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Phase 2 mine > ICS pharmacology > Flashcards

ICS pharmacology Flashcards

1
Q

What are some issues with drug delivery ?

A

Absorption, distribution, metabolism and excretion

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2
Q

What is important to note about absorption in drug levels in thebody?

A

The rate at which it is absorbed as that will contribute to the peak

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3
Q

What can affect the distribution of a drug?

A

Binding to proteins or not

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4
Q

What can affect metabolism?

A

which pathway the drug takes normally and how this is affected by other substances

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5
Q

What is pharmacodynamics?

A

How the drug affects the body

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6
Q

What is pharmacokinetics?

A

Describes the disposition of a compound within an organism and includes ADME

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7
Q

What is drugability?

A

ability of proteins to bind small molecules with high affinity

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8
Q

What do most drugs target?

A

Proteins such as receptors, enzymes, transporters, ion channels

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9
Q

What is an exogenous ligand?

A

A substance that comes from outside the body

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10
Q

What is an endogenous ligand?

A

A substance from the body like a neurotransmitter or a hormone that binds to a receptor

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11
Q

What are the types of receptors?

A

Ligand-gated ion channels, Gprotein coupled receptors, kinase-linked receptors, cytosolic/nuclear receptors

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12
Q

What are types of drug interaction?

A

Synergy, antagonism or other like potentiation

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13
Q

What are patient risk factors for drug interactions?

A

polypharmacy age genetics

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14
Q

What is the theraputic window?

A

The range of doses that can give an effect without being toxic

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15
Q

What are the adsorptive affects of drugs?

A

Motility of the GI, Acidity, solubility, complex formation, direct action on enterocytes

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16
Q

What is celation?

A

Binding of substances together

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17
Q

Which enzymes are involved with drug handling?

A

CYP40

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18
Q

What is metronidazole problems?

A

blocks alcohol dehydrogenase so can get bad side effects

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19
Q

Which drugs have a lot of interactions?

A

Anti-psychotic drugs

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20
Q

What are the type of antagonists?

A

Competitive or non-competitive

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21
Q

How to avoid interactions?

A

Use the BNF and prescribe rationally. Ask ward pharmacists and Patient information leaflet

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22
Q

What are kinase-linked receptors?

A

The ligand binds to the outside of the protein and the proteins are affected inside to phospho-tyrosine docking site

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23
Q

What is an agonist?

A

A ligand that binds to a receptor to activate it

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24
Q

What is an antagonist?

A

A compound that reduces the effect of an agonist

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25
Q

What is EC50?

A

What dose gives 50% of maximal effect

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26
Q

What should an antagonist do?

A

not cause a response in the molecule and should block the effect of an agonist

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27
Q

What factors govern drug action?

A

Receptor related affinity efficacy tissue related receptor number and signal amplification

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28
Q

What are agonists and antagonist properties?

A

both have high affinity byt antagonist has no efficacy

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29
Q

What is receptor reserve?

A

Dont need all receptors to get maximall response.

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30
Q

What is a partial agonist?

A

It cannot illicit a maximal response

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31
Q

What is signal amplification?

A

The level that the initial signal is amplified by receptor mediated reactions inside the cell

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32
Q

What are the types of enzyme inhibition?

A

Irreversible inhibitors and reversible inhibitors

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33
Q

What are unintentional non adherance?

A

Forgetting, can’t pay for drugs, can’t understand instructions, problems using treatment

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34
Q

What are intentional non-adherence?

A

patient’s beliefs about their health, beliefs about treatments personal preferences

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35
Q

What is necessity-concerns framework?

A

Validated questionnaire look at their beliefs about medicine

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36
Q

What are the main routes of drug administration?

A

Oral, intravenous, intra arterial, intramuscular, subcutaneous, inhalational, topical sublingual rectal and intrathecal

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37
Q

How can drugs cross membranes?

A

Passive diffusion, ion channels diffusion, facilitated diffusion, pinocytosis engulfing of the molecule

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38
Q

What stops drugs passively diffusing?

A

Being repelled by the membrane because its not lipid soluble

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39
Q

What uses diffusion channels?

A

Lithium

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40
Q

What can carrier mediated transport do to drugs?

A

Some can remove drugs from cytoplasm and others can inhibit certain pumps to change effectiveness of a drug

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41
Q

What does OAT1 do?

A

Penicillin secretion and uric acid probenecid can stop this excretion

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42
Q

What is drug ionsiation?

A

Drugs are often weak acids or bases this can effect how they bind to receptors

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43
Q

Why is pH and acidity of drugs important?

A

Aspirin overdose, urine us usually lower pH than plasma so weak acid will be unionised and reabsorbed into plasma, if alkalinise urine with bicarbonate more will be excreteed

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44
Q

Why is oral route often used?

A

High blood flow and surface area of drugs, easy and convenient but are obstacles

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45
Q

What problems are there with oral route?

A

Drug structure, drug formulation, gastric emptying and first pass metabolism

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46
Q

How does drug structure affect absorption in the intestine?

A

Lipid doluble to be absorbed, highly polarised drugs tend to be only partially absorbed with much being passed in faeces, some are unstable at pH or with enzymes so can have to be given by other routes

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47
Q

What is a problem with opioids?

A

addiction and become tolerant to it

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48
Q

What are some opiate derivatives?

A

Morphine coedine, diamorphine, oxycodone

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49
Q

What is the antagonist of morphine?

A

Naloxone

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50
Q

What happens to morphine in the liver?

A

The liver absorbs 50% of it

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51
Q

What are the routes of administration for morphine?

A

orally, subcutaneously, intramuscularly, iv, epidural

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52
Q

What is the controlled drugs legislation?

A

need two signatures for controlled drug prescriptions be careful writing prescriptions for them

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53
Q

How do opioids work?

A

descending inhibition of pain they stop the perception of pain. its part of fight or flight mecanism and isnt designed for sustained use

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54
Q

What do opioids act on?

A

4 different opioid receptors

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55
Q

What is the difference between potency and efficacy?

A

Potency is how many mg you need of it how well it binds to the receptor. Efficacy is how well the receptor gives a response

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56
Q

What is tolerance vs dependance?

A

Down regulation of receptors with prolonged use need higher doses to achieve the same effect. Dependency is the reliance upon it

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57
Q

What are the side effects with opioids?

A

Respiratory depression, sedation, nausea vomiting, constipation, itching.

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58
Q

What to do in respiratory depression?

A

naloxone carefully and support breathing

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59
Q

How quickly can they lose effectiveness?

A

Within weeks

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60
Q

When should opioids be used?

A

cancer pain and surgery

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61
Q

What is coedine?

A

Need an enzyme to convert it to the morphine. Don’t use it in children or breastfeeding women

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62
Q

What is the excretion pathway for metabolismof morphine?

A

Morphine goes to morphine 6 glucuronide which is more potent excreted by kidney but with poor kidney function it can cause a serious issue

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63
Q

What is tramadol?

A

Weak opioid it is a prodrug needs to be activated. can interact with SSRIs

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64
Q

What is the oral bioavailability of morphine?

A

50%

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65
Q

What is drug formuation?

A

The mechanism for drug delivery some tablets dissolve slowly

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66
Q

How can gastric emptying affect the drugs?

A

the amount of time the stomach takes can affect how you absorb it

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67
Q

What is first pass metabolism?

A

how the drug gets to the target site and how its modified on its way

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68
Q

What can be involved in the first pass metabolism?

A

The intestinal lumen, the lungs, the liver.

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69
Q

How can the intestinal lumen affect the drug?

A

Contains digestive enzymes and peptide drugs can be broken down by proteases and colonic bacteria can reduce drugs transport back into the lumen

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70
Q

how does the liver affect drug absorption?

A

The liver can remove substances or modify them which can

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71
Q

What is a way to avoid the liver metabolism?

A

rectally or sublingually or skin

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72
Q

Why use transcutaneous?

A

Slow continued absorption, need potent drugs though

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73
Q

Why use intradermal or subcutaneous?

A

Skips waterproof layer limiited by blood flow and only small volume but also local effects and limits rater of blood flow

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74
Q

Why use intramuscular?

A

Depends on blood flow and watersoluble. can be slow releasing if deposited with lipid stuff

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75
Q

Why would you use intranasal?

A

fast and for it to be local

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76
Q

Why inhalation?

A

Large SA, can be toxic to alveoli though

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77
Q

What is the importance of distribution of the drugs?

A

Lots goes to well perfused tissues like the brain and the liver and lungs. then to other less perfused tissues then redistribution from hilgly perfused to low perfusion takes place.

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78
Q

How can protein binding affect drugs?

A

Albumin can bind to drugs and can lower free concentration and can’t be released back into the blood

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79
Q

Which drugs can pass to the brain?

A

lipid soluble drugs easily pass to it but can transport drugs out of the brian

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80
Q

What happens with drugs and pregnancy?

A

The drugs to the mother will end up going to the baby as well so have to be careful and liver can struggle to deal with it

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81
Q

What is involved with elimination?

A

Metabolism and excretion

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82
Q

What is a phase 1 reaction?

A

Makes it more hydrophillic by exposing OH or adding molecules to make it more soluble

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83
Q

What can affect CYP?

A

Grapefruit, foods and alcohol and smoking alcohol and smoking speed them up

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84
Q

what is a phase 2 reaction?

A

Involves joining of drugs with a metabolite to have active groups to make them more soluble

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85
Q

Which ways can drugs be excreted?

A

Fluids like urine bile sweat tears breast milk. Solids faecal elimination which is important for high molecular weifh and hair gases as well like volatile substances

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86
Q

What affects urine excretion?

A

Secretion and absorption in the kidney

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87
Q

What is first order kinetics?

A

Taking a blood sample where it reduces by the same fraction over time eg it has a half life

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88
Q

What is it called when an enzyme system is saturated?

A

Zero order kinetics because it is removed at the same rate whatever the concentration eg alcohol

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89
Q

What is a good measure for first order kinetics drugs?

A

Half life

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90
Q

What is bioavaoilability?

A

How much of the drug reaches the the blood stream unmodified

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91
Q

What is adrenergic and cholinergic pharmacology important?

A

Control of hypertension, control of heart rate, anaesthetic agents, regulation of airway tone, pressure in the eye, control of GI function

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92
Q

Why does it matter that cholinergic pharmaceuticals?

A

They can affect all aspets of the body as well as the desired system

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93
Q

What are the types of autonomic receptors?

A

Muscarine and atropine opposes it and nicotinic receptors and curare

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94
Q

What are the sympathetic ganglia like?

A

They occur close to the spinal cord and have long post ganglionic neurons

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95
Q

What do the post-synaptic nerve fibres of parasympathetic use as a transmiter?

A

Acetylcholine that affects muscarinic receptors

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96
Q

What do the post synaptic nerve fibres of sypathetic nervous system use as neurotransimttters?

A

alpha/beta adrenergic receptors activated by noradrenaline

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97
Q

Which organs are innervated by only sympathetic nervous system?

A

sweat glands and blood vessels

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98
Q

Which organs are only parasympathetic innervation?

A

Bronchial smooth muscle

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99
Q

What are the things to interfere with pharmacologically in the autonomic nervous system?

A

Acetylecholine used in both, noradrenaline used in sympathetic

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100
Q

At which stage is the same neurotransmitter released in both systems?

A

they both release acetylcholine in the first junction

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101
Q

What is released in post-ganglionic parasympathetic fibres?

A

acetylcholine that acts on muscarinic receptors

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102
Q

What is released at the sympathetic post ganglionic fibre end?

A

noradrenaline acting on alpha and beta adrenoreceptors although sweat glands it is Ach and muscarinic

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103
Q

What are other pathways?

A

Non-adrenergic, non-cholinergic autonomic transmitters such as NO vasoactive intestinal eptide or ATP and neuropeptide Y

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104
Q

What does nicotine stimulate?

A

Nicotine stimulates all autonomic ganglia by nicotinic receptors

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105
Q

Where does muscarine act?

A

Activates the muscarinic receptors of the parasympathetic nervous system

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106
Q

What type of receptor are muscarinic receptors?

A

7 transmembrane protein g coupled receptor with Trimeric g proteins

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107
Q

Where are the 5 muscarinic types of receptor found?

A

M1 M4/5 mainly in brain and CNS. M2 is mainly in heart to slow the heart and can block to stop too much slowing. M3: glandular and smooth muscle causing bronchoconstriction sweating and salivary gland secretion

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108
Q

What are some muscarinic agonists?

A

Pilocarpine stimulates salivation, contracts iris smooth muscle to treat glaucoma but it can slow the heart

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109
Q

What are some muscarinice antagonists?

A

Atropine can block parasympathetic hyoscine, local delivery can give specificity

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110
Q

What is the use of a muscarinic antagonist?

A

To prevent bradycardia and BP drop and dry sectetions or to treat excessive betablockers

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111
Q

What drugs are used for treatment of bronchoconstriction?

A

anti-muscarines like ipratropium bromide short acting and tiotropium (mainly blocks M3 receptors) glycopyrrhonium

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112
Q

What is the use of anticholinergics in palliative care?

A

In stopping painful spasms of the GI tract

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113
Q

where is Ach used outside of the autonomic system?

A

In memory formation tends to treat nausea and used in sceletal muscle nicotinic receptors

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114
Q

What are common side effects of anticholinergics?

A

memory loss and confusion constipation dryng of the mouth and tachycardia and

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115
Q

What are cholinergic side effects?

A

muscle twitching and paralysis, salivation and confusion

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116
Q

What is the difference between noradrenaline and adrenaline?

A

Adrenaline is released by the adrenal glands in the figt and flight management of anaphylaxis noradrenalin is released fro sympathetic nerve fibre ends beloved in the management of shock in the intensive care unit

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117
Q

Where are alpha 1 receptors found?

A

blood vessels but not brain lung and heart

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118
Q

Where are alpha 2 receptors?

A

In nose

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119
Q

Beta 2 receptors?

A

in the lungs smooth muscle

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120
Q

Where are beta 1 receptors?

A

increase in heart rate

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121
Q

Why are beta 2 agonists good?

A

They cause bronchial smooth muscles to relaxi and can affect the heart as well

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122
Q

What do beta blockers do?

A

they slow heartrate reduce tremmors but can casuse a wheeze, can lower blood pressure,

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123
Q

What is clearance?

A

The amount of blood cleared of the drug completely per unit of time

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124
Q

Why is clearance important?

A

If you want a constant effect from the drug you need to be able to calculate what the repeated drug dose should be.

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125
Q

How many half lives does it take to reach 95% f steady state concentration?

A

4-5 half lives

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126
Q

How can steady state be calculated?

A

Rate of infusion/Clearance

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127
Q

What is involved in oral dosing calculations?

A

bioavailability the dose and clearance rate and the dosing interval

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128
Q

What is a loading dose?

A

Give a large dose to begin with to load the system to speed up getting to steady state.

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129
Q

What is an allergy?

A

Abnormal response to a harmless foreign material

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130
Q

What does Atopy mean?

A

Tendancy to develop allergies

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131
Q

Which allergies are not allergies?

A

intolerances such as lactose

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132
Q

What are some allergic disease?

A

anaphallaxis, allergic asthma, food allergies, dermatitis

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133
Q

What immunoglobulins can be used in allergic reactions?

A

IgE, IgG4 and IgA occasionall

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134
Q

What causes allergy?

A

Genetic factors and mast cells

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135
Q

Which are the main cells involved with allergic response?

A

Mast cells eosinophils and basophils

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136
Q

How strongly does IgE interact with its receptor?

A

It is quite high and has short half life because it bnds to receptors so hard

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137
Q

What is the low affinity IgE receptor?

A

it is involved with IgE production

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138
Q

which is the most importance cell for allergic reaction?

A

Mast cells variable around the body and involved in many disease proceses and involved in many disease processes

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139
Q

What are found in the mast cell granules?

A

histamine, chemotactic factors proteases cytokines tryptase chymase and proteoglycans, also release over longer time they leukotrieinds

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140
Q

What are the effects of mast cells?

A

Eosinophil attraction and activation, capillary leakage bronchochonstriction

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141
Q

How can mast cells be activated?

A

IgE receptor mediated, by an allergen perhaps, bacterial/viral antigens,

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142
Q

What cells are involved in allergy?

A

Lymphocytes, dendritic cells, neurons, epithelial cells fibriblasts

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143
Q

Why are some antigens allergenic?

A

They are about the size of cells they stimulate PAMPs but only weak ones their delivery is oral or by skin often. very low doses of them

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144
Q

What happens in anaphylaxis?

A

ABCDE very rapid reaction

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145
Q

How can you diagnose anaphalaxis serologically?

A

IgE or direct activation serum tryptase histamine elevated

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146
Q

What are the risk factors for anaphalaxis?

A

Young female drugs fods diagnostic agents

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147
Q

What are the main trestment stratergies of allergies?

A

Avoid allergens, desensitisation, prevent IgE interaction and production

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148
Q

What is desensitisation?

A

Introduce antigen to the skin, in increasing doses but is very dangerous and isn’t that effective in asthma

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149
Q

How can IgE production be done?

A

Get Th1 route activated, give Th1 cytokines antagonise IL4 for Th2 Activation

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150
Q

what can reduces mast cell activation?

A

Beta 2 agonists, glucocorticoids and others

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151
Q

How does an epipen work?

A

epinephrine has

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152
Q

What is the importance of being aware of adverse drug reactions?

A

5% of hospital admissions, 10-20 percent of cases in hospitals

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153
Q

what are the types of adverse drug reactions?

A

Toxic effects beyond therpeutic range, collaterl effecs in the range and hypersusceptibilit effects below the therapeutic range

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154
Q

Why might you get toxic effects of a drug?

A

If its not removed as fast as it could be by kidney, interaction with other drugs.

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155
Q

What are some collateral effects?

A

Beta blockers cause bronchoconstriction, antibiotics causin c difficile and pseudomembranous colitis

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156
Q

What are hypersuceptibility reactions?

A

Anaphalyaxis and penicillin

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157
Q

What are time independent reactions?

A

Ones that take place at any time during treatment

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158
Q

What are the types of time dependant reactions/

A

Rapid reactions, first dose reactions, early reactions, intermediate reactions, late reactions and delayed reactions

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159
Q

What are the classifications of adverse drug reactions?

A

Augmented pharmacological Type A B bizarre or idiosyncratic, Chronic delayed end of treatment or failure of therapy

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160
Q

What does DoTS system mean?

A

Dose relatedness, timing eg fast infusions hearing loss patient susceptibility

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161
Q

What is a type A reaction?

A

augmented the intended effect is too much, more than would be expected

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162
Q

What is type B reactions?

A

Not predictble not dose dependant and can’t be reversed easily, usually lifethreatening

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163
Q

What is a type C reaction?

A

Uncommon cumulative dose reaction, nephropathy from overuse of drugs

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164
Q

What is type D?

A

Uncommon can be very delayed, eratogenesis, carcinogenic

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165
Q

What is type F?

A

failure to have the required response

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166
Q

What are most common anaphalactic causing drugs?

A

Antibiotics anti cancer, NSAIDS CNS drugs

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167
Q

What are the most common systems to be affected?

A

GI, renal, metabolic, deratologic, endocrine, haemorrhagic

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168
Q

What is MHRA?

A

Medicines and healthcare products regulatory agency

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169
Q

What is the yellow card scheme?

A

Collects adverse drug reactions, and records them

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170
Q

Why should we report adverse drug reactions?

A

to help point out things missed in safety testing

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171
Q

What is a black triangle?

A

Undergoing additional surveillance

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172
Q

What goes on a yellow card?

A

The drug involved the reaction, patient’s details and reporter details

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173
Q

What is required for an allergic reaction to drugs?

A

need an exposure then a re-exposure, doesn’t have to be serious

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174
Q

What is important when a patient says they are allergic?

A

are they allergic or intollerant how serious

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175
Q

What are the two types of drug hypersenstivity?

A

Anaphalaxis from immunological or non-immuological cause

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176
Q

What mediates type 1 hyperensiticity?

A

IgE mediated

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177
Q

What happens in type 1 hypersensitivity?

A

IgE mediated after exposure then causes mast cell degranulate and repease substances causing a response

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178
Q

What happens in anaphalaxis?

A

vasodilation increased vascular permeability, bronchoconstriction, urticaria, angio-oedema swelling of face and mouth

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179
Q

What is a type 2 reaction?

A

Antibody dependant cytotoxicity, IgG or IgM and antibodies activate complement

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180
Q

What are the main features of anaphalaxis?

A

Immediate response(tablet within hour) rash not always, swelling of lips and face, wheeze, hypotension cardiac arrest

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181
Q

What is the management of anaphalaxis?

A

ABC airways, breathing, circulation. Adrenaline given first time (500micrograms IM or epipen is 300mg), High flow oxygen, IV fluid, IV antihistamine chlorphenamine, IV hydrocortisone if in shock may need IV adrenaline

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182
Q

What does adrenaline do to affect anaphalaxiss?

A

Vasoconstriction Beta 1 adenoreceptors for heart, reduces oedema bronchodilates and attenuates mediators

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183
Q

Is IgE involved with complement?

A

no

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184
Q

Which cells respond to lots of IgE?

A

Mast cells Eosinophils and basophils

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185
Q

Which type of immunity are mast cells involved with?

A

both

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186
Q

How can Th2 response be suppressed?

A

IL-12-18 redices IgE production in mice. Anti-IgE therapy with monoclonal antibodies anticytokine antibodies

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187
Q

What is a commensal organism?

A

one that can colonise the hostwith normal circumstances

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188
Q

What is an opportunist pathogen?

A

Only causes disease if defences are compromised

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189
Q

How are bacteria names?

A

Genus then species

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190
Q

What are the shapes of bacteria?

A

Coccus round or bacillus rod,

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191
Q

What are the morphologies of bacteria?

A

Diplococcus, streptococcus(long chain), staphylococcus clusters. chain of rods curves rods vibrio, spiral rod spirochaete

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192
Q

What makes a bacterium gram negative or positive?

A

2 membranes gram negative one membrane gram positive

193
Q

What is the outermost layer of a bacteriu?

A

Capsule

194
Q

What are Ziehl-neelsen stain used for

A

Mycobacteria acid-fast bacilla

195
Q

What is the bacterial cell envelope like of gram positive?

A

Cell membrane with peptidoglycan on the outised with a capsule occasionally

196
Q

What is the bacterial cell envelope like for gram negative bacteria?

A

inner membrane then lipoprotein and peptidoglycan layer then an outer membrane with lipopolysaccharide layer which is endotoxin

197
Q

What are bacterial spores?

A

They can protect the bacteria from heat because it holds their DNA

198
Q

What can bacteria live in?

A

large range of temperature pH.

199
Q

What is doubling time of most viruses?

A

less than an hour

200
Q

Why is it slow to diagnose mycobacteria?

A

Their doubling time is very long

201
Q

Which type of bacteria have endotoxins?

A

Gram negative bacteria

202
Q

What is an exotoxin?

A

Secreted by bacteria

203
Q

What is the difference between endotoxins and exotoxins?

A

Protein endotoxins vs lipopolysaccaride xotoxis are specific heat labile strong antigenicity produced by both and can bec converted to toxoid

204
Q

What is bacterial conjugation?

A

Transfer of genetic material between two of them by sex pilli

205
Q

How can bacteria be classified?

A

if they have to live inside a cell, with or without cell walls single cells and then shape and staining and anaerobic and aerobic

206
Q

What are the sages of gram staining?

A

Crystal-violet staining then washing with alcohol and then another stain to be able to see gram negative

207
Q

What is the structure of the outer membrane of gram-negtive bacteria/

A

Inner layer of bilayer is phospholipid, the outer part is lipid layer A zone then R core short chain of sugars, repeating polysaccaride sugar on the outside this is endotoxin

208
Q

What is the envelope structure of mycobacteria?

A

They ajve am iter lipit bilayer with mycolic acids they have no proteoglycans

209
Q

Which are importang gram negative phyla of bacteria?

A

Proteobacteria, chlamydiae, spirochaetae and bacteroidetes

210
Q

Which are the important positive bacteris?

A

Actinobacteria, firmicutes, tenericutes

211
Q

What is virulence determinants?

A

An aspect that contributes to pathogenicity of an organism

212
Q

What are some factors of virulance?

A

Adhesisns, invasins nutrient aquisition defence against the host and toxins that usually secrete protein substances

213
Q

What are enterobacteria?

A

Most motile and are rod shaped, anaerobic but can be aerobically ssome colonise the intestinal tract

214
Q

What is Shigella flexnei?

A

Causes GI infections not motile. cannot use lactose

215
Q

What is Escherichia coli?

A

Can use lactose unlike salmonella and is motile causes GI infections

216
Q

How is the use of Macconky-actose agar useful?

A

has pH indicator if Lactose is used as substrate it produces lactic acid changing colour of the pH so must be E. coli

217
Q

How can flagella and other structures be detected?

A

Using antibodies to detect structures

218
Q

What are serovars?

A

Organisms of the same species but with different strains as they have different surface antigens

219
Q

What is often an infection caused by E.Coli?

A

Wound infections, UTI, gastroenteritis, traveller’s diarrhoea, bacteraemia sepsis syndrome, meningitis occasionally

220
Q

What makes some E.coli pathogenic?

A

Have a commonDNA sequences but cna aquire a pathogenic variant of new genes from other bacteria from lateral gene transfer causing pathogenicity islands

221
Q

What do enterotoxigenic E.coli do?

A

Heat labile and heat stable toxins. they adhere to apical surface of enterocytes and they produce a toxin which is taken into the cell and does ADP ribose a G protein and they cause activation of adenylate cyclase causing cAMP causing CFTR protein to release chloride and water into gut Heat stable toxin which mimics guanine and causes CFTR to activate

222
Q

How do EHEC and EPEC wor?

A

Inect a protein into the cell and then attach itself usin that receptor to attach itelf

223
Q

What are Enetoinvasive bacteria?

A

they don’t release a toxin

224
Q

What are symptoms of shigella?

A

Blood in diarrhoea and frequent stool passage

225
Q

How does Shigella get to the enterocytes?

A

They enter thrugh M cell to destroy undrlying macrophage and then pass through the cells disctroying gut epithelium

226
Q

What toxin does shigella do?

A

Shigatoxin made of catalytic subunit in centre and B subunits that bind to it and allow it to bind to membranes. It hydrolyses a rucleotide in rRNA and removes a purine it inhibits protein synthesis in the cell. Can cause kidney problems

227
Q

What are three main types of salmonella poisoning?

A

Frequent cause of food poisoning highest number of food-related hospitalisations/deaths 6 hour-36hour incubations localised infection susually
Enteric fever systemic disease typhoid, bavteraemia cholerasuis and Dublin uncommon

228
Q

How is gastroenteritis mediated?

A

bacteria is endocytoses, induction of chemokine release neutrophil recruitment and migration, neutrophil induced tisssue injury and fluid and electolyte loss through diarrhoea and inflamation of the Gut lining

229
Q

What happens in enteric fever?

A

The infection spreads in macrophages around the body causing systemic infection

230
Q

What does proteas mirabilis do?

A

It travels and can swim it breaks down urea and cause kidney stones long term

231
Q

What is vibrio cholerae?

A

causes pandemics, from salt water environments, from contaminated water by shell fish

232
Q

How does cholera spread?

A

Faecal-oral but not person to person as a high dose is required. From leaks into sewage and clean water areas. Incubation a few hour to 5 days to give watery stools often death due to dehydration no blood or puss or fever

233
Q

How is the cholera pathogenic?

A

It adheres to the TCP pilli cholera toxin which goes into cells and activates CFTR again to give diarrhoea

234
Q

What does Pseudomonsa aeruginosa do?

A

Localised infection UTI catheters, eye infection, systemic in blood leading to sepsis more likely in neutropenic patients ICU patients on ventialtors, it is chronic in CF patientes

235
Q

What happens in P. aeruginosa in CF patients?

A

It mutates in their lungs during chronic infection and leads to mucous producing bacteria that make F worse

236
Q

How many fungi are pathogenic to mammals?

A

150

237
Q

How common is an invasive disease of fungi?

A

1%

238
Q

How dangerous are fungal infections?

A

They kill more globally than breast cancer

239
Q

What type of infections are fungal ones normally?

A

oportunistic

240
Q

What is endemic mycoses?

A

fungal diseases that are often only found in tropical regions

241
Q

What forms do fungal infections take?

A

Skin infections including keratitis, mucosal infection mild but occasionally debilitating, invasive infection that is very likely to cause death

242
Q

What are the natural reservoir of fungal infection/

A

animal vectors, commensal they live just on the body, most are environmental organisms

243
Q

Why are fungal infections more common in fish than animals?

A

They don’t survive well at our body temperature

244
Q

Where do most fungal infections go?

A

into the upper layers of the skin onlyand feed of keratin

245
Q

What is fungal eye keratitis?

A

Ulceratve corneal infection, common cause of blindness.

246
Q

What are fungal wound infections like?

A

Traumatic injury rare complication of chronic wounds they are devastating

247
Q

What are the major fungal disease?

A

Candida oral thrush, three main species with one new one which is resistant to anti microbial agents

248
Q

What is aspergillosis?

A

in the environment found in warmer temperatures like compost heaps, conidial fungus with spores.

249
Q

What disease can aspergillosis cause?

A

causes invasive disease in immunocompromised allergic response, chronic pulmonary can happen with compromised immunity

250
Q

What is pneumocystis pneumonia?

A

Parasite of the lung only not sure how it transmitted mild or subclinical infection lots of uncontrolled HIV

251
Q

What is cryptococcus?

A

in a ring and have a capsule cause meningitis, found in the environment

252
Q

What is the theory behind treating fungal disease?

A

Selective toxicity, kill fungi or inhibit more than standard cells

253
Q

Why is it hard to target fungi?

A

DNA/RNA synthesis is similar they are more similar to us than bacterial cells

254
Q

What do antifungals work on?

A

Echinocandins to attack the cell wall, amphotericin, azoles, terbinafine that dammage ergosterol the human cell membrane

255
Q

How can the cell membrane be attacked?

A

Polyenes form a pore in the membrane to allow he contents to leave the fungal cell
Ergosterol synthetic pathway inhibitors

256
Q

What do Azoles do?

A

Stop formation of ergosterol, originally for candida but can act in other organisms

257
Q

What are the side effects of azoles?

A

GI symptoms can have reversible visual disturbances photosensitivity CYP450 interaction depending on relative affinity of drugs for individual enzymes

258
Q

What are problems with echinocandins stop cell wall synthesis?

A

Not too many but generally not too many interactions, fungicidal, susceptible to yeasts fungistatic to moulds. IV only. type 1 hypersensitivity only sometimes

259
Q

What is febrile?

A

Feverish

260
Q

Why is it hard to diagnose fungal disease/

A

the tequniques in blood culture etc is quite hard to diagnose fungal compared to bacteria

261
Q

What is the best way to detect fungal infection?

A

using aspirated or biopsy

262
Q

What is the most common fungal infection?

A

Fungal nail disease, dont tend to cause infection systemically from too high temperature, sometimes caused by non dermatophytes

263
Q

What are differentials for nail infection?

A

psoriasis lichen planus trauma eczema yellow nail syndrome, lamellar onychoshizia, periungual squamous cell malignant meanoma alopecia areata

264
Q

What is Onychomycosis?

A

Nail fungal infection, poor treatment outcomes take a long time to act due to nail growth being slow

265
Q

What usually causes osteomyelitis?

A

staphylcoccus aureus

266
Q

How can staphylococcus be further divided?

A

Into coagulase positive or negative that can protect the bacteria from phagocytosis

267
Q

How are staphylcoccus aureus spread?

A

Carriers and shedders, coughing and sneasing

268
Q

What is MRSA?

A

resistant to beta lactams, gentamicin erythromicin tetracycline.

269
Q

How is staph. aureus virulent?

A

Pore forming toxins, PVL and allows contents to leave
Proteases such as exfoliatin that attacks the desmosomes
Toxic shock syndrome toxin with inflammatory reaction
Protein A immunoglobulins bind backwards so can’t be recognised by the body

270
Q

What are the three types of conditions associated with staph aureus?

A

Pyogenic, Toxin mediated, Coagulase negative

271
Q

What are virulence factors for coagulase negative staphylcocci?

A

opportunistic in catheters, ability to form persistent biofilms some can produce kidney stones

272
Q

What is beta haemolytic?

A

destry RBC completely

273
Q

What is alpha haemolysis?

A

it splits haemaglobin by release of H2O2

274
Q

What are the ways you can group streptococci?

A

Haemolysis, Lancefield typing and biochemical properties

275
Q

What is special about haemophilus influenzae?

A

Causes meningitis sinuses, bronchopneumonia bacteraemia, pneumonia

276
Q

Which plate can show factor Y?

A

Chocolate agar

277
Q

What are the benefits to a bacterium having a capsule?

A

Can penetrate the nasopharengeal epithelium and resistance to phagocytosis and complement system

278
Q

What does haemopholus influenza LPS do?

A

Avoids activation of complement, inflammation

279
Q

What are sources of Legionella pneumophila?

A

warm man made aquatic environments

280
Q

What does leigonella do to the macrophages?

A

It lives in it and protects itself in the phagosome and then go back to individual form then leave macrophage

281
Q

What does fastidious organism mean?

A

Need nutrient rich environment

282
Q

What toxins do pertussis produce?

A

pertussis toxin, and a shiga-like toxin that stops adenylate

283
Q

What are neisseria?

A

Diplococci, gonorrhoea and meningitidis

284
Q

Where are you likely to find outbreaks of meningitis?

A

In person to person transmision in areas of high population

285
Q

What is the pathogenesis of Neisseria meningitidis?

A

they can cosss from the pharynx into the blood and causing septicaemia or meningitis if it gets into the CSF requires very fast treatment

286
Q

What are the virulence determinants of meningitis?

A

Capsule has anti-phagocytic properties, LPS causes cytokine cascade and sepsis

287
Q

What are the properties of gonorrhoea?

A

Person to person only, higly asymptomatic, can infect genitalia and also eye occasionally non-capsulated

288
Q

What are campylobacter?

A

Spiral rods, they are unipolar or bipolar flagella. cause a lot of food poisoning low infective dose can shed for 3 weeks

289
Q

What is helicobacter pylori?

A

Spiral morhology polar tuft, found in 50% but doesn’t usually cause disease, major role in gastritis and peptic ulcer disease 80-90% of ulcers

290
Q

What are bacteroides?

A

They are commensals of the large intestine can cause opportunistic tissue injury

291
Q

What are chlamydia and chlamydophila?

A

They are very small bacteria and non-motile and obligate intracellular parasites. often live asymptomatically in symbiotic organisms cannot culture them

292
Q

What is the lifecycle of chalmidia?

A

live in two forms the elementary body and reticulate body. EB taken up by mucosal cells in tract and replicate and differentiate in a phagosome and stops lysosome from joining. then goes back to EB and exits the cell by exocytosis

293
Q

What are the types of chlamydia?

A

serotypes A-C can have eye infections leading to scarring and blindness. gebtal forms D-K, most common std, can cause PID infertility , lympho granuloma venerum biovar tyes L1-L3 invasive urogental or anorectal infection then migrates to lymph nodes

294
Q

What are spirochaetes?

A

Long spiral bacteria often free living and non-pathogenic 3 are pathogenic

295
Q

What the purposes of endoflagellum?

A

Good for moving through viscous fluids

296
Q

What are important spirochetes?

A

Lymes disease, borrelia burgdorferi, leptospira interrogans, leptospirosis Weil’s disease, siphyllis

297
Q

What are stages of syphilis?

A

primary wount ulcer, secondary lyph infection and teriary where dammage is not reversible

298
Q

What shape are mycobacteria?

A

Rods

299
Q

What damage can mycobacteria produce?

A

Ulcers bone destruction, nodule, deforming

300
Q

How big is the burden of TB?

A

very big much more than other diseases as it has been around a long time?

301
Q

How do you treat TB?

A

Treatment of Antibiotics for 2 months and then others for 4 months and can have hepatotoxicity and neuropathy

302
Q

What is the problem with TB?

A

It is becoming drug resistant there are some totally drug resistant strains

303
Q

How does TB infect the body?

A

Airborn transmision, person to person, only need very few to infect a person, alveolar macrophages take them up but then taken to lymphatics and

304
Q

How does TB infect the body?

A

Airborn transmision, person to person, only need very few to infect a person, alveolar macrophages take them up but then taken to lymphatics and can get latent TB sometiems in T cells

305
Q

What does the TB do to the lungs?

A

Granulomas around bacilli that settle in the apex of the lung with more air with less blood flow

306
Q

What is the primary complex?

A

Granuloma, lymphatics, lymph nodes

307
Q

What are the common tissues TB infects?

A

Meningits, bone and joints, kidney etc

308
Q

Where does mycobacteria sit?

A

Technically gram positive but it doesnt stain neeed to use Ziehl-Neelsen stain acid fast positive

309
Q

How is TB usually detected?

A

augumented staining

310
Q

What is different about the cell envelope of mycobacteria?

A

waxy coating outside the other layers

311
Q

How long does it take for mycobacteria to replicate?

A

15-20hours making hard to target replication in antibiotic treatment

312
Q

What does the body do to respond to mycobacteria/

A

Macrophage and t cell mediated. Bacteria taken in into lysosome and then gets into cytosol can be killed by antimicrobial agents inside cells CD4 t cells generate interferon gamma to activate intracellular killing in macrophages

313
Q

What is a granuloma?

A

It is a way the body tries to stop the bacteria spreading everywhere. they can have macrophages that become epithelial cells and can fuse to form giant cells, t cells infiltrate, fibroblasts wall it of . central tissue dies of lack of oxygen

314
Q

What can destabilise a granuloma?

A

TNF alpha depletion, HIV,

315
Q

Which diseases cause granulomas?

A

Leprocy and TB

316
Q

What are the forms of leprosy?

A

Tuberculoid leprosy, lepromatous leprosy.

317
Q

How can TB be diagnoses?

A

Solid or liquid culture but takes a lot of time as selective antibiotics to remove others takes weeks, Nucleic acid detection PCR detection

318
Q

How can latent TB be detected?

A

T cell response use tuberculin skin test SC derivatives of TB that can give skin swelling and redness if you already have it

319
Q

How can TB be studied?

A

in animal models like mouse Guinea pig and rabbit also zebrafish, and Primates

320
Q

What are some serious virus?

A

Flu viral stomach infection HIV/AIDS

321
Q

What are some globally important viruses?

A

Spanish flu, Ebola MERS

322
Q

What are the importance viral problems for the uk?

A

Miscarriages and birth defects(CMV,varicella virus herpes simplex and rubella) Flu, cancer causing viruses epstein barr birus hep bc HIV HPV, immunosupressed patients and stigma

323
Q

Why are immunosuppressed patients problems?

A

They can get CMV or EBV can reactivate afterwards

324
Q

What is a virus?

A

An infectious obligate intracellular parasie and has DNA or RNA surrounded by a coat and or a membrane

325
Q

What are the shapes of viruses?

A

Helical icosahedral, complex

326
Q

What size are viruses?

A

They are much smaller than bacteria but they have a large size variation

327
Q

How do viruses replicate?

A

They attach to host cell via receptors, they enter the cell and release the genetic material into the cytoplasm, it migrates to the nucleus and uses host ribosome and nucleotides insde the cell then it produces its own structural proteins and genome and assembles itself then exit by bursting the cell which causes cell death or but out of the cell exocytosis

328
Q

How do viruses cause destructio of cells?

A

Infects a cell population and splits the ell after the viruus has replicated

329
Q

How do viruses cause change to host cells?

A

They can cause chages in the cells eg atrophy of villi causing problems with the functioning of the cells

330
Q

How can viruses cause immine issues?

A

Heapatitis attacks the cells and displays its viral antigen on the cell and then the immune system attacks the cells

331
Q

How do viruses cause proliferation?

A

The virus goes into the cell, expresses some proteins integrates viral DNA into the host chromosome, continuous expression of oncoproteis that can lead to cancer in those cells through dysplasia and neoplasia

332
Q

How do viruses evade host defences/

A

Nerve root ganglion by hiding there VZV and herpes, through lymphoid cells like EBV and HHV-8, And myeloid cells HHV6,7, and CMV

333
Q

What is secondary infection

A

When a latent virus can come back up an eg chicken pox can cause shingles

334
Q

How else can host defence be evaded?

A

Can spread cell to cell spread to infect lots of cells like Measals and HIV, antigenic variability, Flu, prevening host cell apoptosis, downregulate interferron

335
Q

How can viruses be detected?

A

PCR shows viral DNA is present, serological testing looking for immune memory to a specific virus, histopathology to look for characteristic changes of viral infection, owls eyes in nuclei, viral culture and electron microscope but not used much

336
Q

What is the most important staphylococcus?

A

It is gram positive, Saureus is coagulase positive it is found in the nose and skin

337
Q

How is staph.aureus spread?

A

aerosol and touch

338
Q

What are characteristics of streptococcus pyogenes?

A

beta haemolytic facultatively anaerobic penicillin sensitive

339
Q

How are streptococi classified?

A

Haemolysis and lancefield typing (for coag negative)

340
Q

What is anti SLO test?

A

To look at antibodies for SLO to test for streptococcal antibodies

341
Q

What are the virulence factors for S pyogenese?

A

Hylauronidase to aid with spreading, streptokinase breaks down clots C5a peptidase reduces chemotaxis toxins stretolisins bind to cholesterol and erythrogenic toxin causes an exaggerated response

342
Q

Which bacteria form draughtsman colonies?

A

Strep pneumonia,

343
Q

What can S.pneumoniae cause?

A

pneumonia, otitis media, sinusitis, meningitis

344
Q

What are the virulence factors for strep pneumoniae?

A

polysaccharide capsule, inflammatory wall constituent teichoic acid and peptidoglycan and it produces pneumolysin a cytotoxin

345
Q

What are the most virulent viridans streptococci?

A

milleri group s intermedius s angiosus and s constellatus

346
Q

What are protozoa?

A

One celled animals, 5 main groups

347
Q

What are the main classifications of protozoa?

A

Flagellates, amoebae, microsporidia, sporozoa and cilliates

348
Q

Which disease is sleeping sickness?

A

African Trypanosomaisis,

349
Q

What is african trypanosomaisis?

A

From tsetse fly bite, causes flu like symptoms, CNS involvement, coma and death diagnoses with blood sample

350
Q

What is American trypanosomaisis?

A

Chagas disease flu like symptoms can cais cardiomyopathy megaoesophagus and megacolon long term

351
Q

What is Giardiasis?

A

faeco-oral spread, diarrhoesa bloating flatulance with history of recent travel cysts or trophozoites seen in the stol treat with metroidazole

352
Q

What symptoms can amoeba cause?

A

Dysentry colitis liver and lung abscesses

353
Q

When do you worry about malaria?

A

Recent travel and fever? anaemia jaundice hepatosplenomegaly

354
Q

What is Entamoeba hystolytica?

A

causes sever dysentry, more in tropical areas and sanitation one of the bad amoeba in the gut

355
Q

How is Amaoebosis treated?

A

Metronisazol

356
Q

What is romana’s sign?

A

a swelling of the eyelid

357
Q

What are the 3 types of leishmaniais?

A

Cutaneous mucocutaneous and visceral

358
Q

What is Trichomonas vaginalis?

A

STI sores in genital areas, more in woamen that men,

359
Q

Which form of malaria lies dormant in the liver?

A

Plasmodium vivax and ovale

360
Q

How does plasmodium get into humans?

A

Sporosites are injected by mosquito and travel toliver and infect the cells then become Shizonts

361
Q

What hapens in the liver to schizonts?

A

They rupture and release merozoites into the blood, merozoites go into RBC, enter ring stage trophozoite

362
Q

What hapens after entering the ring stage of malaria?

A

The trophozoits mature into schizonts then reuptrue releaseing merzoites and so on some immature trophozoits differentiate into sexual phase that can lead to infection in mosquito

363
Q

How is malaria transmitted?

A

The gametocytes mature in mosquito over 9 days

364
Q

what causes symptoms in malaria/

A

Parasite develops in the RBC producing waste products and toxic factors, infected cells lyse releaseng the surface proteins and hemosoin into blod that stimulates macrophages to produce pro inflammatory cytokines and mediators

365
Q

What is bad about Pfalciparum?

A

Causes cytoadherance. rosetting to be protected and swquestration. can cause clots

366
Q

What are haemotalogical changes in malaria/

A

haemolytic anaemia, haemoglobin uria and jaudice reduced platelets from all the clotting factors

367
Q

Where can malaria cause complications?

A

Cerebral malaria, renal failure, ARDS, Bleeding and shock

368
Q

How is malaria diagnosed?

A

using thick and thin films

369
Q

What is the treatment for complicated malaria?

A

IV artesunate

370
Q

What is split into coagulase positive and negative?

A

Staphylococci, S aureus is positive

371
Q

Why are coagulase positive dangerous?

A

They can coagulase blood and can cause a worse infection

372
Q

What is a biofilm?

A

When bacteria stick togethr to form a community that can work together and share immunity and protects against attacks

373
Q

What attacks bacteria?

A

IgA, AB C3b Complement and Antibodies toneutralise toxins

374
Q

What cell mediated substance can cause fever?

A

TNF alpha

375
Q

How do worms evade host defences?

A

They can establish hyporesponsiveness in the host so that it can’t respond to the infection

376
Q

What kind of infections can be caused by staphylococcus aureus?

A

Wound infectons abcesses, impetigo, septicaemia osteomyelitis pneumonia, endocarditis

377
Q

What are virulence factors for S.pyogenes?

A

Hyaluronidase to help with spreading streptokinase to break clots C5a peptidase reduces chemotaxis

378
Q

What are Beta-lactams?

A

Cell wall killers break down peptidoglycan walls

379
Q

What are some beta lactams?

A

Cefuroxime ceftriaxone cefotaxime, piperacillim-tazobactam penicillins and cephalosporins

380
Q

What is different about cephalosporins?

A

Good for penecillin allergy better for ressistant bugs get into other parts of the body

381
Q

Why do gram negative bacteria need a different typ of antibiotic?

A

They are thincell walled and a different structure to gram positive

382
Q

What can you attack using antibiotics?

A

The cell walls, inibit protein synthesis, inhibit nucleic acid synthesis, anti-metabolites, inhibitors of membrane function

383
Q

What are macrolides?

A

They inhibit protein synthesis and work on gram positives and atypical pneumonia pathogens

384
Q

What to tetracyclines do?

A

They inhibit protein syntheis doxycycline, Broad spectrum mainly positive can be used in cellulitis and chest infections

385
Q

What does lincosamides do?

A

for grampisttves and can turn of toxins made by gram positives

386
Q

What is used or gram negatives?

A

Ciproflocain, nitrofurantoin and trimethroprime

387
Q

What are antibiotics?

A

a molecule produced by an organism that kills others

388
Q

What do beta lactams do?

A

break down the cell wall

389
Q

Which drugs are beta lactams?

A

Penicillins cephalosporins carbapenems and monobactams, vancomycin also

390
Q

What do beta lactams do?

A

They disrupt peptidoglycn production by binding covalently and irreversibly to the PBP casuing lysis

391
Q

How could the patient have resistant bacteria?

A

If they have been on antibiotics in the last few weeks

392
Q

Why might people not be able to take antibiotics?

A

Pregnancy breast milk, drug interatcions, renal and liver function, age, side effects allergy anaphylaxis risk of C. difficile

393
Q

What are betalactamases?

A

they are drugs that break down beta lactams to stop them working

394
Q

What is special about amoxicillin-clavulanate piperacillin-tazobactam meropenem and cephalosporins?

A

They inhibit beta lactamase or dont get broken down it. cephalosporins are not bad for penicillin allergies and get into different parts.

395
Q

What do you use for skin and soft tisue S. aurius?

A

Flucloxacillin, becasue lots can break down penacillins

396
Q

What is the limitation of penicillin V?

A

It oly gets enough in the throat if orally so only for throught symptoms

397
Q

Why can penicillin be used in strep throat?

A

there is no resistance to it

398
Q

What are glycopeptides?

A

Vancomycin and teicoplanin IV they only do gram positive, they are cell wall weapons

399
Q

What are glycopeptides?

A

Vancomycin and teicoplanin IV they only do gram positive, they are cell wall weapons

400
Q

What are gram negative rods that are lactose fermentingg?

A

Keibmosis, E. coli

401
Q

What is gentamicin used for?

A

IV only broad against gram negative. synergistic with other drugs it inhibits protein synthesis, its used in UTI, need measurements of levels in blood

402
Q

What is quinolones of?

A

DNA synthesis oral or IV affects gram negative, usually used in penicillin and UTI and intra-abdominal infections

403
Q

What is the problem with nitrofurantoin?

A

It is only good in Lower UTI doesn’t get to other parts

404
Q

What are beta lactams most effective against?

A

rapidly multiplying organisms

405
Q

What does metronidazole do?

A

Nucleic acid synthsis

406
Q

What antibiotics target ribsimes?

A

Tetracyclines macrolides, lincosamids, aminoglycosides

407
Q

What are we trying to achieve in antibiotics?

A

Kill bacteria or stop them being hostile

408
Q

What are bacteriostatic antibiotics?

A

They inhibit replication, but do effectively kill them somewhat

409
Q

What is Minimum bactericidal concentration?

A

Lowest concentration that required to give a bacteriocidal level

410
Q

When are bacterocidal antibiotics most important?

A

In time sensitive ones like meningitis

411
Q

WWhy might a baceriostatic antibacterial work better?

A

Redce toin production, less of an endotoxin surg and reducsed repease of bacterial components

412
Q

Which antibiotics are time dependant?

A

beta lactams, clindamycin macrolides and oxazolodonones

413
Q

What is a time dependant antibiotic?

A

One that needs extra time to work on the bacteria

414
Q

What is a concentration dependant drug?

A

One that simply requires high levels of the drug to wor not a long time

415
Q

What are the phases pf HIV infection?

A

1 acute primary infection can have acute seroconversion illness then asymtomatic phase and early symptomatic HIV finally AIDS when CD4<200

416
Q

What happens to viral levels and CD4 in primary infection?

A

viral load increases rapidly and CD4 drops and then recovers viral load can drop again

417
Q

WWhat happens when AIDS starts?

A

CD4 has dropped below 200 and virus increases rapidly

418
Q

What are examples of AIDS related conditins?

A

Candidiasis oesophageal or lung, extra-pulmonary cryptopcoccosis, CMV, mycobacterium TB, HSV muco-cutansoud ulcer, recurring bacterial pneumonia. Invasive cervical carinoma, kaposi’s carcinoma, primary CNS lymphoma HIV dementa HIV associated wasting

419
Q

What is likely to occur in Primary HIV infection?

A

2-4 weeks get abrupt onset of non-specific symptoms, fever weight loss lethargy depression aseptic meningitis and oportunistic infections but unlikely

420
Q

What are early symptomatic HIv symptoms?

A

oral vaginal candida, oral hairy leukoplakia, VAV mroe episodes or multiple dermatomes, cervical dysplasia, peripheral neuropathy, bacillary angiomatosis, Immune-mediated thrombocytopanic purpura PID listeriosis constitutional symptoms for greater than 1 month

421
Q

When should you consider testing for HIV?

A

recurrant shingles, candidaisis especially if with risk factors for HIV

422
Q

Where do HIV drugs act?

A

Fusion inhibitors reverse transcriptase inhibitors and protease inhibitors

423
Q

If a patient has TB what should test for as well?

A

HIV

424
Q

What is HAART?

A

Highly active antiretroviral therapy

425
Q

How does HIV develop resisstance?

A

Non-adherence, Drug-Drug interactions lanzoprazol,

426
Q

What type of virus is HIV?

A

Retrovirus and a lentivirus

427
Q

What are the types of HIV?

A

Main Outlyin and New, there are lots of types A-K B is predominant in europe

428
Q

What are the stages of virus replication for HIV?

A

Attachment via cell receptors, cell entry carrying the nucleic acid and some proteins, interaction with host cells, replication, assembly of the virus, and release by exocytosis overtime

429
Q

What is the function of reverse transcriptase?

A

It turns RNA into singlestranded DNA then into doublestranded DNA

430
Q

Which cells can HIV infect?

A

CD4+ cells like t cells, macrophages and maybe dendritic cells

431
Q

What is the bodys humoral immunity to HIV?

A

Poor slow to develop antibodies the glycoprotein on HIV is poorly immunogenic

432
Q

What is the bodys cell mediated response to HIV?

A

CD8 cells initially do have an effect but are not produced in high enough concentrationt to remove the virus,

433
Q

Why is an HIV vaccine not already around?

A

Not identified a protective immune response against HIV so can’t expect to sensitise the body to it

434
Q

What are long term non-progressors in HIV?

A

Hetrogenous indivduals who dont get AIDS, genetic factors and high CTL responses and MHC HLA difference may be the cause

435
Q

What are the consequences on the immune system on HIV?

A

Excessive and inappropriate activation of immune system. Decreased proliferation in response to antigens, Skewing of CD4 t cell receptors and more memory cells CD8 cells are less cytolytic, B vell show enhanced activation and decreased proliferation with decreased antibody secretion

436
Q

What are the 3 type of genes in HIV?

A

Structural regulatory and accessory

437
Q

What is CCR5?

A

chemokine receptor that HIV uses to bind after CD4

438
Q

What is the error-prone replication?

A

HIV has at least 1 error per replication

439
Q

What is a key driving force for HIV infection?

A

The immune response

440
Q

What makes HIV-1 hard for immune system to respond to?

A

Has human like sugars, the key parts of envelope cover the antigenic parts of the virus, there are very few docking parts

441
Q

Why is treated HIV life expectancy lower?

A

The immune systems response

442
Q

Which countries are increasing in HIV infections?

A

Eastern europe from IV drug use, africa

443
Q

When are viral infections most dangerous?

A

in the first few days of getting symptoms

444
Q

Which groups can viral infections affect the most?

A

immunocompromised patients, pregnant women, smokers, infants

445
Q

What are the stages of VZV rashes?

A

Macule then raisted spot, fluid filld spots, puss filled spots then crust over and fall off

446
Q

How can chicken pox be distinguished from other viral infection?

A

rash distribution is over the hot areas of the body. Cropping where lesions are at different stages

447
Q

Where are the small pox rashes?

A

The extremities

448
Q

How can you test for chicken pox?

A

green viral swab, prick vesicle and swab it

449
Q

What are some complications of chicken pox?

A

Dehydration, haemorragic change, cerebellar ataxia, encephalitis pneumonia, soft tissue infections more happen in adults

450
Q

What is foetal varicella syndrome?

A

Foetal infection occurs in 10-15% of cases of chicken pox in pregnancy, can get shingles in first year can have sever defects, limb hypoplasia, visceral ad cocular lesions, microcephaly and growth retardation cicatricial skin scaring

451
Q

How can mother be protected from foetal varicella syndrome?

A

Test for immunity

452
Q

What is hutchinsons sign?

A

skin on nose has shingles as can affect the eye

453
Q

What is enteroviruses?

A

hand foot and mouth pustules, can cause cardiomyopathy

454
Q

What gives lesions on palm?

A

Secondary Syphilis, enterovirus

455
Q

What is parvovirus B19?

A

slapped cheeks rash body more affected in adults. reticular virus. Can cause haemolytic anaemia from destroying reticulocytes

456
Q

What does herpes simplex look like?

A

Vesicles occur on the mucosa of lips and skin. can have antiviral therapy

457
Q

What do you see in Primary CMV?

A

can have rash and lymphadenopathy, CMV can cause end organ failure

458
Q

What is the problem with measals?

A

Morbilliform rash, sparing on pressure points, coplic spots on throat. R is very high. needs reporting to PHE

459
Q

What is dengue shock syndrome?

A

When the tourniquet put on get a lot of bruising

460
Q

What are the groups of worms?

A

Nematodes (round worms)
Trematodes (flatworms of flukes)
Cestodes (tapeworms)

461
Q

What is worm like in UK?

A

Rare in UK, adult worms cannot usually reproduce without a period outside the body. produce a lot of larvae

462
Q

What is pre-patent period?

A

The time between infection and the eggs exiting body

463
Q

What are intestinal nematodes?

A

Soil-transmitted varieties, all are transmitted human to human via eggs

464
Q

What are ascariasis?

A

20-30cm worms round worm can get through meatloop through lung mucosa then get swallowed again

465
Q

What are the signs and symptoms of roundowrms?

A

Loeffler’s sydrome from lungs couch fever CXR infiltrates, wheeze eosinophilia, can cause obstructions

466
Q

How are roundworms treated?

A

oyrantel mebendozole vert treatable

467
Q

What are hookworm?

A

Very thin worms very small but 40-100 days before see eggs coming out, crawl through the skin pulmonary symptoms

468
Q

What is commonest reason for anaemia?

A

hookworms

469
Q

What is the most common worm in UK?

A

enterobius vermicularis pinworm or threadworm. contact with foamites get eggs then eat then replcates in bowel and lay eggs outside body then ingested by next host

470
Q

What are the clinical symptoms of pinworms?

A

Puritis ani affects whole families,

471
Q

What are whipworms?

A

Quite large 3cm. straining to the toilet, can cause bowel prolapse 1,000 cases a year in UK 70-90 day incubation

472
Q

What is an example of way to diagnose worms?

A

Eosinophils high

473
Q

What is Toxicaris cannis?

A

Comes from dog poo and infects children, can infect the eye, hepatomegaly, splenomegaly.

474
Q

What is Anisakiasis?

A

From eating raw fish

475
Q

What are dracunculus, medinensis?

A

1 meter long. guinaeworm. comes out of skin when ready erupts whilst showering. comes from fresh water from a crustacean.

476
Q

What is filaria?

A

Insect born, commonest cause of elephantiatis, Ear blood sample.DEC and ivermectin

477
Q

What is Loa loa?

A

eyeball worm west africa

478
Q

What are tapeworm like?

A

Live in beef, some take as weight loss, can be not too bad

Phase 2 mine (13 decks)

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