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Phase 2a Sheffield Medicine > Introduction to Clinical Science > Flashcards

Introduction to Clinical Science Flashcards

1
Q

What are the 4 signs of inflammation?

A

Rubor - redness
Calor - heat
Tumor - swelling
Dolor - pain

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2
Q

What is inflammation?

A

A reaction to injury or infection involving cells such as macrophages and neutrophils

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3
Q

What is the difference between Acute and Chronic inflammation?

A

Acute - short lasting, sudden, usually resolves.

Chronic - long lasting, slow onset, may not resolve

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4
Q

Give one example of Chronic and acute inflammation

A

Acute - Appendicitis

Chronic - TB

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5
Q

What cells are involved in inflammation?

A 
Neutrophils
Macrophages
Lymphocytes 
Endothelial cells
Fibroblasts
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6
Q

What is the role of Neutrophils in inflammation?

A

Cytoplasmic granules w/ enzymes to kill bacteria and can signal for macrophages.

They are the first there and first to die at the site.

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7
Q

What is the role of Macrophages in inflammation?

A

Long lasting, phagocytic and can present antigens.

They ingest bacteria and carry it away.

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8
Q

What is the role of Lymphocytes in inflammation?

A

Long lasting - produce chemicals to attract other inflam cells.

They provide immunological memory for past infections.

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9
Q

What is the role of Endothelial cells in inflammation

A

They line capillary blood vessels.

They become sticky, allowing adhesion of inflam cells, can also become porous to let cells pass into tissue.

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10
Q

Is inflammation always good?

A

It can be during infection/injury.

It is problematic in hypersensitivity reactions or AI disease.

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11
Q

What are endogenous chemical mediators of inflammation (with examples)

A

They are secreted and mediate the inflammatory response.

Examples - histamine, prostaglandins, bradykinin and Nitric Oxide.

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12
Q

How would you treat inflammation?

A

You need to treat the route cause e.g. bact infection w/ antibiotics.

You would prescribe NSAIDs which inhibit prostaglandin synthetase.

You could also prescribe Corticosteroids to down regulate chemical mediators.

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13
Q

Why might somebody be refered for an autopsy?

A

Medico legal reasons - coronial
Hospital autopsy - teaching/confirmation of COD.

(Presumed natural, presumed unnatural and presumed iatrogenic)

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14
Q

Who can make request an autopsy?

A

Relatives, police, registrar of BDM, coroner.

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15
Q

What is an embolus?

A

Mass of material in the vascular system able to become lodged within a vessel and block it.

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16
Q

What are three causes of Emboli?

A

Thrombus
Air
Cholesterol Crystals

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17
Q

How do the lungs act as a filter for venous emboli?

A

BV from the lungs are capillaries which means that it cannot reach the arteries as it will get caught in the vein/cap network.

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18
Q

What is Thrombosis?

A

solid mass of blood constituents formed within an intact vascular system during life.

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19
Q

What is Virchow’s triad?

Reasons for Thrombotic formation

A

Change in vessel wall
Change in blood flow
Change in blood constituents

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20
Q

Process of Thrombus formation

A
  1. Damage to endothelial cells cause platelets to stick to collagen –> Platelet aggregation, + Feedback
  2. Endothelial injury disrupts laminar flow

Formation of a thrombus causes fibrin polymerase to be released –> keeps it together.

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21
Q

What is the reason clots are fairly rare?

A

Laminar flow - blood travels in the center and doesn’t touch the side.

Endothelial cells are not sticky when healthy.

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22
Q

What are the outcome of Thromboses?

A

Break down and lysis
Recanalisation - new capillaries grow through it
Break off and embolise

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23
Q

How can you prevent thrombosis?

A

Exercise
Stockings
Aspirin - inhibits platelet aggregation.

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24
Q

What is Ischaemia?

A

Reduction of blood flow to a tissue without any other implications.

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25
Q

What is the risk of Reperfusion post ischaemia?

A

Can produce super oxide radicals which damage the cells.

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26
Q

What is the difference between Ischaemia and Infarction?

A

In Ischaemia there is reduction of blood flow w/o implications and in infarction there is tissue death.

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27
Q

What is Infarction?

A

Reduction in blood flow means that cell’s cannot support maintenance and will die.

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28
Q

Is Infarction always deadly?

A

No

Some organs have two artery supplies e.g. COW, Liver, Lung whereas others only have one.

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29
Q

What is usually the cause of infarction?

A

Thrombosis breaking off from other areas or a tumour.

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30
Q

What is granulation tissue?

A

Composed of small BV in a connective matrix with myofibroblasts.

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31
Q

What is a granuloma?

A

An aggregate of epitheliod histocytes

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32
Q

What are the definitions of Resolution and Repair?

A

Resolution - initiating factor is removed and the tissue regenerates.

Repair - the initiating factor is still present, tissue is damaged and unable to regenerate.

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33
Q

What cells can regenerate?

A 
Hepatocytes
Pneumocytes
All blood cells 
Epithelium of Gut and Skin
Osteocytes
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34
Q

What cells cannot regenerate?

A

Myocardial cells

Neurones

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35
Q

What is the process of Repair?

A

replacement of damaged tissue by fibrous tissue which is collagen produced by fibroblasts.

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36
Q

What produces collagen?

A

Fibroblasts

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37
Q

What is lobar pneumonia?

A

Pneumonia specific to one lobe in the Lungs, can recover as pneumocytes can regenerate.

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38
Q

What is the process of Skin repair?

A

Abrasion - scab formation - epidermis grows and is protected by the scab.

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39
Q

What is the process of Skin repair post surgery?

A

Exudation of fibrinogen causes a weak fibrin joint. Epidermal growth causes collagen synthesis –> stronger collagen joint

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40
Q

What is Atherosclerosis?

A

A disease in which plaque builds up in the artery.

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41
Q

Who tends to get Atherosclerosis more often?

A

Men in industrial areas.

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42
Q

Where do Atheroma’s develop?

A

In arteries with high pressure, e.g. the aorta, and less in the arteries with low pressure e.g. pulmonary arteries.

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43
Q

What increases the risk of Atherosclerosis?

A

Smoking - damages endothelium using free radicals
Hypertension - shearing forces on endothelial cells
Diabetes ( poorly controlled) - super anions damage cells
Hyperlipidaemia - direct damage to endothelial cells.

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44
Q

What is the Endothelial Damage theory?

A

Recurrent endothelial cell injury causes microthrombi formation which builds atheroscleroma over years.

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45
Q

What are some of the Complications of Atherosclerosis?

A

MI
Gangrene
Peripheral Vasc disease
Aneurysm

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46
Q

How can you reduce the risk of Atherosclerosis?

A

Low dose aspirin can prevent platelet aggregation.

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47
Q

What is Apoptosis?

A

Programmed cell death

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48
Q

What is Necrosis?

A

Traumatic cell death which is unprogrammed

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49
Q

What are some examples of Necrosis?

A

Avascular necrosis of bone
Pancreatitis
Frost bite

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50
Q

What are the different types of Necrosis?

A

Caseous necrosis - linked w/ TB
Liquifactive necrosis - thin liquid
Coagulation necrosis - thick and goey

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51
Q

What is a disease in which too much apoptosis occurs?

A

HIV (gets rid of T helper cells)

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52
Q

What is a disease in which too little apoptosis occurs?

A

Cancer

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53
Q

What protein Initiates apoptosis?

A

P53

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54
Q

What is the role of Capases?

A

They are the effectors of apoptosis

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55
Q

What are the effectors of apoptosis?

A

Capases

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56
Q

What switches on Capases?

A

BAX protein

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57
Q

What switches off Capases?

A

Bcl2 protein

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58
Q

What can trigger apoptosis?

A

DNA damage

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59
Q

What is the process of apoptosis?

A
  1. A trigger causes a release of enzymes

2. These enzymes cause the nucleus to shrink and organelles are carried out by vesicles

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60
Q

Why don’t adult cells divide very often?

A

The telomeres get shorter after every division.

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61
Q

What causes cells to ‘wear out’?

A

Free radical generation
Free radical absorption
Cross linking of proteins via UV light
Shortening telomeres

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62
Q

What are some diseases associated with aging?

A

Deafness –> Ciliated hair cells are not replaceable
Osteoporosis - bone matrix is decreased
Senile dementia –> brain atrophy
Sarcopenia –> loss of skeletal muscle mass

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63
Q

Define congenital

A

Present at birth

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64
Q

Define Inherited disease

A

Caused by an inherited genetic abnormality, not always present early e.g. huntingtons

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65
Q

Define acquired disease

A

caused by non-genetic environmental factors e.g. FAS

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66
Q

What is a homeobox gene?

A

A gene sequence that codes for different parts of the body.

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67
Q

What is Mendelian inheritance?

A

Single gene inheritence

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68
Q

What is autosomal inheritance?

A

Non sex cell, autosomal dominant (FAP) and recessive (CF)

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69
Q

What is polygenic inheritance?

A

When one characteristic is associated with two or more genes.

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70
Q

What is Hypertrophy, with an example?

A

Increase in size of tissue caused by an increase in size of constituent cells.

e.g. Muscles getting bigger.

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71
Q

What is Hyperplasia, with an example?

A

Increase in size of a tissue caused by an increase in number of the constituent cells

e.g. Benign prostatic hyperplasia.

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72
Q

What is Atrophy, with an example?

A

Decrease in size of a tissue caused by a crease in the number of constituent cells or a decrease in their size .

e.g. Muscular atrophy and alzheimers.

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73
Q

What is metaplasia, with an example?

A

Change in differentiation of a cell from one fully differentiated type to a different fully differentiated type.

e.g. change from cilliated columnar epithelium to squamous in bronchi (barretts oesophagus thanks to smoking)

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74
Q

What is Dysplasia, with an example?

A

Imprecise term for the morphological changes seen in the progression to becoming cancer.

e.g. epithelial cells changing as a precursor to cancer.

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75
Q

Define carcinogenesis.

A

The transformation of normal cells to neoplastic cells through permanent alterations/mutations.

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76
Q

Define Oncogenesis

A

Formation of benign and malignant tumours

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77
Q

Define Mutagenic

A

Something which acts on the DNA

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78
Q

How much of cancer is due to the environment?

A

85%

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79
Q

What are some behavioral risks of cancer?

A

Smoking - Lung cancer

Rubber industries - bladder cancer

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80
Q

What is radiating energy?

A

ionising radiation w/ long term effects

e.g. Thyroid cancer post chernobyl and exposure to UV –> Increase in skin cancer, BCC and melanoma

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81
Q

What are the classes of Carcinogens?

A 
Chemical
Viral
Ionising/non ionising radiation
Host
Miscellaneous
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82
Q

What is a chemical carcinogen?

A

It has no common structure, some act directly some need to be metabolised from pro-carcinogenic to ultimate carcinogenic.

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83
Q

Examples of Chemical carcinogens

A

Polycyclic aromatic HC - lung and skin cancer - smoking
Aromatic amines - bladder cancer - rubber workers
Nitrosamines - gut cancer
Alkylating agents - Leukaemia

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84
Q

Miscellaneous examples of carcinogens

A

Asbestos and metals

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85
Q

What are Host factors?

A

Race - oral cancer in indians
Diet
Constitutional factors - increases w/age, inherited predisposition + gender
premalignant lesions - Ulcerative collitis

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86
Q

What are the Biological factors?

A

Hormones - Oestrogen - mammary/endometrial cancer
Mycotoxins - alfatoxin B1 - Hepatocellular Carcinoma
Parasites - Clonorchis sinesis - Cholanginocarcinoma

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87
Q

What does Asbestos cause?

A

Malignant Mesothelioma
Lung cancer
Asbestosis

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88
Q

What is Basal cell carcinoma and how would you treat it?

A

Only invades the skin locally, doesn’t spread to other parts of the body. You can excise it locally.

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89
Q

How is leukemia spread around the body?

A

WBC circulate around the body and so will any tumour of the WBC.

Chemotherapy is the appropriate treatment

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90
Q

What is a Carcinoma?

A

They spread to the lymph nodes that drain the site of the carcinoma (can spread from blood to bone)

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91
Q

What cancers can be spread from blood to bone?

A 
Breast
Prostate
Lung
Thyroid
Kidney
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92
Q

How would you treat Breast cancer?

A
  1. Confirm the cancer using a biopsy
  2. Check if its spread to the axilla - if so clear it.
  3. if it’s spread to the body chemo
  4. If it hasn’t surgery w/wo axillary clearence
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93
Q

What is adjuvant therapy?

A

Extra treatment given post surgical excision to prevent a secondary tumour.

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94
Q

What is the route of mets?

A
  1. Through BM to EC
  2. EC to vessels, travels in to the vessels
  3. Adheres and breaks int othe EC then grows
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95
Q

What is the growth of mets limited to, and what is it dependent on?

A

1mm in diameter.

GF and blood supply

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96
Q

What is required to invade the basement membrane?

A

Requires collagenase and cell motility

Collagenase required to break through the collagen layers of the BM

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97
Q

What is required to enter the blood stream (Intravasation)?

A

Collagenase + cell motility

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98
Q

What is required to exit the blood stream?

A

Adhesion
Cell motility
Collagenase

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99
Q

How does a tumour hide from the immune system?

A

Shed surface antigens
adhese to other cells
aggregate w/ platelets.

100
Q

What are 2 angiogenesis promoters?

A

Vascular endothelial growth factor

Basic fibroblast growth factor

101
Q

What are 3 angiogenesis inhibitors?

A

Angiotensin, endostatin, vasculostatin

102
Q

How could a cancer spread to the lung?

A

Tumour enters vein and R side of heart to capillary level which acts a filter so it goes to the Lung

103
Q

How could a cancer spread to the liver?

A

PV to liver which branches to capillary level and acts as a filter

Colon stomach and pancreatic can all spread via PV.

104
Q

What is chemotherapy suitable for?

A

Fast dividing tumours - lymphoma, acute leukemia, germ cell tumour of testis

Not good for slow dividing.

105
Q

What is conventional chemotherapy and what are some problems?

A

Not selective to tumour cells

It will hit normal cells that are dividing - hair loss myelosuppresion and diarrhea

106
Q

What is the difference between conventional chemotherapy and targeted chemotherapy?

A

Targeted is more effective and comes w/ less side effects.

107
Q

What is a tumour?

A

Any abnormal swelling - could be down to hyperplasia, hypertrophy, neoplasm or inflammation.

108
Q

What is a neoplasm?

A

A lesion resulting from relatively autonomous abnormal growth of cells that persist after the initiating stimulus is removed.

109
Q

What is the structure of a Neoplasm?

A

Neoplastic cells - derivded from nucleated cells, growth pattern and activity is related to parent cells

Stroma - connective tissue framework w/ mechanical support and nutrition.

110
Q

Why might central necrosis of a tumour occur?

A

Due to a lack of blood supply.

111
Q

How would you classify neoplasms?

A

Treatment and prognosis

112
Q

Why should we classify neoplasms?

A

Appropriate treatment and informed prognosis

113
Q

What is a benign neoplasm?

A

Localised, low mitotic activity, non invasive and often bare close resemblance to normal tissue.

They are exophytic (grow up and out)

Rare necrosis + ulceration.

114
Q

Is necrosis and ulceration more common in benign or malignant tumours?

A

Malignant.

115
Q

Why would a benign neoplasm cause worry?

A

Pressures adjacent structures, can become malignant, can produce hormones and causes anxiety.

116
Q

Why would a malignant neoplasm cause worry?

A

Destruction of adjacent tissue, mets, blood loss from ulcers + obstruction of flow, can also produce hormones and causes anxiety.

117
Q

What is a malignant neoplasm?

A

Invasive, mets with a rapid growth rate.

They have hyperchromatic + pleomorphic nuclei

Poorly defined with variable resemblance to the normal tissue

Endophytic growth (grow down and in)

118
Q

What can neoplasms arise from?

A

Epithelial cells
connective tissues
Lymphoid/haemopoietic regions

119
Q

What is a papilloma?

A

Benign tumour of non secretory, non glandular epithelium - prefixed with its origin.

e.g. squamous cell papilloma

120
Q

What is a adenoma?

A

Benign tumour of secretory or glandular epithelium, prefied with its origin.

e.g. Thyroid adenoma.

121
Q

What is a carcinoma?

A

Malignant tumour of epithelial cells, prefixed by the epithelial cell type.

Adenocarcinoma (glandular)

122
Q

What are 2 benign epithelial neoplasms?

A

Papilloma and Adenoma.

123
Q

What is a metastatic epithelial neoplasm?

124
Q

What are the benign neoplasms of the connective tissue?

A

Lipoma - adipocytes
chondroma - cartilage
Osteoma - bone
Angioma - vascular

Rhabdomyoma - striated muscle
leiomyoma - smooth muscle

125
Q

What is a neuroma?

A

Benign neoplasm of the nerves

126
Q

What is an aplastic tumour?

A

When the cell type of origin is unknown.

127
Q

How are tumours classified?

A

Often by their degree of differentiation.

128
Q

What are some malignant connective tissue neoplasms?

A 
Liposarcoma - adipose
Rhabdosarcoma - striated muscle
Leiomyosarcoma - Smooth muscle
Chondrosarcoma - cartilage 
Osteosarcoma - bone
Angiosarcoma - vascular
129
Q

What is innate immunity?

A

Instinctive, non specific not dependent on lymphocytes.

130
Q

What is adaptive immunity?

A

Specific acquired immunity, requiring lymphocytes

131
Q

Where do leukocytes originate from?

A

Multipotent haematopoietic stem cells (haemocytoblast)

132
Q

Give 3 examples of Polymorphonuclear leukocytes

A

Neutrophils
Eosinophils
Basophils

133
Q

Give 3 examples of mononuclear Leukocytes

A

Monocyte
T cell - thymus
B cell - Bone marrow

134
Q

What do monocytes turn into usually in tissue?

A

Macrophages

135
Q

What do B cells turn into usually?

A

Plasma cells that secrete Ab

136
Q

What do T cells turn into usually?

A

T reg cells
T Helper Cells (CD4)
Cytotoxic T cells (CD8)

137
Q

What are mast cells?

A

Natural killer cells e.g. Langerhans/dendritic cells.

138
Q

What are the soluble factors in the blood?

A

Complement
Antibodies
Cytokines
Chemokines

139
Q

What is complement?

A

Group of proteins secreted by the liver that needs to be activated to work.

140
Q

What are the 3 functions of complement?

A

Lysis
chemotaxes of leukocytes
Opsonisation

141
Q

What do antibodies bind to?

142
Q

What are immunoglobulins bound to?

A

B cells

They are soluable and secreted.

143
Q

Which Immunoglobulin is secreted?

144
Q

Give 3 functions of antibodies

A
  1. Neutralise toxins
  2. Opsonisation of pathogens
  3. Activation of complement system (classical)
145
Q

What are the 2 most common Ig?

A

IgG and IgM

146
Q

What region of an antibody binds to an antigen?

A

Fab region.

147
Q

What region of an antibody binds to a B cell?

A

Fc region.

148
Q

Where is IgD present?

A

mature B cells

149
Q

Where is IgE present?

A

On basophils and Mast cells.

150
Q

What are cytokines?

A

Proteins secreted by immune and non-immune cells.

151
Q

Give 4 examples of Cytokines

A

Interferons
Interleukins
Colony stimulating factors
Tumour Necrosis Factors

152
Q

What do Interferons do?

A

Induce Anti-viral resistance in non affected cells.

153
Q

What do Interleukins do?

A

Pro or anti-inflammatory affects

154
Q

What do Colony stimulating factors do?

A

Directs division + differentiation of bone marrow and stem cells.

155
Q

What does Tumour Necrosis Factor do?

A

mediates inflammation.

156
Q

What are Chemokines?

A

Substances that attract leukocytes to the site of infection e.g. CXCL - Neutrophils.

157
Q

What are 3 O2 dependent ways of microbial killing?

A

Using ROI

Superoxides can be converted to H2O2 and OH Free radicals

NO causes vasodilation and increased extravascation.

158
Q

What are 3 O2 independent ways of microbial killing?

A

Enzymes

Proteins - defensins + TNF

pH

159
Q

What is the process of phagocytosis?

A
  1. Pathogen binds to macrophage/neutrophil
  2. Engulfment of pathogen
  3. Phagosome formation then phagolysosome
  4. Pathogen is destroyed.
160
Q

What are the 3 complement activation pathways?

A

Classical - Antibody binds to microbe

Alternative - C binds to microbe.

Lectin - activated by mannose binding lectin bound to microbe.

161
Q

How can pathogens be sensed?

A

Pathogen associated molecular patterns (PAMP) (on microbe)

Pattern Recognition Receptors (PRR) (On cells)

162
Q

How can microbes be sensed;

a - in the blood
b - in tissues

A

in the blood - monocytes+neutrophils

in tissues - macrophages + dendritic cells

163
Q

What are the Hallmarks of inflammation?

A

Increased vasc supply
increased vasc permeability
Increased leukocyte migration

164
Q

What are some physical and chemical barriers?

A

Skin
Mucocillary escalator
Gastric acid
Lysozymes and pH

165
Q

What does a lysozyme do?

A

Destroy bacterial cell walls

166
Q

What is the inflammatory response?

A
  1. Coagulation

2. Acute inflammation

167
Q

What is the purpose of the inflammatory response?

A

Kill pathogens, stop the spread and neutralise toxins.

Proliferation of cell to repair damage
Removal of clot - remodelling extracellular matrix
Establish normal tissue function.

168
Q

What are some of the defence mechanisms in innate immunity?

A

Physical + chemical barriers
Blood proteins - complement
Phagocytic cells - Macrophages + neutrophils.

169
Q

What is extravasation?

A

WBC migration across the endothelium

170
Q

What do macrophages secrete to initiate Extravasation?

171
Q

Describe the process of Extravasation

A
  1. Macrophages release TNFa
  2. Endothelium stimulated to express adhesion molecules + stimulate chemokines
  3. Neutrophils bind to adhesion molecules - roll, slow and get stuck.
  4. Neutrophils are activated by chemokines
  5. Neutrophils pass through endothelium to combat infection
172
Q

Why do we need cell mediated immunity?

A

Some viruses evade innate immunity.

IC Viruses + bacteria hide from innate immunity.

Needs memory to a specific antigen when it happens again.

173
Q

What Cells are responsible for cell mediated immunity?

A

T cells - intracellular microbes

174
Q

What cells are responsible for humoral immunity?

A

B cells - Extracellular microbes

175
Q

Give 3 examples of APC

A

Dendritic cells
Macrophages
B cells

176
Q

What is cell mediated immunity?

A

Occurs between APC and T cells and requires intimate cell to cell contact.

It controls Ab responses via contact w/ B cells to kill infected ones.

177
Q

Which cells express MHC 1?

A

Glycoproteins on all nucleated cells

178
Q

Which cells express MHC 2?

A

Glycoproteins only on APC.

179
Q

What does MHC 1 bind to?

A

CD8 cell –> killer cell –> induce apoptosis when they bind.

180
Q

What does MHC 2 bind to?

A

CD4 cells –> helper cells –> TH1 Secretes cytokines and TH2 Produces antibodies against extracellular pathogens.

181
Q

What happens to B cells that can recognise self?

A

They are killed in the bone marrow as they mature.

182
Q

Describe the process of a T helper cell binding to a B cell.

A

B-cell Ab binds to Ag

Epitope is displayed on the surface of B-cell bound MHC2

TH2 binds to b cell –> cytokine secretion causes B cell clonal expansion

Differentiation of plasma cells and memory B cells.

183
Q

What happens to T cells that recognise self?

A

They are killed in thymus, they only respond to IC presented antigens.

184
Q

Which T cell would respond to an IC/intrinsic antigen?

185
Q

Which T cell would respond to an EC/Ex antigen?

186
Q

What is needed for Cell mediated immunity?

A

Intimate contact between T and APC cells.

Intrinsic/endogenous/IC antigens OR Extrinsic/exogenous/EC antigens.

This helps recognise self from non-self.

187
Q

What is a type one hypersensitivity reaction?

A

IgE binds to mast cells which releases histamine

e.g. Pollen and anaphylaxis

188
Q

What is a type two hypersensitivity reaction?

A

IG bind to surface antigens

e.g. Transplant rejection and grave disease

189
Q

What is a type three hypersensitivity reaction?

A

The activation of complement by a fungus.

190
Q

What is a type four hypersensitivity reaction?

A

T cell mediated

E.g. TB

191
Q

How can you diagnose Atopy?

A

Skin prick or Ras Test

192
Q

Where would IgM be the highest?

A

at the beginning of Infection

193
Q

What is IgE made against?

A

Made to things that we are allergic too

194
Q

What is active immunity?

A

When you make your own antibodies post exposure to a pathogen.

195
Q

What is passive immunity?

A

When you artificially gain the antibodies

196
Q

Why are vaccines good?

A

Save lives, prevents disability and saves money.

197
Q

What is an adverse drug reaction?

A

A noxious and unintended response to a drug

198
Q

What is Rawlin-thompsons classification?

A

Way of classifying different drug reactions

199
Q

What is a Type A RT?

A

Augmented, very common and predictable –> dose related

200
Q

What is a Type B RT?

A

Bizzare, unpredictable, immunological in nature –> often allergy related

201
Q

What is a Type C RT?

A

Chronic, occurs after long term therapy

202
Q

What is a Type D RT?

A

Delayed and happens after many years of treatment

203
Q

What is a Type E RT?

A

End of use, withdrawal action

204
Q

What are 3 causes of ADR?

A

Receptor abnormality
Immunological
Abnormalities in drug metabolism

205
Q

What are 3 risk factors for ADR?

A

Being a woman
Elderly
Poly-pharmacy
Many allergies

206
Q

What is the difference between active and passive immunity?

A

Active - making your own antibodies post infection

Passive - Artificially gaining the antibodies

207
Q

How can synthetic peptides be used as vaccines?

A

They stimulate T cell development.

208
Q

What is the process of active immunisation?

A

Engage the immune system
Elicits danger signals and triggers PAMPs
Engage TLR
Activate specialist APC -> Langerhans
Engage the adapative immune system - generates T+B memory cells and activates T cell helpers.

209
Q

Give 3 examples of active immunity

A
  1. Induces immunological memory
  2. Produces high affinity AB
  3. Produces a protective response against pathogens
210
Q

Give 2 advantages of passive immunity

A

Immediate effect

Useful for acute dangers

211
Q

Give 3 disadvantages of passive immunity

A

Short term
No Immunological memory
Possible

212
Q

What is the first immune response to initial exposure?

A
  1. Innate immune response
  2. IgM predominates
  3. Low affinity
213
Q

What is the second immune response to a previously met pathogen?

A
  1. Rapid and larger than the first
  2. Higher affinity IgG
  3. Adaptive immunity - T cell help
214
Q

What are 5 Features of an Ideal vaccine?

A 
Safe
Induces a suitable immune response 
Shouldn't require boosters 
Generates immunological memory 
Stable and easy to transport
215
Q

What is the role of an adjuvant?

A

A substance added to a vaccination to stimulate an immune response.

216
Q

What is an example of an adjuvant?

A

Toxoids, proteins and chemicals.

217
Q

What are the advantages of an inactivated vaccine?

A

No risk of infection

Storage is less critical

218
Q

What are the disadvantages of an inactivated vaccine?

A

Response is weak
Boosters are needed
Tend to only activate humoral response –> Lack of T cell involvement.

219
Q

Where are atherosclerotic plaques found?

A

Peripheral and coronary artery

220
Q

What leads to neointima forming?

A

Atherosclerosis causing increased wall thickness.

221
Q

What is the function of thyroid hormone?

A
  1. Food metabolism
  2. Protein synthesis
  3. Increased sympathetic action e.g. CO and HR
  4. Heat production
  5. Needed for growth and development
222
Q

How long does Thyroxine (t4) last?

A

Half life is 5-7 days

223
Q

How long does Triiodothyronine last?

A

Half life is only 1 day

224
Q

What does ADH do?

A

Acts on the CD of the nephron and increases the insertion of aquaporin 2 channels –> Causes H2O retention.

225
Q

What are two things ADH is inhibited by?

A

Caffeine and Alcohol

226
Q

When is ADH release triggered?

A

High osmolality and Low blood vol, nausea, vomiting, stress and exercise

227
Q

What are two characteristics of Iodothyronines?

A

Not water soluble

99% Bound to proteins

228
Q

How are Iodothyronines formed?

A

Iodine + tyrosine = Iodothyronines

229
Q

How is Thyroxine (t4) formed?

A

Iodothyronines are conjugated to make T4.

230
Q

Where is the posterior pituitary derived from?

A

The floor of the ventricles

231
Q

Name two hormones that are secreted from the posterior pituitary

A

Oxytocin and ADH

232
Q

Give two functions of oxytocin

A

Milk secretion

Uterine contraction

233
Q

What 4 cells make up the islets of Langerhans?

A

Beta cells (70%)
Alpha cells (20%)
Delta cells 8%
Polypeptide secreting cells

234
Q

What is an example of a water soluble hormone?

A

Peptides e.g. TRH,LH,FSH

235
Q

Are water soluble hormones stored in vesicles or synthesised on demand?

A

Water soluble hormones e.g. peptides are stored in vesicles.

236
Q

How do water soluble hormones e.g. peptides get into cells?

A

They bind to cell surface receptors.

237
Q

Give an example of a fat soluble hormone

A

Steroids e.g. cortisol

238
Q

Are fat soluble hormones stored in vesicles or synthesised on demand?

A

Synthesised on demand

239
Q

Give an example of an amine hormone

A

Noradrenaline and adrenaline

240
Q

Where are hormones secreted from the posterior pituitary bound to?

A

Stored in colloid and bound to thyroglobulin.

241
Q

What stimulates the movement of colloid into a secretory Cell?

A

TSH it allows T3–>T4.

242
Q

Describe the pathway for noradrenaline synthesis

A

Phenylalanine –> L-tyrosine –> L-dopa –> Dopamine –> NAd and Ad

243
Q

What two enzymes break down catecholamines

A

MAO and COMT

244
Q

What are noradrenaline and adrenaline broken down into?

A

Normetadrenaline and metadrenaline

245
Q

Where in a cell are peptide cell receptors located?

A

on the cell membrane

246
Q

Where in a cell are thyroid/vit A and D cell receptors located?

A

Thyroid, Vit A and D and oestrogen act on nuclear receptors.

Phase 2a Sheffield Medicine (10 decks)

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