
Q

Name 3 drugs used as osteoporosis treatments ?

A

Bisphosphonates, SERMS (Raloxifene), Estradiol (semisynthetic oestrogen)

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50
Q

What does DENOSUMAB do ?

A

It targets RANK-L and inhibits bone resorption, it is a monoclonal antibody

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51
Q

What does ROMOSUMAB do ?

A

It’s inhibits sclerostin, increasing bone formation and decreasing bone resorption

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52
Q

How much does osteoporosis treatment reduce fracture risk by ?

A

Half

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53
Q

How man kg of Ca are there in the body ?

A

1

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54
Q

What percentage of serum calcium is free ?

A

47%

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55
Q

What is the adjusted calcium equation ?

A

Ca (adj) = Ca(tot) + [0.02[45-alb)]

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56
Q

What is a normal Ca (adj) value ?

A

2.2-2.6 mmol/L

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57
Q

What are the main organs involved in Ca homeostasis ?

A

Kidney , gut, bone , parathyroid glands

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58
Q

What are the main hormones involves with metabolic control of calcium ?

A

PTH, vit D (active 1.25DHCC form)

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59
Q

What’s are the WHOs 6 Domains of QOL ?

A

Physical, environment, social relationships, psychological, level of dependence, spiritual

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60
Q

Name the 3 common musculoskeletal ageing syndromes

A

Joints = osteoarthritis
Bone = osteoporosis
Muscles = Sarcopenia

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61
Q

What makes healing of articulation cartilage slow ?

A

No innervation, vascularisation or macrophages

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62
Q

What cells are in articulate cartilage ?

A

Chondrocytes

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63
Q

What percentage of chondrocytes are lost between 40-80 years old ?

A

50%

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64
Q

What maintains swelling pressure of proteoglycans ?

A

ECM contains hydrophilic proteoglycans

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65
Q

Define osteoarthritis

A

A disorder of synovial joints which occurs when damage triggers repair processes leading to structural damage within a joint

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66
Q

Name 3 features of osteoarthritis

A

Localised loss of cartilage
Osteophyte formation
Mild synovitis

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67
Q

How long does morning stiffness last for osteoarthritis?

A

Wither no morning stiffness or less than 30 minutes

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68
Q

What growth hormone is responsible for differentiating osteoblasts ?

A

IGF-1

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69
Q

What is the rate of rapid bone loss in the first 5 years after menopause ?

A

2-3%

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70
Q

What are the most common fragility fractures ?

A

Spine , hip and wrist

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71
Q

Outline the SARC-F screening tool for sarcopenia

A

Strength
Assistance walking
Rise from chair
Climb stairs
Falls

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72
Q

What is subluxation?

A

Dislocation if a joint where contact to some of the articulating surfaces remains

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73
Q

What is grade 1 ligament injury ?

A

Fibres stretched but normal range on stressing

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74
Q

What is grade 2 ligament injury ?

A

More fibres involved, laxity on stressing but definite end point

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75
Q

What is grade 3 ligament injury ?

A

Complete tear, excessive laxity and no end point. May be pain free as nerve fibres torn

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76
Q

Outline management of grade 1 and 2 ligament injury

A

Promote tissue healing, prevent joint stiffness, protect against further damage, strengthen muscles

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77
Q

Outline management of grade 3 ligament injury ?

A

Protective bracing or surgical repair/ reconstruction

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78
Q

What e muscles are most commonly affected by strains and tears ?

A

Hamstrings, quadriceps femora’s and gastrocnemius

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79
Q

What tendon is most likely to rupture ?

A

The quadriceps tendon

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80
Q

What is the treatment for hamstrings rupture ?

A

NSAIDs, electrotherapy, strength and stretching (physio), surgery ??

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81
Q

What happens in muscles contusion ?

A

Local damage and bleeding, due to direct blow

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82
Q

What is myositis ossificans ?

A

Ossification due to severe contritions, haematoma calcification

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83
Q

What are the 2 most common tendon injury sites ?

A

Achilles tendon and supraspinatus

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84
Q

What are the 2 common nerves injured in sport ?

A

Ulnar nerve at elbow, common fibular/personal nerve at the neck of the fibula

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85
Q

Outline tendon composition

A

20% = cellular-tenocytes
70% = water
30% solids = collagen 1, ground substance, elastin, other collagen (collagen 3)

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86
Q

What is tendinopathy ?

A

Painful conditions that arise in and around tendons, in response to overuse

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87
Q

What are the 3 phases of tendon healing ?

A

Inflammation (day 0-7), repair (day 3-60), organisation and remodelling (day 28-180)

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88
Q

What is the function of a tendon ?

A

To transmit force

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89
Q

What happens in the inflammation step of tendon healing ? (Day 0-7)

A

Inflammatory cells migrate
Defect filled with granulation tissue, haematoma and tissue debris
Matrix proteins laid down as scaffolding for collagen synthesis

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90
Q

What happens during the repair step of tendon healing? (Day 3-60)

A

By day 5 = fibroblast/tenocyte migrate and begin to synthesise collagen 3 (laid in random orientation)

During 4th week = fibroblasts proliferate synthesising and reabsorbing collagen, collagen switched to type 1, vascular ingrowth via fibronectin scaffolding

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91
Q

What happens during the remodelling phase of tendon healing ? (Day 28-180)

A

Cross linking between fibrils increases tendon tensile strength, final stability reached

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92
Q

What is the composition of ECM ?

A

50% water, proteins, glycoproteins, proteoglycans, glucosaminoglycans, collagen

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93
Q

Where is type 1 collagen found ?

A

Skin, bone, tendons, ligaments, cornea, internal organs

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94
Q

Where is type 2 collagen found ?

A

Cartilage, IVD, notochord

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95
Q

Where is type 3 collagen found ?

A

Skin, blood vessels, internal organs

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96
Q

Where is type 4 collagen found ?

A

Basal lamina

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97
Q

What is collagen structure described as ?

A

Triple helix , 3 polypeptide chains

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98
Q

What is osteogenesis imperfecta ?

A

Brittle bone disease, collagen type 1

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99
Q

What are the 5 derivatives of the mesoderm ?

A

Notochord, paraxial mesoderm, intermediate mesoderm, lateral plate mesoderm, extraembryonic mesoderm

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100
Q

What mesoderm forms somites ?

A

Paraxial mesoderm

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101
Q

What does the intermediate mesoderm form ?

A

Genitourinary system

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102
Q

What does the lateral plate mesoderm form ?

A

The parietal and visceral layers of mesoderm

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103
Q

What muscles aren’t formed by the mesoderm ?

A

Pupil, mammary and sweat gland smooth muscles, there’s are from the ectoderm

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104
Q

What can you use somite numbers for ?

A

To determine the age of an embryo

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105
Q

What regulates somitogenesis?

A

Clock and wave mechanism - FGF family, Wnt, Notch act as alarms (clocks)

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106
Q

How many somite pairs are present by the end of week 5 development ?

A

42-44 pairs, these go on to form the axial skeleton

107
Q

What is a somite?

A

Paired blocks of mesoderm cells that are located on either side of the neural tube. They give rise to the axial skeleton

108
Q

What do sometimes differentiate into ?

A

Sclerotome and dermomyotome

109
Q

What does the sclerotome turn into ?

A

Ribs and vertebrae

110
Q

What does the dermomyotome split into ?

A

The dermatome and the myotome

111
Q

What does the dermatome turn into ?

A

Dermis and CT

112
Q

What does the myotome turn into ?

A

Muscle

113
Q

What are myoblasts ?

A

Myocyte precursors

114
Q

What controls myoblast cell division ?

A

The presence of growth factors

115
Q

What happens to myoblasts when growth factors are depleted ?

A

They stop dividing
Fibronectin secreted onto ECM, binding via integrins
Myoblasts align into chains and fuse, cell membranes disappear, multi-nucleated primary myotubes

116
Q

What mediates myoblasts differentiation ?

A

Myogenin

117
Q

In the neural tube, what does Wnt and BMP do ?

A

Activate MYOD in the dermomyotome, creates a group of muscle cell precursors which express MYF5

118
Q

In the notochord, what do SHH and Noggin induce?

A

Sclerotome formation

119
Q

In the lateral plate mesoderm, what do Wnt and BMP do ?

A

Activate MYOD/MYF5

120
Q

What do MYOD/MYF5 do ?

A

Activate muscle specific genes

121
Q

What happens if both MYF5 and MYOD1 are present ?

A

This is a loss of function mutation, causes complete lack of skeletal muscle formation

122
Q

What genes control differentiation in the 3 muscle types (smooth,skeletal and cardiac) ?

A

Skeletal = MYOD, MYF5, Myogenin
Smooth = Serum Response Factor (SRF)
Cardiac = MYOD NOT involved

123
Q

What type of mesoderm do the 3 types of muscle develop from ?

A

Skeletal = paraxial mesoderm
Smooth = splanchnic mesoderm
Cardiac = splanchnic mesoderm

124
Q

Below what age is scaphoid fracture unlikely to occur (and why) ?

A

10 years old, the scaphoid is mostly cartilage up until this point

125
Q

What is Torus fracture ?

A

Caused by falling onto hand, bone bends but doesn’t break through (buckles)

126
Q

What is a green stick fracture ?

A

Bone is only fracture on one side, fracture isn’t the full way through the bone

127
Q

What is a plastic bowing fracture ?

A

Only occurs in long bones, bone bends but doesn’t snap in any location

128
Q

What is the Salter-Harris classification ?

A

A method used to grade fractures that occur in children involving the epiphyseal growth plate

129
Q

What are the classifications of Salter-Harris (salter mnemonic) ?

A

Separated growth plate = I
Above the growth plate = II
Lower than the growth plate = III
Through the growth plate = IV
ERasure of growth plate (crush) = V

130
Q

What type of fracture in infants is classed as non-accidental injury ?

A

Bucket handle fracture , causes injury to the metaphysis

131
Q

What is Rickets ?

A

Softening of the bones due to deficiency or impaired metabolism of Vitamin D. Causes leg bowing and other skeletal problems.

132
Q

What is the Trendelenburg test ?

A

Detects weakness of gluteus medius and minimus, standing on each leg in turn. If hip affected, pelvis will tilt by dropping at the opposite side and the body leans away from affected side.

133
Q

What are menisci ?

A

C-shaped wedges of fibrocartillage, there is a medial and lateral menisci. They improve the fit of the knee joint and act as shock absorbers

134
Q

Which of the collateral ligaments is NOT attached to the joint capsule ?

A

FCL (fibular collateral ligament)

135
Q

What is the TCL (tibial collateral ligament) attached to ?

A

The joint capsule and medial meniscus

136
Q

What is the angle between the femur and tibia called ?

A

The Q angle (approx 15 degrees)

137
Q

What is Genu Varum?

A

Bow leg, angle between longitudinal axis of bones is <17 degrees

138
Q

What is Genu Valgum?

A

Knock knee, angle between longitudinal axis of bones >17 degrees

139
Q

What is the crown to rump length at 24 weeks ?

A

200 mm

140
Q

What are the 6 zones present in developing bones ?

A

Resting cartilage
Proliferation of chondrocytes
Maturation (no more mitosis)
Hypertrophy (vacuole formation)
Cartilage Degeneration
Osteogenic activity

141
Q

What is the definition of differentiation ?

A

Changing one cell type to another

142
Q

What regulates cell differentiation?

A

Transcription factors

143
Q

What can differentiation affect ?

A

Cell : Shape, size, membrane potential, metabolic activity and responsiveness to signals

144
Q

When do limb buds become visible ?

A

By the end of week 4

145
Q

When does limb morphogenesis take place ?

A

Week 4-8

146
Q

Which limbs develop slowest ?

A

Lower limb, but they catch up

147
Q

What is the 1st sign of limb musculature ?

A

Mesenchyme near the limb buds

148
Q

What is mesenchyme compromised of ?

A

A matrix of Collagen fibres
Hyaluronic acid
Glycoproteins

149
Q

Are there nerves in the early limb bud?

A

No

150
Q

What does the limb bud consist of ?

A

Mesenchymal core with a covering cubital ectoderm layer

151
Q

What does ectoderm thickening at the distal border form ?

A

Apical Ectodermal Ridge (AER)

152
Q

What do AER cells differentiate into ?

A

Cartilage and muscle

153
Q

What is limb outgrowth initiated by ?

A

Secretion of FGF10

154
Q

What does the dorsal ectoderm express?

A

Radical fringe

155
Q

What does the ventral ectoderm express ?

A

Engrailed-1

156
Q

Once the AER is established what does it express and why ?

A

FGF4 and FGF8, to maintain the undifferentiated zone at the distal end

157
Q

Which transcription factor designates the upper limb ?

A

TBX-5

158
Q

Which transcription factor designates the lower limb ?

A

TBX-4

159
Q

What happens at 6 weeks in limb development ?

A

Terminal portion of the buds flatten to form hand and foot plates

160
Q

What separates the segments of the developing limb ?

A

Constriction

161
Q

What are the 3 components of the developing limb ?

A

Stylopod = humerus + femur
Zeugopod = radius/ulna + tibia/fibula
Autopod = carpals/metacarpals/digits + tarsals/metatarsals/digits

162
Q

What are HOX genes ?

A

Genes that regulate the positioning of the body structures

163
Q

What HOX genes position the limbs ?

A

9-13

164
Q

What is polydactyly ?

A

Extra digits cause by mesoderm defect due to mutation of HOX genes, SHH or Wnt

165
Q

What causes the AER to separate into 5 digits?

A

Cell death in the AER

166
Q

What day in development is digit separation complete ?

A

Day 56

167
Q

What happens during week 7 of limb development ?

A

The upper and lower limbs rotate in opposite directions, occurring from coronal to parasagittal plane then along the axis

168
Q

Which direction and angle do limbs rotate by ?

A

Upper = 90* laterally
Lower = 90* medially

169
Q

What drives mesenchyme condensation and differentiation into chondrocytes ?

A

BMP expression

170
Q

What is cell proliferation, increased density, differentiation and cell death induced by in joint formation ?

A

WNT 14

171
Q

By what week are primary centres of ossification present in all long bones ?

A

Week 12

172
Q

What does calcified cartilage matrix not allow?

A

Diffusion of nutrients

173
Q

What does the lack of nutrients cause in calcified cartilage matrix ?

A

Cells to die, leaving spicules which act as scaffolding on which bone can be deposited

174
Q

What happens when blood vessel grow into the bones periosteum ?

A

It brings progenitor cells

175
Q

What happens to progenitor cells in periosteum ?

A

They form osteoblasts, osteoclasts and osteocytes

176
Q

What does intramembranous bone growth do ?

A

Increases bone width (diameter) by replacing bone in the medullary cavity

177
Q

What does endochondral bone growth do ?

A

Increases bone length, cartilage is ossified at the epiphyseal growth plates

178
Q

What is Achondroplasia?

A

A disorder of bone girth affecting endochondral ossification in the long bones of arms and legs

179
Q

Outline the inheritance of achondroplasia

A

Autosomal dominant, normally sporadic mutation

180
Q

What is achondroplasia caused by ?

A

Mutations in the FGF3 receptor, meaning it is permanently expressed resulting in reduced chondrocyte activity

181
Q

What drug can be used in achondroplasia to promote growth ?

A

Vosoritide

182
Q

What are the 4 medial ankle ligaments ?

A

Tibiocalcaneal, tibionavicular, tibiotalar (anterior and posterior), plantar calcaneonavicular

183
Q

What are the 3 lateral ankle ligaments ?

A

Talofibukar (post and ant), calcaneofibular

184
Q

What is an ankle sprain ?

A

Damage to ligaments

185
Q

What is an ankle strain ?

A

Damage to muscle or tendon

186
Q

What are the 3 retinacula groups of the ankle?

A

Flexor
Extensor (sup and inf)
Fibular (sup and inf)

187
Q

What maintains the foot arch ?

A

Plantar aponeurosis

188
Q

What else in involved in foot arch maintenance?

A

Calcaneonavicular ligament aka SPRING ligament

189
Q

How many veins is each artery surrounded by ?

A

2

190
Q

What are the top 5 most common autoimmune diseases ?

A

Graves’ disease , RA, Thyroiditis, vitiligo , type 1 diabetes

191
Q

What are the multi factorial causes of autoimmunity ?

A

Genetic, infection and environment exposure, immune regulation

192
Q

Name 3 possible autoimmunity genotypes ?

A

HLA-DR4 alleles, PTPN22, CTLA4 ( and cytokines)

193
Q

What is positive thymic selection ?

A

When T-cells survive despite reaction to self-antigens

194
Q

What is negative thymic selection ?

A

When T-cells undergo cell death for responding to self-antigens

195
Q

What is the treatment for FOXP3 gene mutation ?

A

Bone marrow transplant, immunosuppressant therapies

196
Q

What MHC gene is RA associated with ?

A

DR4

197
Q

What MHC gene is Crohn’s disease associated with ?

A

CARD15

198
Q

What is the specific target of Graves’ disease ?

A

TSH receptor

199
Q

What does Graves’ disease lead to ?

A

Overproduction of thyroid hormones

200
Q

What happens is Myastenia gravis ?

A

Antibody blocks acetylcholine receptors, no Na+ influx occurs and therefore no muscle contraction

201
Q

What are 3 examples of organ specific autoimmunity ?

A

Addison’s disease, MS, Guillain-Barre Syndrome

202
Q

What are 3 examples of non-organ specific autoimmunity?

A

RA, Scleroderma, systemic lupus

203
Q

What does Gillian-Barre syndrome cause ?

A

Acute paralysis

204
Q

What is the formula for hydroxyapatite ?

A

Ca10(PO4)6(OH)2

205
Q

What are the 3 possible pathologies of metabolic bone disorders ?

A

Loss of mineralisation
Bone mass (low or high)
Turnover (low or high)

206
Q

What are biochemical tests for metabolic bone disorders ?

A

Serum Ca/PO4(3-)
PTH
Vit.D activity
Alkaline phosphates

207
Q

What is the difference between menopausal osteoporosis and normal osteoporosis ?

A

Menopausal involves reduces mineral mass whereas normal involves reduced total bone mass

208
Q

What do corticosteroids effect in bone remodelling?

A

They increase bone resorption rate and depth , and inhibit osteoblasts activity

209
Q

What causes high calcium and high PTH ?

A

Primary hyperparathyroidism

210
Q

What causes low calcium and high PTH ?

A

Secondary hyperparathyroidism due to renal impairment or Vit D deficiency

211
Q

What cause low calcium and low PTH ?

A

Hypoparathyroidism due to autoimmunity, surgical thyroid removal and radiotherapy

212
Q

What causes high calcium and low PTH ?

A

Malignancy, excessive intake, medications, granulomatous disorders

213
Q

What happens if corrected calcium is above 2.8?

A

Test for PTH levels = undetectable suggests malignancy, detectable or high suggests primary hyperparathyroidism

214
Q

What is Paget’s disease ?

A

Rapid bone turnover , both resorption and formation are increased. Causes disorganised bone

215
Q

What is an example of a selective NSAID ?

A

Celecoxib

216
Q

What is the benefit of Celecoxib for the GI tract ?

A

Decreased risk of GI side effects ( increased risk of CV side effects)

217
Q

What are corticosteroids useful for treating ?

A

RA, Lupus, Acute Leukaemia, Asthma, Psoriasis, Anaphylaxis, Transplantation, Addison’s disease, UC, Crohn

218
Q

What are the key symptoms of RA?

A

Joint pain, stiffness in the morning, swelling, fatigue (in systemic weight loss and fevers)

219
Q

What immune system is responsible for RA (primarily) ?

A

ADAPTIVE

220
Q

What type of gut bacteria is enriched in early RA ?

A

Prevotella Copri

221
Q

What type of T cells are defected in RA?

A

CD4

222
Q

What treatments are used for RA?

A

NSAIDs, corticosteroids, DMARDs (methotrexate)

223
Q

What is seen as the conductor in RA ?

A

TNF-alpha (produces cytokine signalling)

224
Q

Give an example of an anti-TNF drug ?

A

Infliximab

225
Q

Describe costovertebral joints ?

A

Rib articulating with superior Demi-facet of corresponding vertebrae + inferior Demi-facet of vertebrae superior

226
Q

Describe costotransverse joints ?

A

Tubercle of rib articulates with corresponding transverse process of vertebrae

227
Q

What are the openings at the top and bottom of the ribcage called ?

A

Superior + inferior thoracic aperture

228
Q

What can occur in cervical rib ?

A

Compression of underlying nerves and vessels, can present similar to Klumpke’s syndrome

229
Q

How much does the diaphragm move in quiet breathing ?

A

1-2 cm

230
Q

How much does the diaphragm move in forced breathing ?

A

6-10 cm

231
Q

From anterior to posterior, what structures pass through the diaphragm?

A

IVC
Oesophagus
Aorta

232
Q

What nerve supplies the diaphragm ?

A

Phrenic nerve

233
Q

What vertebrae does the phrenic nerve arise from ?

A

C3, 4 + 5 (keeps the diaphragm alive)

234
Q

From internal to external, outline the layers if a blood vessel

A

Tunica intima
Internal lamina
Tunica media
External lamina (with adventitious fibroblasts)
Nerves
Perivascular adipose tissue (PVAT)

235
Q

What does eutrophic mean ?

A

Normal blood vessel structure

236
Q

What does hypotrophic mean ?

A

Widening of blood vessels, either due to less wall tissue or adventitious widening

237
Q

What does hypertrophic mean ?

A

Narrowing of a vessel, due to increased wall tissue or widening adventitia

238
Q

What makes up blood vessel walls ?

A

Endothelium, collagen (type 1) elastic fibres and other cells

239
Q

What is key in vascular remodelling ?

A

Angiotensin

240
Q

Outline the beginning steps of atherosclerosis

A

Insult to vascular endothelium
Increased adhesion and transmigration of leukocytes
Increased lipid permeability
Generation of cytokines
Inflammation focus established

241
Q

What happens during fatty streak formation ?

A

Lipid-laden foam cells form under endothelium

242
Q

What causes an advanced lesion in blood vessels to form ?

A

Macrophage accumulation
Formation of necrotic core
Fibrous cap formation

243
Q

What causes thrombosis ?

A

Fibrous cap thins, intraplaque haemorrhage occurs and the vessel becomes blocked

244
Q

What is cholesterol essential for ?

A

Cell membranes, maintaining membrane permeability + steroid and fat-soluble vitamin formation

245
Q

What is the livers role in cholesterol?

A

Monitors levels, regulates (through synthesis, absorption and bile secretion)

246
Q

What is VLDL ?

A

LDL precursor, carries synthesised TGs from liver to adipose tissue

247
Q

What is LDL ?

A

Major cholesterol reservoir, taken up via endocytosis by LDL receptors
BAD

248
Q

What is HDL ?

A

GOOD cholesterol, absorbs cholesterol released by dying cells
Acts as reverse transport to take cholesterol back to liver

249
Q

Exogenous cholesterol pathway

A

Intestine - chylomicron - capillary (can become adipose) - chylomicron remnant - bind to receptors on liver - cholesterol produced

250
Q

What blood vessels does PVAT not surround ?

A

Cerebral

251
Q

Outline PVAT composition and nerve supply

A

Adipocytes (+ fibroblasts and immune)
Nerve supply = adrenergic nerve fibres
They release adipokines

252
Q

Endogenous pathways of cholesterol transport

A

Liver VLDL - capillary (can become adipose) - IDL - IDL to LDL - LDL binds to receptors and deposits cholesterol

253
Q

What is familial hypercholesterolaemia ?

A

Reduced LDL receptors on liver
VDL is converted to IDL in the capillaries

254
Q

What are the signs of FH ?

A

Xanthomas = fatty deposits in skin (elbows,knees,buttocks and tendons)
Xanthelasmas = fatty deposits in the eyelids
Arcus senilis = a white ring around the cornea

255
Q

What do statins do ?

A

They are competitive inhibitors of the rate-limiting stem in cholesterol biosynthesis
Less cholesterol may stimulate LDL receptor up-regulation

256
Q

What are the 5 main causes of hypertension ?

A

Smoking!
Obesity !
Diet!
Exercise (lack of) !
Genetics

257
Q

What are the risks of hypertension ?

A

Atherosclerosis, stroke, myocardial infarction, heart failure, renal failure , retinopathy

258
Q

What is the BP calculation ?

A

BP = TPR x CO

CO= HR x SV

259
Q

Outline beta-adrenoceptor blockers

A

Propranolol (B1+B2) and Atenolol (B1)
Completive reversible antagonists
Lower BP by blocking sympathetic tone on heart
lowering HR,SV and CO

260
Q

Outline alpha-adrenoceptor blockers ?

A

Phentolamine (a1+a2) and Doxazosin,Prazosin (a1 selective)
Competitive reversible antagonists
Lower BP by lowering sympathetic tone in arterioles
Lowers TPR

261
Q

Outline ACE inhibitors

A

Captopril and Enalapril
Reduce angiotensin II formation - lowers TPR
Reduces aldosterone formation (stimulated by angiotensin II) - lowers blood volume

262
Q

Outline diuretics

A

Bendroflumethiazide
Lowers BP by reducing blood volume
Reduces renal reabsorption of Na+ and water

263
Q

Outline Calcium channel blockers

A

Verapamil, Diltiazem, Nifedipine
Block Ca entry into vascular smooth muscle causing vasodilation - lowers TPR
Block Ca entry into cardia muscle - lowers HR,SV and CO

Y1 Medicine (5 decks)

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