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MBChB1 Phase 1 > Week 4 > Flashcards

Week 4 Flashcards

1
Q

What are some functions of the skeleton?

A

Support
Protection
Locomotion
Mineral reserve
Haematopoesis

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2
Q

Which minerals are present in bone?

A

Calcium salts and phophate

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3
Q

What is produced from bone marrow?

A

RBCs, WBCs and platelets

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4
Q

Where is red bone marrow found in children?

A

All bones

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5
Q

Where is red bone marrow found in adults? Yellow BM?

A

Red: skull, vertebral collumn, pelvis
Yellow: long bones

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6
Q

What is yellow bone marrow composed of?

A

Adipose tissue

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7
Q

What are osteons?

A

Layers of bone in circular layers

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8
Q

What is the composition of bone?

A

30% organic type I collagen
70% inorganic calcium and phophate salts

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9
Q

Function of calcium in bone?

A

Tensile strength
Allows bending
When ca is low in blood it can be taken from bone

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10
Q

Function of minerals in bone?

A

Compressive sytrength: makes bones sturdy

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11
Q

What is rickets?

A

Vitamin D deficiency - lack of sun exposure or calcium in diet
Vit D required for calcium absorption: lack of circulating calcium so cannot be taken up as calcium hydroxyaptite
Bones are overly flexible as they lack minerals

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12
Q

What is osteogensis imperfecta?

A

Gentic disorder
Affects collagen production - mutations in type I collagen
Brittle bones which frature easily
Brittle bone disease

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13
Q

Structure and Function of epiphyses in bone?

A

Articular surfaces of joints
Mostly spongy bone but compact on surface

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14
Q

Structure of diaphyses?

A

Mostly compact bone, strong but a little flexible

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15
Q

Function of epiphyseal growth plate?

A

Seperates epiphyses and diaphyses
Site of growth

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16
Q

What happens in bones when growth is complete? What line is made?

A

Growth plate ossifies
Makes epiphyseal line

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17
Q

What is the periosteum? What does it attach?

A

Covers outer surface of bone
Site of attachment for tendomns

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18
Q

Endosteum function?

A

Lines intrnal surfaces of cavities in bones

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19
Q

What does the medullary cavity contain?

A

Bone marrow

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20
Q

Structure of skull bones?

A

Flat bones
No medullary cavity
2 sheets of compact bone with cancellous bone in the middle
Filled with red bone marrow

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21
Q

What is spongy bone formed from and what is found in its spaces?

A

Trabeculae struts
Red bone marrow

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22
Q

Examples of long bones?

A

Femur, humerus

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23
Q

Examples of short bones?

A

Carpals, tarsals

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24
Q

Examples of flat bones?

A

Skull, sternum, scapula, ribs

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25
Q

Examples of irregular bones?

A

Vertebrae, sacrum, facial bones

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26
Q

Functions of sesamoid bones in tendons?

A

Protect tendons and increase movement

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27
Q

Which bone is sesamoid?

A

Patella

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28
Q

How many bones in adult body?

A

206

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29
Q

How many bones in newborns?

A

270

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30
Q

3 types of joints? Examples?

A

Fibrous e.g. sutures
Cartilaginous e.g. IVDs
Synovial e.g. humerus

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31
Q

What makes up the axial skeleton?

A

Skull
Vertebral collumn
Ribs
Sternum

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32
Q

What makes up the appendicular skeleton?

A

Upper and lower limbs

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33
Q

What makes up the upper limb?

A

Pectoral girdle
Bones of arms/hands

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34
Q

What makes up the lower limb?

A

Pelvic girdle
Bones of hands/feet

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35
Q

How many skull bones are there?

A

22

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36
Q

How many bones are in the vertebral collumn?

A

33

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37
Q

How many pairs of ribs are there?

A

12

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38
Q

Function of skull?

A

Houses brain and special sense organs

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39
Q

What is the viscerocranium and how many bones does it contain?

A

Facial skeleton
14

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40
Q

What is the neurocranium and how many bones does it contain?

A

Surround brain
8

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41
Q

What are the 5 parts of the vertebral collumn and how many bones are in each?

A

Cervical 7
Thoracic 12
Lumbar 5
Sacrum 5 fused
Coccyx 4 fused

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42
Q

Structure of cervical bones?

A

Small and mobile

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43
Q

Which part of vertebral column is most susceptible to dislocation?

A

Cervical

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44
Q

What does the thoracic collumn articulate with and why does it have long processes?

A

Ribs
For mucle attachment

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45
Q

Which body of vertebral collumn is the largest and susceptible to herniated IVDs?

A

Lumbar as it bears weight

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46
Q

What does the sacrum articulate with?

A

Hip bones

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47
Q

What is the structure and function of the pectroal girdle?

A

Clavicle and scapula
Attaches UL to body

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48
Q

Which bone connnects UL to axial skeleton? Why?

A

Clavicle
Allows large range of movement

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49
Q

What makes up the UL?

A

Humerus
Radius and ulna
Carpals
Metacarpals
Phalanges

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50
Q

What makes up the lower limb?

A

Femur
Tibia and fibula
Tarsals
Metatarsals
Phalanges

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51
Q

How many carpals are there?

A

8

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52
Q

How many metacarapals are there?

A

5

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53
Q

How many phalanges are in the hands/feet?

A

14 each

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54
Q

How many tarsals are there?

A

7

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55
Q

How many metatarsals are there?

A

5

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56
Q

What is a condyle?

A

Rounded bone forming joint surfaces and muscle attachemnts

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57
Q

What are foramens?

A

Holes

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58
Q

What are fossas?

A

Dips in bones

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59
Q

What does the iliac crest help you locate? Significane?

A

Inigual ligamnt
Hernia locaion

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60
Q

Function of ribs?

A

Surrounds and protects thoracic organs

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61
Q

How are ribs made flexible?

A

Costal cartilages

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62
Q

Which level is the sternal angle?

A

T4/5

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63
Q

What does the sternal angle help locate? Why?

A

2nd ribs
Auscultation
Boundary of mediastinum: aorta/trachea splitting
Imaging

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64
Q

What are SIPCEPs?

A

Standard infection control precautions
Used by all staff at all times for all patients

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65
Q

Sources of potential infection?

A

Blood/body fluids
Secretions/excretions, not sweat
Non-intact skin
Mucus membranes
Any contaminated equipment

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66
Q

What are the standard precations?

A

Hand hygiene at 5 moments
Disposal of sharps
Use of PPE for potential infectious substances
Clean environemnt
Safe waste disposal
Safe used linen management

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67
Q

Why do we wash hands?

A
  • healthcare environemnt is contaminated
  • hands spread germs
  • some patients are very vulnerable to infection and not washing hands could spread germs
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68
Q

What should you do before performing hand hygeiene?

A
  • expose forearms
  • remove all jewellery
  • nails clean and short
  • cover cuts with waterproof dressing
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69
Q

When should you perform hand hygeiene?

A

Before touching patient
Before aseptic procedure
After body fluid exposure
After touching patient
After touching patient surroundings

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70
Q

When should you wash hands with soap and water?

A
  • hands are visibly soiled
  • patient has suspected GI infection e.g. norovius/c. diff
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71
Q

When are hand wipes used?

A

When no running water is available

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72
Q

What is a healthcare associated infection?

A

Infection acquired as a result of healthcare related intervention or during healthcare that the patient would usully not catch

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73
Q

Most common healthcare associated infections?

A

GI infections
UTIs
Resp infections
Surgical site

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74
Q

Why is resp and cough hygeiene used?

A

To minimise risk of cross contamination of resp illness

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75
Q

How to do resp and cough hygeiene?

A

Cover mouth and nose with tissue when sneezing, coughing, wiping and blowing nose
Dispose of tissues into bin
Wash hands with liquid soap and water when coughing, sneesing, using tissues
Keep contaminated hands away from eyes, nose, mouth

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76
Q

Examples of PPE?

A

Gloves disposable/sterile
Aprons disposable/sterile
Eye protection
Masks/respirators

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77
Q

All PPE should…

A
  • located close to point of use
  • stored to prevent contamination in clean/dry area
  • single use
  • disposed of after use correctly
  • reusable PPE should be decontaminated after usw
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78
Q

What are transmission based precautions?

A

Additional; infection control precautions taken with patients known or suspected to be infected with organisms posing a significant risk to other patients

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79
Q

4 types of transmission based precautions?

A

Contact
Enteric (intestines)
Droplet
Airborne

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80
Q

Examples of high risk fluids?

A

CSF
Pleural fluid
Semen
Synovial fluid
Vaginal secretion
Breast milk
(any body fluid containing visible blood)

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81
Q

Which body fluids are not high risk unless bloodstained?

A

Urine
Feces
Saliva
Sweat
Vomit

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82
Q

What is the most likely route of infection for healthcare workers?

A

Needlestick inury
Blood splashing onto broken skin

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83
Q

Examples of blood borne disease?

A

HIV, AIDS, Hep B, Hep C

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84
Q

Which receptor does COVID bind to?

A

ACE2

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85
Q

Symptoms of covid?

A

Cough, fever, shortness of breath, loss of senses

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86
Q

What is the R0?

A

The number of new cases oof infection arising from a single case

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87
Q

What R number is covid?

A

R3

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88
Q

What is covid spread by?

A

Droplets e.g. coughing sneezing
Surfaces
Aerosols

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89
Q

What PPE should you use when COVID is confirmed in a patient?

A

Eye protection
Fluid repellent face mask
Gloves
Apron

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90
Q

What is requird when aerosol generated infecton is present?

A

Filtering face piece

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91
Q

Order of putting on PPE?

A

Apron
Face mask
Eye protection
Gloves

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92
Q

What should you do before putting on PPE?

A

Hydrate
Tie hair back
Remove jewellery
Clean hands with gel rub

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93
Q

How is cortical bone arranged?

A

In osteons

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94
Q

Why do osteons have central canals?

A

For blood vessels

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95
Q

What are lamellae?

A

Circular layers of bone

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96
Q

Function of trabeculae?

A

Help to transfer weight through bone
Present in spongy bone

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97
Q

What are osteoprogenitor cells?

A

Stem cells differentiating into osteoblasts and osteocytes

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98
Q

Function of osteoblasts?

A

Lay down new bone

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99
Q

Function of osteocytes? Where are they found?

A

Mature osteoblasts trapped in bone matrix
In caves called lacunae
Respond to mechanical strain and send signals to intiate bone formation/resorption

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100
Q

Function of osteoclasts?

A

Break down bone

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101
Q

What is required for hardness and strength in bone?

A

Calcium hydroxapitate

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102
Q

What is decalcification?

A

Removing inorganic calcium salts from bone matrix

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103
Q

Why are bone shafts hollow?

A

To allow unrestricted movement of the thigh
Stronger than solid bar
Aids blood supply of bone

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104
Q

How are trabeculae arranged and why?

A

Lattice work
Even spread of weight

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105
Q

How does bone grown?

A

Appositional growth
Bone laid down on surface
Osteoblasts lay down osteoid (organic)
It is mineralisied (inorganic)
Osteoblasts trapped - become osteocytes

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106
Q

How can cartilage grow?

A

Appositional and interstitial growth

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107
Q

How does growth occur in epiphyseal plate?

A

Interstitial growth - cartilage expands and is replaced by bone

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108
Q

How does cartilae recieve nutrients?

A

Diffusion as its avascular

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109
Q

What are the 5 zones of the growth plate?

A

R - resting/reserve chondrocytes which replicate slowly
P - proliferation zone, cells divide rapidly
H - hypertrophy zone, chondrocytes mature and expand
C - calcification zone. cells become calcified and die via apoptosis, forms calcified matrix
O - blood vessels and bone cells invade calcified cartilage and replace it with bone

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110
Q

Which cartilage is growth plate formed from?

A

Hyaline

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111
Q

When willl bone stop growing in length?

A

When cartilage growth plate stops proliferating and is replaced entirely with bone

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112
Q

What is ossification?

A

The process by which bone is made

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113
Q

What is endochondral ossification?

A

Cartilage model made first and replaced e.g. long bones

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114
Q

What is intramembranous ossification?

A

Bone formed directly in mesenchyme e.g. skull bones

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115
Q

What is the primary ossification centre?

A

First part to form e.g. diaphyses in long bones
Allows flexibility

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116
Q

What is the secondary ossification centre?

A

Epiphyses

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117
Q

What are fontanelles? Function?

A

Soft spots between skull bones
Allow flexibility in birth
Allow rapid growth of brain in first 2 years of life

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118
Q

What can timing of bone fusion be affected by?

A

Males and females
Populaiton differences
Stress
Nutrition
Usually fuse in predictable pattern

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119
Q

Function of knowing ossification times?

A

Age fraud in sports
Age estimation in refugees

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120
Q

What are sutures? Which type of joints are these?

A

Joints between bones of the skull - fibrous joints, limited movement

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121
Q

What is osteoperosis?

A

Bone removed faster than laid down
Bone density reduced and more susceptible to fracture

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122
Q

When is OI common and why?

A

Post menopausal women
Oestrogen promotes osteoblast activity which reduces in menopause

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123
Q

What happens when you have osteoperosis in spine?

A

Trabeculae struts disappear
Kyphosis of thoracic spine - hunchback
Vertebral bodies collapse

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124
Q

What are enthesophytes?

A

Abnormal bony projections at attachment of tendon/ligament

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125
Q

What are osteophytes?

A

Abnormal bony projections in joint spaces

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126
Q

Symptoms of enthesophytes/osteophytes?

A

Pain/stiffness in back
Numbing/weakness in limbs

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127
Q

What is periostitis?

A

Inflammation of periosteum

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128
Q

Causes of periostisis?

A

Acute infection
Trauma/stress to bone (chronic)

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129
Q

Examples of perostitis causes?

A

Staph bacteria
Congenital syphilis
Leukaemia/cancer
Shin splints
Osgood-schlatter disease

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130
Q

What is the most common cancer in Scottish women?

A

Breast

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131
Q

What is the most common cancer in Scottish men?

A

Prostate

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132
Q

What is the most common cancer in Scotland overall?

A

Lung

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133
Q

What is a neoplasm?

A
  • new growth
  • abnormal
  • uncontrolled cell division
  • aka tumor
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134
Q

What does benign mean?

A

Grows slowly
Remains localised to site of origin

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135
Q

What does malignant mean?

A

Invades and spreads to different sites
Aka cancer

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136
Q

What is metastasis?

A

Tumor cells move from primary site to colonise secondary site

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137
Q

What are some characteristics of cancer cells?

A

Large variable shaped nuclei
Many dividing cells
Disorganised
Varied size and shape
Loss of normal features

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138
Q

What is anaplasia?

A

Loss of normal features in a cell

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139
Q

Why do cancer cells stain more basophilic aka blue than normal cells?

A

There is higher metabolic activity in the cell so more acidic molecules are present e.g. rRNA and mRNA

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140
Q

Describe the multistep development of cancer

A

Initiation: environmental carcinogens e.g. smoking
Mutation occurs
Oncogenes activated
Loss of tumor suppressors
Proliferation increases
Further mutations occur
One cell passes threshold of malignancy

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141
Q

Name molecules which are mutated in colon cancer

A

Beta catenin (e-cadherin)
K-ras pathway
p53

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142
Q

What are the six characteristics of cancer and molecules involved

A

Uncontrolled Proliferation: self sufficiency in growth factors due to oncogenes e.g. was, bcr-abl, HER-2
Increased growth capacity: tumor suppressor genes inactivated e.g. Rb
Evasion of apoptosis: increased BCL-2
Limitless replication potential: telomerase
Sustained angiogenesis:VEGF
Tissue invasion: cadherin, proteases

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143
Q

Function of platelet derived growth factor?

A

Matrix formation (inc fibroblasts)
Remodelling (produce proteases)

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144
Q

Function of vascular endothelial growth factor?

A

Angiogenesis - endothelial cell proliferation and migration

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145
Q

Function of colony stimulating factors?

A

Myeloid lineage in haematopoeisis

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146
Q

Function of erythropoeitin?

A

Produces red blood cells

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147
Q

Function of thrombopoietin?

A

Produces platelets

148
Q

Which transduction pathway is present in keratinocyte proliferation?

149
Q

How is a cell response signalled in a normal pathway?

A

Extracellular signal binds to receptor
This causes signal transduction
Nucleus eventually targeted and it is signalled to transcribe new molecules

150
Q

What is an oncogene?

A

A gene who’s product is involved In inducing cancer

151
Q

How is an oncogene formed?

A

Mutated proto-oncogene

152
Q

What is a proto-oncogene?

A

A normal gene involved in regulation of cell growth and proliferation, when mutated becomes oncogene

153
Q

What is a tumor suppressor gene?

A

Inhibits cell proliferation and progression through cell cycle

154
Q

What happens when TSGs lose their function?

A

They are oncogenic - cells can proliferate without checkpoints

155
Q

How does uncontrolled cell proliferation occur in cancer?

A

Molecules that initiate/speed up proliferation are switched on
Molecules that slow/halt prolifeeration are turned off

156
Q

What are some receptors that are protooncogenes?

A

EGFR
HER2 - amplified HER2
c-met

157
Q

What are some cytoplasmic signalling molecules that are protooncogenic?

A

Ras, kI-RAS IN COLON CANCER
BRAF
Abl - bcr-abl in chronic myeloid leukaemia

158
Q

Which nuclear molecules are protooncogenic?

A

Cyclin D - amplification
Myc - translocation

159
Q

How does was become an oncogene? Usual role?

A

G protein transfusing signals from cell receptors
Point mutation
Ras signalling pathway switched on constantly so the cell will no longer need a growth factor

160
Q

How does BRAF become an oncogene? Usual role?

A

Kinases transfusing signals from cell receptors
Point mutation
Switched on all the time so cell no longer needs growth factor

161
Q

What is BRAF usually activated by?

162
Q

How does EGFR become an oncogene? Usual role?

A

Cell surface receptor receiving extracellular signal
Point mutation deletes extracellular portion
Active in absence of EGF so constant cell proliferation

163
Q

Which gene is amplified to induce cancer?

164
Q

Which 2 genes undergo Philadelphia translocation (chromosome rearrangement) to form a gene present in chronic myeloid leukaemia?

A

BCR and ABL
forms bcr-abl
Persistently active kinase activity

165
Q

Which cancers form when Rb is inactivated?

A

Bladder, breast, lung

166
Q

Which cancers form when p53 is inactivated?

A

Brain, breast, colon, liver, lung, oesophageal
Most commonly mutated gene in cancer

167
Q

Which cancers form when BRCA1 is inactivated?

A

Breast/ovarian

168
Q

What is the two hit hypothesis of tumor formation?

A

Both copies of tumor suppressor gene must be mutated to induce cancer

169
Q

What happens if there is no growth factor (Rb)?

A

Rb binds to E2F and the cell cycle is arrested

170
Q

What happens if there is a growth factor (Rb)?

A

Rb is phosphorylated and the cell enters the cell cycle

171
Q

What happens when Rb is lost?

A

There is unregulated entry into cell cycle as rb doesn’t bind to e2f

172
Q

What happens when Rb is mutated?

A

It can’t bind to e2f and the cell cycle is unregulated

173
Q

What is Li-farumeni syndrome caused by? What is it?

A

p53 mutation
increases risk of developing cancer

174
Q

How do cancer cells avoid apoptosis?

A

Increased expression of BCL-2 which inhibits apoptosis

175
Q

Function of telomeres?

A

Caps that protect ends of chromosomes
Prevent chromosomes fusing with other chromosomes
Ensure DNA is correctly copied

176
Q

Why are telomeres unregulated in cancer?

A

They increase cell replication potential by protecting the chromosome

177
Q

Why do cancer cells need their own blood supply?

A

They (tumors) initially get nutrients by diffusion but they become hypoxic (low oxygen) and can’t proliferate without nutrients

178
Q

How do tumor cells sustain angiogenesis?

A

Hypoxia stimulates them to produce VEGF so blood vessels are stimulated to grow near tumor

179
Q

Which parts of adherens junctions become altered/defective in cancer?

A

Integrins
E-cadherin
Both form part of adheres junction

180
Q

How do proteases aid in metastasis?

A

MMP-8 breaks down collagen in basement membrane
uPA activates plasmin which is a protease

181
Q

What therapy is used in breast cancer?

A

Herceptin aka trastuzumab targets ERB B2

182
Q

What therapy is used in colorectal cancer and non small cell lung cancer?

A

Bevacizumab targets VEGF

183
Q

What therapy is used in chromic myeloid leukaemia?

A

Imatinib tagets ABL

184
Q

What is targeted in melanoma?

185
Q

What is BRCA1 normally involved in?

A

DNA repair - tsg

186
Q

What is embryology?

A

Study of development of embryo
From fertilisation to fetal stage

187
Q

When is the preimplantation stage and what happens?

A

Week 1
First week after fertilisation
DFertilised embryo hasn’t yet embedded into uterus

188
Q

What happens in week 2-8 of pregnancy?

A

Embryonic stage aka organogenesis
Connection between embryo and uterus
All organ systems of body established
Placenta develops

189
Q

What happens in week 9-38 of pregnancy?

A

Fetal stage
Fetus grows and organ systems differentiate and develop

190
Q

How does fertilisation occurs?

A

Ovary release one oocyte every month
Oocyte leaves ovary, if in contact with sperm fertilisation occurs

191
Q

What is a zygote?

A

Fertilised egg

192
Q

By which day does the zygote reach the uterus?

193
Q

What is cleavage? Week 1

A

Mitotic divisions of fertilised oocyte
Overall size remains the same as each division creates smaller cells

194
Q

How is cell division triggered in the zygote?

A

When the paternal and maternal genome fuse

195
Q

What is the isthmus?

A

Narrowest part of uterine tube

196
Q

Function and structure of zone pellucidA?

A

Touch glycoprotein coat preventing premature implantation and allows passage down isthmus

197
Q

What is a morula? What is it held together by?

A

Cells maximising contact with each other
Forms cluster of cells
Held together by tight junctions

198
Q

What are the first signs of cellular differentiation?

A

Inner cell mass and outer cell trophoblasts

199
Q

What happens when the embryo enters the uterine cavity?

A

Fluid enters via the zona pellucid and into the spaces of inner cell mass
Fluid filled blastocyst forms

200
Q

Wha does the inner cell mass go on to form?

A

Embryo and embryonic tissues

201
Q

What do trophoblasts form?

A

Placental structures

202
Q

Why does the blastocyst implant?

A

It begins to run out of nutrients

203
Q

How is implantation facilitated?

A

ICM cells proloferate
Fluid builds up in cavity
Blastocyst hatches from zone pellucida

204
Q

What is implantation an interaction between?

A

Embryo and endometrial layer of uterus
Connection becomes placenta

205
Q

What is decidualisation and what does it trigger?

A

Changes in endometrium to prepare it for pregnancy - making cells bigger and longer
Triggers production of molecules to promote trophoblast cells to become invasive

206
Q

What do trophoblast cells differentiate into in week 2?

A

cytotrophoblast - inner layer
synctiotrophoblast - outer invasive layer, establishes blood supply connection with placenta

207
Q

What does the ICM differentiate into in week 2?

A

epiblast and hypoblast
bilaminar disc

208
Q

Which molecule does synctiotrophoblasts produce?

A

HCG, early indicator of pregnancy

209
Q

Summarise week 2 of pregnancy?

A

implantation occurs forming connection between embryo and maternal endometrium
icm forms 2 layers making bilaminar disc
trophoblast differentiates to form 2 placental layers

210
Q

What is ectopic pregnancy?

A

Implantation occurs in abnormal sites

211
Q

Why does ectopic pregnancy occur?

A

Slow transit in uterine tube
Premature hatching of blastocyst

212
Q

When and where is ectopic pregnancy common?

A

ivf
- ovary surface
- uterine tube
- wall of go tract

213
Q

What happens if ectopic pregnancy isn’t treated with surgery/pill?

A

Trophoblast cells can cause life threatening haemorrhage
Uterine tube sometimes removes

214
Q

What are the 4 extra embryonic membranes?

A

Amnion
Chrorion
yolk sac
allantois

215
Q

Where is amnion found?
Function?
Life span?

A

Continous with epiblast of bilamiar disc
Lines amniotic cavity
Protects embryo
Up until birth

216
Q

Structure and location of chorion?
Function?

A

Double layered membrane
Formed by trophoblast and extra embryonic membranes
Lines chorionic cavity in early pregnancy but disappears when amniotic cavity expands

217
Q

Location of yolk sac?
Function?
Life span?

A

Continuus with hypoblast of bilaminar disc
Nutrient transfer in week 2-3
Disappears in week 20
Important in blood cell formation and gut formation

218
Q

Structure and function of allantois?

A

Forms as outgrowth of yolk sac
Contributes to umbilical arteries and connects to fetal bladder

219
Q

What is gastrulation?

A

Process of cell division resulting in 3 germ layers

220
Q

What is the trilaminar embryo formed from?

A

bilaminar epiblast

221
Q

What are the three germ layers?

A

ectoderm
mesoderm
endoderm

222
Q

What are 3 important structures in trilmainar embryo?

A

primitive streak
notochord
neural tube

223
Q

How are the three germ layers formed?

A

Epiblast cells proliferate - move towards primitive streak and push downwards to create new layers (invagination)
Epiblast forms ectoderm
Invaginating cells creates mesoderm
Epiblast cells push hypoblast to side to create ectoderm

224
Q

Examples of ectoderm structures?

A

Outside things
Nervous system (nerve cells in skin)
Epidermis
Cornea
Tooth enamel
Adrenal medulla

225
Q

Examples of mesoderm structures?

A

Notochord
Skeletal system
Muscular system
Excretory system
Circulatory/lympatic system
Dermis
Adrenal coortex

226
Q

Examples of endoderm structures?

A

Epithelium of disgtive tract
Epithelium of resp system
Lining of urine system and reproductive system
Liver
Pancreas
Thymus
Thyroid glands

227
Q

What is a teratoma?

A

Tumor with tissue/organ components resembling derivitaes of germ layers usually ectoderm

228
Q

What are germ cell teratomas?

A

Develop from germ cells that have failed to differentiate from oocyte/sperm
Found in gonads - testes/ovary

229
Q

What us cryptorchidism? Risks?

A

Failure of testes to descend into scrotal sac
Risk to develop germ cell tumours

230
Q

What are embryonal teratomas and where do they appear?

A

Congenital - baby born with it
Appear on midline of body

231
Q

Example of cels that don’t divide?S

A

Stratum granulosum cells, neutrophils, eythrocytes

232
Q

Which cells only divide sometimes?

A

Lymphocytes

233
Q

What is G0?

A

Phase when cells are not actively dividing
Not always permanent as cells can re enter cell cycle if their conditions are met

234
Q

What is G0 a response to?

A

External signal

235
Q

Examples of g0?

A

After antigen presentation, T lymphocyte undergoes clonal expansion and differentiation to memory and effector T cells
Erythrocytes permanently in G0

236
Q

How long is G1, S, G2 and M phase?

A

11, 8, 4, 1 hours

237
Q

What is interphase?

A

Growth and preparation for cell division
G1, S, G2

238
Q

What happens in S phase?

A

dna synthesis

239
Q

What happens in G1? What is it dependent on?

A

growth in size
rna and protein synthesis - prepare for s
needs growth factors

240
Q

What happens in G2?

A

further growth
cell organelle replication

241
Q

What happens in prophase?

A

chromatin condensation
nucleolus disappears
centrioles move to poles

242
Q

What happens in pro metaphase?

A

nuclear membrane dissolves
chromosomes attach to microtubules

243
Q

what happens in metaphase?

A

spindle fibres align the chromosomes along middle of cell nucleus aka metaphase plate

244
Q

what happens in anaphase?

A

paired chromosomes separate and move to opposite ends of cell

245
Q

what happens in telophase?

A

chromatids arrive at opposite ends of cell
new membrane form around daughter nuclei
chromosomes decondense
spindle fibres disperse

246
Q

Function of CDKs?

A

regulate progression through cell cycle

247
Q

what are CDKs regulated by?

A

cyclins
phosphorylation/dephosphprylation
CKIs

248
Q

What are cyclins?

A

activator proteins up or down regulated depending on stage of cell cycle
unstable

249
Q

What are CKIs?

A

Small proteins blocking cyclin/cdk activity
bind directly to cdk to form inactive complex or act as competitive ligand

250
Q

3 families of CKIs?

A

p21 cip
p27 kip
p16 ink

251
Q

What is progression to M phase dependent on?

A

cdk1/cyclin b

252
Q

When do cyclin b levels rise?

253
Q

What 3 things does MPF phosphorylate to induce mitosis?

A
  • lamins to destroy nuclear envelope
  • condensins/histones to condense chromeosomes
  • microtubule associated proteins to form spindles
254
Q

What do cell checkpoints monitor?

A

Precense of growth factors
sufficient growth
dna damage
replication errors
spindle attachment
chromosome integrity

255
Q

3 cell cycle checkpoints?

A

restriction point (g1)
dna damage checkpoints (late g1 and g2)
metaphase/spindle checkpoint

256
Q

What is progression of the cell cycle dependent on?

A

Growth factors

257
Q

When does the cell commit to cell division?

A

restriction point in g1

258
Q

What is progression to S phase dependent on?

A

accumulation of cyclin D

259
Q

What is the gatekeeper of restriction point?

260
Q

What happens when a growth factor is detected in restriction point?

A

Ras pathway produces cyclin D and activates cdk 4/6, kinases phosphorylate Rb and doesnt bind to E2F, so E2F can now transcribe genes for S phase

261
Q

Function of Rb?

A

maintains integrity of genome
causes cell cycle arrest in abnormally dividing cells and repairs DNA damage

262
Q

Function of p53?

A

Arrests cell cycle in DNA damage or apoptosis in irreparable damage

263
Q

What are examples of dna damage?

A

chemical mutagens
radiation
replication errors

264
Q

How does p53 arrest the cell cycle in response to DNA damage?

A

produces cdk inhibitor p21 which binds to sdks to inactivate them

265
Q

What is the metaphase/spindle checkpoint?

A

delays anaphase
checks all chromosomes are attached to spindle fibres
anaphase promoting complex inhibited until all chromosomes are attached

266
Q

What is pathology?

A

Using knowledge of cel biology to determine how illness arises

267
Q

What is ‘the patient journey’?

A

symtoms
investigations
diagnosis
management

268
Q

What are some general common investigation?

A

bloods
imaging
cultures

269
Q

What are some pathology specific investigations?

A

fluid sampling
tissue biopsy
genetic profiling

270
Q

What is neoplasia?

A

Excessive irreversible uncontrolled growth which persists even after withdrawal of stimuli that caused it

271
Q

What are 3 branches of neoplastic disease?

A

benign disease
dysplasia
malignancy

272
Q

4 reactions to normal tissue undvrstress?

A

hyperplasia - cells increase in number
hypertrophy - cells enlarge
atrophy - cells get smaller
metaplasia - cells change from one type to another
all reverible

273
Q

What are some irreversible cell changes to stress?

A

apoptosis - programmed cell death
necrosis - uncontrolled cell death
inflammation. reaction to cell death
neoplasia

274
Q

Qualities of benign disease?

A

localised
well encapsulated
slow growing
resembles tissue of origin
regular nuclei

275
Q

What is dysplasia?

A

anormal/atypical cells due to failure of differentiation

276
Q

Three qualities of dysplasia?

A

disordered architecture of tissue - loss of normal structure
disordered cellular features: pleomorphic nuclei (larger and misshapen)
mitotic figures (nuclei in stages of mitosis)

277
Q

Qualities of malignancy?

A

Invasive
Can metastasise
Grows fast
Dysplasia features
May not resemble tissue of origin

278
Q

How is colon tissue arranged?

279
Q

3 ways metastasis can spread?

A

through lymphatics
through blood
transcoelomic - spreading across body cavity e.g. pleural/pericardial cavity

280
Q

What is cancer of unknown primary?

A

Metastasis that you cannot easily identify the site of origin

281
Q

Which pathway does HER2 work via?

A

Receptor tyrosine kinase

282
Q

What does an over expression of HER2 in breast cancer suggest?

A

A more aggressive cancer

283
Q

How are breast cancers tested for HER2?

A

immunohistochemistry

284
Q

What is immunohistochemistry?

A

shows where certain proteins are expressed and in what quantities

285
Q

What is microsatellite instability and when does it occur?

A

Higher chanvce of mutation and therefore cancer caused by failure of mismatch repair system
When theres a failure of the mechanism to repair damaged DNA in the cell cycle

286
Q

What is microsatellite instability in colon cancer associated with?

A

lynch syndrome

287
Q

What is neoplasm grading?

A

How closely the neoplasm corresponds with normal cells for that tissue
Higher dysplasia = higher grade

288
Q

What is neoplasm staging?

A

How far the neoplasm has spread through the body

289
Q

How is neoplasm staging measured?

A

Tumour - measures local invasion
Node - measures spread to lymph nodes
Metastasis - measures spread to distant tissues

290
Q

Local effects of neoplasm

A

symptoms e.g. pain, lump, mass
ulceration
bleeding/anaemia
compression of surrounding structures

291
Q

Metastatic effects of neoplasm?

A

depends on site
brain - swelling, raised pressure, stroke, seizure

292
Q

Systemic effects of neoplasm?

A

weight loss
appetite loss
fever
infection

293
Q

What cyclin and cdk is associated with G1?

A

cyclin d
cdk 4/6

294
Q

What cyclin/cdk is associated with g1/s?

A

cyclin e
cdk2

295
Q

What cyclin/cdk is associated with s phase?

A

cyclin a
cdk 2/1

296
Q

What cyclin/cdk is associated with m phase?

A

cyclin b
cdk1

297
Q

Examples of signals?

A

nutritional status e.g. glucose level
oxygen supply
temperature
pathogens
hormones
growth factors

298
Q

Examples of responses to signals?

A

die
grow
divide
differentiate
migrate
change shape
produce protein
release hormones

299
Q

Example of a morphogen?

A

Sonic hedgehog - substance secrete from cell to surroundings, cell closer to signal will recieve more of signal than those far away

300
Q

What is cyclopean?

A

failure of SHH signalling in development
only have one eye

301
Q

Why do we need signals?

A

coordinating development
maintaining normal physiological function
to avoid disease

302
Q

What happens when there is high blood sugar?

A

insulin released
glucose taken into cells and used/stored as glycogen

303
Q

What happpens when there is low blood sugar ?

A

Glucagon released
glycogen turned back into glucose in the liver and released into the blood stream

304
Q

What is the cause of type I and type II diabetes?

A

Type I - lack of sufficient insulin production
Type II - reduced responsiveness to insulin in target cells

305
Q

Which signals mutation causes pancreatic cancer?

A

k-ras is too active and causes cells to grow/divide/survive in absence of growth signals

306
Q

Which drug and target is involved in asthma relief?

A

salbutamol
beta 2 receptor

307
Q

Which drug and target is involved in chronic myeloid leukaemia?

A

Gleevec
bcr-abl

308
Q

What does Avastin target in cancer?

309
Q

3 examples of signal types and examples of these?

A

physical - temp and pressure
electrical - nerve cells
biochemical - hormones, growth factors, neurotranmitters

310
Q

2 ways to classify biochemical signals?

A

chemical structure
range of action

311
Q

3 ways to classify hormones and examples?

A

amino acid derivatives
steroid hormones
eicosanoids

312
Q

Examples of amino acid derived hormones

A

adrenaline - modified AA
oxytocin - peptide hormone
insulin - protein hormone

313
Q

Examples of steroid hormones?

A

testosterone, cortisol

314
Q

Examples of eicosanoid, where are they derived from?

A

prostaglandin
lipids

315
Q

4 ranges of action in biochemical signals?

A

long distance, endocrine: via blood
nearby cells, paracrine: via diffusion
neighbouring cell, juxtacrine: cell to cell contact
same cell, autocrine

316
Q

example of juxtacrine?

A

apc mediated T cell activation

317
Q

example of autocrine?

A

activated T cell sending information to effector t cells

318
Q

What are 3 stages of signal transduction?

A

detecting signal via receptor
transfusing signal from site of detection to part of cell that will respond
responding - activation of cellular response

319
Q

How do intracellular receptors get activated? Examples?

A

Hydrophobic signalling molecules diffuse through plasma membrane
steroid hormones, nitric oxde

320
Q

Explain how steroid hormones alter gene expression?

A
  • bind directly to intracellular receptor proteins
  • hormone receptor complex acts as transcription factor
  • complex binds to DNA and alters gene expression
321
Q

How do cell surface receptors cause a cellular response? Examples?

A

Signal binds to receptor, it is activated, alters shape/activity which causes a cellular response
Insulin/adrenaline

322
Q

3 types of cell surface receptors?

A

ion-channel linked
gpcr linked
enzyme linked

323
Q

how do ion channel linked receptors cause a response in the cell?

A

when signal binds, the channel pens and ions move along concentration gradient in or out of the cell
this changes electrical properties of the cell

324
Q

example of ion channel linked cells?

A

glutamate neurotransmitter

325
Q

How do G protein linked receptors cause a response in the cell?

A

when signal binds it activates a g protein which activates an enzyme and passes a signal onto the cell

326
Q

Examples of GPCR molecules?

A

adrenaline
serotonin
glucagon

327
Q

How do enzyme linked receptors cause a response in a cell?

A

When a signal binds to an inactive receptor it brings the two parts of the receptor together and causes activation of an enzyme inside the cell

328
Q

Which type of molecule is usually present in enzyme linked receptors?

329
Q

Give an example of an enzyme linked binding signal?

A

insulin, growth factors

330
Q

Which type of receptor are rtfs usually?

A

enzyme linked

331
Q

What type of protein dephosphorylates?

A

Protein phosphatases

332
Q

What is the reason for kinase to phosphorylate a protein? What is required?

A

alters protein function
atp

333
Q

What type of receptor does EGF use?

334
Q

Which molecules are produced when signals are transduced?

A

Relay molecules

335
Q

What are two main methods of signal amplification?

A

Enzyme cascades
Second messengers

336
Q

Example of an enzyme cascade?

A

MAPK cascade

337
Q

When are MAPK cascades activated?

A

In response to growth factor RTK activation e.g. EGF

338
Q

Explain how a EGF MAPK kinase cascade would be activated

A

EGF binds to RTK receptor
Relay proteins activate ras
Ras activates MAP KINASE cascade
Enzyme cascade amplifies signal and transcription factors are phosphorylated

339
Q

What is a second messenger?

A

Small molecule produced in large amounts inside cell after receptor activation

340
Q

Example of second messenger?

341
Q

Example of adrenaline second messenger process?

A

Binds to GPCR
GPCR activates cAMP
cAMP activates PKA
PKA activates effector proteins by phosphprylation

342
Q

Examples of responses to signal transduction?

A

gene expression
protein ectivity e.g. phosphorylation
protein binding e.g. to DNA or activor/inhibitor proteins
protein localisation e.g. transcription factor activated by moving from cytosol to nucleus

343
Q

Which pathways are often overactive in cancer?

A

RTK pathways

344
Q

What drug type is Herceptin?

345
Q

What drug targets VEGF in colorectal cancer?
Drug type?

A

Avastin
Antibody

346
Q

What drug targets EGFR in lung cancer? Drug type?

A

Odessa
inhibitor

347
Q

How to treat overactive RTK pathways?

A

inactivating antibodies, small molecule kinase inhibitors

348
Q

How does adrenaline cause fight or flight reaction?

A

Sympathetic nervous system is active when seeing a threat
This activates arenal cortex to produce adrenaline

349
Q

What is adrenaline?

A

Hormone produced in acute stress response

350
Q

3 outcomes of adrenaline?

A

inc heart rate
inc respiration
inc blood glucose

351
Q

Examples of GPCRS?

A

Adrenaline
Rhodopsin
Glutamate

352
Q

How are GPCRS activated?

A

Ligand binds to receptor
Conformational change in cytoplasmic domain
Conformational change allows g protein to bind or be activated by receptor
Activated g proteins actuvate intracellular enzyes

353
Q

What happens when gdp vs gtp is bound in GPCR?

A

GDP - inactive
GTP - active

354
Q

What exactly does activated G protein produce?

A

downstream effector proteins

355
Q

What is the off switch for GPCRs?

356
Q

Effect of GPCR activation?

A

secondary messenger molecules are produced
lots of targets activated

357
Q

How are G proteins turned off?

A

RGS hydrolyses GTP to turn it to inactive GDP

358
Q

How does adrenaline converted glucose store to glucose?

A

Adrenaline binds to GPCR
Alpha unit is activated and activates adenylyl cyclase molcule
this activates camp then pka
PKA phosphorylates phosphorylase kinase which activates phosphorylase and converts glycogen store to glucose

359
Q

How does adrenaline stop convert glucose to glycogen store?

A

Adrenaline binds to gpcr
Alpha unit is activated and activates adenylyl cyclase molecule
This activates camp then pka
pka phosphorylates glycogen synthase which stops glucose being turned to glycogen

360
Q

What happens when adrenaline isnt bound to gpcr?

A

gtp hydrolysed to gdp
adenylyl cyclase not made any more
phosphodiesterases break down camp
glucose stored as glycogen

361
Q

Which 3 responses can EGF cause?

A

survival - inhibits apoptosis
proliferation
invasion

362
Q

Which molecule activates p53 in low cell damage?

363
Q

Which molecule activates p53 in high cell damage?

A

ser15 and ser46

364
Q

Which responses can adrenaline cause?

A

glucose release from sekeltal muscle, liver
inc heart rate
vasodilation/constriction
bronchodilation

365
Q

Which cells do adrenaline bind?

A

muscle/liver

MBChB1 Phase 1 (12 decks)

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