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Phase 2A Ikenna > Introduction to clinical sciences > Flashcards

Introduction to clinical sciences Flashcards

1
Q

What is atherosclerosis

A

Accumulation of fibrolipid plaques in systemic arteries

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2
Q

Risk factors for atherosclerosis

A

hypertension
hyperlipidaemia
cigarette smoking
poorly-controlled diabetes mellitus

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3
Q

Does atherosclerosis occur in low pressure arteries

A

No

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4
Q

Main lipid in atherosclerosis

A

Cholesterol

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5
Q

Things within an atherosclerosis

A

Lipids-Cholesterol
Lymphocytes

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6
Q

Can atherosclerosis’ kill organs

A

Yes, if the organ only has 1 source of blood flow

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7
Q

What causes atherosclerosis risk in cigarette smoking

A

Free radicals
Carbon monoxide
nicotine

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8
Q

How does hypertension cause risk of atherosclerosis

A

Shearing forces on endothelial cells

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9
Q

How does diabetes cause risk of atherosclerosis

A

superoxide anions
glycosylation products

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10
Q

How does hyperlipidaemia cause risk of atherosclerosis

A

Lipids cause direct damage to endothelial cells

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11
Q

What does accumulated endothelial damage cause

A

Atherosclerosis

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12
Q

What are caspases

A

Family of protease enzymes with essential roles in apoptosis regulation

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13
Q

What is apoptosis

A

Programmed cell death

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14
Q

Function of apoptosis

A

prevents cells with accumulated genetic damage from dividing and potentially becoming cancer cells

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15
Q

Function of p53 protein

A

Can detect DNA damage and can the trigger apoptosis

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16
Q

What is Necrosis

A

It is wholesale destruction of large numbers of cells by some external factor

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17
Q

Clinical examples of necrosis

A

Infarction e.g myocardial
Frostbite
Toxic venom
Pancreatitis

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18
Q

What cells phagocytose dead cells following necrosis and replace necrotic tissue

A

Macrophages

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19
Q

myelomeningocele

A

Nerves bulge out with meninges

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20
Q

What is an inherited disease caused by

A

An inherited genetic abnormality

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21
Q

Acquired disease is caused by

A

Non-genetic environmental factors

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22
Q

What is hypertrophy

A

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

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23
Q

What is hyperplasia

A

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

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24
Q

What is a congenital disease

A

Disease present at birth

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25
Q

What is a meningocele

A

Outpouching of meninges

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26
Q

Polygenic inheritance is the inheritance of….

A

Many genes

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27
Q

benign prostate hyperplasia

A

muscle in prostate

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28
Q

What is mixed hypertrophy/hyperplasia

A

increase in the size of an organ due to increase in size and number of its constituents

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29
Q

Atrophy

A

Decrease in size of an organ due to decrease in size or number of its constituent cells or both

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30
Q

What is metaplasia

A

Change in cell differentiation from one fully differentiated type to another fully differentiated type

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31
Q

What is Dysplasia

A

Morphological changes that may be seen in cells (often epithelium) in the progression on to development of cancer(neoplasia)

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32
Q

Why would skin cells from older people divide less than those from younger people

A

The telomere region at the end of chromosomes shortens and eventually becomes so short that it is not possible for the chromosomes to divide and replicate so the cell can no longer divide.

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33
Q

Effects of ageing on skin

A

Wrinkling

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34
Q

Effects of ageing on eyes

A

Cataracts

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35
Q

Effects of ageing on osteoporosis

A

Loss of bone matrix

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36
Q

Effects of ageing on brain

A

Dementia (e.g Alzheimers)

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37
Q

Effects of ageing on muscle

A

Loss of muscle (sarcopaenia)

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38
Q

Effects of ageing on hearing

A

Causes deafness

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39
Q

What happens to growth hormone with age

A

decreased

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40
Q

What happens to testosterone with age

A

Decreased

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41
Q

What happens to catabolic cytokines with age

A

Increased

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42
Q

What are catabolic cytokines

A

Catabolic proinflammatory cytokines play a key role in mediating biochemical changes associated with many pathophysiological states

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43
Q

Where does a basal cell carcinoma invade/ spread to

A

only invades locally

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44
Q

Cure for basal cell carcinoma

A

Complete local excision

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45
Q

Cure for leukaemia

A

systemic chemotherapy

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46
Q

Where do carcinomas spread to

A

The lymph nodes that drain the site of the carcinoma

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47
Q

Can carcinomas spread through the blood to bone

A

Yes

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48
Q

Common cancers that commonly spread to the bone

A

Breast, prostate, lung, thyroid and kidney

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49
Q

What is adjuvant therapy

A

Extra treatment given after surgical excision

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50
Q

Can micro metastases be present even if a tumour is completely excised

A

Yes

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51
Q

What is a neoplasm

A

An abnormal mass of tissue that forms when cells grow and divide more than they should or do not die when they should

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52
Q

What is the name of the main effector cell in acute inflammation

A

Neutrophil polymorph

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53
Q

What is the name of the cells that produce collagen in fibrous scarring

A

Fibroblasts

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54
Q

Example of acute inflammation

A

Appendicitis

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55
Q

Does granulomatous inflammation occur in Crohn’s disease

A

Yes

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56
Q

What is granulomatous inflammation

A

When immune cells clump together and create tiny nodules at the site of the infection or inflammation

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57
Q

Example of a process that is a chronic inflammatory process from its start

A

Infectious mononucleosis

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58
Q

Example of hyperplasia

A

Benign prostate enlargement

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59
Q

Examples of apoptosis

A

Loss of cells from tips of duodenal villi
Loss of cells during embryogenesis
Graft versus host disease

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60
Q

Is a loss of cells from tips of duodenal villi apoptosis

A

YES

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61
Q

Is a loss of cells during embryogenesis apoptosis

A

Yes

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62
Q

Is the brain in dementia atrophy?

A

Yes

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63
Q

Example of necrosis

A

Renal infarction

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64
Q

Drug that inhibits platelet aggregation

A

Aspirin

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65
Q

What process is defined by the formation of a solid mass of blood constituents within an intact vascular system during life?

A

Thrombosis

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66
Q

What is Carcinogenesis

A

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

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67
Q

What does oncogenesis consist of

A

Benign and malignant tumours

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68
Q

Does carcinogenesis apply to malignant neoplasms

A

Yes

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69
Q

What does carcinogenic mean

A

Cancer causing

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70
Q

What does oncogenic mean

A

Tumour causing

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71
Q

What is a carcinogen called when it acts on DNA

A

Mutagenic

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72
Q

What % of cancer risk is environmental

A

85%

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73
Q

5 Classes of carcinogens

A

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

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74
Q

Do chemical carcinogens have any common structural features

A

No

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75
Q

Do chemical carcinogens require metabolic conversion

A

Yes, from pro-carcinogens to ultimate carcinogens

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76
Q

See Carcinogens PPt for examples of carcinogens

A

OK

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77
Q

Hormones that can cause cancer

A

Oestrogen
Anabolic steroids

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78
Q

miscellaneous carcinogens examples

A

Asbestos
Metals

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79
Q

Host factors for cancer

A

Ethnicity
Diet / Lifestyle
Constitutional factors - age, gender etc.
Premalignant lesions
Transplacental exposure

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80
Q

Can a carcinoma in situ in a duct spread

A

No

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81
Q

Can an invasive carcinoma spread

A

Yes

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82
Q

What is a micro-invasive carcinoma

A

When the carcinoma only partially invades the basement membrane

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83
Q

What do cancer cells produce

A

Proteases-matrix metalloproteinases
Collegenase
Cathepsin D
urokinase-type plasminogen activator

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84
Q

Why do cancer cells contain collegenases

A

To break down collagen in Basement membrane

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85
Q

Cancer spread process

A

Invades intracellular matrix
Blood vessel
Lymph tissue
Through blood vessel
through more intracellular matrix
Into another cell

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86
Q

Specific process of cancer spread

A

Invasion of basement membrane
Tumour cell motility
Intravasation
Evasion of host immune defence
Extravasation
Growth at metastatic site
Angiogenesis

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87
Q

What is angiogenesis

A

Formation of new blood cells

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88
Q

What is intravasation

A

Entering blood vessel

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89
Q

Where does a tumour in the IVC end up and why

A

Lung, because blood vessels get smaller here

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90
Q

Where would a tumour of the colon metastasize to

A

Liver via portal venous system

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91
Q

Is conventional chemotherapy best for fast dividing or slow dividing tumours

A

Fast dividing

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92
Q

Is conventional chemotherapy selective for tumour cells

A

No

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93
Q

What is a granuloma

A

A macrophage collection

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94
Q

What is the name of a malignant tumour of a striated muscle?

A

rhabdo myo sarcoma

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95
Q

Does liposarcoma commonly metastasise to bone

A

No

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96
Q

what term describes a cancer that has not invaded through the basement membrane

A

Carcinoma in situ

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97
Q

What is the name of a benign tumour of glandular epithelium

A

Adenoma

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98
Q

What is the name of a benign tumour of fat cells

A

Lipoma

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99
Q

What is the name of a malignant tumour of glandular epithelium

A

adenocarcinoma

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100
Q

What is a neoplasm

A

A lesion resulting from the autonomous or relatively autonomous abnormal growth of cells which persists after the initiating stimulus has been removed

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101
Q

What are neoplastic cells derived from

A

Nucleated cells

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102
Q

Functions of neoplasm stroma

A

Connective tissue framework
Mechanical support
Nutrition

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103
Q

Why do we classify neoplasms

A

To determine appropriate treatment
To provide prognostic information

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104
Q

Methods of classification for neoplasms

A

Behavioural:benign/borderline/malignant

Histogenetic:cell of origin

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105
Q

Features of benign Neoplasms

A

Localised, non-invasive
Slow growth rate
Low mitotic activity
Close resemblance to normal tissue
Circumscribed or encapsulated

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106
Q

Features of malignant neoplasms

A

Invasive
Metastases
Rapid growth rate
Variable resemblance to normal tissue
Poorly defined or irregular border

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107
Q

What can neoplasms arise from

A

Epithelial cells
Connective tissues
Lymphoid/haematopoietic organs

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108
Q

What is a papilloma

A

Benign tumour of non-glandular, non-secretory epithelium

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109
Q

What is an adenoma

A

Benign tumour of glandular or secretory epithelium

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110
Q

What is a carcinoma

A

Malignant tumour of epithelial cells

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111
Q

What does the suffix lipoma suggest

A

Adipocytes

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112
Q

What does the suffix chondroma suggest

A

Cartilage

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113
Q

What does the suffix osteoma suggest

A

Bone

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114
Q

What does the suffix angioma suggest

A

Vascular

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115
Q

What is rhabdomyoma to do with

A

Striated muscle

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116
Q

What is leiomyoma to do with

A

Smooth muscle

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117
Q

What is a neuroma to do with

A

Nerves

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118
Q

Does a basal cell carcinoma metastasize

A

Never

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119
Q

Malignant connective tissue neoplasms and their associated cell types

A

Liposarcoma adipose tissue
Rhabdomyosarcoma striated muscle
Leiomyosarcoma smooth muscle
Chondrosarcoma cartilage
Osteosarcoma bone
Angiosarcoma blood vessels

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120
Q

What does anaplastic mean

A

The cell-type is unknown

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121
Q

Are all -oma suffixes neoplasms

A

No

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122
Q

What is a melanoma

A

Malignant neoplasm of melanocytes

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123
Q

What is a mesothelioma

A

Malignant neoplasm of mesothelial cells

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124
Q

What is a lymphoma

A

Malignant neoplasm of lymphoid cells

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125
Q

What does the suffix -oma mean

A

Neoplasm

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126
Q

TNM classification system for staging of tumours

A

T = tumour size
N = node involvement
M = metastasis
PL = pleural involvement
R = resection, with R0 being the ideal = fully excised

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127
Q

What does tumour staging allow

A

allows decision making with regard to follow-up treatment, particularly if there is evidence of metastasis

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128
Q

Therapies for tumours

A

Biopsy + anti-tumour therapies (molecular signalling pathway inhibitors)
Chemotherapy
Radiotherapy
Surgery

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129
Q

Innate immunity

A

Instinctive, non-specific, does not depend on lymphocytes, present from birth

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130
Q

Adaptive immunity

A

Specific ‘Acquired/learned’ immunity, requires lymphocytes, antibodies

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131
Q

What is serum

A

Plasma without fibrinogen and other clotting factors

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132
Q

What type of immunity are T and B cells used in

A

Adaptive immunity

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133
Q

What are mast cells used in

A

Allergic reaction

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134
Q

WHat are natural killer cells used in

A

Viral + cancer reaction

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135
Q

What type of immunity are macrophages used in

A

Innate Immunity

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136
Q

What are leukocytes

A

White blood cells

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137
Q

Modes of action of complement

A

Direct lysis
Attract more Leukocytes to site of infection
Coat invading organism

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138
Q

What is complement

A

Group of ~20 serum proteins secreted by the liver that need to be activated during an immune response to be functional

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139
Q

Are immunoglobulins antibodies

A

YES

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140
Q

Most common immunoglobulin

A

IgG

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141
Q

What are cytokines

A

Proteins secreted by immune and non-immune cells controlling the growth and activity of other immune system cells and blood cells

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142
Q

Types of cytokines

A

Interferons
Interleukins
Colony stimulating factors
Tumour necrosis factors
Chemokines

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143
Q

Examples of physical barriers to disease

A

Lysozyme in tears
Mucus
cilia
Skin barrier
Fatty acids
Acid(stomach)
pH change

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144
Q

Inflammatory response

A

Stop bleeding (coagulation)
Acute inflammation (leukocyte recruitment)
Kill pathogens, neutralise toxins, limit pathogen spread
Clear pathogens/dead cells (phagocytosis)
Proliferation of cells to repair damage
Remove blood clot – remodel extracellular matrix
Re-establish normal structure/function of tissue

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145
Q

What is chronic inflammation

A

Persistent, un-resolved inflammation

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146
Q

Acute inflammation steps

A

Pathogen is fully eliminated
Resolution of damage
Disappearance of leukocytes
Full regeneration of tissue

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147
Q

What senses microbes in blood

A

Monocytes
Neutrophils

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148
Q

What senses microbes in tissues

A

Macrophages
Dendritic cells

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149
Q

Antigen presenting cells examples

A

Macrophages
Dendritic cells
B cells

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150
Q

What membrane bound immunoglobulins do B cells normally express

A

IgM
IgD

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151
Q

What is APC

A

A type of immune cell that boosts immune responses by showing antigens on its surface to other cells of the immune system

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152
Q

Functions of antibodies

A

Neutralise toxin by binding to it
Increase opsonisation – phagocytosis
Activate complement

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153
Q

What is opsonisation

A

Marking for phagocytosis

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154
Q

What is pharmacodynamics

A

How the drug acts on the body

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155
Q

What is pharmacokinetics

A

What the body does to the drug

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156
Q

What is Physicochemical

A

How the drugs interact regardless of the condition

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156
Q

What is Physicochemical

A

How the drugs interact regardless of the condition

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157
Q

Summation

A

Drugs used together produce the expected result

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158
Q

Synergism

A

Two drugs together have a greater effect than expected

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159
Q

Antagonism

A

One drug has a negative effect on the other

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160
Q

Potentiation

A

One drug is made more potent than the other drug without any alterations to the other drug

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161
Q

Pharmacokinetics acronym:ADME

A

Adsorption
Distribution
Metabolism
Excretion

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162
Q

What is bioavailability

A

How much of a drug is available over a period of time

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163
Q

What drug is given in a paracetamol overdose

A

Activated charcoal

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164
Q

How does activated charcoal help a paracetamol overdose

A

Paracetamol binds to the charcoal to be excreted

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165
Q

What does INR stand for

A

International normalised ratio

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166
Q

What does a high INR mean

A

Blood clots more slowly than desired

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167
Q

Definition of drug

A

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

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168
Q

Pharmacology definition

A

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

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169
Q

What is druggability

A

It describes a biological target that is known to or is predicted to bind with high affinity to a drug

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170
Q

Examples of drug targets

A

Receptors
Enzymes
Transporters
Ion channels

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171
Q

What is a 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

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172
Q

Example of exogenous ligand

A

Drugs

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173
Q

Example of endogenous ligands

A

Hormones
Neurotransmitter

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174
Q

Examples of autacoids

A

Cytokines
Histamine

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175
Q

What is an autacoid

A

Physiologically active substance (such as serotonin, bradykinin, or angiotensin) that is produced by the body

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176
Q

Types of receptors

A

Ligand-gated ion channels
G protein coupled receptors
Kinase-linked receptors
Cytosolic/nuclear receptors

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177
Q

Example of cytosolic/nuclear receptor

A

Steroid receptors

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178
Q

What are ion channels?

A

Ion channelsare pore-formingmembrane proteinsthat allowionsto pass through the channel pore so that the cell undergoes a shift inelectric chargedistribution

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179
Q

What is the largest and most diverse membrane receptor

A

G protein coupled receptors (GPCRs)

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180
Q

Alternative name for G proteins

A

Guanine nucleotide-binding proteins

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181
Q

What are Kinases

A

Enzymes that catalyse the transfer of phosphate groups between proteins-phosphorylation

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182
Q

How do nuclear receptors work

A

By modifying gene transcription

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183
Q

Can imbalance of chemical/receptors lead to pathology

A

Yes

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184
Q

Examples of chemical imbalance leading to pathology

A

allergy-increased histamine
Parkinson’s-reduced dopamine

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185
Q

Examples of Receptor imbalance leading to pathology

A

myasthenia gravis; loss of ACh receptors
mastocytosis; increased c-kit receptor

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186
Q

What is an agonist

A

A compound that binds to a receptor and activates it

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187
Q

What is an antagonist

A

A compound that reduces the effect of an agonist

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188
Q

What is the two-state model of receptor activation

A

Describes how drugs activate receptors by inducing or supporting a conformational change in the receptor from “off” to “on”.

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189
Q

What is intrinsic activity/efficiacy

A

The ability of a drug receptor complex to produce a maximum functional response

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190
Q

What is affinity

A

Describes how well a ligand binds to the receptor

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191
Q

Do both agonists and antagonists show affinity

A

Yes

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192
Q

What is efficacy

A

How well a ligand activates the recptor

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193
Q

What is efficacy

A

How well a ligand activates the receptor

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194
Q

Do antagonists have efficacy

A

No

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195
Q

What is receptor reserve

A

The idea that some agonists needs to activate only a small fraction of the existingreceptors to produce the maximal system response.

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196
Q

Is any receptor response seen for a partial agonist

A

No

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197
Q

Receptor related factors that govern drug action

A

Affinity
Efficiacy

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198
Q

Tissue related factors that govern drug action

A

Receptor number
Signal amplification

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199
Q

What is inverse agonism

A

When a drug that binds to the same receptor as an agonist but induces a pharmacological response opposite to that of the agonist

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200
Q

What is tolerance

A

Reduction in agonist effect over time due to continuously high concentrations

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201
Q

Is any compound truly ever specific

A

NO

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202
Q

What is an enzyme inhibitor

A

A molecule that binds to an enzyme and (normally) decreases its activity

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203
Q

What are the two types of enzyme inhibitors

A

Irreversible inhibitors
Reversible inhibitors

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204
Q

How do irreversible inhibitors work

A

Usually react with the enzyme and change it chemically e.g covalent bond formation

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205
Q

How do reversible inhibitors work

A

Bind non-covalently and different types of inhibition are produced depending on whether these inhibitors bind to the enzyme, enzyme substrate complex or both

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206
Q

What is streptokinase

A

A clot buster

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207
Q

Function of statins

A

Block the rate limiting step in the cholesterol pathway

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208
Q

What does inhibiting Angiotensin converting enzyme (ACE) do

A

Reduces ATII production and therefore causes a reduction in blood pressure

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209
Q

Reason for xenobiotic metabolism

A

generates compounds that are more readily excreted by the body

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210
Q

What are xenobiotics

A

Are compounds foreign to an organism’s normal biochemistry, such any drug or poison

211
Q

What does pharmacokinetics give us

A

Gives us information about how drugs will function at certain doses and for how long

212
Q

What is bioavailability

A

The fraction (%) of an administered drug that reaches the systemic circulation

213
Q

What are CYPs(Cytochrome P450)

A

Major enzymes involved in drug metabolism

214
Q

What percentage of metabolism do CYPs account for

A

75%

215
Q

Which antigen presenting cell is the best at activating lymphocytes

A

Dendritic cells

216
Q

What can monocytes differentiate into

A

Macrophages
Dendritic cells

217
Q

What does adrenergic relate to

A

Adrenaline or noradrenaline and their receptors

218
Q

What does cholinergic relate to

A

Acetylcholine and its receptor

219
Q

Afferent definition

A

Carries signals towards brain or spinal cord

220
Q

Efferent definition

A

Carries signals away from the brain or spinal cord

221
Q

How many neurons between CNS and skeletal muscle in somatic NS

A

Single neuron

222
Q

What does the somatic NS innervate

A

Skeletal muscle

223
Q

Does the somatic NS excite or inhibit

A

Excite

224
Q

How many neurons are there in the autonomic NS chain

A

Two

225
Q

What does the autonomic NS innervate

A

Smooth muscle
Cardiac muscle
Glands
GI neurons

226
Q

Does the autonomic NS lead to excitation or inhibition

A

Both

227
Q

Is fight or flight sympathetic or parasympathetic

A

Sympathetic

228
Q

Is rest or digest parasympathetic or sympathetic

A

Parasympathetic

229
Q

What separates the two neurons in the ANS

A

The autonomic ganglion

230
Q

Where is the autonomic ganglion in the parasympathetic system

A

Close to the effector organ

231
Q

Where is the autonomic ganglion in the sympathetic system

A

Within a chain adjacent to the spinal cord

232
Q

Preganglionic neurotransmitter

A

Acetylcholine

233
Q

Postganglionic neurotransmitters

A

Acetylcholine (parasympathetic)
Noradrenaline (sympathetic)

234
Q

What receptor does acetylcholine act on preganglionic

A

Nicotinic receptor (sympathetic and parasympathetic)

235
Q

What receptor does acetylcholine act on postganglionic

A

Muscarinic receptors (parasympathetic)

236
Q

What receptors does noradrenaline act on postganglionic

A

Alpha and beta receptors (sympathetic)

237
Q

Are muscarinic receptors receptive to drug targeting

A

Yes

238
Q

What are the 5 types of muscarinic receptors

A

M1: Brain
M2: Heart
M3: All organs with parasympathetic innervation
M4: Mainly CNS
M5: Mainly CNS

239
Q

How do muscarinic receptors activate intracellular processes

A

Through G-proteins

240
Q

What does activation of M2 receptors on heart SA node cause

A

Decrease in heart rate

241
Q

What does activation of M2 receptors on heart AV node cause

A

Decrease in conduction velocity
Induces AV node block (Increases PR interval)

242
Q

M3 Receptors stimulation in respiratory system effects

A

Produces mucus
Induces smooth muscle contraction (bronchoconstriction)

243
Q

M3 Receptors stimulation in GI tract effects

A

Increase saliva production
Increases gut motility
Stimulates biliary secretion

244
Q

M3 Receptors stimulation in Skin effect

A

Sweating

245
Q

Where is the only place the sympathetic system releases ACh

A

Skin

246
Q

M3 Receptors stimulation in urinary system effects

A

Contracts detrusor muscle
Relaxation of internal urethral sphincter

247
Q

M3 Receptors stimulation in Eye effects

A

Causes myosis
Increases drainage of aqueous humour
Secretion of tears

248
Q

What is myosis

A

Excessive constricting of pupil

249
Q

What does blockage of normal transmission of ACh lead to

A

Skeletal muscle weakness-myaesthenia Gravis

250
Q

What is the precursor of adrenaline and noradrenaline

A

Dopamine

251
Q

See Cholinergic and adrenergic PPt for alpha and beta receptor info

A

OK

252
Q

What does alpha 1 receptor activation cause

A

Vasoconstriction (mainly in the skin)

253
Q

Alpha 2 receptor activation causes..

A

Mixed effects on vascular smooth muscle

254
Q

What do alpha 1 blockers do

A

Lower blood pressure

255
Q

Where are beta 1 receptors usually found

A

Heart
Kidney
Fat cells

256
Q

What does agonism of beta 1 receptors cause

A

Tachycardia
Increase in stroke volume
Renin release (increase in vascular tone)
Lipolysis and hyperglycaemia

257
Q

Beta blockers effects

A

Reduce heart rate
Reduce stroke volume
Reduce myocardial oxygen demand and help remodelling in heart failure or post-myocardial infarction

258
Q

Examples of naturally occurring opioids

A

Morphine
Codeine

259
Q

Opioid antagonist

A

Naloxone

260
Q

Synthetic partial agonists for opioids

A

Buprenorphine

261
Q

How long does a single dose of morphine last for

A

3-4 hours

262
Q

Routes of administration for opioids

A

Sub-cutaneous
IV
IM (intra-muscular)

263
Q

What is opium made up of

A

Morphine and codeine

264
Q

What drug class are opioids

A

Class A drugs

265
Q

How do opioids work

A

Inhibit the release of pain transmitters at spinal cord and midbrain and modulate pain perception in higher centres
Changes the emotional perception of pain

266
Q

What does sustained activation by opioids lead to

A

Tolerance and addiction

267
Q

What is potency

A

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

268
Q

What is efficacy

A

Looking at if it is possible to get a maximal response with the drug or not

269
Q

Biological definition of tolerance

A

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

270
Q

Side effects of opioids

A

Respiratory Depression
Sedation
Nausea and Vomiting
Constipation
Itching
Immune Suppression
Endocrine Effects

271
Q

What is morphine metabolised to

A

Morphine 6 glucuronide

272
Q

What happens in renal failure (morphine related)

A

Morphine 6 glucuronide builds up as it isn’t cleared and may cause respiratory distress

273
Q

What is tramadol

A

A weak opioid agonist, stronger than codeine

274
Q

Oral availability for morphine

A

50%

275
Q

Type 1 hypersensitivity reaction

A

Allergy
Primarily IgE dependent

276
Q

Type 2 hypersensitivity reaction

A

Primarily IgG-dependent cytotoxicity

277
Q

Type 3 hypersensitivity reaction

A

IgG/IgM-dependent immune complex formation

278
Q

Type 4 hypersensitivity reaction

A

Delayed type hypersensitivity (DTH)
Cell dependent (Th1/ cytotoxic T cells/macrophages)

279
Q

Which hypersensitivity reactions are antibody mediated

A

Type 1-3

280
Q

What does IgE in type 1 hypersensitivity reaction induce

A

Mast cell activation

281
Q

Which hypersensitivity reactions are directed against soluble antigens

A

1 and 3

282
Q

Which hypersensitivity reaction is directed at a cell or matrix associated antigen

A

Type 2

283
Q

Clinical allergy indications for skin

A

Swelling
Itching
Reddening

284
Q

Clinical allergy indications for airways

A

Anaphylaxis
Excessive mucus production
Bronchoconstriction

285
Q

Clinical allergy indications for GI

A

Abdominal bloating
Vomiting
Diarrhoea

286
Q

What is allergy

A

Abnormal response to harmless foreign material (allergens)

287
Q

What is atopy

A

Tendency to develop allergies

288
Q

Examples of allergic diseases

A

Anaphylaxis
Allergic asthma
Allergic rhinitis (hay fever)
Atopic dermatitis
Allergic conjunctivitis
Oral allergy syndrome (food allergy)
Angioedema (not idiopathic)

289
Q

Cells involved in allergic diseases

A

Mast cells, eosinophil, basophil
Lymphocytes, dendritic
Epithelial cells
Smooth muscle, fibroblast

290
Q

Mediators of allergic diseases

A

Cytokines
Chemokines
Lipids
Small molecules

291
Q

Low affinity Ige receptor

A

FceRII
CD23

292
Q

Function of FceRII, CD23

A

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

293
Q

3 major cell types that express a high affinity IgE receptor

A

Eosinophil
Mast cell
Basophil

294
Q

What is CD117 (c-kit)

A

Cell surface receptor for Stem Cell Factor

295
Q

What is the function of stem cell factor

A

Causes Stem blood cells to change into different types of blood cells

296
Q

What does histamine cause

A

Arteriolar dilation
Capillary leakage

297
Q

How do T cells work

A

T cells ‘polarise’ according to the threat detected and this determines the nature of the adaptive immune response

298
Q

What does mast cell activation cause

A

Production of modulators of IgE synthesis

299
Q

Anaphylaxis pneumonic (ABCDE)

A

Airway
Breathing
Circulation
Disability
Exposure

300
Q

Anaphylaxis cardiovascular effects

A

Vasodilation
Increased vascular permeability
Lowered BP

301
Q

Slow Anaphylaxis response

A

Pain
Vomiting
Gi related etc

302
Q

Anaphylaxis respiratory effects

A

Bronchial smooth muscle contraction
Mucus

303
Q

Anaphylaxis SKin effects

A

Rash
Swelling

304
Q

Anaphylaxis biological effect

A

Mast cell or basophil activation
IgE or direct activation
Serum tryptase and histamine elevated

305
Q

What is serum tryptase

A

A marker of mast cell degranulation

306
Q

Chronic asthma

A

Non Th2 T cell mechanisms
CD8 (regulatory) T cell eosinophil responses

307
Q

Function of Xolair(Omalizumab)

A

Inhibits binding of IgE to High- affinity IgE receptor (FcεRI)

308
Q

What is omalizumab

A

Monoclonal antibody

309
Q

What is IL-5

A

An interleukin produced by type-2 T helper cells and mast cells

310
Q

Function of Glucocorticoids

A

Inhibit gene transcription

311
Q

What is pavementing

A

Adhesion of neutrophils to vascular endothelium at site of acute inflammation

312
Q

What is an adverse drug reaction

A

Unwanted or harmful reaction following administration of a drug or combination of drugs under normal conditions of use

313
Q

What does an adverse drug reaction have to be

A

Noxious and unintended

314
Q

What is a side effect

A

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

315
Q

What is nephrotoxicity

A

Damaging or destructive to the kidneys

316
Q

What is ototoxicity

A

Has a toxic effect on the ear or its nerve supply

317
Q

What is dysarthria

A

A speech disorder

318
Q

What is ataxia

A

A lack of muscle coordination

319
Q

What causes toxic effects of drugs

A

If the dose is too high
Or if drug excretion is reduced by impaired renal or hepatic function
By interacting with other drugs

320
Q

patient risk factors for adverse drug reactions

A

Gender (F>M)
Elderly
Neonates
Polypharmacy (21% 5 or more drugs)
Genetic predisposition
Hypersensitivity/allergies
Hepatic/renal impairment
Adherence problems

321
Q

Drug risk factors for adverse drug reactions

A

Steep dose-response curve
Low therapeutic index
Commonly causes ADR’s

322
Q

Causes for adverse drug reactions

A

Pharmaceutical variation
Receptor abnormality
Abnormal biological system unmasked by drug
Abnormalities in drug metabolism
Immunological
Drug-drug interactions
Multifactorial

323
Q

Adverse drug reactions (ABCDEF)

A

Type A (Augmented pharmacological)
Type B (Bizarre or idiosyncratic)
Type C (Chronic)
Type D (Delayed)
Type E (End of treatment)
Type F (Failure of therapy)

324
Q

Most common drugs to have ADR

A

Antibiotics
Anti-neoplastics
Cardiovascular drugs
Hypoglycaemics
NSAIDS
CNS drugs

325
Q

Common ADRs

A

Confusion
Nausea
Balance problems
Diarrhoea
Constipation
Hypotension

326
Q

What does the yellow card scheme do

A

Collects spontaneous reports of ADRs
Collects suspected adverse drug reactions

327
Q

Is the yellow card scheme a voluntary reporting scheme

A

Yes

328
Q

What does the black triangle mean on a yellow card scheme

A

It indicates that a medicine is undergoing additional monitoring

329
Q

Information that must be included on a yellow card report

A

Suspected drug(s)
Suspect reaction(s)
Patient details
Reporter details
Additional useful information

330
Q

Is hypersensitivity caused by immunologic or non-immunologic mechansism

A

Both

331
Q

What is cytopenia

A

When one or more of your blood cell types is lower than it should be

332
Q

What is angioedema

A

Swelling underneath the skin

333
Q

What happens in a type 2 hypersensitivity reaction

A

Drug or metabolite combines with a protein
Protein gets treated as foreign and the body forms antibodies (IgG, IgM)
Antibodies combine with antigen and complement activation damages the cells

334
Q

Type 3 hypersensitivity process

A

Antigen and antibody form large complexes and activate complement
Small blood vessels are damaged or blocked
Leucocytes attracted to the site of reaction and release pharmacologically active substances leading to an inflammatory process

335
Q

Type 4 hypersensitivity process

A

Antigen specific receptors develop on T-lymphocytes
Subsequent admin, adminstration leads to local or tissue allergic reaction

336
Q

What are the effects of adrenaline

A

Vasoconstriction
Stimulation of Beta1-adrenoceptors positive ionotropic and chronotropic effects on the heart
Reduces oedema and bronchodilates via beta2-adrenoceptors
Attenuates further release of mediators from mast cells and basophils by increasing intracellular c-AMP and so reducing the release of inflammatory mediators

337
Q

Function of vasoconstriction

A

Vasoconstriction- increase in peripheral vascular resistance, increased BP and coronary perfusion via alpha1-adrenoceptors

338
Q

What is a commensal

A

An organism which colonises the host but causes no disease in normal circumstances

339
Q

What is an opportunist pathogen

A

Microbe that only causes disease if host defences are compromised

340
Q

What is virulence/pathogenicity

A

The degree to which a given organism is pathogenic

341
Q

What is asymptomatic carriage

A

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

342
Q

What is a pathogen

A

Organism that causes or is capable of causing disease

343
Q

What are small round bacteria called

A

Cocci

344
Q

What are rod shaped bacteria called

A

Bacilli

345
Q

What are bacteria if they stain red

A

Gram negative

346
Q

What are bacteria if they stain blue

A

Gram positive

347
Q

Example of bacteria that don’t stain with Gram stain

A

Tb which is mycobacteria

348
Q

What stain stains Tb

A

Ziehl-Neelsen stain

349
Q

What structure do gram negative bacteria have that isnt in gram positive bacteria

A

Lipopolysaccharide(endotoxin)

350
Q

What does Lipopolysaccharide(endotoxin) contain

A

Terminal sugars
O antigen
Lipid A

351
Q

BActeria environment (temp, Ph)

A

-80C to 80C
Ph:4-9

352
Q

What is an endotoxin

A

Component of the outer membrane of bacteria, eg lipopolysaccharide in Gram negative bacteria

353
Q

What is exotoxin

A

Secreted proteins of Gram positive and Gram-negative bacteria

354
Q

See endotoxin and exotoxin table in bacteria as causes PPT

A

OK

355
Q

Typical bacterial chromosome base number

A

Typically 2-4 x 10*3 kb

356
Q

Can plasmids be transferred between bacteria

A

Yes

357
Q

Mutation causes for genetic variation in bacteria

A

Base substitution
Deletion
Insertion

358
Q

Gene transfer causes for genetic variation in bacteria

A

Transformation eg via plasmid
Transduction eg via phage
Conjugation eg via sex pilus

359
Q

What is conjugation

A

The process by which one bacterium transfers genetic material to another through direct contact

360
Q

What is transduction

A

The process by which a virus transfers genetic material from one bacterium to another

361
Q

What is transformation

A

The process by which an organism acquires exogenous DNA from its natural environment

362
Q

Examples of Gram positive cocci

A

Streptococci
Staphylococcci

363
Q

Features of gram positive cocci

A

Thick cell wall

364
Q

What is staphylococcus aureus

A

Gram positive cocci in clusters

365
Q

What is coagulase

A

An enzyme produced by bacteria that clots blood plasma

366
Q

Is Staphylococcus aureus coagulase positive

A

Yes

367
Q

Why is coagulase important

A

Forms a fibrin clot around bacteria and may protect it from phagocytosis

368
Q

Example of coagulase negative bacteria

A

Staphylococcus epidermis
S.saprophyticus

369
Q

Normal habitat of staphylococcus

A

Nose and skin

370
Q

Main virulence factor of s.epidermis

A

Ability to form persistent biofilms

371
Q

What is alpha haemolysis due to

A

Due to the production of hydrogen peroxide, which reacts with haemoglobin to form the green compound met-haemoglobin

372
Q

What is beta haemolysis due to

A

It is due to the production of two pore-forming toxins – streptolysin O and S. Streptolysin O which is oxygen sensitive and is very antigenic

373
Q

Function of streptokinase

A

Breaks down clots

374
Q

Function of Streptolysins O&S

A

binds cholesterol

375
Q

Function of M protein

A

Surface protein that encourages complement degredation

376
Q

What is a pathogen’s ability to infect or damage its host tissues determined by

A

Virulence factors

377
Q

What are virulence factors

A

The molecules that assist the bacterium to colonize the host at the cellular level

378
Q

What does C.tetani cause

A

Tetanus

379
Q

What does c.botulinum cause

A

Botulism

380
Q

What does C.difficile cause

A

antibiotic associated diarrhea
pseudomembranous colitis

381
Q

Examples of anaerobic Gram positive bacilli

A

C.tetani
C.Botulinum
C.Difficile

382
Q

Examples of aerobic Gram positive bacilli

A

Listeria monocytogenes
Bacillus anthracis
Corynebacterium diphtheriae

383
Q

What is an epitope

A

The part of an antigen to which the antibody attaches itself

384
Q

2 main examples of mycobacteria

A

TB
Leprosy

385
Q

What is mycobacteria

A

Aerobic, non-spore forming, non-mobile bacilli

386
Q

What stain is used for mycobacteria

A

Ziehl-Neelsen stain
Acid fast bacteria stain red
Non-acid fast stains blue

387
Q

Why is Mycobacteria resistant to Gram stain

A

Its cell wall has a high lipid content with mycolic acids

388
Q

Are mycobacteria fast or slow growing

A

Slow growing

389
Q

Primary tuberculosis

A

Initial contact made by alveolar macrophages
Bacilli taken in lymphatics to hilar lymph nodes

390
Q

Latent tuberculosis info

A

Cell mediated immune response from T-cells
Primary infection is contained but Cell mediated immunity persistss

391
Q

What happens in pulmonary tuberculosis

A

Granuloma forms around Bacilli that have settled in the apex
In apex of the lung there is more air and less blood supply so less white blood cells
Necrosis results in abscess forming and caseous material coughed up

392
Q

What does miliary mean

A

Accompanied by a rash with lesions

393
Q

How does TB affect us

A

Aerosol transmission
Primary TB in lung
Latent TB can remain for decades
Can spread beyond lungs

394
Q

What is a virus

A

An infectious, obligate intracellular parasite comprising genetic material (DNA or RNA) surrounded by a protein coat and/or a membrane

395
Q

What does obligate intracellular mean

A

Totally dependent on living cells for their replication and existence

396
Q

Shapes of viruses

A

Helical
Icosahedral
Complex
Enveloped
Non-enveloped

397
Q

What are viruses called when not insde an infected cell

A

Virions

398
Q

Examples of non enveloped viruses

A

Adenovirus
Parvovirus

399
Q

Examples of enveloped viruses

A

Influenza
HIV

400
Q

How do viruses replicate

A

Attachment to specific receptor
Cell entry(uncoating of virion within cell)
Host cell interaction + replication
Assembly of virion
Release of new virus particles

401
Q

What happens in host cell interaction+ replication

A

Migration of genome to cell nucleus
Transcription to mRNA using host materials
Translation of viral mRNA to produce structural proteins, viral genome and non-structural proteins e.g enzymes

402
Q

How do viruses cause disease

A

Direct destruction of host cells
Modification of host cell
Over reactivity of immune system
Damage through cell proliferation (when viruses burst out of cell)
Evasion of host defences

403
Q

Example of a virus that causes direct destruction of host cells

A

Poliovirus

404
Q

Example of virus that causes modification of the host cell

A

Rotavirus (atrophies villi and flattens epithelial cells)

405
Q

Example of viruses that causes over-reactivity of immune system

A

Hepatitis B
SARS-CoV-2

406
Q

Example of virus that causes damage through cell proliferation

A

Human papillomavirus (causes cervical cancer)

407
Q

why do viruses vary wildly in the range of clinical syndromes they can cause

A

Due to different host cells and tissues that they can infect
Different methods of interaction with the host cell

408
Q

Two types of immunity

A

Active
Passive

409
Q

Two types of active immunity

A

Cell-mediated immunity
Antibody-mediated immunity

410
Q

What are the 5 types of immunoglobulin

A

G,M,A,D and E

411
Q

Is passive immunity temporary

A

Yes

412
Q

What is passive immunity

A

Protection provided from the transfer of antibodies from immune individuals

413
Q

Examples of passive immunity

A

Cross-placental transfer of antibodies from mother to child
Transfusion of blood or blood products including immunoglobulin

414
Q

What are vaccines made from

A

Inactivated (killed) (e.g. pertussis, inactivated polio)
Attenuated live organisms (e.g. yellow fever, MMR, polio, BCG)
Secreted products (e.g. tetanus, diphtheria toxoids)
The constituents of cell walls/subunits (e.g. Hep B) or
Recombinant components (experimental)

415
Q

Function of vaccination

A

Stimulates immune response and memory to a specific antigen/infection

416
Q

What is primary vaccine failure

A

When a person does not develop immunity from the vaccine

417
Q

What is secondary vaccine failure

A

When a person’s immune system initially responds but protection wanes over time

418
Q

5 major groups of protazoa

A

Flagellates
Amoebae
Microsporidia
Sporozoa
Cilliates

419
Q

Example of flagellate protazoa diseases

A

African Trypanosomiasis (AKA sleeping sickness)
American Trypanosomiasis (Chagas disease)
Leishmaniasis
Giardiasis
Trichomonas vaginalis

420
Q

African trypanosomiasis symptoms

A

Chancre
Flu like symptoms
CNS involvement(sleepy, confusion, personality change)
Coma and death

421
Q

How is African trypanosomiasis diagnosed

A

On blood film or CSF

422
Q

Acute symptom of American Trypanosomiasis

A

Flu like symptoms

423
Q

Chronic symptoms of American Trypanosomiasis

A

Cardiomyopathy
Megaoesophagus
Megacolon

424
Q

3 clinical pictures of Leishmaniasis

A

Cutaneous
Mucocutaneous
Visceral

425
Q

What does Cutaneous and mucocutaneous Leishmaniasis cause

A

Ulceration and destruction

426
Q

Symptoms of visceral Leishmaniasis

A

Fever
Weight loss
Massive splenomegaly
Hepatomegaly
Anaemia
High fatality without treatment

427
Q

Symptoms of giardasis

A

Diarrhoea
Cramps
Bloating
Flatulence

428
Q

How is giardasis treated

A

metronidazole

429
Q

Examples of amoebae diseases

A

Amoebiasis

430
Q

Symptoms of amoebiasis

A

Dysentry
Colitis
Liver and lung abcesses

431
Q

How is Amoebiais spread

A

Faeco-oral

432
Q

How is amoebiasis treated

A

Metronidazole

433
Q

Examples of sporozoa diseases

A

Cryptosporidiosis
Toxoplasmosis
Malaria

434
Q

If someone has a fever and has travelled recently what disease are they likely to have

A

Malaria

435
Q

Symptoms of Cryptosporidiosis

A

Diarrhoea (Watery, no blood)
Vomiting
Fever
Weight loss

436
Q

When is Cryptosporidiosis severe

A

In the immunocompromised

437
Q

5 species of anopheles mosquitos that cause malaria

A

Plasmodium falciparum
Plasmodium ovale
Plasmodium vivax
Plasmodium malariae
Plasmodium knowlesi

438
Q

How do you test for malaria

A

Blood film!!

439
Q

Signs of malaria

A

Anaemia
Jaundice
Hepatosplenomegaly
‘Black Water Fever’
Fever symptoms

440
Q

Stages of malaria

A

Mosquito bite
Abdominal pain
Cyclical fever
Hameolysis

441
Q

What does haemolysis cause

A

Anaemia
Jaundice
Haemoglobinuria

442
Q

What does P.Falciparum cause

A

Obstructed microcirculation> complicated malaria

443
Q

Cerebral malaria symptoms

A

Drowsy
Increased intracranial pressure
Seizures
Coma

444
Q

What is complicated malaria

A

When particular organs are seen to be compromised

445
Q

What is acute respiratory distress syndrome

A

A life-threatening condition where the lungs cannot provide the body’s vital organs with enough oxygen

446
Q

Symptoms of complicated malaria

A

Cerebral malaria
ARDS
Renal failure
Bleeding
Shock

447
Q

Malaria treatment

A

IV artesunate
IV quinine + doxycycline

448
Q

Supportive measures for different aspects of complicated malaria

A

Cerebral: antiepileptics
ARDS: oxygen, diuretics, ventilation
Renal failure: fluids, dialysis
Sepsis: broad spectrum antibiotics
Bleeding/Anaemia: blood products
Exchange transfusion if huge parasite burden

449
Q

What is used to treat acute infection

A

Broad spectrum antibiotics
Chloroquine
Primiquine to kill hypnozoites

450
Q

What happens in malaria relapse

A

P. ovale and vivax can form hypnozoites in the liver

451
Q

How to eliminate hypnozoites

A

Primiquine

452
Q

Key attributes of pathogens

A

Infectivity
Virulence
Invasiveness

453
Q

What is infectivity

A

The ability to become established in host, can involve adherence and immune escape

454
Q

What is virulence

A

The ability to cause disease once established

455
Q

What is invasiveness

A

The capacity to penetrate mucosal surfaces to reach normally sterile sites

456
Q

Four stages of pathogenesis

A

Exposure (contact)
Adhesion (colonisation)
Invasion
Infection

457
Q

5 groups of agents that cause infectious disease

A

Viruses
Bacteria
Fungi
Protozoa
Helminths (worms)

458
Q

Do viral infections need rapid cell entry

A

Yes

459
Q

What response do viral infections elicit

A

Humoral (antibody mediated) response
And cell mediated response

460
Q

Viral infection humoral response

A

Antibodies (IgG, A, M) -Block binding, Block virus host cell fusion, are involved in opsonisation

IgM-Agglutinates particles

Complement-Opsonisation, lysis

461
Q

What cells does influenza/RSV virus affect

A

Respiratory epithelium

462
Q

What cells does Varicella Zoster virus affect

A

Skin cells

463
Q

What cells does Yellow Fever virus affect

A

Liver cells

464
Q

What cells does HIV affect

A

T helper cells

465
Q

What is viral evasion

A

The process by whichviruses evadethe immune system and interferes with specific or non-specific defence

466
Q

What is antigenic drift

A

Spontaneous mutations, occur gradually giving minor changes in HA (haemagglutinin) and NA (neuraminidase). Epidemics.

467
Q

What is antigenic shift

A

Sudden emergence of new subtype different to that of preceding virus. Pandemics.

468
Q

How does a bacterial infection enter a host

A

Respiratory tract
Gastrointestinal tract
Genitourinary tract
Skin/mucous membrane break

469
Q

What response does a bacterial infection elicit

A

An antibody response unless intracellular bacteria which causes cell-mediated immunity response

470
Q

Function of ahesins

A

Help bacteria bind to mucosal surfaces

471
Q

Types of adhesins

A

Fimbriae and pili filamentous proteins e.g. Neisseria gonorrhoeae
Non fimbrial proteins e.g. Fibronectin binding protein of Treponema pallidum
Lipid e.g. lipid teichoic acid of Streptococcus pyogenes
Glycosaminoglycans of Chalmydia sp.

472
Q

Complement function in bacterial infection

A

Cell lysis
Prevents proliferation

473
Q

What is delayed type hypersensitivity

A

An immune response that occurs through direct action of sensitized Tcellswhen stimulated by contact with antigen

474
Q

What is an antibiotic

A

A molecule that works by binding to a target site on a bacteria

475
Q

Examples of beta lactams

A

Penicillins
Cephalosporins
Carbapenems
Monobactams

476
Q

What do penicillin drugs end in

A

-illin

477
Q

Function of beta lactam antibiotics

A

Disrupt peptidoglycan production by binding covalently to penicillin binding proteins

Cell wall is disrupted and lysis occurs

478
Q

What type of bacteria is more succeptible to beta lactams

A

Gram positive

479
Q

What causes the difference in activity of beta lactam antibiotics

A

Due to different affinities for different penicillin binding proteins

480
Q

Are penicillins ineffective in the treatment of intracellular pathogens

A

Yes

481
Q

What is the minimum inhibitory concentration

A

The amount of antibiotic needed to inhibit bacterial growth

482
Q

What are the two major determinants of antibacterial effects

A

Concentration and the time the antibiotic remains on the binding sites

483
Q

Antibiotics use in the body

A

Its release from the dosage form;
Its absorption from the site of administration into the bloodstream;
Its distribution to various parts of the body, including the site of action
Its rate of elimination from the body via metabolism (LIVER) or excretion (KIDNEY) of unchanged drug.

484
Q

What enzyme hydrolyses the beta lactam ring of penicillins and cephalosproins

A

Beta lactamase

485
Q

What is MRSA

A

Methicillin resistant Staphylococcus aureus

486
Q

What is MRSA resistant to

A

B-lactam antibiotics
Methicillin=flucloxacillin

487
Q

What are the two main ways antibiotics can be administered

A

Intravenously
Orally

488
Q

What factors are considered when deciding if an antibiotic is safe to prescribe

A

Intolerance, allergy and anaphylaxis
Side effects
Age
Renal and Liver function
Pregnancy and breast feeding
Drug interactions
Risk of Clostridium difficile

489
Q

What is the cell wall also known as

A

Peptidoglycan

490
Q

Why are cephalosporins usually used

A

Good for people with penicillin allergy
Work against some resistant bacteria
Get into different parts of the body e.g. meningitis

491
Q

What is known as a simple cell wall weapon

A

Beta-lactams

492
Q

When are IV Vancomycin and Teicoplanin used

A

For gram positive bacteria resistant to beta-lactams
Or due to a penicillin allergy

493
Q

Examples of gram-positive bacteria resistant to beta lactams

A

MRSA
Enterococci
Some coagulation negative staph

494
Q

5 types of bacteria weapons

A

Inhibitors of cell wall synthesis
Inhibitors of protein synthesis
Inhibitors of nucleic acid synthesis
Anti-metabolites
Inhibitors of membrane function

495
Q

What do Macrolides affect

A

Protein synthesis
Mainly for gram positive bacteria(S. aureus, β haemolytic strep)

496
Q

Examples of Macrolides

A

Clarithromycin
Erythromycin
Both oral and IV

497
Q

What drugs affect bacteria protein synthesis

A

Macrolides
Lincosamides
Tetracyclines

498
Q

Example of Lincosamide

A

Clindamycin (oral & IV)

499
Q

Example of tetracycline

A

Doxycycline(oral)

500
Q

Do gram positive bacteria have a thick or thin cell wall

A

Thick cell wall

501
Q

Do gram negative bacteria have a thick or thin wall

A

Thin cell wall

502
Q

Chickenpox virus name

A

Varicella Zoster virus

503
Q

What is prmary infection of varicella zoster virus called

A

Varicella (chickenpox)

504
Q

What is secondary reactivation of varicella zoster virus called

A

Herpes zoster (shingles)

505
Q

Who is chickenpox serious in

A

Immunocompromised and patients who have had transplants
Adults
Pregnant women
Smokers
Infants

506
Q

Who is shingles most common in

A

The elderly

507
Q

Process of aquiring sihingles

A

Primary infection-widespread chickenpox
Viral dormancy in dorsal root or cerebral ganglion
Localised reactivation-shingles

508
Q

What are the two forms of fungi

A

Yeast-single cell that divide via budding
Moulds- form multicellular hyphae or spores

509
Q

What is the cell wall of fungi made up of

A

Chitin and glucan

510
Q

What do antifungal drugs target

A

Cell wall
Plasma membrane

511
Q

What is the suffix for drugs used generally to treat fungi

A

-azole drugs

512
Q

Two common fungal infections

A

Candida albicans
Aspergillus fumigatus

513
Q

What does Candida albicans cause

A

Vaginal and oral infections
Sepsis(candidiasis)
Line/catheter infections

514
Q

Does candida albicans kill quickly or slowly

A

Rapidly

515
Q

What does Aspergillus fumigatus cause

A

Mainly lung infections
Allergic disease

516
Q

Does aspergillus fumigatus kill quickly or slowly

A

Slowly

517
Q

What type of virus is HIV

A

A retrovirus (RNA virus)

518
Q

How does HIV get its DNA into an infected cell

A

It uses reverse transcriptase to make a DNA copy that becomes integrated into the DNA of the infected cell

519
Q

What does HIV infect

A

CD4+ T cells and macrophages

520
Q

How is HIV transmitted

A

Via bodily fluids

521
Q

What are Highly acting anti-retroviral therapies (HAART) used for

A

HIV infection

522
Q

What are direct acting antivirals (DAA) used for

A

Hepatitis C infection

523
Q

What does HIV being a retrovirus mean

A

It encodes a reverse transcriptase for an extra life cycle step where RNA is transcribed into DNA, a protease and integrase

524
Q

Slow dividing tumours

A

Lung
Colon
Breast

Phase 2A Ikenna (5 decks)

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