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Phase 2a Medicine > Introduction to clinical sciences > Flashcards

Introduction to clinical sciences Flashcards

1
Q

What are the 2 types of autopsy

A

Hospital Autopsy
Medico-legal Autopsy

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2
Q

What are hospital autopsies useful for, and what % of UK autopsies are they

A

Useful for audit, teaching, governance, research
10% of all UK autopsies

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3
Q

What are Medico-legal autopsies useful for, and what % of UK autopsies are they

A

Coronial autopsies – standard
Forensic autopsies – deaths involving crime
90% of all autopsies in the UK

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4
Q

What is presumed natural death (coroners)

A

Cause of death not known
Not seen by doctor with recent illness (last 14 days)

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5
Q

what is presumed iatrogenic death (coroners)

A

Peri/postoperative deaths
Anaesthetic deaths
Abortion
Complications of therapy

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6
Q

What are presumed unnatural deaths (coroners)

A

Accidents
Industrial death
Suicide
Unlawful killing (murder)
Neglect
Custody deaths

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7
Q

What is Inflammation

A

the local physiological response to tissue injury.

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8
Q

What are beneficial effects of Inflammation

A

Destruction of invading microorganisms
The walling off of an abscess cavity, thus preventing spread of infection

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9
Q

What are problems caused by inflammation

A

An abscess in the brain would act as a space-occupying lesion compressing vital surrounding structures
Fibrosis resulting from chronic inflammation may distort the tissues and permanently alter their function

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10
Q

What are the cells involved in inflammation

A

Neutrophils
Macrophages
Lymphocytes
Endothelial cells
Fibroblasts

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11
Q

Role of Neutrophils in inflammation

A

Short lived cells
First on the scene of acute inflammation
Cytoplasmic granules full of enzymes that kill bacteria
Usually die at the scene of inflammation
Release chemicals that attract other inflammatory cells such as macrophages

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12
Q

Role of Macrophages in inflammation

A

Long lived cells (weeks to months)
Phagocytic properties
Ingest bacteria and debris
May carry debris away
May present antigen to lymphocytes

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13
Q

What are the names of macrophages based on location (liver, skin, bone, brain.)

A

Kupffer cell (liver), melanophage (skin), osteoclast (bone), microglial cell (brain)

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14
Q

Role of Lymphocytes in inflammation

A

Long lived cells (years)
Produce chemicals which attract in other inflammatory cells
Immunological memory for past infections and antigens

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15
Q

Role of Endothelial cells in inflammation

A

Line capillary blood vessels in areas of inflammation
Become sticky in areas of inflammation so inflammatory cells adhere to them
Become porous to allow inflammatory cells to pass into tissues
Grow into areas of damage to form new capillary vessels

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16
Q

Role of Fibroblasts in inflammation

A

Long lived cells
Form collagen in areas of chronic inflammation and repair

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17
Q

What is Acute Inflammation

A

the initial and often transient series of tissue reactions to injury
Sudden onset
Short duration
Usually resolves

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18
Q

What are the 3 processes of Acute inflammation

A

Vascular component: dilatation of vessels
Exudative component: vascular leakage of protein – rich fluid
Neutrophils recruited to the tissue

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19
Q

What are the potential outcomes of Acute Inflammation

A

Resolution
Suppuration
Organisation
Progression to chronic inflammation

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20
Q

What is Resolution (acute inflammation)

A

the complete restoration of the tissues to normal after an episode of acute inflammation.

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21
Q

What is Supperation (acute inflammation)

A

(e.g. abscess) – the formation of pus, a mixture of living, dying and dead neutrophils and bacteria, cellular debris and globules of lipid.

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22
Q

What is Organisation (Acute inflammation)

A

the process whereby specialised tissues are repaired by the formation of mature fibrovascular connective tissue. It occurs by the production of granulation tissue and the removal of dead tissue by phagocytosis.

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23
Q

What are 6 causes of Acute Inflammation

A

Microbial infections e.g. viruses
Hypersensitivity reactions e.g. parasites
Physical agents e.g. trauma/ radiation
Chemicals e.g. corrosives/ acids
Bacterial toxins
Tissue necrosis e.g. ischaemic infarction

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24
Q

What is Chronic inflammation

A

the subsequent and often prolonged tissue reactions following the initial inflammatory response
Slow onset
Long duration
May never resolve

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25
Q

What are the causes of chronic inflammation

A

Primary chronic inflammation
Transplant rejection
Progression from acute inflammation
Recurrent episodes of acute inflammation

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26
Q

What are the main cells involved in chronic inflammation

A

macrophages, Lymphocytes, plasma cells

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27
Q

What are the main cells involved in Acute inflammation

A

Neutrophils

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28
Q

What are Granulomas

A

a collection of epithelioid histiocytes (macrophages).

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29
Q

What is Granulation tissue

A

repair phenomenon, it is loops of capillaries supported by myofibroblasts which actively contracts to reduce wound size, this may leave a structure present

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30
Q

What does Ibuprofen do?

A

inhibit prostaglandins synthetase, decrease inflammation

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31
Q

What are Prostaglandins

A

chemical mediators of inflammation

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32
Q

describe the process and recovery for Lobar pneumonia

A

Affects a lobe of the lung rather than the whole thing (bronchopneumonia)
Alveoli filled with neutrophil polymorphs (acute inflammation) rather than air
Pneumocyte that line the alveoli can regenerate so the lung can be regenerated – the pneumocytes divide and reline the alveoli

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33
Q

Describe what skin abrasions are and their process of healing

A

The most superficial skin wounds e.g. road rash
Normal skin -> abrasion -> scab formed over surface -> epidermis growing out from adnexa, produced by scab -> thin confluent epidermis -> final epidermal regrowth

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34
Q

What is healing by 1st intention for incised skin wounds

A

An incision causes very little damage to the tissues on either side of the cut, so if the two sides are brought together accurately the healing can proceed quite quickly.
1st intention – can suture up the cut
Incision -> exudation of fibrinogen -> weak fibrin join -> epidermal regrowth and collagen synthesis -> strong collagen join

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35
Q

What is healing by 2nd intention for tissue loss injuries

A

A tissue loss injury or another reason that the wound margins are not apposed requires another mechanism for repair.
Can’t bring the skin edges together the cut is too deep
Loss of tissue -> granulation tissue -> organisation -> early fibrous scar -> scar contraction
Phagocytosis to remove any debris
Granulation tissue to fill in defects and repair specialised tissues lost
Epithelial regeneration to cover the surface

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36
Q

What is repair (vs healing)

A

Initiating factor still present
Tissue damaged and unable to regenerate
Replacement of damaged tissue by fibrous tissue
Collagen produced by fibroblasts

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37
Q

What cells don’t regenerate

A

Myocardial cells
Neurones

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38
Q

What cells regenerate

A

Hepatocytes
Pneumocytes
All blood cells
Gut epithelium
Skin epithelium
Osteocytes – help remodel bone fractures

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39
Q

Why are blood clots rare in normal physiology

A

Laminar flow – cells travel in the centre of arterial vessels and don’t touch the sides
Endothelial cells which line vessels are not ‘sticky’ when healthy

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40
Q

Define Thrombus

A

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

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41
Q

What are the steps of thrombus formation

A
  1. Damage to endothelial cells in the vessel causes some of the cells to lift away from the vessel wall, exposing collagen.
  2. Platelets then begin to stick to this exposed collagen, and release the chemicals which cause platelet aggregation. Platelet aggregation also starts off the cascade of clotting proteins in the blood.
  3. Red blood cells then get trapped within the aggregating platelets
  4. Clotting factors join the red blood cells and platelets, and the clotting cascade forms a large protein molecule fibrin, which then gets deposited and forms the clot.
  5. Positive feedback loop -> can end up causing a thrombus (thrombosis), blocking the artery
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42
Q

What is the Virchow triad

A

the causes of thrombosis:
Change in vessel wall
Change in blood flow
Change in blood constituents

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43
Q

How does low dose Aspirin work

A

Low dose aspirin inhibits platelet aggregation, so this can be prescribed to reduce the risk of thrombosis.

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44
Q

Define Embolism

A

the process of a solid mass in the blood being carried through the circulation to a place where it gets stuck and blocks the vessel

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45
Q

define Embolus

A

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

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46
Q

What are the common types of embolus

A

Usually caused by a thrombus from a blood vessel
Air
Tumour
Amniotic fluid (rare in pregnant women)
Fat (severe trauma with fractures)

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47
Q

define Ischaemia

A

reduction of blood flow to a tissue, reducing perfusion but not causing cell death

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48
Q

define Infarction

A

a reduction of blood flow to a tissue that is so reduced that it cannot even support mere maintenance of the cells in that tissue so they die

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49
Q

define End artery supply

A

an organ that only receives blood supply from one artery.

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50
Q

Why is end arterial supply problematic

A

As when a blood clot forms,the whole blood supply to that organ is cut off leading to infarction.

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51
Q

Atheroma

A

degeneration of the walls of the arteries caused by accumulated fatty deposits and scar tissue, and leading to restriction of the circulation and a risk of thrombosis.

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52
Q

Define Apoptosis

A

programmed cell death

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53
Q

Apoptosis in cancer

A

lack of apoptosis – mutated p53 gene producing faulty p53 protein, p53 gene important in apoptosis

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54
Q

Apoptosis in HIV

A

too much apoptosis – kills the antibodies in the blood so the body can’t defend itself.

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55
Q

What is apoptosis triggered by

A

DNA damage such as:
Single-strand break
Base alteration
Cross-linkage

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56
Q

define Necrosis

A

death of most or all of the cells in an organ or tissue due to disease, injury, or failure of the blood supply

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57
Q

Name 5 clinical examples of necrosis

A

Toxic spider venom
Frostbite
Cerebral infarction
Avascular necrosis of bone – femur has single arterial supply through the neck of the femoral head
Pancreatitis

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58
Q

define Hypertrophy

A

increase in size of a tissue cause by an increase in size of the constituent cells
(the size of the cell/tissue/organ increases without an increase in the number of cells)

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59
Q

define Hyperplasia

A

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

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60
Q

define Atrophy

A

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

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61
Q

define Metaplasia

A

change in differentiation of a cell from one fully-differentiated type to a different fully-differentiated type

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62
Q

define Dysplasia

A

imprecise term for the morphological changes seen in cells in the progression to becoming cancer

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63
Q

What change caused by cell division causes ageing

A

telomeres get shorter after each cell division – limiting the amount of division that can occur (hence ageing occurs)

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64
Q

What is Dermal elastosis

A

Accumulation of abnormal elastic in the dermis of the skin
Result of prolonged/ excessive sun exposure – photoaging
UV light causes protein cross-linking

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65
Q

What is Cataracts

A

Result of the formation of opaque proteins within the lens which usually also results in a loss of lens elasticity
UV-B light causes protein cross-linking

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66
Q

Define Carcinogenesis

A

the transformation of normal cells to neoplastic cells through permanent genetic alterations or mutations

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67
Q

What is the difference between oncogenesis and carcinogenesis

A

Oncogenesis applies to benign and malignant tumors, carcinogenesis applies only to malignant

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68
Q

what are carcinogens?

A

Agents known or suspected to cause cancer, they act on DNA so are Mutagenic

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69
Q

Define Oncogens

A

Agents known or suspected to cause tumours

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70
Q

Give 2 examples of occupational risks for cancer

A

Scrotal cancer – increased incidence in chimney sweeps
Bladder cancer – increased incidence in aniline dye and rubber industries

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71
Q

what are the 5 classes of Carcinogens

A

Chemical
Viral
Ionising and non-ionising radiation
Hormones, parasites and mycotoxins
Miscellaneous

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72
Q

What are pro-carcinogens and ultimate carcinogens

A

Chemical carcinogens pre and post metabolic conversion
most chemical carcinogens require metabolic conversions

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73
Q

What are three examples of groups affected by radiation carcinogens

A

Skin cancer in radiographers
Lung cancer in uranium miners
Thyroid cancer in Ukrainian children

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74
Q

What are the 5 classes of Host factors for cancer

A

Race
Diet
Constitutional factors
Premalignant conditions
Transplacental exposure

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75
Q

What % of cancer risks are inherited

A

15%

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76
Q

give 2 examples of how race affect cancer risk

A

Decreased skin cancer in black people (melanin)
Increased oral cancer in India, SE Asia (reverse smoking)

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77
Q

How do constitutional factors affect cancer risk

A

Age – incidence increases with age
Gender – breast cancer F:M = 200 (more common in women)

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78
Q

Define tumour

A

any abnormal swelling e.g. neoplasm, inflammation, hypertrophy, hyperplasia

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79
Q

Define Neoplasm

A

a lesion resulting from the autonomous or relatively autonomous abnormal growth of cells which persists after the initiating stimulus has been removed – a new growth.
(all neoplasms are tumours but not all neoplasms are tumours)

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80
Q

What are the 3 classifications of Neoplasms

A

Benign
Borderline
Malignant

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81
Q

How can Neoplasms cause morbidity and mortality

A

Pressure on adjacent structures
Obstruct flow
Production of hormones
Transformation to malignant neoplasm
Anxiety

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82
Q

How can malignant neoplasms cause morbidity and mortality

A

Destruction of adjacent tissue
Metastases
Blood loss from ulcers
Obstruction of flow
Hormone production
Paraneoplastic effects
Anxiety and pain

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83
Q

define Papilloma

A

benign tumour of non-glandular, non-secretory epithelium

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84
Q

Define Adenoma

A

benign tumour of glandular or secretory epithelium

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85
Q

Define Carcinoma

A

malignant tumour of epithelial cells

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86
Q

4 examples of how benign connective tissue neoplasms named

A

Lipoma – adipocytes
Chondroma – cartilage
Osteoma – bone
Angioma – vascular

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87
Q

What are solid neoplasms composed of

A

Solid Neoplasms are composed of neoplastic cells and stroma (supporting network of cells)

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88
Q

Give 2 examples of Benign neoplasms

A

Fibroid
Tubulovillous adenoma

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89
Q

give 2 examples of Malignant neoplasms

A

Prostate cancer
Squamous cell carcinoma

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90
Q

define Carcinoma in situ

A

a malignant epithelial neoplasm that has not yet invaded through the original basement membrane

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91
Q

define Invasive carcinoma

A

a carcinoma that has breached the basement membrane – it can now spread elsewhere

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92
Q

define Micro-invasive carcinoma

A

has breached the basement membrane but hasn’t invaded very far away from the original carcinoma

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93
Q

what is the process of invasion

A

neoplastic cells spread directly through tissue and gain access to blood vessels and lymphatic channels

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94
Q

What is invasion dependent on

A

decreased cellular adhesion,
abnormal cellular motility
the production of enzymes with a lytic effect on the surrounding tissues

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95
Q

What is metastasis

A

Process by which a malignant tumour spreads from its primary site to produce secondary tumours at distant sites

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96
Q

what routes can metastasis occur through

A

via blood vessels, lymphatics, across body cavities, along nerves or as a result of direct implantation of neoplastic cells during a surgical procedure

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97
Q

What are the 7 steps of the metastatic cascade

A

Detachment
Invasion
Intravasation
Evasion of host defences
Arrest
Extravasation
Vascularisation

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98
Q

What is the maximum diameter a tumour can grow before it requires vascularisation

A

1mm

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99
Q

Name two angiogenesis promoters

A

Vascular endothelial growth factors
Basic fibroblast growth factor

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100
Q

Name 3 types of angiogenesis inhibitors

A

Angiostatin, endostatin, vasculostatin

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101
Q

What is Haematogenous metastsis

A

The route of metastasis by the blood stream – forms secondary tumours in organs perfused by blood that has drained from a tumour

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102
Q

What is lymphatic metastasis

A

the route of metastasis by lymph channels – form secondary tumours in the regional lymph nodes

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103
Q

What is Trans-coelomic metastasis

A

rputeof tumour metastasis across cavities such as pericardial and peritoneal cavities

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104
Q

Which tumours commonly metastasise to the lung

A

sarcomas and any common cancers

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105
Q

Which tumours commonly metastasise to the liver

A

colon, stomach, pancreas, and carcinoid tumours of intestine

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106
Q

which tumours commonly metastasise to bone

A

prostate, breast, thyroid, lung and kidney

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107
Q

Name two treatment options for breast cancer

A

Anti-oestrogen drugs
Herceptin

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108
Q

Why and when to use anti-oestrogen drugs for breast cancer

A

Giving drugs that block the oestrogen receptors on the cancer cells which inhibits their growth. The tumours are stained in the lab for oestrogen receptors so that oncologists can decide whether a breast cancer is likely to respond to anti-oestrogen therapy.

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109
Q

why use herceptin for breast cancer

A

Herceptin is a drug that binds to the Her2 protein on the outside of the cell membrane.
Tumours overexpress a growth factor receptor on their cell surface called Her2 protein. This is coded for by the HER2 gene.
This drug binding to the protein on the surface of the cancer cells reduces their rate of growth

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110
Q

What is the main requirement of the immune system

A

to discriminate self from non-self

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111
Q

What are the 2 categories of immunity

A

Innate immunity
Adaptive immunity

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112
Q

What is innate immunity

A

non-specific, instinctive, does not depend on lymphocytes

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113
Q

What is adaptive immunity

A

specific ‘acquired’ immunity, requires lymphocytes, antibodies
Is made up of cells and soluble proteins (humoral)

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114
Q

What is the stem cell that every blood cell in the body originates from

A

Haematopoietic pluripotent stem cell (haemocytoblast)

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115
Q

What are Polymorphonuclear leukocytes

A

Cells with multi-lobed nuclei-
neutrophils, eosinophils and basophils

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116
Q

What are Mononuclear leukocytes

A

Cells with single-lobed nuclei-
monocytes (kidney shaped nuclei), T-cells and B-cells (lymphocytes)

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117
Q

What is the role of Neutrophils in immunity

A

Plays an important role in innate immunity (phagocytosis)
2 main intracellular granules
Primary lysosomes – can kill microbes by secreting toxic substances
Secondary granules- may have regulatory functions outside the cell

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118
Q

Role of Monocytes in immunity

A

Plays an important role in innate AND adaptive immunity (phagocytosis and Ag presentation)
Differentiate into macrophages in the tissues
Main role – remove anything foreign (microbes) or dead

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119
Q

Role of Macrophages in immunity

A

Play important role in innate and adaptive immunity (phagocytosis and Ag presentation)
Reside in tissues, lifespan – months/years e.g. Kupffer cells – liver, microglia – brain
Most often first line of non-self recognition
Main role – remove foreign (microbes) and self (dead/tumour cells)
Present Ag to T-cells

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120
Q

Role of Eosinophil in immunity

A

Mainly associated with parasitic infections and allergic reactions
Lifespan 8-12 days
Granules stain for acidic dyes (eosin)
Activates neutrophils, induces histamine release from mast cells and provokes bronchospasm

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121
Q

Role of basophil in immunity

A

Mainly involved in immunity to parasitic infections and allergic reactions
Lifespan 2 days
Granules stain for basic dyes
Very similar to mast cells
Binding of IgE to receptor causes de-granulation releasing histamine – main cause of allergic reactions

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122
Q

role of mast cells in immunity

A

Only in tissues (precursor in blood)
Very similar to basophils
Binding to IgE to receptor causes de-granulation releasing histamine – main cause of allergic reactions

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123
Q

role of T-lymphocytes in immunity

A

Play major role in adaptive immunity
Lifespan hours-years
Mature in thymus
Found in blood, lymph nodes and spleen
Recognise peptide Ag displayed presenting cells (APC)

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124
Q

What are the 4 types of T-cell and their roles

A

T helper 1 (CD4 – help immune response intracellular pathogens)
T helper 2 (CD4 – help produce antibodies extracellular pathogens)
Cytotoxic T cell (CD8 – can kill cells directly)
T regulator – regulate immune responses

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125
Q

Role of B lymphocytes in immunity

A

Play major role in adaptive immunity
Lifespan hours – years
Mature in bone marrow
Recognise Ag displayed by antigen presenting cells (APC)
Differentiate into plasma cells that make antibodies
Found in blood, lymph nodes and spleen

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126
Q

Role of Natural killer cells

A

Part of innate immune response
Account for 15% of lymphocytes
Found in spleen, tissues
They recognise and kill by apoptosis;
Virus infected cells
Tumours cells

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127
Q

What are the 4 soluble factors involved in immunity

A

Complement, antibodies, cytokines and chemokines

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128
Q

What are complement factors and how do they work

A

Classical – Ab bound to microbe
Alternative – C binds to microbe
Mode of action
Direct lysis
Attract more leukocytes to site of infection (chemotaxis)
Coat invading organisms (opsonisation)

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129
Q

What is an antibody

A

protein produced in response to an antigen. It can only bind with the antigen that induced its formation – i.e. specificity.

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130
Q

What are immunoglobulins (antibodies) and what are the 5 classes

A

Ig’s are soluble glycoproteins, with distinct classes : G, A, M, D, E

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131
Q

What is IgG

A

Predominant in human serum, 70-75% of total Ig in serum
Crosses placenta

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132
Q

What is IgA

A

Accounts for 15% of Ig in serum
Predominant Ig in mucous secretions such as saliva, milk and bronchiolar secretions.

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133
Q

What is IgM

A

Accounts for 10% of Ig in serum
Mainly found in blood (they’re big so they can’t cross the endothelium)
Mainly primary response, initial contact with Ag

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134
Q

What is IgD

A

Accounts for 1% of Ig in serum
A transmembrane monomeric form is present on mature B cells

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135
Q

What is IgE

A

Accounts for ~0.05% of Ig in serum
Basophils and mast cells express an IgE-specific receptor that has high affinity for IgE – binding triggers release of histamine
Associated with allergic response and defence against parasitic infections

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136
Q

Define Antigen

A

a molecule that reacts with preformed antibody and specific receptors on T and B cells.

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137
Q

Define Epitope

A

the part of the antigen that binds to the antibody/ receptor binding site

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138
Q

Define Affinity

A

measure of binding strength between an epitope and an antibody binding site. The higher the affinity the better.

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139
Q

define cytokines

A

proteins secreted by immune and non-immune cells. Substances produced by one cell that influence the behaviour of another, thus effecting intercellular communication.

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140
Q

What are the 4 types of Cytokines

A

Interferons (IFN)
Interleukins (IL)
Colony stimulating factors (CSF)
Tumour necrosis factors

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141
Q

What is the role of interferons

A

induce a state of antiviral resistance in uninfected cells and limit the spread of viral infection

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142
Q

What is the role of interleukins

A

produced by many cells, over 30 types.
Can cause cells to divide, to differentiate and to secrete factors

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143
Q

What is the role of colony stimulating factors

A

Involved in directing the division and differentiation on bone marrow stem cells – precursors of leukocytes

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144
Q

What is the role of tumour necrosis factors

A

Mediate inflammation and cytotoxic reactions

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145
Q

What are Chemokines

A

Group of approx. 40 proteins that direct movement of leukocytes from the blood stream into the tissues or lymph organs by binding to specific receptors on cells.
They attract leukocytes to sites of infection/inflammation – like magnets

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146
Q

What is the role of the Skin in innate immunity

A

is an anatomical barrier
Sebum (skin secretions)
Intact skin – prevents penetration, prevents growth

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147
Q

What is the role of mucous membranes in innate immunity

A

physical barrier
Saliva
Tears – lysozyme in tears and other secretions
Low pH and commensals of vagina
Mucous secretions
Mucous – entrapment
Cilia – beating removes microbes
Commensal colonies – attachment, nutrients

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148
Q

Define commensals

A

those type of microbes that reside on either surface of the body or at mucosa without harming human health.

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149
Q

Physiological barrier

A

High body temperature
Fever response inhibits micro-organism growth
pH changes
Gastric acidity

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150
Q

Define Extravasation

A

a discharge or escape, as of blood, from a vessel into the tissues. Usually lymph from blood into tissues

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151
Q

Define opsonisation

A

the coating of pathogens with antibodies in order to increase their susceptibility to ingestion by phagocytes.

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152
Q

What is C3b

A

Part of Complement component 3, is an important molecule in opsonisation

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153
Q

What is the major histocompatibility (MHC)

A

a group of genes that encode proteins on the cell surface that have an important role in immune response. they display self or non-self proteins.

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154
Q

What are the three MHC classes

A

MHC I- glycoproteins on all nucleated cells
MHC II- glycoproteins only on APC
MHC III- code for secreted proteins- not fully understood

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155
Q

What is an APC

A

Antigen presenting cell works in conjugation with MHC II to present antigens to T cells

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156
Q

Role of MHC I

A

Intrinsic (intracellular) – present intracellular proteins on surface to alert immune system, interacts with cytotoxic T (CD8) cells

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157
Q

Role of MHC II

A

Presents extracellular proteins to T helper (CD4) cells, initiates antigen specific immune response

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158
Q

What is T cell selections

A

T cells that recognise self are killed in the foetal thymus as they mature

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159
Q

Summarise B cell activation

A

B cells become activated upon binding with an antigen. These then go to the lymph nodes where clonal expansion takes place with the cells differentiating into plasma cells. These secrete Ab (usually IgM) which later turn into IgG. B cells divide – clonal expansion and differentiate into plasma cells and memory B cells. Re-stimulation of memory B cells lead to secondary response.

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160
Q

What do T helper (CD4) cells do

A

help coordinate the immune response by stimulating other immune cells, such as macrophages, B lymphocytes (B cells), and CD8 T lymphocytes (CD8 cells), to fight infection.

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161
Q

What do cytotoxic T (CD8) cells do

A

kill virus-infected cells and produce antiviral cytokines such as interferon gamma.

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162
Q

What are Pattern Recognition Receptors (PRRs)

A

proteins capable of recognizing molecules frequently found in pathogens. these are :
Pathogen-Associated Molecular Patterns-PAMPs
or Damage-Associated Molecular Patterns-DAMPs which are molecules released by damaged cells

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163
Q

What are the 2 types of PRRs

A

Secreted and circulating PRRs
Cell-associated PRRs (more traditional receptors)

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164
Q

What are Secreted and circulating PRRs

A

Antimicrobial peptides secreted in lining fluids from epithelia
Lectins and collectins (carbohydrate-containing proteins that bind carbohydrates or lipids in microbe walls. Activate complement, improve phagocytosis.

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165
Q

What are Cell-associated PRRs

A

Receptors that are present on the cell membrane or in the cytosol of the cells
Recognise a broad range of molecular patterns
TLRs are the main family (toll-like receptors)

166
Q

Role of TLRs

A

a class of pattern recognition receptors (PRRs) that initiate the innate immune response by sensing conserved molecular patterns for early immune recognition of a pathogen

167
Q

What are the 3 types of vaccines

A

whole killed, toxoids, live attenuated

168
Q

Define passive immunisation

A

Passive immunity is a short-term immunity which results from the introduction of antibodies from another person or animal.

169
Q

What are the pros and cons of Passive immunisation

A

Advantages:
Gives immediate protection
Effective in immunocompromised patients

Disadvantages:
Short-lived
Possible transfer of pathogens

170
Q

Define Vaccines

A

antigenic substance prepared from the causative agent of a disease

171
Q

What are whole killed vaccines and their limitations

A

These vaccines do not cause infection but the antigens contained in it induce an immune response which protects against infection.
The organisms must be grown to high titre in vitro
Whole pathogens often cause excessive reactogenicity
Usually need at least 2 vaccinations

172
Q

What are live attenuated vaccines

A

The organisms replicate within the host, and induce an immune response which is protective against the wild-type organism

173
Q

What are toxoids

A

Non-living vaccines can also be cell-free toxoids (inactivated toxins

174
Q

What are the pros and cons of Live attenuated vaccines

A

Advantages:
Lower doses are required, so the scale of in vitro growth needed is lower
Immune response more closely mimics that following real infection
Route of administration may be more favourable
Fewer doses may be required

Limitations:
Often impossible to balance attenuation and immunogenicity
Reversion to virulence
Transmissibility
Live vaccines may not be so attenuated in immunocompromised

175
Q

What are the stages of vaccination

A

Engage the innate immune system
Danger signals that activate the immune system, triggers such as molecular fingerprints of infection – PAMPs (pathogen associated molecular patterns)
Engage TLR receptors
Activate specialist APC

Engage the adaptive immune system
Generate memory T and B cells
Activate T cell help

176
Q

General features for Tumours in immunity

A

Tumours express antigens that are recognised as foreign by the immune system of the tumour-bearing host
Immune responses frequently fail to prevent growth of tumours
The immune system can be activated by external stimuli to effectively kill tumour cells and eradicate tumours

177
Q

Define immuno-surveillance

A

immune system can recognise and destroy nascent transformed cells, normal control

178
Q

Define Cancer immunoediting

A

Immune system can kill and also induce changes in the tumour resulting in tumour escape and recurrence.

179
Q

What are the 2 types of tumour antigens

A

Tumour specific antigens (TSA)
Tumour associated antigens (TAA)

180
Q

What are the features of Tumour specific antigens (TSA)

A

Are only found on tumours
As a result of point mutations or gene rearrangement
Derive from viral antigens

181
Q

What are the features of Tumour associated antigens (TAA)

A

Found on both normal and tumour cells, but are overexpressed on cancer cells
Developmental antigens which become de-repressed
Differentiation antigens are tissue specific
Altered modification of a protein could be an antigen

182
Q

Define Tumour escape

A

immune responses change tumours such that tumours will no longer be seen by the immune system.

183
Q

Define immune evasion

A

tumours change the immune responses by promoting immune suppressor cells.

184
Q

Define Cancer immunotherapy

A

induce an immune response against the tumour that would discriminate between the tumour and normal cells

185
Q

What are the types of Immunotherapy vaccines

A

Killed tumour vaccine
Purified tumour antigens
Professional APC-based vaccines
Cytokine – enhanced vaccines
DNA vaccines
Viral vectors (augmentation of host immunity to tumours with cytokines and costimulators)

186
Q

What is tumour hypoxia

A

Hypoxia is a prominent feature of malignant tumours
Inability of the blood supply to keep up with growing tumour cells
Hypoxic tumour cells adapt to low oxygen

187
Q

Why does tumour hypoxia = poor patient prognosis

A

Stimulates new vessel growth
Suppressed immune system
Resistant to radio and chemotherapy
Increased tumour hypoxia after therapy

188
Q

What is a synergic drug interaction

A

interaction of drugs such that the total effect is greater than the sum of the individual effects (1+1>2)

189
Q

What is an antagonistic drug interaction

A

an antagonist is a substance that acts against and blocks an action (2 drugs opposed to each other) (1+1=0)

190
Q

What is a summation drug interaction

A

different drugs used together to have the same effect as a single drug would (1+1=1)

191
Q

What is a potentiation drug interaction

A

enhancement of one drug by another so that the combined effect is greater than the sum of each one alone (1+1=1+1.5)

192
Q

Define Pharmacodynamics

A

the effect the drug has on the human body

193
Q

Define pharmacokinetics

A

what the body does with the drug (the disposition of a compound within an organism)

194
Q

What are risk factors of a drug need to be considered for administration

A

Narrow therapeutic index
Steep dose/response curve
Saturable metabolism

195
Q

What is ADME

A

the mechanisms of pharmokinesis:
Absorption, Distribution, Metabolism, Excretion

196
Q

What factors affect absorption (pharmacology)

A

Motility – if the gut has slowed digestion, the drugs won’t work as well (oral contraceptive pill and antibiotics is the most common interaction)
Acidity – pH and pKa interactions.
Solubility
Complex formation

197
Q

What are the factors affecting distribution (pharmacology)

A

Drugs can go into the proteins, other tissues or the effect site
Protein binding
If you give 2 highly protein bound drugs, they will make each other strong and increase their effect so you always make sure you know what drugs the patient has taken before giving them new drugs

198
Q

What are the factors affecting metabolism (pharmacology)

A

CYP450 proteins- these metabolise many substrates
inhibition- Drug A blocks metabolism of drug B, leaving more free drug B in the plasma so it has an increased effect
induction- Drug C induced CYP450 isoenzyme leading to increased metabolism of drug D so it has a decreased effect

199
Q

What affects excretion (pharmacology)

A

Renal:
-pH dependant
-Weak bases – cleared faster if urine acidic
-Weak acids – cleared faster if urine alkali

Billary (minor)

199
Q

What are the receptor based pharmacodynamic mechanism types

A

Agonists
Partial agonists
Antagonists:
-Competitive
-Non-competitive

200
Q

What is signal transduction

A

the process by which a chemical or physical signal is transmitted through a cell as a series of molecular events

201
Q

What are 2 examples of drug interactions to be aware of

A

Warfarin – lots of interactions – enzyme induction
Acute kidney injury – NSAIDs, ACEi

202
Q

Define Drug

A

a medicine or other substance which has a physiological effect when ingested or otherwise introduced into the body

203
Q

Define pharmacology

A

the branch of medicine concerned with the uses, effects and modes of action of drugs

204
Q

What are the 4 major drug target proteins

A

Receptors
Enzymes
Transporters
Ion channels

205
Q

define receptor

A

a component of a cell that interacts with a specific ligand and initiates a change of biochemical events leading to the ligands observed effects.

206
Q

What conditions involve an imbalance of chemicals/receptors

A

Chemicals
Allergy; increased histamine
Parkinson’s; reduced dopamine

Receptors
Myasthenia gravis; loss of ACh receptors
Mastocytosis; increased c-kit receptor

207
Q

What are the 4 classes of receptor

A

ligand-gated ion channels
G-protein coupled receptors
kinase-linked receptors
cytosolic/ nuclear receptors

208
Q

define ligand

A

a molecule that binds to another (usually larger) molecule

209
Q

Define Agonist

A

a compound that binds to a receptor and activates it

210
Q

define antagonist

A

a compound that reduces the effect of an agonist

211
Q

What are the two categories of cholinergic receptors

A

nicotinic and muscarinic

212
Q

What are the antagonist and receptor for muscarine

A

Atropine and mAChR

213
Q

What are the antagonist and receptor for nicotine

A

Curare
nAChR

214
Q

define affinity

A

describes how well a ligand binds to the receptor

215
Q

define Efficacy

A

describes how well a ligand activates the receptor

216
Q

Signal transduction

A

a basic process involving the conversion of a signal from outside the cell to a functional change within the cell

217
Q

what is allosteric modulation

A

When an allosteric ligand binds to a different site on the molecule and prevents the signal from being transmitted.

218
Q

How do ACE inhibitors work

A

RAAS increases blood pressure by increasing the amount of salt and water the body retains.
Inhibiting ACE reduces angiotensin II production, which causes a reduction in blood pressure.

219
Q

What are the 3 main types of protein ports

A

Uniporters – use energy from ATP to pull molecules in
Symporters – use the movement in of one molecule to pull in another molecule against a concentration gradient
Antiporters – one substance moves against its gradient, using energy from the second substance (mostly Na+, K+ or H+) moving down its gradient

220
Q
A
221
Q

What are CYPs

A

(e.g. cyP450) are the major enzymes involved in drug metabolism (75%)
Most drugs undergo deactivation by CYPs, either directly or by facilitated excretion from the body.

222
Q

define druggability

A

the ability of a protein target to bind small molecules with high affinity (sometimes called ligandability).

223
Q

What are 8 sources for drug development

A

Medicines from plants
Inorganic elements
Organic molecules
Bacteria/fungi/moulds
Stereoisomers
Immunotherapy antibodies
Medicines from animals
Gene therapy

224
Q

What are 6 examples of recombinant proteins in clinical use

A

Insulin
Erythropoietin
Growth hormone
Interleukin 2
Gamma interferom
Interleukin 1 receptor

225
Q

Describe gene therapy

A

Gene therapy consists of a recombinant nucleic acid used in or administered to a human being with a view to regulating, replacing, adding or deleting a genetic sequence
Its effect relates directly to the recombinant nucleic acid sequence it contains or to the product of genetic expression of this sequence

226
Q

What is rational drug design

A

The process of finding new medications based on the knowledge of a biological target

227
Q

define adherence

A

the extent to which the patient’s actions match agreed recommendations

228
Q

Necessity beliefs

A

perceptions of personal need for treatment
-concerns about a range of potential adverse consequences

229
Q

define Pharmacokinetics

A

the action of the body on the drug (ADME)

230
Q

What is drug ionization

A

property of weak acid or base drugs- pH of environment changes absorption through drugs changing between ionized and unionized form

231
Q

How does drug structure affect absorption

A

Drugs need to be lipid soluble to be absorbed from gut
Some drugs unstable at low pH or in presence of digestive enzymes so have to be given by alternative route

232
Q

How does drug formulation affect absorption

A

The capsule/ tablet must disintegrate and dissolve to be absorbed
Some formulated to dissolve slowly or have a coating that is resistant to the acidity of the stomach

233
Q

How does gastric emptying affect drug absorption

A

Rate of gastric emptying determines how soon a drug taken orally is delivered to small intestine
Can be slowed (food/drugs) or sped up (gastric surgery)

234
Q

What is first pass metabolism for oral administration and the 4 barriers

A

any loss of the administered material by transmucosal or hepatic means after absorption and before reaching the systemic circulation,
Intestinal lumen
Intestinal wall
Liver
Lungs

235
Q

What are 4 reasons to use intradermal or subcutaneous methods

A

Avoids barrier of stratum corneum
Mainly limited by blood flow
Small volume can be given
Use for local effect or to deliberately limit rate of absorption

236
Q

What affects IM absorption and why use it

A

Depends on blood flow and water solubility
Increase in either enhances removal of drug from injection site
Can make a depot injection by incorporating drug into lipophilic formulation which releases drug over days or weeks

237
Q

What affects inhalational absorption and why use it

A

Large SA and blood flow but limited by risks of toxicity to alveoli and delivery of non-volatile drugs
Largely restricted to volatiles such as general anesthetics and locally acting drugs such as bronchodilators in asthma
Asthma drugs non-volatile so given as aerosol or dry powder

238
Q

What is protein binding and what affects it

A

Many drugs can bind to plasma or tissue proteins
This may be reversible or irreversible
The most common reversible binding occurs with the plasma protein albumin
Binding lowers the free concentration of drug and can act as a depot releasing the bound drug when the plasma concentration drops through redistribution or elimination
Some drugs bind irreversibly and cannot re-enter the circulation and is equivalent to elimination

239
Q

the relationship between drug structure, the brain and placenta

A

Lipid soluble drugs easily pass from blood to brain
The brain does little metabolizing and drugs are removed by diffusion into plasma, active transport in the choroid plexus or elimination in the CSF
Lipid soluble drugs readily cross placenta
Large molecules do not cross placenta
Foetal liver has low levels of drug metabolizing enzymes, so relies on maternal elimination

240
Q

Define elimination

A

The removal of a drugs activity from the body, either by metabolism to an inactive form or by excretion

241
Q

What is drug metabolism needed for

A

Necessary for the elimination of lipid soluble drugs
They are converted to water soluble products that are readily removed in the urine

242
Q

What is Phase 1 metabolism

A

these reactions involve the transformation of the drug to a more polar metabolite
done by unmasking or adding a functional group
oxidations are the commonest reactions catalyzed by CP450

243
Q

What is phase 2 metabolism

A

involves the formation of a covalent bond between the drug or its phase 1 metabolite and an endogenous substrate
Resulting products are usually less active and readily excreted by the kidneys

244
Q

What methods of drug excretion are there

A

Fluids – important for low molecular weight polar compounds (urine, bile, sweat, tears, breast milk)
Urine excretion: Total excretion = glomerular filtration + tubular secretion – reabsorption
Solids – faecal elimination
Gases – expired air important for volatiles

245
Q

What is first order drug kinetics

A

Concentration declines exponentially

246
Q

What is zero order drug elimination

A

occurs when the metabolising enzyme is saturated, the rate of drug elimination is constant

247
Q

What is Bioavailability

A

Fraction of the administered drug that reaches the systemic circulation unaltered (F)
F=1 for IV
for any drugs with first pass metabolism F<1

248
Q

Define distribution

A

Rate and extent of movement of a drug into tissues from blood

249
Q

What factor affects rate of distribution for water soluble drugs

A

rate of passage across membranes

250
Q

What factor affects rate of distribution of lipid soluble drugs

A

blood flow to tissues that accumulate the drug

251
Q

What is volume of distribution

A

the total amount of drug in body (dose)/ plasma concentration

252
Q

Define clearance

A

the volume of blood or plasma cleared of drug per unit time

253
Q

What is the relationship between elimination and volume of distribution

A

inversely proportional
k= Clearance/ Vd

254
Q

What is steady state

A

the balance between drug input and elimination (Css)

255
Q

Give an example of the difference in doseage dictated by route of administration

A

50% of oral morphine is metabolized by the first pass metabolism. Halve the dose if given IM/ IV

256
Q

Mechanism of opioids

A

use the existing pain modulation system
The opioid receptors are coupled to G1 proteins and the actions of the opioids are mainly inhibitory. decrease neuronal excitability.

257
Q

Define drug potency

A

whether a drug is ‘strong’ or ‘weak’ relates to how well the drug binds to the receptor, the binding affinity.

258
Q

define efficacy

A

the concept of full or partial agonists

259
Q

define tolerance

A

down regulation of the receptors with prolonged use. Need higher doses to achieve the same effect

260
Q

What is the timeframe of opioid withdrawal

A

starts within 24 hours, lasts about 72 hours

261
Q

What are some side effects of opioids

A

Respiratory depression
Sedation
Nausea and vomiting
Constipation
Itching
Immune suppression
Endocrine effects

262
Q

Why do opioids have side effects

A

Opioid receptors exist outside the pain system e.g. digestive tract, respiratory control centre
normally delivered systemically so activate these

263
Q

How is morphine removed from the body

A

Morphine is metabolized to morphine 6 glucuronide which is more potent than morphine and is renally excreted.

264
Q

Why does renal function affect morphine doseage

A

metabolised and cleared by the kidney
With normal renal function this is cleared quickly
In renal failure it will build up and may cause respiratory depression
Be careful in patients with <30% renal function (creatinine clearance <30). Reduce dose and timing interval

265
Q

What is cholinergic and adrenergic pharmacology responsible for

A

Control of blood pressure
Control of heart rate
Anaesthetic agents
Regulation of airway tone
Pressures in the eye
Control of GI function

266
Q

What is the structure of the parasympathetic nervous system

A

Cranial nerves like the oculomotor nerve, facial nerve and vagus nerve carry signals to the body
A further sacral outflow innervates the pelvis
Short post-synaptic nerve fibres reach the targets and release acetylcholine (ACh), which acts on muscarinic receptors of various subtypes

267
Q

What is the structure of the sympathetic nervous system

A

Regulates the fight-and-flight response
Nerve fibres originating in the spinal cord terminate in ganglia near the cord, then send out long nerve fibres to blood vessels, muscles etc.
They release noradrenaline which activates adrenergic receptors, of which there are two main types (alpha/ beta) with subtypes

268
Q

what is involved with the parasympathetic and sympathetic fibres immediately out of the CNS

A

Parasympathetic and sympathetic fibres coming out of the CNS both release ACh, which acts on nicotinic receptors

269
Q

What mediators and receptors are involved in post-ganglionic parasympathetic interactions

A

The post-ganglionic parasympathetic fibres release more acetylcholine, acting on muscarinic receptors

270
Q

What mediators and receptors are involved in post-ganglionic sympathetic interactions

A

The post-ganglionic sympathetic fibres release noradrenaline, acting on alpha and beta adrenoceptors

270
Q

What type of receptors are muscarinic receptors

A

G-Protein-Coupled Receptors
G proteins can activate various types of second messenger signals

271
Q

Where are muscarinic receptors M1-5 located

A

M1: mainly in the brain
M2: mainly in the heart. (their activation slows the heart, so we can block these)
M3: glandular and smooth muscle. (cause bronchoconstriction, sweating, salivary gland secretion
M4/5: mainly in the CNS

272
Q

What are some side effects of anticholinergic drugs

A

In the brain, anticholinergics worsen memory and may cause confusion
Peripherally, may get constipation, drying of the mouth, blurring of the vision, worsening of glaucoma

273
Q

How do alpha 1 agonists act

A

Alpha 1 activation causes vasoconstriction, particularly in the skin and splanchnic beds: less so in brain, lung, heart

274
Q

What receptor does adrenaline act on

A

Alpha 1, causes vasoconstriction

275
Q

What are the reponses of blood pressure to alpha1/2 agonists

A

Alpha 1 activators raise blood pressure
Alpha 2 activators lower blood pressure

276
Q

What do agonists of Beta 1 receptors do

A

Beta 1 activation will increase heart rate and chronotropic effects, and may increase risk of arrhythmias

277
Q

What do agonists of Beta 2 receptors do

A

Beta 2 activation is life saving in asthma, causes bronchodilation, relaxing of smooth muscle

278
Q

What do beta blockers do

A

Lower blood pressure (reduction in cardiac output reduction in central sympathetic outflow activity)

279
Q

What are 5 clinical indications for allergy

A

Epithelial – eczema, itching, reddening
Excessive mucus production
Airway constriction
Abdominal bloating, vomiting, diarrhoea
Anaphylaxis

280
Q

Define allergy

A

an abnormal response to harmless foreign material

281
Q

What 4 immune cells are involved in allergy

A

Mast, eosinophil, lymphocytes, dendritic

282
Q

what 3 non-immune cells are involved in allergy

A

Smooth muscle, fibroblasts, epithelia

283
Q

What are 4 mediators in allergy

A

Cytokines, chemokines, lipids, small molecules

284
Q

What process is required for IgE receptors to cause signalling

A

clustering

285
Q

Which cells express low affinity IgE recpetors

A

B cells, T cells, monocytes, eosinophils, platelets, neutrophils

286
Q

What is the function of IgE receptors

A

Regulation of IgE synthesis
Triggering of cytokine release by monocytes
trigger Antigen presentation by cells

287
Q

Which cells express high affinity IgE receptors

A

Eosinophils, mast cells and basophils

288
Q

What are 3 indirect activators of mast cells and what mediates this

A

Allergens e.g. wasp venom, pollen
Bacterial/viral antigens
Phagocytosis of enterobacteria
mediated by IgE

289
Q

What are direct activators of mast cells

A

Cold/mechanical deformation
Aspirin, preservatives, latex

290
Q

What are adverse drug reactions

A

unwanted or harmful reactions following the administration of drugs or combination of drugs under normal conditions of use and is suspected to be related to the drug

291
Q

What are side effects

A

an unintended effect of a drug related to its pharmacological properties and can include unexpected benefits of treatment

292
Q

Give an example of an adverse drug reaction

A

Beta blockers
Bradycardia and heart block are primary adverse effects
Bronchospasm is a secondary pharmacological adverse effect

293
Q

What is the classification model for adverse drug reactions

A

Rawlins Thompson classification

294
Q

What is a type A ADR

A

Type A – (augmented pharmacological) – predictable, dose dependent, common

295
Q

What is a type B ADR

A

Type B – (bizarre or idiosyncratic) – not predictable and not dose dependent

296
Q

What is a type C ADR

A

Type C – (chronic) –steroids causing osteoporosis

297
Q

What is a Type D ADR

A

Type D – (delayed) – malignancies after immunosuppression

298
Q

What is a type E ADR

A

Type E – (end of treatment) – occur after abrupt drug withdrawal

299
Q

What is a type F ADR

A

Type F – (failure of therapy) – failure of oral contraceptive pill in presence of enzyme inducer

300
Q

What are 3 causes of ADRs

A

Pharmaceutical variation
Receptor abnormality
Drug-drug interactions

301
Q

What are 4 signs of an ADR

A

Symptoms soon after a new drug is started
Symptoms after a dosage increase
Symptoms disappear when the drug is stopped
Symptoms reappear when the drug is restarted

302
Q

Describe the yellow card system

A

The first ADR reporting scheme
Collects spontaneous reports
Acts as an ‘early warning system’ for identification of previously unrecognised reactions
Provides information, about factors which predispose patients ADRs
Continual safety monitoring of a product throughout its life span as a therapeutic agent

303
Q

What are the 4 critical pieces of information to include on a yellow card

A

Suspected drug
Suspect reaction
Patient details
Reporter details

304
Q

What is type 1 hypersensitivity

A

Type 1 – IgE mediated hypersensitivity

305
Q

What is the mechanism of type 1 hypersensitivity

A

Prior exposure to the antigen
IgE becomes attached to mast cells or leukocytes, expressed as cell surface receptors
Re-exposure causes mast cell degranulation and release of pharmacologically active substances

306
Q

What is type 2 hypersensitivity

A

Type 2 – IgG mediated cytotoxicity

307
Q

What is the mechanism of type 2 hypersensitivity

A

Antibody dependent cytotoxicity
Drug or metabolite combines with a protein
Body treats it as a foreign protein and forms antibodies
Antibodies combine with the antigen and complement activation damages the cells

308
Q

What is type 3 hypersensitivity

A

Type 3 – immune complex deposition

309
Q

What is the mechanism of type 3 hypersensitivity

A

Immune complex mediated
Small blood vessels are damaged or blocked
Leucocytes attracted to the site of reaction release pharmacologically active substances leading to an inflammatory process

310
Q

What is type 4 hypersensitivity

A

Type 4 – T cell mediated

311
Q

What is the mechanism of type 4 hypersensitivity

A

Lymphocyte mediated
Antigen specific receptors develop on T-lymphocytes
Subsequent administration leads to local or tissue allergic reactions

312
Q

Define anaphylaxis

A

an acute allergic reaction to an antigen to which the body has become hypersensitive

313
Q

What are the main features of anaphylaxis

A

Exposure to drug, immediate rapid onset rash
Swelling of lips, face, oedema, central cyanosis
Hypotension
Cardiac arrest

314
Q

What is the management of anaphylaxis

A

Commence basic life support
Adrenaline – IM 500µg
High flow oxygen

315
Q

How does adrenaline work

A

Vasoconstriction – increase in peripheral vascular resistance, increased BP and coronary perfusion
Stimulation of beta1-adrenoceptors positive ionotropic and chronotropic effects on the heart
Reduces oedema and bronchodilates via beta2-adrenoceptors

316
Q

Define pathogen

A

Organism that causes or is capable of causing disease

317
Q

define commensal

A

Organism which colonises the host but causes no disease in normal circumstances

318
Q

define opportunist pathogen

A

Microbe that only causes disease if host defenses are compromised

319
Q

Define virulence/pathogenicity

A

The degree to which a given organism is pathogenic

320
Q

Define asymptomatic carriage

A

When a pathogen is carried harmlessly at a tissue site where it causes no disease

321
Q

What are the outcomes of the gram stain

A

positive= purple
negative= pink

322
Q

What is a coccus

A

Ball shaped bacteria

323
Q

what is the apperance streptococcus bacteria

A

chain of cocci

324
Q

What is the appearance of staphylococcus bacteria

A

cluster of cocci

325
Q

What is the appearance of diplococcus bacteria

A

pairs of cocci

326
Q

What is a bacillus

A

rod shaped bacteria

327
Q

What is a vibrio

A

curved rod shaped bacteria

328
Q

What is a spirochaete

A

Spiral rod shaped bacteria

329
Q

What is the structure of gram negative bacteria

A

has 2 membranes – an inner and outer membrane, which are separated by lipoprotein, periplasmic space and peptidoglycan

330
Q

What is a bacterial endotoxin

A

component of the outer membrane of bacteria, e.g. lipopolysaccharide in gram negative bacteria

331
Q

What is a bacterial exotoxin

A

secreted proteins of gram positive and gram negative bacteria

332
Q

What is the structure of gram positive bacteria

A

only an inner membrane, surrounded by thick layer of peptidoglycan

333
Q

What are the two methods of genetic variation in bacteria

A

Mutation
Gene transfer

334
Q

What are the 3 mechanisms of gene mutation in bacteria

A

Base substitution
Deletion
Transfer

335
Q

What are the 3 mechanisms of gene transfer in bacteria

A

Transformation e.g. plasmid
Transduction e.g. via phage
Conjugation e.g. via sex pilus

336
Q

What is the process of gram staining

A

Apply a primary stain such as crystal violet (purple) to heat fixed bacteria
Add iodide which binds to crystal violet and helps fix it to the cell wall
Decolourise with ethanol or acetone
Counterstain with safranin (pink)

337
Q

What is the purpose of the coagulase test

A

Distinguishes S.aureus from other staphylococci – coagulase positive

338
Q

What are the three outcomes of the haemolytic bacteria classification

A

alpha, beta, gamma

339
Q

What is alpha haemolysis

A

haemolysis causing by production of hydrogen peroxide oxidising haemoglobin – the agar appears green

340
Q

What is Beta haemolysis

A

complete haemolysis results because of lysis of red blood cells by haemolysis such as Streptolysin O produced by S.pyogenes - so clear agar

341
Q

What is gamma haemolysis

A

implies no haemolysis

342
Q

What is the oxidase test

A

Tests if micro-organism contains a cytochrome oxidase – implies organism able to use oxygen as the terminal electron acceptor

343
Q

What are 6 important examples of gram positive bacteria

A

Staphylococcus Aureus, S.epidermis, S.pyogenes, S.pneumoniae, viridans streptococci, C.diphtheriae

344
Q

What is the classification process for streptococci

A

gram staining
Haemolysis
Lancefield typing
Biochemical properties

345
Q

What is lancefield grouping

A

a method of grouping catalyse negative, coagulase negative bacteria based on bacterial carbohydrate cell surface antigens

346
Q

What are the main determinants of virulence

A

Colonization factors: adhesins, invasins, nutrient acquisition, defense

Toxins (effectors): usually secreted proteins -> damage, subversion

347
Q

What are the 4 major groups (phyla) of gram-negative pathogens

A

Proteobacteria – all are rod-shaped
Bacteroids – rod-shaped
Chlamydia – round pleimorphic
Spirochaetes – spiral/ helical

348
Q

What are the 3 groups of worms

A

Nematodes (roundworms)
Trematodes (flatworms, flukes)
Cestodes (tapeworms)

349
Q

Where are the 3 types of nematodes

A

Intestinal – ascaris lumbricoides
Larva migrans- skin
Tissue (filaria)

350
Q

What are the 4 types of trematodes

A

Blood
Liver
Lung
intestinal

351
Q

what are the 2 types of cestodes

A

Non-invasive
Invasive

352
Q

What is the pre-patent period for worms

A

the interval between infection and the appearance of eggs in the stool

353
Q

What are 7 mycobacteria of clinical importance

A

M.tuberculosis – tuberculosis
M.leprae – leprosy
M.avium – disseminated infection in AIDS, infections in patients with chronic lung disease
M.kansasii – chronic lung infection
M.marinum – fish tank granuloma
M.ulcerans – buruli ulcer
Rapidly growing mycobacteria – skin and soft tissue infections

354
Q

What is the microbiology of mycobacteria

A

Aerobic, non-spore forming, non motile bacillus
Cell wall contains high molecular weight lipids
Weakly gram-positive or colourless
Survive inside macrophages, even in low pH environment
Slow reproduction
Slow response to treatment
Slow growing
M tuberculosis generation time 15-20h vs. 1h for common bacterial pathogens

355
Q

What are acid fast bacilli

A

stain used to identify organisms with wax-like, thick cell walls e.g. mycobacteria (resistant to gram stain)

356
Q

What are 4 characteristics of viruses

A

Non-cellular structure – do not have membranes or any cell organelles
Consist of an outer protein coat and a strand of nucleic acid, either DNA or RNA
Come in a variety of shapes
Do not carry out metabolic reactions on their own – require the organelles and enzymes of a host to carry out such reactions

357
Q

What are the 6 steps of viral replication

A

Attachment: viral and cell receptors e.g. HIV
Cell entry: only central viral core carrying the nucleic acid and some associated proteins enter host cell
Interaction with host cells: use cell materials (enzymes, amino acids, nucleotides) for their replication
Replication: may localize in nucleus, cytoplasm or both
Assembly: occurs in nucleus, in cytoplasm or at cell membrane
Release: bursting open of cell, or by leaking from the cell over a period of time

358
Q

what are 4 ways viruses cause disease

A

Damage by direct destruction of host cells e.g. HIV
Damage by modification of host cell structure or function e.g. rotaviruses
Damage involving over-reactivity of the host as a response to infection e.g. hepatitis B
Damage through cell proliferation and cell immortalization e.g. HPVs

359
Q

What are 4 main features of fungi

A

Eukaryotic
Chitinous cell wall
Heterotrophic- gets it food from other organisms
Move by means of growth or through the generation of spores, which are carried through air or water

360
Q

What is the fungal cell wall made of

A

mannoproteins
B1,3 and B 1,6 glucan
chitin

361
Q

What drugs target fungal cell walls

A

echinocandins

362
Q

what drug targets DNA/RNA and protein synthesis in fungi

A

flucytosin

363
Q

What are fungal plasma membranes made of

A

ergosterol (instead of cholesterol in humans)

364
Q

What drugs target ergosterol in fungi

A

amphotericin
Azoles
Terbinafine

365
Q

What is the diference between yeasts and moulds

A

Yeasts are small single celled organisms that divide by budding
Moulds form multicellular hyphae (branching filaments) and spores

366
Q

What are dimorphic fungi

A

Some fungi exist as both yeasts and moulds switching between the two when conditions suit

367
Q

What are features of selective toxicity in regards to treating fungal disease

A

Target does not exist in humans
Target is significantly different to human analogue
Drug is concentrated in organism cell with respect to humans
Increased permeability to compound
Modification of compound in organism or human cellular environment
Human cells are ‘rescued’ from toxicity by alternative metabolic pathways

368
Q

What are 3 key features of pathogens

A

infectivity
virulence
invasiveness

369
Q

What are the two types of responses to viruses

A

Humoral response
cell mediated response

370
Q

What is the mechanism of humoral response to viruses

A

Antibody (IgA) – blocks binding
Opsonisation- coating for phagocytosis
Complement cascade prepares for removal

371
Q

What is the mechanism of cell-mediated response against viruses

A

Antiviral action
Kill infected cells
Macrophages clear up

372
Q

What is the usual time-frame for viral disease

A

Peaks at 7-10 days then declines

373
Q

What is viral evasion

A

Interfere with specific or non-specific defence
Influenza changes coat antigen
Antigenic drift: spontaneous mutations, occur gradually giving minor changes = Epidemics
Antigenic shift: sudden emergence of new subtype different to that of preceding virus =Pandemics

374
Q

How do bacteria enter the body

A

via:
Respiratory tract
Gastrointestinal tract
Genitourinary tract
Skin break

375
Q

How is the defence mechanism affected by number of pathogens and virulence

A

Low number or virulence – phagocytes active
High number of virulence – immune response

376
Q

Give 2 examples of bacterial evasion

A

Mycobacterium – escape from phagolysosome, live in cytoplasm
M.avium – blocks phagosome

377
Q

What does the immune response to parasites depend on

A

Location in host:
Blood stage – humoral immunity
Tissue stage – cell mediated immunity

378
Q

What are 3 types of protozoan evasion

A

Surface antigen variation
Intracellular phase
Outer coat sloughing

379
Q

Why doesnt the immune system remove worms

A

Do not multiply in humans
Not intracellular
Few parasites carried
Poor immune response
Immune response not sufficient to kill

380
Q

What are 2 types of worm evasion

A

Decreased antigen expression by adult
Glycolipid/ glycoprotein coat (host derived)

381
Q

What is passive immunization and its 3 types

A

preformed antibody transferred
Transplacental transfer
Inject preformed antibody
Colostrum- milk at start of breast feeding

382
Q

What is active immunization and its 2 types

A

Elicitis – protective immunity – immunological memory
Achieved by natural infection – vaccine administration

383
Q

What are protozoa

A

The first animals
Single-celled eukaryotic organisms
Main biological role: consumers of bacteria, algae, microfungi
Important parasitic and symbiotic relationships
All engulf food by phagocytosis and then digest it in intracellular

384
Q

What are the 5 major groups of protozoa

A

Flagellates
Amoebae
Sporozoans
Ciliates
Microsporidia

385
Q

What are the features of flagellates

A

Flagellum as main locomotory organelle
Usually reproduce by binary fission
Intestinal flagellates or other body sites

386
Q

How do amoeba move

A

by means of flowing cytoplasm and production of pseudopodia

387
Q

What are the features of sporozoans

A

the pathogen in malaria
No locomotory extensions
All species parasitic
Most intracellular parasites
Reproduce by multiple fission

388
Q

What are the features of ciliates

A

Cilia that beat rhythmically at some stage in lifecycle
2 types of nuclei – macro/micronucleus

389
Q

What are the features of microsporidia

A

Production of resistant spores
Unique polar filament; coiled inside spore

390
Q

What is malaria

A

Protozoan infection caused by Plasmodia sporozoan.
Transmitted by bite of female Anopheles mosquitoes
5 different species

391
Q

What are the clinical features of malaria

A

Very varied
Fever almost invariable
Other common;
Chills and sweats
Headache
Myalgia
Fatigue
Nausea and vomiting
Diarrhoea
all these symptoms common to all species

392
Q

Define antibiotics

A

agents produced by micro-organisms that kill or inhibit the growth of other micro-organisms in high-dilution.

393
Q

What are 5 target sites of antimicrobials

A

Penicillin-binding proteins in cell wall
Cell membrane
DNA
Ribosomes
Topoisomerase IV or DNA gyrase

394
Q

What are the 7 key groups in infection prevention and control

A

Infection prevention and control team
Ward teams
Microbiology/ virology laboratories
Trust management
Estates
Domestic services
Pharmacy

395
Q

What is the most effective method of preventing cross infection

A

Hand hygiene

396
Q

When to wash hands ( 5 times)

A

Before and after handling patients/ clients
After handling any item that is soiled
After using the toilet
Before and after an aseptic procedure
After removing protective clothing including gloves

397
Q

When to use alcohol gel (2 times)

A

Following hand washing, prior to a ward based invasive procedure
Following hand washing, when caring for a patient with barrier precautions

398
Q

What are endogenous diseases

A

Infection of a patient by their own flora
Important in hospitalized patients, especially those with invasive devices or surgical patients

399
Q

What is the 90/90/90 goal for aids

A

90% of people living with HIV being diagnosed
90% diagnosed on ART (antiretroviral therapy)
90% viral suppression for those on ART by 2020

400
Q

What are the 3 transmission routes for HIV

A

Blood
Sexual
Vertical

401
Q

What are the 6 main benefits of knowing HIV status

A

Access to appropriate treatment and care
Reduction in morbidity and mortality
Reduction in mother-to-child-transmission (MTCT)
Reduction of sexual transmission
Public health
Cost-effective

402
Q

What are the symptoms of HIV

A

Acute generalized rash
Glandular fever
Indicators of immune dysfunction
Unexplained weight loss or night sweats
Recurrent bacterial infections including pneumococcal pneumonia

403
Q

What are the 9 steps of HIV replication

A

Attachment
Entry
Uncoating
Reverse transcription
Genome integration
Transcription of viral RNA
Splicing of mRNA and translation into proteins
Assembly of new virions
Budding

404
Q

What are the receptors and mechanism involved in HIV infection

A

HIV infects cells that express CD4
Binding of gp120 to CD4 induces a conformational change in gp120
The co-receptor binding site includes a conserved bridging sheet and also amino acids in the V3 loop

405
Q

How does HIV damage the immune system

A

through depletion of CD4 T-cells

406
Q

What are the 2 markers used to monitor HIV infection

A

CD4 cell count
HIV viral load

407
Q

What is the most common oppurtunist infection in HIV

A

PCP (pneumocystis pneumonia)

408
Q

Who are the 7 high risk groups for HIV

A

Men who have sex with men
Heterosexual women
Injecting drug users
Commercial sex workers
Heterosexual men
Truck drivers
Migrant workers

Phase 2a Medicine (10 decks)

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