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2A > Pathology, Immunology & Pharmacology > Flashcards

Pathology, Immunology & Pharmacology Flashcards

1
Q

what causes thrombus formation?

A

endothelial tissue damage - cells lift and expose collagen and platelets bind and aggregate
fibrin is formed and can entrap red blood cells

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2
Q

what is the definition of thrombosis?

A

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

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3
Q

what promotes thrombosis?

A

change in vessels wall
change in blood flow
change in blood constituents

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4
Q

why does smoking promotes thrombosis?

A

smoke/nicotine damage endothelial cells

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5
Q

what is laminar flow?

A

cells travel in the centre of arterial vessels and don’t touch the sides

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6
Q

what does asparin do?

A

inhibit platelet aggregation - can prevent thrombosis

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7
Q

what is an embolus?

A

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

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8
Q

what causes embolus?

A

thrombus most commonly
also air, cholesterol crystals, tumour, amniotic fluid, fat

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9
Q

what is ischemia?

A

reduction in blood flow

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10
Q

what is infarction?

A

reduction in blood flow with subsequent death of cells

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11
Q

what is the difference between resolution/repair of tissue

A

resolution - initiating factor removed. Tissue undamaged or able to regenerate
repair - –initiating factor still present. Tissue damaged and unable to regenerate

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12
Q

what cells regenerate?

A
  • hepatocytes
  • pneumocytes
  • all blood cells
  • gut epithelium
  • skin epithelium
  • osteocytes
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13
Q

what cells don’t regenerate?

A

*myocardial cells
* neurones

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14
Q

what happens during tissue repair?

A

replacement of damaged tissue by fibrous tissue
collagen produced by fibroblasts

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15
Q

how is inflammation classified?

A

acute/chronic

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16
Q

What cells are involved in inflammation?

A

*Neutrophil polymorphs
* Macrophages
* Lymphocytes
* Endothelial cells
* Fibroblasts

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17
Q

what is special about neutrophil polymorphs?

A
  • polylobed nucleus
  • contain lysosomes
  • phagocytose
  • first in acute inflammation, phagocytosed by macrophages
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18
Q

what is special about macrophages in inflammation?

A
  • Phagocytic properties
  • carry materials away to lymph nodes and lymphocytes
  • different names in different areas, eg kupffer cells, osteoclasts, microglia
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19
Q

what are fibroblasts?

A

Produce collagenous connective tissue in scarring following
some types of inflammation

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20
Q

what cells are present in acute/chronic inflammation?

A

acute - neurophils & macrophages
chronic - macrophage & lymphocytes, then usually fibroblasts

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21
Q

what is an example of acute inflammation?

A

appedicitis
frostbite
burns
infection
allergy

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22
Q

what are some examples of chronic inflammation

A

fibromyalgia
lupus
autoimmune disease
rheumatoid arthritis

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23
Q

what are granulomas?

A

type of chronic inflammation with collections
of macrophages/histiocytes surrounded by lymphocytes
- may be due to myobacterial infection eg TB
- also seen in Crohn’s disease, sarcoidosis and around foreign material

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24
Q

what are the vascular and exudative components of inflammation?

A

dilation of vessels
vascular leakage of protein rich fluid

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25
Q

what are the outcomes of inflammation?

A

resolution
suppuration - pus formation
organisation
progression to chronic inflammation

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26
Q

what is atherosclerosis?

A

accumulation of fibrolipid plaques in systemic arteries, reducing blood flow

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27
Q

what are modifiable/non-modifiable risk factors for atherosclerosis?

A

Smoker
Lack of exercise
Weight
(Borderline) Diabetes (type 2)
HTN
High cholesterol

Age
Gender
Race
Family History
Diabetes (Type 1)

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28
Q

what explains the pathogenesis of atherosclerosis?

A

endothelial damage theory
- LDL/cholesterol can enter endothelial wall when damaged causing plaque build up
- macrophages take up LDL - causing foam cells - releases more LDL when they die

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29
Q

how can diabetes lead to atherosclerosis?

A

High glucose levels = Increased Free radicals = Increased oxidation of LDLs
- Loss of nitric oxide (NO) - normally allows relaxation of vessel +
increased flow - Promotes platelet aggregation

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30
Q

what are the 3 major stages of plaque formation?

A

1) the fatty streak, which represents the initiation
2) plaque progression, which represents adaption
3) plaque disruption, which represents the clinical complication of atherosclerosis

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31
Q

what are the 5 key stages of atherogenesis?

A

1) endothelial dysfunction
2) formation of lipid layer or fatty streak within the intima
3) migration of leukocytes and smooth muscle cells into the vessel wall
4) foam cell formation
5) degradation of extracellular matrix

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32
Q

what is the difference between apoptosis vs necrosis?

A

apoptosis - programmed cell death
necrosis - cell death by damage/ external factors

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33
Q

why can hypertension lead to atherosclerosis?

A

Increased pressure causes increased damage of the endothelial cell wall

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34
Q

what are some complications of atherosclerosis?

A

blocked arteries
- can lead to infarction and embolism

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35
Q

what are some primary/secondary preventative measures for atherosclerosis?

A

primary
● Exercise more
● Eat more healthily -Less salt + sat fats, Less sugar- diabetes risk
● Stop smoking
secondary
● Statin
● Antihypertensives
● DM control: carbs, meds
● Social prescribing - Weight loss groups, Gym vouchers

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36
Q

what is the difference between apoptosis vs necrosis?

A

apoptosis - programmed cell death
necrosis - cell death by damage/ external factors

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37
Q

what protein detects DNA damage?

A

p53

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38
Q

why is apoptosis important?

A
  • development
  • cell turnover eg. intestinal villi
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39
Q

name 2 diseases where apoptosis is abnormal

A

cancer - cells in tumours don’t apoptose - mutated p53
HIV - virus induces apoptosis in CD4 helper cells

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40
Q

what is hypertrophy?

A

increased size of tissue due to increased size of cells

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41
Q

what is hyperplasia?

A

increassed size of tissue due to increased number of cells

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42
Q

where does hypertophy/hyperplasia occur?

A

hypertrophy - in organs where cells cannot divide eg. skeletal muscles
hyperplasia - in organs where cells can divide eg. benign prostatic hyperplasia, endometrial hyperplasia

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43
Q

where/when does mixed hypertrophy and hyperplasia occur?

A

smooth muscle cells of uterus during pregnancy

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44
Q

what is atrophy?

A

decrease in size of tissue due to decreased number of cells or their size

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45
Q

what is metaplasia?

A

change in differentiation of a cell

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46
Q

give an example where metaplasia occurs?

A

bronchial epithelium
- from ciliated columnar epithelium to squamous epithelium due to smoking

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47
Q

what is dysplasia?

A

abnormal organization of cells within a specific tissue
- can lead to cancer

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48
Q

why is there a limit on how many times cells can divide?

A

telomeres get shorter each time until they’re too short for a cell to divide - hayflicks limit

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49
Q

what are some effects of ageing on the body?

A
  • dermal elastosis
  • osteoporosis
  • cataracts
  • dementia
  • sarcopaenia - loss of muscle mass
  • deafness
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50
Q

Do basal cell carcinoma of skin spread?

A

No! only invades locally

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51
Q

what is the definiton of carciogenesis

A

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

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52
Q

what cancers most commonly spread to bone?

A

breast, prostate, lung, thyroid and kidney

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53
Q

what is oncogenesis?

A

formation of benign/malignant tumours

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54
Q

what are the classes of carcinogens?

A

chemical
viral
radiation
Hormones, parasites and mycotoxins
Miscellaneous

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55
Q

what are some examples of chemical carcinogens and what can they cause?

A

polycyclic aromatic hydrocarbons -smoking/minerals -lung/skin cancer
aromatic amines - rubber/dye - bladder cancer
nitrosamines - animals - gut cancer
alkylating agents - leukaemia

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56
Q

what are some examples of DNA virus carcinogens?

A

HHV8 - kaposi sarcoma
EBV (Epstein Barr) - lyphoma, nasopharyngeal
HBV - hepatocellular carcinoma
HPV - squamous cell carcinomas
MCV - merkle cell carcinoma

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57
Q

what are some exaples of RNA virus carcinogens?

A

HTLV-1 - t-cell leukemia
HCV - hepatocellular

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58
Q

what do anabolic steroids increase the risk of?

A

hepatocellular carcinoma

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59
Q

what is a myotoxin that causes hepatocellular carcinoma?

A

Aflatoxin B1

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60
Q

what parasites are carcinogenic

A

Chlonorchis sinensis → cholangiocarcinoma
Shistosoma → bladder cancer

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61
Q

what are some examples of miscellaneous carcinogens?

A

asbestos
metals

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62
Q

what is micro-invasive carcinoma?

A

cancer has only invaded partially past basement membrane

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63
Q

what is the difference between innate and adaptive immunity?

A

innate - non-specific, doesn’t require lymphocytes
adaptive - acquired/learned, requires lymphocytes

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64
Q

what are Polymorphonuclear
leukocytes?

A

neurophils, eosiphils, basophils

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65
Q

what are Mononuclear
leukocytes?

A

monocytes (macrophages), t-cells, b-cells

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66
Q

what other cells (apart from white blood cells) make up immune system?

A

mast cells, natural killer cells, dendritic cells, kupffer cells, langerhans cells

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67
Q

what are complement soluble factors?

A

group of 20 proteins made by liver that need to be activated.
Action - lysis, attract leukocytes, coat invading organisms

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68
Q

what are the 5 classes of antibodies?

A

igG(1-4), igA(1&2), igM, igD, igE

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69
Q

what is the most predominant Ig in human serum?

A

IgG

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70
Q

what is IgM responsible for?

A

primary immune response

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71
Q

where is IgA found?

A

mucous secretions

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72
Q

where is IgD found?

A

mature B cells

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73
Q

where is IgE found?

A

basophils and mast cells - allergic response

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74
Q

what specific region on antigen bind to antibodies?

A

epitope

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75
Q

what are some examples of cytokines?

A

interferons - limit viral infections
interleukins - IL1-pro-inflam, IL10-anti-inflam
colony stimulating factors
tumour necrosis factors - TNFalpha

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76
Q

what are chemokines?

A

direct movement of leukocytes - different for different cells

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77
Q

what is inflammation?

A

A series of reactions that brings cells and molecules of the immune system to sites of infection or damage

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78
Q

what are the hallmarks of inflammation?

A

increased blood supply
increased vascular permeability
Increased leukocyte transendothelial migration ‘extravasation

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79
Q

what are Pattern Recognition Receptors?

A

located on cells, recognise bacteria/pathogens

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80
Q

what are Pathogen-Associated Molecular Patterns?

A

found on microbes

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81
Q

how are complement serum factors activated?

A

Ab binds to microbe
alternative pathway - C’ binds to microbes
lectin pathway - mannose binding lectin bound to microbe

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82
Q

what does C3b do?

A

activated complement factor 3
- marks cells for phagocytosis
- amplifies complement response

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83
Q

what do C3a and C5a do?

A

chemotaxs - attract macrophages

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84
Q

what is E-selectin?

A

endothelial cell surface molecule makes endothelium ‘sticky’ - binds to CD15 on neutrophils

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85
Q

what are the 2 pathways to kill pathogens?

A

O2 dependent - ROIs (reactive oxygen intermediates)
O2 independant - enzymes, proteins, pH

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86
Q

what does cell-mediated immunity require?

A

MHCs - major histocompatibility complexs
intrinsic antigens
extrinsic antigens

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87
Q

what is T cell selection?

A

T cells that recognise self are killed in foetal thymus

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88
Q

what is the difference between MHC1 and MHC2?

A

MHC1 - on all cells - present foreign protein antigen to cytotoxic t cells (CD8+)
MHC2 - on APC - present foreign protein antigens to helper t cells (CD4+)

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89
Q

what do Th1 and Th2 cells produce?

A

1 - IFN-gamma helps kill intracellular pathogens
2 - antibodies

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90
Q

what do CD8 T cells do?

A

Kill Intracellular pathogens directly

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91
Q

what activates CD4 Th1 cells?

A

high levels of IL-12

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92
Q

how do T cells help B cells?

A

Th2 cells bind to B cells presenting Ag.
Th2 cell then secrete cytokines
causing B cell clonal expansion - plasma cells (secrete Ab) and B memory cells

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93
Q

where do activated B cells go for clonal expansion?

A

lymph nodes

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94
Q

what do Th1 and Th2 activate

A

macrophages
b cells

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95
Q

what are DAMPs?

A

Damage associated molecular patterns - molecules created to alert the host to tissue injury and initiate repair.

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96
Q

give some examples of Secreted and circulating PRRs (pattern recognision receptors?

A

pentraxins - proteins like CRP (c reactive protein)
lectins and collectins - eg. Surfactant proteins A and D - bind to oligosaccharide structure or lipids that are on the surface of microorganisms

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97
Q

what are TLRs (toll-like repectors)?

A

cell-associated PRRs

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98
Q

what do TLRs do?

A

bind to ligand and activate a tailored signalling cascade in response to pathogen

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99
Q

what are mannose receptors?

A

PRRs on macrophages

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100
Q

what is dectrin-1?

A

PRRs on various phagocytes/myeloids

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101
Q

what are RIG-I-like Receptors (RLRs)?

A

detect viral RNA in cytoplasm

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102
Q

what are NOD-like Receptors (NLRs)?

A

detect cytoplasmic bacteria
22 NLRs in humans

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103
Q

what are NOD1&2 activated by?

A

specific motifs (mostly muropeptides) present in bacterial peptidoglycan
1 - sense meso-DAp mainly in gram -ve
2 - sense MDP (Muramyl dipeptide in both gram-ve/+ve)

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104
Q

what is the definition of allergy?

A

type 1 hypersensitivity via IgE

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105
Q

what does der p 1 (found in dust mites) cause when affecting protease activity?

A

type1 hypersensitivity reaction using IgE

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106
Q

what are the 4 pharmacokinetic processes?

A

absorption
distribution
metabolism
excretion

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107
Q

what are the 3 ways drugs permeate membranes?

A

Passive diffusion through hydrophobic membrane - most common
Passive diffusion aqueous pores
Carrier mediated transport

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108
Q

what are the 2 factors affecting drug absorption?

A

lipid solubility
drug ionisation
- ionised drugs have poor lipid solubility - poorly absorbed

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109
Q

where are weak acid and weak bases best absorbed?

A

acids - stomach
bases - intestine

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110
Q

what factors affect oral drug absorption in stomach?

A

Gastric enzymes - drug molecule may be digested (peptides, proteins)
Eg. insulin and biologicals
Low pH - molecule may be degraded (benzylpenicillin)
Food (full stomach will generally slow absorption)
Gastric motility (altered by drugs and disease state)
Previous surgery (eg gastrectomy)

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111
Q

what factors affect oral drug absorption in intestine?

A

drug structure - size, solubility
medicine formulation - capsule/tablet effects rate of release
P-glycoprotein - substrates moved back into lumen

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112
Q

what is first pass metabolism?

A

metabolism of drugs preventing them reaching systemic circulation

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113
Q

what is bioavailability (F) in drugs?

A

Proportion of administered drug which reaches the systemic circulation

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114
Q

what is bioavailability not affected by?

A

rate of absorption

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115
Q

what is bioavailability dependent on?

A

extent of drug absorption from GI tract and extent of first pass metabolism

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116
Q

what are transdermal drugs only suitable for?

A

lipid soluble drugs

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117
Q

what affects a drugs ability to distribute around body?

A

molecule size
lipid solubility
protein binding

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118
Q

what is volume distribution (Vd)

A

Theoretical volume a drug will be distributed in the body
Volume of plasma required to contain the total administered dose

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119
Q

what does a high and low Vd show?

A

high Vd - drug’s well distributed ( small & lipophyllic)
low Vd - poorly distributed

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120
Q

what are 3 ways for drugs to reach CNS and cross BBB?

A

high lipid solubility
Intrathecal administration
inflammation - cases BBB to be leaky

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121
Q

how does Vd change as you get older?

A

smaller Vd of water soluble drugs - higher plasma conc

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122
Q

what is phase 1 in drug metabolism?

A

Oxidation/reduction/hydrolysis to introduce reactive group to chemical structure

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123
Q

what is phase 2 drug metabolism

A

Conjugation of endogenous functional group (glycine, sulfate, glucuronic acid) to produce hydrophilic, inert molecule.
Hydrophyllic metabolite can then be renally excreted.

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124
Q

what enzyme is responsible for most phase 1 metabolism?

A

Cytochrome P450

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125
Q

what is paracetamol toxicity treated with?

A

IV N-acetylcisteine (NAC)

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126
Q

how are drug molecules transported out in kidneys?

A

glomerular filtration
carrier system - organic anion/cation transporters
passive reabsorption

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127
Q

what is first order kinetics?

A

Rate of elimination is proportional to the plasma drug concentration
- most drugs
A constant % of the plasma drug is eliminated over a unit of time

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128
Q

what is zero order kinetics

A

Rate of elimination is NOT proportional to the plasma drug concentration
A constant amount of the plasma drug is eliminated over a unit of time

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129
Q

what is half-life dependant on?

A

clearance of drug
volume of distribution - A drug with large Vd will be cleared more slowly than a drug with a small Vd

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130
Q

what is IV bioavailability?

A

100%

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131
Q

why is a short half life significant?

A
  • requires more frequent dosing
  • increases risk of withdrawal
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132
Q

how does reduced clearance affect half life and what does it mean?

A

increases half life
time to Css increases
reduced dosing required

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133
Q

what are Drugs with a narrow therapeutic window?

A

Drugs with a narrow window between MEC (Minimum effective concentration) and MSC (maximum safe concentration)

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134
Q

is conventional chemotherapy better used in fast dividing or slow dividing tumours?

A

fast dividing

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135
Q

what is different about growth factor A receptors in cancer?

A
  • more receptors
  • receptors constantly activated
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136
Q

how can monoclonal antibodies effect growth factor A?

A

bind to recepters so less activation

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137
Q

what gene is amplified in 20-30% of breast cancers?

A

HER-2

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138
Q

what is PD1?

A

programmed cell death protein 1
- involved in immune response

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139
Q

what is a tumour?

A

any abnormal swelling
- can be neoplasm, inflammation, hypertrophy, hyperplasia

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140
Q

what are neoplasms?

A

a lesion resulting from autonomous abnormal growth of cells which persists after taking away initial stimulus

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141
Q

what is the structure of neoplasms?

A

neoplastic cells surrounded by a stroma that supports growth

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142
Q

what does central necrosis signify in a tumour?

A

that the tumour is growing faster and larger than the blood supply

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143
Q

is neoplasia benign or malignant?

A

both

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144
Q

what is angiogenesis?

A

forming new blood vessels

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145
Q

what are characteristics of benign neoplasms?

A
  • localised, slow growth rate
  • low mitotic activity
  • non-invasive
  • resembles normal tissue
  • circumscribed or encapsulated
  • growth on mucosal tissue is exophytic
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146
Q

how can benign neoplasms cause damage?

A
  • pressure on tissue
  • obstruct flow
  • produce hormones autonomosly
  • transform to malignant neoplasm
  • cause anxiety for patient
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147
Q

what are the features of malignant neoplasms?

A
  • invasive (defining feature)
  • metastases - spread
  • rapid growth rate
  • poorly defined/irregular border
    -hyperchromatic, pleomorphic nuclei
  • growth is endophytic
  • necrosis and ulceration is more common
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148
Q

what affects do malignat neoplasms have on the body?

A
  • destruction of tissue
  • metastases
  • blood loss from ulcers
  • obstruct flow - by narrowing lumen
  • paraneoplastic effects
  • produce hormones
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149
Q

what is the behavioural classification of neoplasms?

A

benign or malignant

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150
Q

what is the histogenetic classification of neoplasms?

A

the specific cell of origin of neoplasm

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151
Q

what cell types can neoplasms originate from?

A

epithelial cells
connective tissue
lymphoid/haematopoietic

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152
Q

what suffix is used for neoplasm

A

‘oma’

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153
Q

what is a papilloma?

A

benign neoplasm of non-glandular non-secretory epithelium

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154
Q

what is an adenoma?

A

benign neoplasm of glandular/secretory epithelium

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155
Q

what is a benign cartilage neoplasm called?

A

chondroma

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156
Q

what are benign skeletal muscle neoplasms called?

A

rhabdomyoma

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157
Q

what are benign smooth muscle neoplasms called?

A

leiomyoma (more common than skeletal)

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158
Q

what are nerve benign neoplasms called?

A

neuroma

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159
Q

what is sarcoma?

A

malignant connective tissue neoplasm

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160
Q

what are anaplastic neoplasms?

A

neoplasms where the cell of origin can’t be identified

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161
Q

what is carcinoma?

A

malignant epithelial cells neoplasm

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162
Q

what are the exeptions to neoplasms that don’t contain carcinoma/sarcoma in name but are malignant?

A
  • melanoma
  • mesothelioma
  • lymphoma
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163
Q

what is the difference between TSAs and TAAs?

A

tumour specific - only on tumours
tumour associated - on both normal and tumour cells but overexpressed in cancer

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164
Q

what is tumour escape?

A

when the immune responses change tumours so they’re no longer seen

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165
Q

what is tumour evasion?

A

tumours change the immune response by promoting immune suppressor cells

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166
Q

Give examples of active immunotherapy in cancer

A

killed tumour vaccine
purified tumour antigens
APC based vaccines
DNA vaccines
cytokine vaccines

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167
Q

Give examples of passive immunotherapy in cancer

A

adaptive cellular therapy - T cells
anti-tumour antibodies - HER-2

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168
Q

what is cell-based therapy?

A

they activate patients immune system to attack cancer

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169
Q

what cells are used in therapy for cancer?

A

dendritic cells - APC
T cells - killer cells
natural killer cells, stem cells, tumour cells

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170
Q

why does tumour hypoxia decrease patient prognosis?

A
  • stimulates new vessel growth
  • suppresses immune system
  • resistant to radio/chemotherapy - increases tumour hypoxia
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171
Q

what is passive immunisation?

A

administration of pre-formed immunity

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172
Q

what are the adv/disadv of passive immunisation?

A

+ve immediate protection
-ve short-lived, possible transfer of pathogens

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173
Q

give examples of passive immunisations against diseases

A

human tetanus
human rabies specific Ig
human hep B Ig
varicella zoster

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174
Q

what are 3 whole-microbe approach of vaccines?

A
  • inactivated vaccine
  • live-attenuated vaccine
  • viral vector
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175
Q

what are disadvantages of whole killed vaccines?

A

can cause excessive reactions
need more than 2 shots usually

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176
Q

what are live attenuated vaccines?

A

The organisms replicate within the host and induce an immune response which is protective against the wild-type organism but does not cause disease

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177
Q

what are advantages of live-attenuated vaccines?

A

immune response more closely mimics real infection
lower does required and fewer
can be oral administration

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178
Q

what are disadvantages of live-attenuated vaccines?

A

in immunocompromised hosts vaccine may not be so attenuated
- Often impossible to balance attenuation and immunogenicity
- Reversion to virulence
- Transmissibility

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179
Q

what proteins do most drugs target?

A

receptors
enzymes
transporters
ion channels

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180
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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181
Q

give 4 examples of receptors

A

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

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182
Q

how are g protein coupled receptors regulated?

A

By factors that control abilitty to bind/hydrolyse GTP to GDP

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183
Q

what catalyse the exchange of GDP to GTP

A

GPCRs

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184
Q

what are kinase enzymes responsible for?

A

catalyze the transfer of phosphate groups between proteins - phosphorylation

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185
Q

how do nuclear receptors work?

A

modify gene transcription
ie by zinc fingers

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186
Q

give an example of a nuclear receptor

A

steroid hormone receptors
- tamoxifen - SERN

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187
Q

give an examle where there is increase/decrease of receptors

A

Mastocytosis (Mast cells); increased c-kit receptor
myasthenia gravis; loss of ACh receptors

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188
Q

what is an agonist?

A

a compound that binds to a receptor and activates it

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189
Q

what is an antagonist?

A

a compound that reduces the effect of an agonist

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190
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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191
Q

what is the EC50 of a drug?

A

the concentration that gives half the maximal response

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192
Q

what is the intrinsic activity of a drug?

A

the ability of a drug-receptor complex to produce a maximum functional response

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193
Q

how do antagonists effect receptors?

A

they don’t activate them
- they only reverse agonists

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194
Q

what are non-competitive antagonist?

A

Binds to an allosteric (non-agonist) site on the receptor to prevent activation of the receptor

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195
Q

what are the two categories of cholinergic receptors?

A

nicotinic (n) and muscarinic(m)

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196
Q

what are the antagonists to nicotinic (n) and muscarinic(m) receptors?

A

atropine
curare - muscle relaxant

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197
Q

what factors affect drug action

A

Receptor-related
affinity
efficacy

Tissue-related
receptor number
signal amplification

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198
Q

what is affinity?

A

Describes how well a ligand binds to the receptor

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199
Q

what is efficacy?

A

Describes how well a ligand activates the receptor

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200
Q

what is the efficacy of antagonists?

A

zero

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201
Q

what is a irreversible antagonist?

A

binds to a receptor so that the receptor becomes inactive

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202
Q

what is reverse agonism?

A

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

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203
Q

what is drug tolerance?

A

slow onset
reduction in agonist effect over time
due to continuous, high-dose use

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204
Q

what is drug desensitisation?

A
  • induces tolerance to drug
    rapid onset, uncoupled, internalized, degraded
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205
Q

what are statins also know as?

A

HMG-CoA reductase inhibitors

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206
Q

how do statins work?

A

Block the rate limiting step in the Cholesterol pathway

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207
Q

give an example of a peripheral DDC inhibitor ( that make dopamine)

A

carbidopa

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208
Q

what does the Peripheral COMT Inhibitor do?

A

prevents breakdown of L-DOPA to 3-methyl dopa
(in periphery)
- treat parkinsons

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209
Q

what do central COMT inhibitors do?

A

Function within the CNS to keep Dopamine levels up

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210
Q

what do Mono Amine Oxidase B (MAO-B) Inhibitors do?

A

Prevents Dopamine breakdown and increases availability

treat depression

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211
Q

what do Central Dopamine Receptor Agonists do?

A

Antagonise dopamine receptors (not enzyme inhibitors) in CNS

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212
Q

what are the 3 main types of protein ports?

A

uniports
symporters
antiporters

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213
Q

what are uniporters?

A

use energy from ATP to pull molecules in

214
Q

what are symporters?

A

use the movement in of one molecule to pull in another molecule against a concentration gradient

215
Q

what are antiporters?

A

one substance moves against its gradient, using energy from the second substance (mostly Na+, K+ or H+) moving down its gradient

216
Q

give examples of some ion channels

A

Epithelial (Sodium) – heart failure
Voltage-gated (Calcium, Sodium) – nerve, arrhythmia
Metabolic (Potassium) – diabetes
Receptor Activated (Chloride) - epilepsy

217
Q

what are ENaC epithelial sodium channel blocked by?

A

high affinity diuretic amiloride (often used with Thaizide).

218
Q

what does thaizide target?

A

Na+Cl− cotransporter
-reabsorbs Na and Cl from tubular fluid

219
Q

what does amlodipine do?

A

angioselective
- blocks Ca channel & inhibits contraction eg. of heart and smooth muscle
- lowers BP

220
Q

what drug blocks the transmission of an AP in voltage gated sodium channels?

A

lidocaine

221
Q

how do Repaglinide, nateglinide and sulfonylureal lower blood glucose levels?

A

blocking K+ channels to stimulate insulin secretion

222
Q

what do GABA A receptors do?

A

open Cl- channels - induce hyperpolarisation

223
Q

what does Sodium Pump (Na/K ATP-ase) do?

A

pumps 3 Na out, 2 K in
requires ATP

224
Q

what inhibits the Na+/K+ ATPase pump?

A

digoxin

225
Q

when is digoxin used

A

to decrease HR
- lengthens cardiac AP
- increases intracellular Na and so Ca

226
Q

what is the proton pump of the stomach?

A

The gastric hydrogen potassium ATPase or
H+/K+ ATPase

227
Q

what does the Proton Pump (K/H ATP-ase) in Stomach do?

A

exchanges potassium from the intestinal
lumen with cytoplasmic hydronium
- acidification

228
Q

what is the current legislation for control drugs?

A

misuse of drugs act 1971

229
Q

what is the difference between tolerance and dependance?

A

tolerance - down regulation of receptors - need a higher dose
dependance -psychological, craving

230
Q

what are the side effects of opiods

A

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

231
Q

what is codeine metabolised by, to?

A

CYP2D6, to morphine

232
Q

what population has decreased activity of CYP2D6?

A

10-15% of caucasian population

233
Q

what is morphine metabolised to and how does it compare?

A

morphine 6 glucuronide
- more potent than morphine but cleared quickly

234
Q

when should morphine be prescribed with caution?

A

in renal failure
- may cause respiratory depression

235
Q

what can be used instead of morphine if a patient has <30 renal function?

A

oxycodone

236
Q

what does tramadol inhibit?

A

serotonin reuptake and noradrenaline
reuptake

237
Q

what is tramadol metabolised to, to be active?

A

o-desmethyl tramadol

238
Q

what is oral bioavailability for oral morphine?

A

50%

239
Q

what is an antagonist for opioids?

A

naloxone

240
Q

what is alpha-1 receptor in sympathetic nervous system responsible for?

A

vasconstriction

241
Q

what is alpha-2 receptor in sympathetic nervous system responsible for?

A

negative feedback - suppresses noradrenaline release

242
Q

what is beta-1 receptor in sympathetic nervous system responsible for?

A

increases HR and contractibility

243
Q

what is beta-2 receptor in sympathetic nervous system responsible for?

A

bronchodilation

244
Q

what do beta blockers do?

A

block effect of sympathetic nervous system on the heart
- decrease HR and contractibility and workload

245
Q

what do alpha 2 agonists do?

A

reduce amount of noradrenaline released
- They work as antihypertensives, sedatives and analgesics

246
Q

what is the most commonly used alpha 2 agonist?

A

clonidine

247
Q

how does adrenaline work?

A

stimulates all sympathetic receptors
- short duration

248
Q

what are antagonists for both sympathetic alpha receptors?

A

phenoxybenzamine
phentolamine

249
Q

what are antagonists for both sympathetic beta receptors?

A

propranolol
carvedilol

250
Q

what are antagonists for sympathetic alpha-1 receptors?

A

prazosin
doxazosin

251
Q

what are antagonists for sympathetic beta-1 receptors?

A

metoprolol
atenolol

252
Q

what are agonists for both sympathetic alpha receptors?

A

adrenaline (noradrenaline precuser)

253
Q

what are agonists for sympathetic alpha-1 receptors?

A

phenylephrine
metaraminol

254
Q

what are agonists for sympathetic alpha-2 receptors?

A

clonidine
dexmedetomidine

255
Q

what are agonists for sympathetic beta-1 receptors?

A

dobutamine

256
Q

what are agonists for sympathetic beta-2 receptors?

A

salbutamol

257
Q

as prescribers, in terms of drug interactions we need to…

A
  • Avoid co-prescribing drugs with clinically significant interactions
  • Appropriately monitor patients taking interacting drugs
  • Recognise drug interactions and take appropriate action
258
Q

what is pharmacodynamic drug interaction?

A

Occur when drugs have an effect on the same target or physiological system

259
Q

what is pharmacokinetic drug interaction?

A

Occur when a drug affects the pharmacokinetics (absorption, distribution, metabolism or excretion) of another drug

260
Q

what are the 2 types of pharmacodynamic interactions?

A

synergistic or antagonistic

261
Q

how may Pharmacokinetic drug interactions affect absorption?

A

Drugs which alter pH of GI tract (ionised/unionised drugs)
Formation of insoluble drug complexes
P-glycoprotein induction/inhibition (P-gp transport toxic substances out)

262
Q

give an example of a drug that upregulates P-gp?

A

carbamazepine

263
Q

how do Pharmacokinetic drug interactions affect distribution?

A

when drugs compete for albumin binding in plasma
- eg warfarin has high protein binding - need to monitor INR

264
Q

how do Pharmacokinetic drug interactions affect metabolism?

A

drugs can work as cytochrome enzyme inducers (increase metabolism of enzyme substrate) or inhibitors (decrease metabolism of enzyme substrate and can cause toxicity)

265
Q

how do Pharmacokinetic drug interactions affect elimination?

A

drug Competition for renal tubular secretion
by OAT or OCT

266
Q

what foods interact with drugs?

A

grapefruit - CYP3A4 inhibitor
Milk - affects absorption due to insoluble complex formed with Ca
Vitamin k - apposes warfarin
cranberry juice - CYP2C9 inhibitor

267
Q

what is the definition of an adverse drug reaction?

A

A response to a medicinal product, or combination of medicinal products, which is noxious and unintended

268
Q

how are ADRs classified?

A

a - augmented
b - bizarre
c - chronic
d- delayed
e- end of use/withdrawal
f - failure of treatment
g -genetic

269
Q

what are augmented ADRs?

A
  • most common
  • Exaggerated effect of drugs pharmacology at a therapeutic dose
    Dose dependent and reversible upon withdrawing the drug
270
Q

what are chronic/continuing ADRs?

A

continue after the drug has been stopped

271
Q

what are delayed ADRs?

A

ADRs that become apparent some time after stopping the drug

272
Q

what is another way ADRs can be classified?

A

D - dose-related
T - timing
S - susceptibility

273
Q

what are dose-related ADRs?

A

Hypersusceptibility - subtheraputic doses eg anaphylaxis with penicillin
Collateral effects (side effects)
Toxic effects

274
Q

what is meant by susceptibility in ADRs?

A

Certain patient groups/populations may have a specific susceptibility to ADRs from a drug

275
Q

how are ADRs identified?

A

pre-clinical - eg. animal testing
clinical trial data
post marketing surveillance
pharmacovigilance

276
Q

what are muscarinic receptors M2?

A

cardiac

277
Q

what are muscarinic receptors for exocrine glands and smooth muscles?

A

M3

278
Q

what are muscarinic receptors M4 and M5?

A

CNS

279
Q

what are muscarinic receptors M1?

A

CNS and higher cognative

280
Q

what are nicotinic signs of acetylcholinesterase inhibitor toxicity?

A

Monday = Mydriasis
Tuesday = Tachycardia
Wednesday = Weakness
Thursday = Hypertension
Friday = Fasciculations.

281
Q

what are the muscarinic effects of organophosphate poisoning?

A

D = Defecation/diaphoresis
U = Urination
M = Miosis
B = Bronchospasm/bronchorrhea
E = Emesis
L = Lacrimation
S = Salivation

282
Q

what are the physiological manifestations of atropine overdose

A

“hot as a hare, blind as a bat, dry as a bone, red as a beet, and mad as a hatter”

283
Q

what does atropine block and when is it used?

A

blocks parasympathetic action
- eg in life threatening bradycardia

284
Q

what are nicotinic repectors in parasympathetic system for?

A

vasodilation

285
Q

what are antagonists and agonists for nicotinic receptors?

A

antagonist - trimethaphan (rarely used)
agnostic - nicotine & Ach
neostigmine and organophosphates - Ach Esterase inhibitors

286
Q

what are pilocarpine agonists for?

A

M1, M2, M3

287
Q

what are some antagonists for muscarinic receptors?

A

atropine - (crosses BBB) treat poisoning by muscarinic agents eg organophosphates
glycopyrrolate - inhibit salivary gland and respiratory secretions eg peptic ulcers
hyoscine - treats stomach spasms
ipratopium - for bronchospasms

288
Q

how does botox work?

A

has an irreversible effect on exocytosis of ACh in the pre-synaptic neurone

289
Q

what are the opioid receptors?

A

Mu
delta
kappa
nociceptin (NOP)

290
Q

what receptors do the opioid agonists morphine and fentanyl act on?

A

mu-opioid receptors

291
Q

what can kappa agonists cause?

A

respiratory depression

292
Q

what do allergic reactions to drugs require to happen?

A

subsequent re-exposure

293
Q

what is drug allergy often mistaken for?

A

Drug intolerance
- have to ask patient about symptoms

294
Q

what is immediate vs delayed hypersensitivity?

A

immediate <1hr
delayed >1hr

295
Q

what Ig mediates anaphylactic reactions?

A

IgE
re-exposure causes mast cell degranulation and histamine release

296
Q

what 2 reactions come under the term anaphylaxis?

A

anaphylactic reactions - categorized as IgE-mediated responses
anaphylactoid reactions - categorized as IgE-independent events

297
Q

what causes type 2 hypersensitivity in drugs?

A
  • drug/metabolite combines with protein - treated as foreign body, IgG and IgM form
298
Q

what are type 3 reactions?

A

Antigen and antibody form large complexes and activate complement factors

299
Q

what are type 4 reaction?

A

lymphocyte mediated
- Antigen specific receptors develop on T-lymphocytes

300
Q

what is Non immune anaphylaxis?

A

Anaphylactoid reactions
- Due to direct mast cell degranulation
- caused by some drugs

301
Q

what is the definition of anaphylaxis?

A

a severe, life-threatening, generalised or systemic hypersensitivity reaction which is likely when both of the following criteria are met:
 Sudden onset and rapid progression of symptoms.
 Life-threatening airway and/or breathing and/or circulation problems usually associated with skin and
mucosal changes

302
Q

what blood test can used to clarify an anaphylaxis diagnosis?

A

Serum mast-cell tryptase- (peak at one hour after an anaphylacticreaction, remaining elevated for approximately six hours)
- elevated levels show massive mast-cell degranulation or a condition called mastocytosis
- not in every case - sensitivity/specificity is 95%.

303
Q

what are the signs/symptoms of anaphylaxis?

A
  • Occurs within minutes and lasts 1-2 hours
  • Vasodilation
  • Increased vascular permeability
  • Bronchoconstriction
  • Urticaria (hives)
  • Angio-oedema (rapid, oedema, or swelling, of the area beneath the skin or mucosa)
304
Q

how is anaphylaxis managed?

A

basic life support - ABCDE (disability and exposure)
adrenaline IM 500mg
high flow O2
IV fluids
antihistamines - skin symptoms

305
Q

what are risk factors for hypersensitivity?

A

medication
females more common
EBC, HIV infected patients
uncontrolled asthma
genetic factors - eg. certain HLA groups

306
Q

what is Refractory anaphylaxis?

A

when there is no improvement in cardiovascular or respiratory symptoms after 2 doses

307
Q

what is a commensal?

A

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

308
Q

what is a opportunistic pathogen?

A

Microbe that only causes disease if host defences are compromised

309
Q

what is virulence/pathogenicity?

A

The degree to which a given organism is pathogenic

310
Q

what is asymptomatic carriage?

A

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

311
Q

what is the differnece between coccus and bacillus bacteria?

A

coccus - spherical
bacillus - rod

312
Q

what are the main features of a bacteria cell?

A

cell wall, cell membrane, inner membrane
Chromosome of circular double stranded DNA
pili
capsule - around bacteria

313
Q

what bacteria has lipopolysaccharide and what is it made up of?

A

gram -ve (component of outer membrane)
made of: terminal sugar, o antigen, lipid A

314
Q

what bacteria contains lipoteichoic acid?

A

gram +ve

315
Q

what is the difference between endotoxins and exotoxins from bacteria?

A

endotoxins - Component of the outer membrane of bacteria - LPS in gram -ve, non-specific, stable, weak
exotoxins - Secreted proteins in gram +ve and -ve, strong, specific

316
Q

how is variation created in bacterial genetics?

A

mutations:
- base substitution
- deletion
- insertion
Gene transfer

317
Q

what are the significant genes in a plasmid?

A

transfer promotion genes
Plasmid maintenance genes
Antibiotic or virulence determinant genes

318
Q

how are genes transferred in bacteria?

A

transformation - via plasmid
transduction - via phage
conjugation - via sex pilus

319
Q

what are some examples of obligate intracellular bacteria?

A

chlamydia
coxiella
rickettsia

320
Q

what are bacteria with no cell wall called?

A

mollicutes
- eg mycoplasma pneuomoniae

321
Q

what bacteria with a cell wall grow as filaments?

A

actinomyces
nocardia
streptomyces

322
Q

what bacteria are spirochaetes?

A

leptospira
treponema
borrelia

323
Q

what group of bacteria do staphylococcus and streptococcus belong to?

A

aerobic gram +ve

324
Q

give an example of anerobic gram +ve bacteria (coccus)

A

PEPTOSTREP-TOCOCCUS

325
Q

how is streptococcus bacteria further classified?

A

BETA-HAEMOLYTIC then lancfield grouping
ALPHA-HAEMOLYTIC then optochin test (sensitive vs resistant)
NON-HAEMOLYTIC

326
Q

what bacteria is ZIEHL-NEELSEN
STAIN POSITIVE?

A

mycobacteria
eg M.tuberculosis
M.leprae

327
Q

give some examples of aerobic and anerobic gram +ve rod bacteria

A

anaerobic
- clostridium
- propionibacterium
anerobic
- corynebacterium
- listeria
- bacillus

328
Q

give some examples of gram -ve bacteria

A

anaerobic
- bacteroides
aerobic
- coliforms - salmonella, shigella, citrobacter
- vibro - campylobacter, helicobacter

329
Q

what is coagulase +ve staphylococci bacteria?

A

enzymes produced that clot blood plasma - fibrin clot may protect from phagocytosis
- S.aureus

330
Q

what is the diffeerence between streptococcus and staphylococcus?

A

strep - chain coccus
staph - clusters coccus

331
Q

how is streptococcus bacteria sub-divided?

A

haemolysis - beta/alpha
beta - antigenic group - A, B, C, G
alpha - optochin test - sensitive = S.pneumoniae. Resistant = viridans strep

332
Q

what are staphylococcus aureus virulence factors?

A

pore-forming toxins - a - haemolysin & Panton-Valentine Leucocidin
proteases - exfoliatin
toxic shock syndrome toxin
protein A - binds to Ig in wrong orientation

333
Q

what group does staphylococcus aureus bacteria belong to?

A

spherical gram +ve

334
Q

what diseases does Staphylococcus aureus
cause?

A

wound infections/abscesses
impetigo
septcaemia
osteomyelitis
pneumonia
endocarditis

335
Q

what are 2 examples of Coagulase-negative Staphylococci and what do they cause?

A

S.epidermidis (forms persistant biofilms) - causes infectious endocarditis
S.saprophyticus ( has haemagglutinin for adhesion andurease)
- causes UTIs

336
Q

what are the surface carbohydrate antigens (lancefield grouping) on beta haemolytic streptococcal cells?

A

A-H and K-V
most important…
A (C and G) - s.pyogenes
B - S.agalactiae (neonatal infections)
D - UTIs - enterococci

337
Q

what is the difference in alpha vs beta haemolysis in bacteria?

A

alpha - hydrogen peroxide produced -reacts with haemoglobin - makes green met-haemoglobin (damage of RBCs)
beta - production of two pore-forming toxins – streptolysin O and S. (clear, lysis of RBCs)
gamma - no-lysis

338
Q

give an example of alpha and beta haemolytic bacteria (gram +ve)

A

alpha - s.intermedius
beta - s.pyogenes

339
Q

what are the virulence factors of S.pyogenes?

A

hyaluronidase - spreading
streptokinase - breaks clots
C5a peptidase - reduces chemotaxis
toxins - streptolysins O&S (binds cholesterol) and SPeA (exaggerates response)
hyaluronic capsule layer - non-antigenic
M protein - antiphagocytic protein

340
Q

what infections are caused by S.pyogenes?

A

most commonly tonsillitis and pharyngitis
- also, scarlet fever, impentigo, wound infections

341
Q

what are the virulence factors of S.pneumoniae?

A

capsule - antiphagocytic
Inflammatory wall constituents - teichoic acid (choline) & peptidoglycan
cytotoxin - pneumolysin - pore-forming

342
Q

what is viridan factors streptococci?

A
  • eg S.sanguinis and S.oralis - cause infective endocarditis. Milleri - cause abscesses in deep organs
343
Q

what are some examples of gram +ve bacilli?

A

C.tetani
C.botulinum
C.difficle

344
Q

how do gram +ve and gram -ve bacteria stain?

A

+ve - purple, stain binds to peptidoglycan
-ve - pink

345
Q

why do gram -ve have penicilin resistance

A

thin peptidoglycan - covered by outer membrane

346
Q

what is important in gram -ve bacteria

A

LPS - lipid A released when broken down - toxic - can cause sepsis

347
Q

what shapes do gram -ve bacteria have?

A

rods
cocci
spriochaetes

348
Q

what are coliforms bacteria?

A
  • rod shaped gram -ve bacteria
  • have flagella - very motile
  • facultatively anaerobic
  • colonise intestinal tract (can be good or bad)
349
Q

how are enterobacteriaceae (coliform) differentiated?

A

appearance on MacConkey plate - CLED or XLD - lactose fermentation (acid produced- yellow turns red)
do - Escherichia coli and Klebsiella sp.
don’t - salmonella and shigella
followed by oxidative test

350
Q

what does salmonella reduce that turns black?

A

thiosulphate

351
Q

what are serovars?

A

specific coding for identifying specific bacteria

352
Q

what infections are caused by e.coli?

A

UTIs
wound infections
gastroenteritis
meningitis(infants)

353
Q

what does shigellosis most commonly cause?

A

severe bloody diarrhoea

354
Q

what are features of shigella pathogenesis?

A

entry through M cells in gut
acid-tolerant - low infective dose
self-limiting
shiga toxin inhibits protein synthesis - haemolytic uraemic syndrome - kidney failure

355
Q

what are the 2 salmonella species?

A

s.enterica - common
s.bongori - rare

356
Q

what are the 3 forms of salmonellosis?

A

gastroenteritis/entercolitis - localised
enteric fever - where poor sanitation/water quality
bacteraemia

357
Q

what is the pathogenesis of enteric fever?

A

spread through macrophages and released into blood

358
Q

what is the pathogenesis of salmonella gastroenteritis?

A

interleukin-8 released - causes neutrophil recruitment - tissue injury - fluid and electrolyte loss

359
Q

what is distinctive about Klebsiella pneumoniae?

A

thick capsule
- environmental, opportunistic

360
Q

what is Pseudomonas aeruginosa bacteria?

A

gram -ve rods shaped
- environmental - many antibiotic resistance
- motile

361
Q

what kind of people does P. aeruginosa infect, causing most problems?

A

CF patients, mucoid version secretes thick coating

362
Q

what group does vibrio cholera bacteria belong to?

A

gram -ve rods, facultative anaerobic

363
Q

what is the pathogenesis of cholera?

A

sits on intestinal wall, secretes cholera toxin causing pathogenesis
- can be treated with ORT

364
Q

what bacteria is the most common cause of food poising and what does it look like?

A

campylobacter
- spiral rods, unipolar/bipolar flagella

365
Q

what does helicobacter pylori cause?

A

gastritis, peptic ulcer disease

366
Q

what are the features of haemophilus influenzae?

A

nasopharyngeal carriage
opportunistic infection (smokers & children)
causes: meningitis, brochpneumonia,
non-motile
fastidious - requires factor X and factor Y

367
Q

what are th virulence determinants of H.influenzae?

A

capsule - penetrates nasopharyngeal epithelium, resistance to phagocytosis and complement system
Hi b strain main cause of meningitis
LPS- inflammation, complement resistance

368
Q

what are the features and virulence factors of bordetella pertussis?

A

short rods (coccobacilli)
pertussis - whooping cough
highly contagious - aerosol transmission
toxins: pertussis toxin, CyaA - hypersynthesis of Camp - supresses macrophage phagocytosis

369
Q

where can legionella pneumophila replicate?

A

alveolar macrophages

370
Q

what is the main feature of bacteroides (gram -ve rods) and name one example

A

anaerobes
(non-motile)
b.fragilis

371
Q

what are common gram negative rod bacteria?

A

bacteroids - anaerobic
vibro.cholerae
camplyobacter
helicobacter
haemophilus
bordetella
coliforms - salmonella, e.coli, klebsiella, shigella
pseudomonas

372
Q

what are gram negative cocci bacteria?

A

anaerobic - veillonella
aerobic - neisseria

373
Q

what are the 2 most common species of neiseria?

A

n.meningitidis (meningococcus
n.gonorrhoeae (gonococcus, non-capsulated)

374
Q

what are the 3 common groups of spirochaetes bacteria?

A

leptospira - due to infected rats proximal to water source
treponema (t.pallidum) - syphilis
borrelia (b.burgdorferi - lyme disease - bulls-eye rash, flu-like

375
Q

what are features of spirochaetes?

A

long, slender, helical, highly flexible
most are free-living, non-pathogenic

376
Q

what are the features of the 3 stages of syphilis?

A

primary - localised genital infection. highly transmissible
secondary - systemic. skin rash, swollen lymph, aches/pains, fever (1-3 months post infection)
tertiary - granulomas in bone and soft tissue, cariovascular syphilis, neurosyphilis (several years post infection)
all stages can be treated with antibiotics

377
Q

what are the 3 most common subgroups of obligate intracellular bacteria?

A

chlamydia
rickettsia
coxiella

378
Q

what are the 2 growth cycles of chlamydia?

A

elementary bodies - infectious, enter cell through endocytosis, prevent phagosome-lysosome fusion
reticulate bodies - fragile, replicative, nutrients from host cell

379
Q

what are the 3 important species of chlamydia?

A

c. trachomatis…
- trachoma biovar serotype A-C- eye to eye transmission
- genital tract biovar serotype D-K - STD, infects mucous membrane of urethra (can ascend), conjuctivitis - hand-to-eye transmission
- lympho granuloma venereum LGV biovar serotype L1-L3 - STD, endepic to tropics
c.pneumoniae
c.psittaci - zoonotic infection

380
Q

what group of bacteria does TB belong to?

A

mycobacteria

381
Q

what shape are mycobacteria?

A

beaded bacillia

382
Q

why is Ziehl-Neelsen stain used to stain mycobacteria?

A

High lipid content with mycolic acids in cell wall makes Mycobacteria resistant to Gram stain

383
Q

what are the microbiology features of mycobacteria?

A

weakly gram +ve or colourless
thick lipid cell wall
aerobic, non motile, non-spore forming
slow growth
Mycolic acids
Lipoarabinomannan

384
Q

what are the 3 stages of TB?

A

primary Tb - initial contact - taken in by lymphatics to hilar lymph
latent TB - T cells detected but no disease
pulmonary TB - granulomas form, less blood supply - forms primary complex - necrosis

385
Q

what can TB cause after spreading?

A

genito unrinary TB
bone/joints TB
meningitis TB
miliary TB
plearal TB

386
Q

what cells protect against mycobacteria eg TB?

A

macrophages - phagocytsosis & phagolysosomes
CD4 T-cells - generate interferon gamma

387
Q

when do granulomas (from mycobacteria) become unstable?

A

due to CD4 depletion - eg HIV patients
due to TNF-alpha depletion

388
Q

what cells synthesise INF-y and TNF-a, and what does it do?

A

macrophages
type 1 helper T lymphocytes
- stabalise granuloma

389
Q

why do granulomas form?

A

mycobacteria at centre, when in dormant stage, surrounded by cells

390
Q

why is nucleic acid detection advantageous when testing for bacteria?

A

rapid results to detect mycobacteria
detects rifampicin resistance

391
Q

what is the standaard therapy for TB?

A

isoniazid (INH), rifampicin (RIF), pyrazinamide (PZA) and ethambutol (ETH) x 2 months followed by isoniazid and rifampicin for further 4 months

392
Q

what does Mtb (mycobacterium tuberculosis) produce that interacts with drugs?

A

beta-lactamase

393
Q

what TB is resistant to most commonly used drugs?

A

XDR-TB

394
Q

how is XDR-TB treated?

A

BPaL regimen:
Bedaquiline
Pretomanid
Linezolid
All oral treatments for 6 months
- can fail too in total drug resistance

395
Q

what is a virus?

A

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

396
Q

what are the different structures/shapes of viruses

A

enveloped/non-enveloped
shape - helical, icosahedral, complex

397
Q

what do viruses exist as when not in a cell?

A

virions
- genetic material
- protein coat

398
Q

how do viruses replicate?

A
  • attach to a specific receptor on a cell (they then infect that cell)
  • cell entry - only nucleic acid and proteins enter
  • host cell interaction and replication - migration of genome to cell nucleus, transcription to mRNA using host cell materials
  • assembly of viron (happens in different location of cells)
  • release of new virus - bursts out and cell death or by exocytosis
399
Q

what do HIV drugs traget?

A

NRTIs and NNRTIs (neuclotide Reverse-transcriptase inhibitors) that are involved in transcription of the viral RNA to viral DNA

400
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 - eg HPV
  • Evasion of host defences
401
Q

how does rotavirus cause disease?

A

modifies host cell - atrophies villi and flattens epithelial cells
- also resistant to acidic pH

402
Q

how do viruses evade the immune system?

A

cellular level
- by celll-cell spread
- latency
molecular level
- antigenic variability
- prevention of host cell apoptosis - so virus continues to replicate
- Downregulation of interferon and other intracellular host defence proteins
- Interference with host cell antigen processing pathways

403
Q

what are the causes of meningitis?

A

bacteria eg meningococcus, pneumococcus
viruses eg mumps, herpes
funig, protozoa (rarely)
non-infectious causes:
- medications eg antibiotics
- cancers eg melanoma
- autoimmune disease eg lupus

404
Q

what bacteria causes meningococcal disease?

A

gram -ve diplococci

405
Q

what are the 2 main manifestations of meningococcal disease?

A

Meningitis: a localised infection of the meninges
Septicaemia : a systemic infection with widespread signs, and generalised organ damage

406
Q

what 6 serogroups are responsible for most of the cases of meningitis?

A

A
B
C
W
X
Y

407
Q

what is the tansmission of meningitis?

A

aerosol, direct contact with secretions of URT
frequent/prolonged contact

408
Q

what are some risk factors of meningitis?

A

sickle cell disease
cranial anatomical defects
cochlear implants
overcrowed household
travellers to high risk areas
cancer - eg leukaemia
immunocompromised

409
Q

what are Meningococcal meningitis symptoms?

A

fever
stiff neck
headache
confusion
increased sensitivity to light
naesea/vomiting
babies - poor feeding, slow/inactive, irritable, bulging anterior fontanelle

410
Q

what are Meningococcal septicaemia symptoms?

A

fever/chills
fatigue
vomiting
cold hands/feet
severe aches in muscles/joints
rapid breathing
diarrhoea
pinpoint/non blanching rash - petechiae - later stages is dark purple rash purpura

411
Q

what is important about the onset of meningitis?

A

acute onset, sudden and escalates quickly - can be fatal

412
Q

what specimens should be taken when infected with meningitis?

A

blood sample for culture
CSF for culture and PCR
throat swabs for culture
swabbing family members etc.

413
Q

who do you need to notify if treating meningitis?

A

regional UKHSA health protection team of
Meningitis (any cause)
Meningococcal septicaemia
and notify public health on suspicion
- legal responsibility

414
Q

what is given to carriers/close contact of meningitis and what does it do?

A

chemoprophylaxis or rifampicin - single dose to eradicate throat carriage - not infection (need antibiotics if infected)

415
Q

how long is chemoprophylaxis offered for to housecold contacts of meningitis?

A

4 weeks

416
Q

what diseases are not notifiable?

A

STDs

417
Q

what do notifiable diseases have in common?

A
  • very infectious
  • most have vaccines
  • very unpleasant symptoms/death
  • some have specific control measures - eg food poisoning needs investigation of source
418
Q

what do anifungals target?

A

cell wall - B1, glucan and B1,6 glucan and chitin
cell membrane - ergosterol
DNA/RNA synthesis

419
Q

what targets fungi cell membrane?

A

Polyenes e.g. amphotericin
Azoles
Allylamines e.g. terbinafine

420
Q

what targets fungi cell wall

A

Echinocandins

421
Q

what targets fungi DNA/RNA synthesis/protein synthesis?

A

Flucytosine
Griseofulvin

422
Q

what do dermatophytes cause?

A

many nail/skin fungal diseases

423
Q

what are the 3 main species of dermatophytes?

A

Trichophyton
Microsporum
Epidermophyton

424
Q

what fungal disease is common and can cause significant morbidity?

A

Mucosal candidiasis

425
Q

what is the difference between yeasts and moulds?

A

yeasts - single celled, divide by budding
moulds - multicellular hyphae and spores
(some fungi exist as both - diamorphic fungi)

426
Q

what are Coccidioides fungi?

A

diamorphic fungi that grow in warmer temperatures
- commonly asymtopatic, later manifestations include Cavitatory lung disease

427
Q

what causes Invasive candidiasis (fungi)?

A

most commonly due to infection of prosthetic devices or intra-abdominal disease

428
Q

what can cryptococcus (yeast) cause in people with reduced cell mediated immunity?

A

acute/chronic meningitis

429
Q

what diamorphic fungi can cause meningitis?

A

Histoplasma, Coccidioides, Blastomyces

430
Q

what biomarkers are used to identify fungi?

A

Beta-D-glucan galactomannan
- both not very specific
CrAg LFT - cryptococcal LFT

431
Q

what does Invasive aspergillosis fungi cause?

A

respiratory failure

432
Q

what are Mucoraceous moulds?

A

start in sinuses and spread to brain etc.
eg. Rhinocerebral mucormycosis
- need aggressive antifungal therapy

433
Q

what is Pneumocystis jirovecii?

A

causes pneumonitis with severe hypoxia in the immunocompromised
BDG test +ve

434
Q

what are the 5 groups of protazoa?

A

flagellates
sporozoa
amoebae
cilliates
microsporida

435
Q

what is African Trypanosomiasis and American Trypanosomiasi?

A

sleeping disease
chagas disease - flu like
protozoa, flagellate

436
Q

what is Trichomonas vaginalis?

A

STD
protazoa, flagellate

437
Q

what is Amoebiasis?

A

protazoa - amoeba
Faeco-oral spread
causes: Dysentry, Colitis, Liver and lung abscesses

438
Q

what test is done to diagnose malaria?

A

blood film, thick and thin
thin - shows parasite count and species

439
Q

what is the most signficant symptom of maleria?

A

fever
also, chills, headache diarrhoea etc.

440
Q

what can maleria cause if left untreated?

A

Anaemia
Jaundice
Hepatosplenomegaly

441
Q

what is P. falciparum?

A

complecated maleria due to vascular occulsion
- cerebral maleria
- ARDS
- renal failure
- sepsis
- bleeding/anaemia

442
Q

what is used to treat malaria?

A

IV artesunate
chloroquine

443
Q

what species of maleria cause hypnoizites in the liver and cause relapse of maleria?

A

P. ovale and vivax

primiquine used as treatment - have to check G6PD levels

444
Q

what does aciclovir treat?

A

herpes simplex virus type 1 & 2 and VZV infection

445
Q

how does aciclovir work?

A

Pro-drug, activated to a monophosphate by the viral thymidine kinase only in herpesvirus infected cells
- then added second and third phosphate group
- triphosphate inhibits DNA polymerase

446
Q

where does chickenpox lie dormant to later cause shingles?

A

dorsal root or
cerebral ganglion

447
Q

what is Shingles: Herpes Zoster spectrum red flags?

A

Multiple dermatomes
Haemorrhagic change
Occular involvement
Peripheral/unusual dermatomes affected

448
Q

what does IV acyclovir treat?

A

herpes
shingles
eczema herpeticum

449
Q

what is ganciclovir treat and hoe does it work?

A

CMV infection
- inhibits most herpesvirus, and DNA polymerase

Valganciclovir: L-Valyl ester of ganciclovir

450
Q

what drug is secendaryly used for herpes/CMV

A

foscarnet

451
Q

what is ribvirin used for?

A

hep E
(not hep C as in past)

452
Q

what are symptoms of measels?

A

high fever
morbilliform rash
koplik spots
coryza
cough
diarrhoea
cojuctivitis

453
Q

how are antibiotic classified?

A

by the binding site on bacterium

454
Q

what group of antibiotics inhibit cell wall synthesis?

A

beta lactams - eg penicillins, cephalosporins, carbapenems and monobactams
glycopeptides - eg vancomycin and teicoplanin

455
Q

how do beta lactams work?

A

disrupt peptidoglycan production & cause lysis - must diffuse cell wall first
- gram +ve are more susceptible
- gram -ve have lipopolysaccharide layer - harder to penetrate

456
Q

why is penicillins ineffective in the treatment of intracellular pathogens.?

A

poorly penetrate mammalian cells

457
Q

what antibiotics affect nucleic acid synthesis?

A

DNA gyrase - quinolones
RNA polymerase - rifampin

458
Q

what do antibiotics target when affecting protein synthesis?

A

50s subunits
30s subunits

459
Q

what antibiotic affect folate synthesis?

A

Sulphonamides - Sulphamethoxazole
Trimethoprim - Co-trimoxazole

460
Q

what antibiotics affect cell membrane of bacteria?

A

polymyxins

461
Q

what is the difference between bactericidal antibiotics and Bacteriostatic Antibiotics?

A

kill bacteria
prevent bacteria growth - reduced toxin production

462
Q

what are the 2 major determinants of anti bacterial effects of an antibitic?

A

Concentration & time of antibiotic at binding site on bacteria

463
Q

what antibiotic no longer works on MRSA?

A

flucloxacillin - unable to bind to PBP of staphylococci

464
Q

how are penicillins and cephalosproins inactivated by bacteria?

A

beta lactam ring hyrolysed by beta lactamase - unable to bind to PBP

465
Q

when can Vancomycin and Teicoplanin be used?

A

gram +ve bacteria resistant to beta-lactams eg. mrsa
penicillin allergy

466
Q

what are aminoglycosides antibiotics?

A

eg. gentamicin
- affects protein synthesis
- used against gram -ve and staphs
- for UTIs and infective endocarditis

467
Q

what does CRE stand for in terms of bacteria?

A

Carbapenem Resistant Enterobacteriaceae
(gram -ve bacteria)

468
Q

what are some gram -ve and gram +ve resistant bacteria?

A

+ve - MRSA, VRE (Methicillin resistant Staphylococcus aureus, vancomycin-resistant enterococci)
-ve - ESBL, CRE, AmpC
(extended spectrum beta lactamase)

469
Q

how do ESBL resistant bacteria work?

A

hydrolise oxyimino side chain of antibiotics - (cephalosporins: cefotaxime,ceftriaxone, andceftazidime and monobactams: aztreonam)

470
Q

what are the 4 ways bacteria become resistant to antibiotics?

A
  • change antibiotic target binding site
  • antibiotic is destroyed or inactivated
  • prevent antibiotic access - porin channels on bacteria are modified
  • remove antibiotic from bacteria - protein in bacterial membrane act as efflux pump
471
Q

what does MIC stand for?

A

Minimum Bactericidal Concentration

472
Q

give some examples of beta-lactams

A

Penicillin V
Benzylpenicillin
Flucloxacillin
Amoxicillin
Amoxicillin-clavulanate
Piperacillin-tazobactam
Meropenem
cephalosporins:
Cephalexin
Cefuroxime
Ceftriaxone
Cefotaxime

473
Q

what kind of bacteria do beta-lactams work on?

A

gram +ve

474
Q

what are macrolides antibiotics and what are they used for?

A

Clarithromycin and erythromycin
for gram +ve bacteria
- penicillin allergy
- severe pneumonia

475
Q

what are examples of glyopeptide antibiotic and what are they used for?

A

vancomycin and teicoplanin
- gram +ve ONLY - especiallythose resistant to beta-lactams eg MRSA, or peniclllin allergy

476
Q

what are lincosamides antibiotics? give an example, and when are they used?

A

eg. clindamycin
- affect protein synthesis of bacteria, destroys toxins
- used for gram +ve bacteria eg. S.aureus, beta strep
in cellulitis if penacillin allergy, necrotising fasciitis

477
Q

what are tetracyclines antibiotics?

A

eg. doxycycline
- used for broad spectrum, mainly gram +ve
eg for cellulitis or pneumonia

478
Q

what is ciprofloxacin antibiotic for?

A

gram -ve more than gram +ve
- affects DNA synthesis of bacteria
- used if penicillin allergy, UTIs, itra-abdominal infections

479
Q

how does trimethoprin antibiotic work?

A
  • folate antagonist - affects metabolism of bacteria
  • mainly used for gram -ve
    eg UTIs
480
Q

what are CPEs?

A

carbapenemase producing enterobacteriacease
- bacteria producing enzyme that inactivates carbapenem antibiotics
-enterobacteriacease - colonise large bowl, skin below waist. Most common cause of UTIs and intra-abdominal infections
- eg. e.coli, klebsiella

481
Q

what are some examples of pathegens that need to be controlled through infection control?

A

CPEs
MRSA
Norovirus
Clostridium difficile
Endogenous infections

482
Q

what are sterile parts of the body?

A

blood
CSF
pleural fluid
peritoneal cavity
joints
urinary tract
lower respiratory tract

483
Q

what are non-sterile parts of the body with flora?

A

mouth
skin
vagina
urethra
large intestine

484
Q

what is the 90/90/90 UNAIDS goal?

A

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

485
Q

what is the fast-track cities partnership for HIV?

A

political leadersof affected areas and service providers work together to accelerate response to HIV

486
Q

what are the transmission routes for HIV?

A

sexual
vertical
blood

487
Q

what can be taken before sex if effected with HIV?

A

Pre-exposure prophylaxis of HIV (PreP)

488
Q

what drug is taken after sex if affected with HIV, with 72 hours?

A

PEP - Post-exposure prophylaxis

489
Q

how is HIV most preferably screened for?

A

venous blood sample
- 4th generation HIV tests include p24 antigen and will detect the vast majority of infections at 4 weeks

490
Q

what are HIV POCT (point of care tests)?

A

Finger prick blood
Immediate result
Lower sensitivity and specificity
False positive and negative results
Longer incubation period

491
Q

what kind of virus is HIV?

A

retrovirus, small RNA virus - expresses 10 genes
- uses reverse transcriptase to make DNA copy and insert itself into cell DNA
lentivirus - long incubation time

492
Q

describe the basic pathology of how HIV infects a cell

A
  • glycoprotein gP160 (made of gP120 and gP41)on HIV dock and fuse onto the CD4 and CCR5 receptors
  • viral capsid enters cell, enzymes and nucleic acid released
  • reverse transcriptase converts viral RNA to double stranded DNA
  • viral DNA integrated into cell DNA by integrase enzyme
  • viral proteins are made
  • budding immature virus pushes out of cell with some cell membrane
  • ## maturation protein chains of freed virus cut by protease that combine to form working virus
493
Q

what does pol proetin in HIV do?

A

encodes the enzymes: reverse transcriptase, integrase and protease

494
Q

what does tat do in HIV?

A

contributes to viral replication. Enhances production of host transcription factors e.g NF-kB

495
Q

what does rev do in HIV?

A

binds to viral RNA and allows export from nucleus and also regulates RNA splicing

496
Q

what does gag do in HIV?

A

encodes structural proteins.
Made as a polyprotein and cleaved by HIV protease

497
Q

what are the receprors on the cells that HIV binds to?

A

primary - CD4
co-receptors CCR5 (early) and CXCR4 (later)

498
Q

what do antiretroviral therapies target in the HIV replication cycle?

A

integrase inhibitors
protease inhibitors
reverse transcriptase inhibitors
fusion/entry inhibitors

499
Q

what is the genetic resistance to HIV-1?

A

homozygous 32bp deletion in CCR% gene
- seen in 1% caucasions
- onlt one copy = infected but slow progression

500
Q

why does HIV-1 mutate rapidly?

A
  • error prone replication of reverse transcriptase - 1 error per replication
  • rapid viral replication
  • large population size
  • recombination between subtypes
501
Q

what are the symptoms of acute retroviral syndrome?

A

Glandular fever”-like illness
Fever, lymphadenopathy
Sore throat, oral ulcers
Skin rash (upper trunk)
May include neurological features

502
Q

what is signicicant about the immune response during acute HIV infection?

A

deterime Long-term viral control and Disease progression

503
Q

what cells does HIV affect?

A

range of CD4 + immune cells
- helper T-cells, (including regulatory T-cells, T follicular helper cells, dendritic cells, macrophages and thymocytes)

504
Q

what ultimately happens with immune system when fighting against HIV?

A

immune exhaustion

505
Q

why are antibodies not effective against HIV for mosst people?

A

HIV-1 envelope spike is heavily glycosylated - sugars resemble human type - difficult for antibodies to bind
- envelope protein can change and evolve quickly

506
Q

what are the main targets for broadly neutralising antibodies against HIV-1?

A

CD4 binding site
Membrane-proximal region
V2V3 conformational epitope
Envelope glycans

507
Q

what T cell recognise cells expressing foreign material presented as HLA class 1 molecules?

A

CD8+ cytotoxic T-cells

508
Q

what is released when CD8+ cytotoxic T-cells recognistion is triggered?

A

Cytokines – soluble anti-viral factors
CC- chemokines
(compete with HIV for
the receptor CCR5)
Cytotoxic factors
– kill the cell

509
Q

how does HIV-1 evade T cell recognistion?

A
  • The HIV-1 nef protein reduces cell-surface expression of HLA class I molecules
  • upregulates Fas molecules to kill Cytotoxic T-lymphocytes (CTL)
510
Q

what are Long-term non-progressors (LTNPs) of HIV?

A

survivors with HIV-1 infection for >7-10 years, no therapy, no symptoms and stable CD4+ T-cell count

511
Q

what are elite controllers of HIV

A

HIV-1 infected individuals with plasma VL <50 copies/ml for over one year without ART: VERY RARE

512
Q

where population is HIV concentrated?

A

sex workers and their clients
gay men and other MSM
people who inject drugs
transgender people
prisoners

513
Q

what age group is most at risk of HIV?

A

15-24 year olds

514
Q

how does transmission occur from mother to child?

A

In utero: transplacental, mostly during the third trimester
Intra partum: exposure to maternal blood and genital secretions during delivery
Breast milk: ingestion of large amounts of contaminated milk

515
Q

what are the 2 markers used to monitor HIV infection?

A

CD4 cell count
HIV viral load

516
Q

what are most common symptoms of acute HIV?

A

most common:
Fever
Sore throat
Myalgia
Rash

Vomiting + diarrhoea
Headache
Lymphadenopathy
Weight loss

517
Q

what symptoms would prompt you to ask out sexual history and HIV seroconversion?

A

fever, rash and non-specific symptoms

518
Q

what is clinical latency of HIV?

A

CD4 cell population increases, and the viral load temporarily decreases
then, CD4 declines, causing immunosupression and symptoms

519
Q

what symptoms can be present when HIV is not treated, after clinical latency?

A

shingles
candida - thrush
Oral hairy leucoplakia
Molluscum contagiosum - spots
other bacterial/funal/viral infections

520
Q

you should think about testing for HIV when a patient has a common problem that…

A

is an unexpected patient
That is recurring
That has no clear underlying cause

521
Q

what is CD4 level in AIDS?

A

<200

522
Q

what is the most common AIDS defining illness?

A

Pneumocystis Pneumonia
- fever, dry cough

523
Q

what is the most common oppertunistic infection?

A
524
Q

what are some AIDS defining illnesses?

A

Persistent HSV
Kaposi’s sarcoma
CMV colitis
Candidiasis - oesophageal
HSV oesophagitis
Wasting syndrome
Recurrent salmonella sepsis
Cervical cancer
Primary CNS Lymphoma
Cryptococcal meningitis
CMV retinitis
Recurrent pneumonia
PCP
TB

525
Q

what do all TB patient require to be tested for?

A

HIV

526
Q

how is HIV treated?

A

HAART (Highly Active Anti-Retroviral Therapy
- 3 antiretroviral drugs

527
Q

what are NRTIs?

A

Nucleoside reverse transcriptase inhibitors
- part of HAART regime

528
Q

what sgould be considered in seropositive person with a headache?

A

lumbar puncture

529
Q

why does HIV develop drug resistance?

A
  • Non-adherence
  • Drug-Drug interactions
530
Q

what are 2 classes of drugs that act as entry/fusion inhibitors to HIV and when are they used?

A

maraviroc
enfuvirtide
- used with resistant viral strains

2A (9 decks)

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