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Phase2 > Microbiology and Pathology (before Xmas) > Flashcards

Microbiology and Pathology (before Xmas) Flashcards

1
Q

How do you identify between gram positive and gram negative bacteria?

A

Carry out gram staining and:

Gram positive= purple
Gram negative= pink

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2
Q

What is the significance of the catalase test to gram positive bacteria?

A

positive test = staphylococci
negative test= streptococci

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3
Q

What occurs when a haemolysis test is done to streptococci

A

Beta or alpha
Beta = Clear
Alpha = green

Beta haemolytic strip becomes
Lancfield Group (A(pyogenes), B, C, D, G)

Alpha Haemolytic Strip (complete optochin test)

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4
Q

How do you distinguish Staphylococci bacteria?

A

Coagulase Test

positive= staph. aureus (GOLD on blood agar)
negative= staph. epidermidis

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5
Q

What is Lancefield Grouping?

A

beta haemolytic streptococci differentiation

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6
Q

What organism in lancefield group A is resistant to optochin?

A

strep. pyogenes

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7
Q

How do we differentiate different gram negative bacterias?

A

MacConkey

1) They may be lactose fermenters or
2) Non lactose fermenters

carry out oxidase test also on non-lactose fermenters

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8
Q

Name examples of lactose fermenter gram negative bacteria

A

e. coli
klebsiella

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9
Q

Name some examples of non lactose fermenter gram negative bacteria

A

shigella
salmonella
pseudomonas

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10
Q

Why do gram positive bacteria stain purple

A

Due to a thick layer of peptidoglycan in cell wall

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11
Q

Name the two big groups of gram + bacteria

A

Streptococci
Staphylococci

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12
Q

What is the physical appearance difference between staph and strep

A

strep= chains
staph= clusters

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13
Q

What is inflammation?

A

Local physiological response to tissue injury

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14
Q

Why does inflammation occur?

A

To bring all the cells require for healing to the damaged area

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15
Q

Benefits of inflammation?

A

destruction of invading microbes
infection and injury

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16
Q

Harmful effects of inflammation?

A
  • digestion of normal tissue
  • swelling
  • inappropriate response
  • autoimmunity and over-reaction
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17
Q

ACUTE vs CHRONIC inflammation?

A

sudden vs slow onset

short vs long duration

usually resolves vs may never resolves

hypersensitivity vs autoimmunity

tissue necrosis and infections vs transplant rejection and persistant acute

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18
Q

5 cardinal signs of ACUTE inflammation>

A

1) swelling- oedema
2) redness - dilation of BV’s
3) Heat- hyperaemia (more blood flow)
4) pain- stretch of tissue
5) loss of function

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19
Q

What cells are involved in acute inflammation?

A
  • neutrophils- phagocytosis
  • Macrophages- secrete chemical mediators for chemotaxis
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20
Q

What do chemical mediators do?

A

spread the inflammation response

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21
Q

Where does histamine get released from?

A

mast cells

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22
Q

What is the function of thrombin?

A

increase vessel permeability through platelets

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23
Q

What does histamine and thrombin cause?

A

Neutrophil adhesion to endothelial surface

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24
Q

What are the 3 main stages of Acute Inflammation?

A

1) changes in vessel calibre- (vasodilation so l=blood to the area)

2) Fluid exudate (vasodilation and chemical mediators means permeability increases, this allows proteins to leave= decreased oncotic pressure)

3) Cellular Exudate (accumulation of neutrophils into Extracellular space)

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25
Q

What is Chemotaxis?

A

Attraction of cells to a site through release of chemicals. e.g. neutrophils attracted to mediators released

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26
Q

What are the 3 outcomes of acute inflammation?

A
  • resolution (complete restoration)
  • suppuration (pus formation, granulation tissue and scarring)
  • organisation (tissue replaced with granulation tissue as part of healing process)
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27
Q

What are the 3 primary influences predispose to thrombus formation? (Virchow’s Triad)?

A
  • Stasis of Blood flow (atherosclerosis, aneurysm, AF)
  • Endothelial Injury (MI, atherosclerosis, smoking)
  • Hypercoagulability (genetic and acquired)
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28
Q

What are neutrophil polymorphs?

A
  • short lived cells first on the scene of inflammation
  • cytoplasmic granules with enzymes that kill bacteria
  • release chemicals that attract other cells such as macrophages
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29
Q

What are macrophages

A
  • long lived
  • present antigens to lymphocytes
  • ingest and carry debris
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30
Q

What are lymphocytes?

A
  • long lived
  • produce chemicals to attract other cells
  • can produce memory cells
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31
Q

wHAT ARE ENDOTHELIAL CELLS?

A

Cells that line capillary blood vessels in areas of inflammation
- Sticky= inflammation cells adhere
- Porous= allows inflammatory cells to pass into tissues
- Grow into damaged areas to form new capillary vessels

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32
Q

What are fibroblasts?

A

Long lived cells that form collagen in areas of chronic inflammation

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33
Q

What is the difference between repair and resolution?

A

repair is when tissue is unable to regenerate and is replaced with fibrous tissue. Initiating factor still present

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34
Q

Which cells in the body cant regenerate?

A

Myocardial cells
neurones

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35
Q

What is Thrombosis?

A

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

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36
Q

what is an Embolus?

A

Mass of material in vascular system able to become lodged within a vessel ands block it

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37
Q

What is Ischaemia?

A

Reduction in blood flow

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38
Q

What is infarction?

A

Reduced bllod flow with subsequent death of cells

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39
Q

What is in a Plaque?

A
  • fibrous tissue
  • lipids (cholesterol)
  • lymphocytes
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40
Q

Types of Skin wounds?

A
  • ABRASION
    HEALING BY 1ST INTENSION
  • healing by 2nd intension
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41
Q

What is apoptosis?

A

programmed cell death

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42
Q

What is necrosis?

A

TRAUMATIC CELL DEATH

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43
Q

Definition of acquired?

A

caused by non genetic environmental factors

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44
Q

What is the definition of congenital?

A

present at birth

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45
Q

What is Metaplasia?

A

change in differentiation of a cell. 1 fully differentiated cell changes into another

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46
Q

What is Dysplasia?

A

Morphological changes seen in cells progressing to cancer

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47
Q

Name some evidence of Ageing?

A
  • dermal elastosis
  • osteoporosis
  • cataracts
  • sarcopenia
  • dementia
  • deafness
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48
Q

If there is basal cell carcinoma of the skin, which cells does it invade?

A

only invades locally

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49
Q

How do carcinomas spread?

A

to the lymph nodes that drain the site of carcinoma and can spread from blood to bone

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50
Q

What is Adjuvant Therapy?

A

extra treatment after surgical excision

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51
Q

Which tumours commonly metastasise to the liver?

A

Colon
Stomach
Pancreas
Carcinoid tumour of intestine

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52
Q

which tumours commonly metastasise to bone?

A

Prostate
breast
thyroid
lung
Kidney

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53
Q

What is carcinogenesis?

A

malignant neoplasms

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54
Q

What is oncogenesis?

A

both benign and malignant

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55
Q

What is cancer causing?

A

Carcinogens

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56
Q

What is tumour causing?

A

Oncogens

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57
Q

What is a tumour?

A

abnormal swelling

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58
Q

List examples of chemical carcinogens?

A
  • aromatic amines
  • nitrosamines
  • alkylating agents
  • polycyclic aromatic carbons
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59
Q

Name the classes of carcinogens?

A
  • Viral
  • Ionising/ non radiation
  • hormones
  • parasites
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60
Q

What are host factors?

A

premalignant conditions

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61
Q

What is a neoplasm?

A

a new growth. A lesion that persists after initiating stimulus is removed

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62
Q

What are benign neoplasms?

A
  • non-invasive
  • slow growth
  • low mitotic activity
  • no necrosis/ ulceration
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63
Q

What are malignant neoplasms?

A
  • invasive and rapid growth
  • irregular shape with metastases
  • necrosis and ulceration can be found
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64
Q

How are malignant neoplasms caused?

A

they outgrow their blood supply

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65
Q

Name some types of neoplasm?

A
  • lipoma = adipocytes
  • chondroma = cartilage
  • osteoma = bone
  • angioma = vascular
  • Rhabdomyoma = striated muscle
  • Leiomyoma= smooth muscle
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66
Q

What is a Carcinoma

A

Malignant epithelial neoplasm

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67
Q

What is a sarcoma?

A

Malignant connective tissue neoplasms

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68
Q

What do we call cells of unknown origin?

A

Anaplastic

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69
Q

What is melanoma

A

Malignant neoplasm of melanocytes

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70
Q

What is lymphoma

A

malignant neoplasm off lymphoid cells

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71
Q

Describe the pathology of Metastases?

A

Invasion –erosion of tissue boundaries by enzymes secreted by

  • Intravasion- gain access to metastatic routes e.g. blood/lymph
  • Evasion of host defence
  • Adherence- to endothelium
  • Extravasation- colonisation of new site
  • Angiogenesis- develops its own bloody supply

wow.

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72
Q

What is an adenoma?

A

benign secretory epithelial neoplasm

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73
Q

What is a papilloma?

A

benign non secretory epithelial neoplasm

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74
Q

What are the 3 types of Complement Activation?

A

Classical pathway= Antibody-antigen immune complexes

Alternate pathway= foreign surface antigens

Lectin pathway= mannose binding lectin- mannose residues on pathogen surface

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75
Q

What is the mechanism of action of complement factors?

A

1) Lyse microbes directly (membrane attach complex MAC)

2) Increase chemotaxis (C3a and C5a), and inflammatory response

3) Opsonisation- increase phagocytosis (C3b)

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76
Q

Differences between innate and adaptive immunity.

A

Present at birth vs develops over time
non specific vs specific
no memory vs memory
barriers (skin) vs lymphoid organs (nodes, thymus)
Phagocytes vs Lymphocytes
Natural Killer cells vs
Basophils and eosinophils vs
complement proteins vs antibodies
PAMPS vs Epitopes
Limited receptors vs receptor diversity requires somatic mutation

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77
Q

What is the function of Pattern recognition receptors?

A

Distinguishing foreign bodies by pattern recognition, recognising PAMPs and DAMPs, to then trigger innate response and an inflammatory response

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78
Q

What are PAMPs and DAMPs?

A
  • Pattern associated molecular patterns
  • Damage associated molecular patterns
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79
Q

Name some types of PRR’s?

A
  • Nod like receptors (NLR’s)
  • Toll like receptors (TLR’s- main is TLR4)
  • Secreted and circulating mannose binding lectins and collectins
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80
Q

What happens when the innate response is triggered?

A
  • opsonise pathogen
  • activate complements (mannose binding lectin)
  • activate inflammatory mediators
  • secrete interferons and pro- inflammatory cytokines
  • induce apoptosis of infected cells
81
Q

Signs of chronic inflammation?

A
  • less swelling and exudate
  • inflammation and repair occurring at same time
  • fibrosis (scar formation)
82
Q

Causes of chronic inflammation?

A
  • agent resistant to phagocytes
  • agent indigestible
  • autoimmune disease
  • Crohns/ UC
  • Transplant rejection
83
Q

Cells involved in chronic inflammation?

A
  • B-lymph (differentiate into plasma cells)
  • T-lymph (cell- mediated immunity)
  • Plasma (antibody production)
  • M1 Macrophages (encourage inflammation)
  • M2 Macrophages (decrease inflammation and encourage repair)
84
Q

Fucntion of Macrophages?

A

To eat up debris and display antigen on surface

85
Q

What is a granuloma?

A

Aggregate of Epitheloid Histocytes

86
Q

What do epithelioid Histocytes secrete?

A
  • ACE (which is a blood marker if someone has systematic granulomatosis disease)
87
Q

Function of Lymph Nodes?

A
  • house T cells, B (plasma) and phagocytes
88
Q

What are the two parts of the spleen

A
  • red pulp (old blood cells are destroyed)
  • white pulp= filters blood, antibodies made by B cells, antibody coated bacteria are filtered out
89
Q

function of the thymus

A

involved in the development of T cells and destroys t cells that react to self-antigens

90
Q

What does aspirin do?

A

irreversible COX 1>2 inhibition

91
Q

What does an NSAID do

A

non-selective competitive reversible COX inhibition

92
Q

Overdose management of opiate/ opioid

A

Naloxone

93
Q

overdose management of aspirin

A

Haemodialysis

94
Q

Process of Phagocytosis

A

1) Chemotaxis and adherence of microbe to phagocyte
2) Ingestion of microbe by phagocyte
3) formation of phagosome
4) Fusion of phagosome and lysosome= phagolysosome
5) Digestion of ingested microbe by enzymes
6) Formation of residual body containing indigestible material
7) Discharge of waste material

95
Q

Function of Natural Killer T cells

A

Kill own cells by apoptosis if infected with virus/ become cancerous

96
Q

function of mast cells

A

release: histamine, heparin, chemokines and cytokines

97
Q

function of basophils

A

hypersensitivity reactions and parasitic infections/ release histamine

98
Q

function of eosinophils

A

Raised in allergy and parasitic infections

99
Q

Humoral Adaptive Immunity response control freely circulating pathogens, describe the process

A

1) A B cell binds to its specific antigen
2) B cell differentiates into plasma cell
3) plasma cell proliferates and produce antibodies against the pathogens

100
Q

Cell- mediated Adaptive Immunity controls intracellular pathogens, describe the process

A

1) T cell binds to antigen and this activates its cytokine receptors
2) Helper T cell produces cytokines that cause differentiation into a cytotoxic T cell. These cytokines also influence formation of B cells, macrophages and plasma cells
3) Infected cell is lysed by cytotoxic T cell

101
Q

definition of an antigen

A

a toxin or other foreign substance which induces an immune response in the body

102
Q

Name 3 antigen- presenting cells

A

macrophages, dendritic cells, B cells

103
Q

What are major histocompatibility complexes

A

Proteins that mark a cell as SELF (show antigen)

class 1= all cells
class 2= antigen- presenting cells

104
Q

What do B cells do?

A

proliferate into plasma cells/ memory B cells and recognise soluble antigens in the blood

105
Q

What is a FAB

A

region on antibody that recognises antigen

106
Q

Function of Helper T cells

A
  • stimulate proliferation of other T cells
  • stimulate B cells to produce antibodies
107
Q

WHat is an Epitope?

A

Part of the antigen that binds to an antibodies FAB region

108
Q

How do antibodies protect against infection?

A
  • Neutralisation (specific binding neutralise toxins and form complexes)
  • Opsonisation ( Enhance innate mechanisms; activate classical complement pathway, release of inflammatory mediators by mast cells, enhancing phagocytosis)
109
Q

Immunoglobulin classes and function?

A

IgM- 1st response to antigen, cant cross placenta
IgG- most common, crosses placenta (passive immunity)
IgA- Secreted from mucous membranes
IgD- B cell activation; cant cross placenta
IgE- histamine reactions and allergies

110
Q

What is Pharmacodynamics?

A

How the drug affects the body

111
Q

What is Pharmacokinetics?

A

How the body affects the drug

  • absorption
  • distribution
  • metabolism
  • excretion
112
Q

What is Absorption

A

process of transfer from where the drug was administered to the circulation

113
Q

What is Distribution

A

Drug reversibly leaves blood stream and enters extracellular fluid and tissues

114
Q

What is Metabolism?

A

Transformation of drug molecule into different molecule

115
Q

What is Ecretion?

A

Molecule expelled in liquid, solid or gaseous waste

116
Q

Whats Bioavailability?

A

Fraction of administered drug that reaches the systematic circulation unaltered

117
Q

What is Efficacy?

A

How well a ligand activates a receptor

118
Q

WHat is Potency?

A

The binding affinity

119
Q

What is the difference between parasympathetic receptors and sympathetic receptors on a target organ
?

A

Para= muscarinic
Symp= NAd receptor (alpha or beta)

120
Q

What is a Thrombus?

A

Solid mass of blood constituents

121
Q

What is a Physiological reason for a thrombus?

A

haemostasis/ prevent bleeding
imbalance in blood coagulation system

122
Q

What is a Pathological reason for a Thrombus?

A

imbalance in blood coagulation system

123
Q

Features of Arterial Thrombosis?

A
  • superimposed on atheroma
  • high pressure
  • mainly platelets (white)
  • cause MI/Stroke
124
Q

Features of Venous Thrombosis?

A
  • due to stasis
  • low pressure- mainly coagulation factors&RBC (red)
  • cause DVT/PE
125
Q

Tretament of Thrombosis?

A

Antiplatelet= clopidogrel/ aspirin
Anticoagulants= warfarin, heparin, NOACs

126
Q

Name the process of Atherosclerosis

A

1) Endothelial cells damaged by cholesterol
2) High levels of LDL accumulate on arterial wall
3) Macrophages attract to site- take up lipid to form foam cells
4) formation of fatty streak
5) Cytokines and growth factors released from macrophage
6) Smooth muscle proliferation around lipid core and formation of a fibrous cap

127
Q

What is an EMbolism?

A

Mass of material in vascular system able to get stuck

128
Q

What is Infarction?

A

issue death due to lack of blood supply

129
Q

Name a few inducers and inhibitors of Cytochrome P450

A

inducers: Antiepileptics, smokers, chronic alcohol intake

inhibitors- erythromycin, allopurinol, anti-fungal, SSRI, acute alcohol

130
Q

Name some Enteral routes of Administration

A
  • enteric coated (oral)- intestinal absorption
  • extended release
  • sublingual/ buccal
131
Q

Name some Parenteral routes of administration

A
  • intravenous
  • intramuscular
  • subcutaneous
132
Q

Name mechanisms of Absorption

A
  • diffusion
  • active transport
  • endocytosis
133
Q

Name some variables of Absorption

A
  • pH
  • vascularity
  • surface area
  • contact time
134
Q

how do you work out bioavailability of a drug?

A

AUC oral/ AUC injected x 100 (e.g IV is 100%)

135
Q

NAme some factors of bioavailability

A

first pass hepatic metabolism (liver transforming drug)
solubility
chemical instability (GI breakdown by enzymes)

136
Q

Factors of Distribution

A
  • blood flow
  • capillary permeability
  • plasma binding protein
137
Q

Difference between phase 1 and phase 2 metabolism

A

1= catalysed by cytochrome P450, polarise lipophilic drug (functionalisation by adding chemically reactive group permitting conjugation) (oxidation, reduction, hydrolysis)

2= conjugation by glucuronic acid e.g
to then be excreted by renal/biliary system (add exogenous compound increasing polarity)

138
Q

What is a first order and zero order rate?

A

1st= catalysed by enzymes, rate of metabolism directly proportional to drug conc
zero= enzyme saturated by high drug dose, rate of metabolism is constant

139
Q

How does elimination occur

A
  • excretion by urine, must be sufficiently polar (role of phase 2 and conjugation)
140
Q

What is drug signal transduction?

A
  • binding of drug to EC/IC receptor e.g ligang gated ion channels/ G- protein coupled receptor
  • leads to amplification or down- regulation of signals
141
Q

What does allosteric mean?

A

binds to other site of the cell irreversibly

142
Q

How do opioids work?

A

Inhibitng descending pain signals, all durgs are μ receptor agonists

143
Q

What is naloxone?

A

opioids antagonist used in overdose or respiratory depression

144
Q

side effects of opioids?

A
  • respiratory depression
  • sedation
  • nausea/ vomit
  • constipation
145
Q

effect of Muscarinic receptor M1?

A

mainly brain

146
Q

effect of Muscarinic receptor M2?

A

mainly slowing of the heart

147
Q

effect of Muscarinic receptor M3

A

glandular and smooth muscle

bronchoconstriction

sweating

salivary gland secretion

148
Q

effect of Muscarinic receptor M4 and M5?

A

CNS

149
Q

What is Salbutamol

A

beta 2 adrenoreceptor agonist (SABA)

150
Q

what is the effect when NAd binds to an alpha 1 receptor?

A
  • vasoconstriction
  • mydriasis (pupil dilate)
  • contraction of bladder neck (urinary retention)
  • increased peripheral resistance
151
Q

what is the effect when NAd binds to an alpha 2 receptor?

A
  • inhibits release of NAd and ACh
  • reduces insulin produced from the pancreas
152
Q

what is the effect when NAd binds to a beta 1 receptor?

A
  • positive chronotropic effect on the heart
  • increased renin from the kidney (increased BP)
  • increased lipolysis
153
Q

what is the effect when NAd binds to a beta 2 receptor?

A
  • bronchodilation
  • vasodilation
  • decreased GI motility
  • decreased peripheral resistance
154
Q

what is the effect when NAd binds to a beta 3 receptor?

A
  • increased lipolysis
  • relaxation of the bladder
155
Q

beta blocker side effects?

A
  • wheeze
    -tired
  • bradycardia
  • hypoglycaemia
156
Q

what is a COX enzyme?

A

an enzyme that allows production of thromboxane and prostaglandins

157
Q

how does aspirin work?

A

aspirin inhibits COX1 and COX2 enzymes which stops the production of thromboxane’s and prostaglandins

158
Q

What do thromboxane’s do?

A

cause vasoconstriction and platelet aggregation therefore aspirin stops this occurring

159
Q

what can prostaglandins do?

A

cause inflammation/ anaphylactic reaction and pain! therefore aspirin stops this occurring?

160
Q

which enzyme catalyses thromboxane production?

A

COX1

161
Q

which enzyme catalyses prostaglandin production?

A

COX2

162
Q

Describe the breakdown of paracetamol in the body

A

Paracetamol is converted into a reactive intermediate by CYP450

it then becomes a cellular macromolecule or stable metabolite

It then undergoes cellular necrosis if it become a cellular macromolecule

163
Q

What is bradykinin?

A

a potent vasodilator

164
Q

Alpha 1 agonists?

A

decongestants (phenylephrine)

165
Q

alpha 1 antagonists?

A

Tamsulosin

166
Q

beta 1 agonists?

A

Inotropes (epinephrine and dopamine)

167
Q

BETA 1 ANTAGONISTS?

A

selective/ non selective beta blockers

168
Q

beta 2 agonists?

A

SABA/LABA

169
Q

beta 2 antagonists?

A

non selective beta blockers

170
Q

histamine antagonist?

A

cetirizine
loratidine

171
Q

What are the factors of dose- response relationship?

A
  • drug conc (dose of drug + pharmacokinetic profile)
  • receptor availability (maximal effect once receptors and saturated irrelevant of increased dose)
172
Q

parasympathetic pathway?

A

acetylcholine – nicotinic receptor – acetylcholine – muscarinic receptor

173
Q

sympathetic pathway?

A

acetylcholine – nicotinic receptor – norepinephrine – adrenergic receptor

174
Q

What are type 1 hypersensitivity reactions related to

A

Allergies (anaphylaxis and asthma)
(IgE, mast cells, histamine)

175
Q

What are type 2 hypersensitivity reactions related to

A

Cytotoxic cells, antibody dependant

Ab binds to Ag on target cell and kills it via complement

176
Q

What are type 3 hypersensitivity reactions related to

A

Immune complex disease

Circulating Ab binds to Ag to form a complex. Circulating complex deposited in tissue = inflammation e.g reactive arthritis

177
Q

What are type 4 hypersensitivity reactions related to

A

Delayed type hypersensitivity

Ag presenting cell presents Ag to T cell, T cell activated to Th1, forms memory Th1 cell. When Ag presented again, memory Th1 cell activates macrophages- inflammation

178
Q

Definition of Allergy?

A

Abnormal response to harmless foreign material

179
Q

Definition of Atopy?

A

tendency to develop allergies

180
Q

What is Anaphylaxis?

A

Acute allergic reaction to an antigen to which the body has become hypersensitive.

181
Q

Pathogenesis of Allergies?

A

IgE binds to FceRI on mast cell and basophil
(IgE has high affinity for FceRI 1:1),
this causes degranulation of the cells which releases histamine= bronchoconstriction and arteriolar dilation

182
Q

What is FceRI found on?

A
  • mast cells (tissues)
  • Eosinophils and Basophils (circulating)

Involved in host defence against parasites

183
Q

What are mast cells derived from and where are they found

A

myeloid stem cells and found in tissues

184
Q

Effects of Histamine

A

bronchoconstriction and arteriolar dilation

185
Q

Effects of LT

A

capillary contraction- increasing vascular permeability

186
Q

Effects of PGD2

A

Smooth muscle contraction

187
Q

Effects of Platelet Aggregation Factor (PAF)

A

Increasing vascular permeability and platelet aggregation

188
Q

Describe what happens in anaphylaxis in terms of the CVS, Resp, Skin and GI systems

A

Mast cell/ Basophil activation - IgE activation- histamine elevation

CVS= vasodilation, increased vascular permeability and increased BP
Resp= Bronchial smooth muscle contraction, mucous
Skin= Rash/swelling
GI= pain/ vomiting

189
Q

Treatment of Allergies?

A

1) Avoid allergens
2) Desensitisation to allergens- increase dose of Ag
3) Prevent IgE production- block Th2 cytokines (Lumiluximab)
4) Bind to and inactivate receptor of IgE (omalizumab)
5) Prevent mast cell activation- mast cell membrane stabiliser (prednisolone)
6) Inhibit mast cell products- PT/LT antagonist

190
Q

Describe the Optochin test

A

Differentiate between Alpha haemolytic streps

resistant= s.viridans    (positive) sensitive= s.pneumoniae
191
Q

What bacteria is it if there is a positive oxidase test (gram negative non lactose fermenter)

A

Positive oxidase test= pseudomonas oxidase

192
Q

What antibiotic is given to treat MRSA

A

vancomycin

193
Q

Causes of Chronic Inflammation?

A

Persistent acute
develops from acute

Primary Chronic Inflammation

194
Q

Sarcoidosis blood marker?

A

ACE

195
Q

Final differentiation between bacteria?

A

Serotyping (API strip)

196
Q

Name the leukocytes?

A

Neutrophils, basophils, eosinophils

197
Q

Efficacy and Affinity are receptor related, what do agonists and antagonists show?

A

Agonists = both
Antagonists = just affinity

198
Q

What is Tolerance and Desensitisation?

A

Tolerance - reduction in drug effect over time (continuously repeated high conc)

Desensitisation - receptors become degraded / uncoupled

Phase2 (19 decks)

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