ICS pharmacology Flashcards
1
Q
What are some issues with drug delivery ?
A
Absorption, distribution, metabolism and excretion
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
3
Q
What can affect the distribution of a drug?
A
Binding to proteins or not
4
Q
What can affect metabolism?
A
which pathway the drug takes normally and how this is affected by other substances
5
Q
What is pharmacodynamics?
A
How the drug affects the body
6
Q
What is pharmacokinetics?
A
Describes the disposition of a compound within an organism and includes ADME
7
Q
What is drugability?
A
ability of proteins to bind small molecules with high affinity
8
Q
What do most drugs target?
A
Proteins such as receptors, enzymes, transporters, ion channels
9
Q
What is an exogenous ligand?
A
A substance that comes from outside the body
10
Q
What is an endogenous ligand?
A
A substance from the body like a neurotransmitter or a hormone that binds to a receptor
11
Q
What are the types of receptors?
A
Ligand-gated ion channels, Gprotein coupled receptors, kinase-linked receptors, cytosolic/nuclear receptors
12
Q
What are types of drug interaction?
A
Synergy, antagonism or other like potentiation
13
Q
What are patient risk factors for drug interactions?
A
polypharmacy age genetics
14
Q
What is the theraputic window?
A
The range of doses that can give an effect without being toxic
15
Q
What are the adsorptive affects of drugs?
A
Motility of the GI, Acidity, solubility, complex formation, direct action on enterocytes
16
Q
What is celation?
A
Binding of substances together
17
Q
Which enzymes are involved with drug handling?
A
CYP40
18
Q
What is metronidazole problems?
A
blocks alcohol dehydrogenase so can get bad side effects
19
Q
Which drugs have a lot of interactions?
A
Anti-psychotic drugs
20
Q
What are the type of antagonists?
A
Competitive or non-competitive
21
Q
How to avoid interactions?
A
Use the BNF and prescribe rationally. Ask ward pharmacists and Patient information leaflet
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
23
Q
What is an agonist?
A
A ligand that binds to a receptor to activate it
24
Q
What is an antagonist?
A
A compound that reduces the effect of an agonist
25
What is EC50?
What dose gives 50% of maximal effect
26
What should an antagonist do?
not cause a response in the molecule and should block the effect of an agonist
27
What factors govern drug action?
Receptor related affinity efficacy tissue related receptor number and signal amplification
28
What are agonists and antagonist properties?
both have high affinity byt antagonist has no efficacy
29
What is receptor reserve?
Dont need all receptors to get maximall response.
30
What is a partial agonist?
It cannot illicit a maximal response
31
What is signal amplification?
The level that the initial signal is amplified by receptor mediated reactions inside the cell
32
What are the types of enzyme inhibition?
Irreversible inhibitors and reversible inhibitors
33
What are unintentional non adherance?
Forgetting, can't pay for drugs, can't understand instructions, problems using treatment
34
What are intentional non-adherence?
patient's beliefs about their health, beliefs about treatments personal preferences
35
What is necessity-concerns framework?
Validated questionnaire look at their beliefs about medicine
36
What are the main routes of drug administration?
Oral, intravenous, intra arterial, intramuscular, subcutaneous, inhalational, topical sublingual rectal and intrathecal
37
How can drugs cross membranes?
Passive diffusion, ion channels diffusion, facilitated diffusion, pinocytosis engulfing of the molecule
38
What stops drugs passively diffusing?
Being repelled by the membrane because its not lipid soluble
39
What uses diffusion channels?
Lithium
40
What can carrier mediated transport do to drugs?
Some can remove drugs from cytoplasm and others can inhibit certain pumps to change effectiveness of a drug
41
What does OAT1 do?
Penicillin secretion and uric acid probenecid can stop this excretion
42
What is drug ionsiation?
Drugs are often weak acids or bases this can effect how they bind to receptors
43
Why is pH and acidity of drugs important?
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
44
Why is oral route often used?
High blood flow and surface area of drugs, easy and convenient but are obstacles
45
What problems are there with oral route?
Drug structure, drug formulation, gastric emptying and first pass metabolism
46
How does drug structure affect absorption in the intestine?
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
47
What is a problem with opioids?
addiction and become tolerant to it
48
What are some opiate derivatives?
Morphine coedine, diamorphine, oxycodone
49
What is the antagonist of morphine?
Naloxone
50
What happens to morphine in the liver?
The liver absorbs 50% of it
51
What are the routes of administration for morphine?
orally, subcutaneously, intramuscularly, iv, epidural
52
What is the controlled drugs legislation?
need two signatures for controlled drug prescriptions be careful writing prescriptions for them
53
How do opioids work?
descending inhibition of pain they stop the perception of pain. its part of fight or flight mecanism and isnt designed for sustained use
54
What do opioids act on?
4 different opioid receptors
55
What is the difference between potency and efficacy?
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
56
What is tolerance vs dependance?
Down regulation of receptors with prolonged use need higher doses to achieve the same effect. Dependency is the reliance upon it
57
What are the side effects with opioids?
Respiratory depression, sedation, nausea vomiting, constipation, itching.
58
What to do in respiratory depression?
naloxone carefully and support breathing
59
How quickly can they lose effectiveness?
Within weeks
60
When should opioids be used?
cancer pain and surgery
61
What is coedine?
Need an enzyme to convert it to the morphine. Don't use it in children or breastfeeding women
62
What is the excretion pathway for metabolismof morphine?
Morphine goes to morphine 6 glucuronide which is more potent excreted by kidney but with poor kidney function it can cause a serious issue
63
What is tramadol?
Weak opioid it is a prodrug needs to be activated. can interact with SSRIs
64
What is the oral bioavailability of morphine?
50%
65
What is drug formuation?
The mechanism for drug delivery some tablets dissolve slowly
66
How can gastric emptying affect the drugs?
the amount of time the stomach takes can affect how you absorb it
67
What is first pass metabolism?
how the drug gets to the target site and how its modified on its way
68
What can be involved in the first pass metabolism?
The intestinal lumen, the lungs, the liver.
69
How can the intestinal lumen affect the drug?
Contains digestive enzymes and peptide drugs can be broken down by proteases and colonic bacteria can reduce drugs transport back into the lumen
70
how does the liver affect drug absorption?
The liver can remove substances or modify them which can
71
What is a way to avoid the liver metabolism?
rectally or sublingually or skin
72
Why use transcutaneous?
Slow continued absorption, need potent drugs though
73
Why use intradermal or subcutaneous?
Skips waterproof layer limiited by blood flow and only small volume but also local effects and limits rater of blood flow
74
Why use intramuscular?
Depends on blood flow and watersoluble. can be slow releasing if deposited with lipid stuff
75
Why would you use intranasal?
fast and for it to be local
76
Why inhalation?
Large SA, can be toxic to alveoli though
77
What is the importance of distribution of the drugs?
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.
78
How can protein binding affect drugs?
Albumin can bind to drugs and can lower free concentration and can't be released back into the blood
79
Which drugs can pass to the brain?
lipid soluble drugs easily pass to it but can transport drugs out of the brian
80
What happens with drugs and pregnancy?
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
81
What is involved with elimination?
Metabolism and excretion
82
What is a phase 1 reaction?
Makes it more hydrophillic by exposing OH or adding molecules to make it more soluble
83
What can affect CYP?
Grapefruit, foods and alcohol and smoking alcohol and smoking speed them up
84
what is a phase 2 reaction?
Involves joining of drugs with a metabolite to have active groups to make them more soluble
85
Which ways can drugs be excreted?
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
86
What affects urine excretion?
Secretion and absorption in the kidney
87
What is first order kinetics?
Taking a blood sample where it reduces by the same fraction over time eg it has a half life
88
What is it called when an enzyme system is saturated?
Zero order kinetics because it is removed at the same rate whatever the concentration eg alcohol
89
What is a good measure for first order kinetics drugs?
Half life
90
What is bioavaoilability?
How much of the drug reaches the the blood stream unmodified
91
What is adrenergic and cholinergic pharmacology important?
Control of hypertension, control of heart rate, anaesthetic agents, regulation of airway tone, pressure in the eye, control of GI function
92
Why does it matter that cholinergic pharmaceuticals?
They can affect all aspets of the body as well as the desired system
93
What are the types of autonomic receptors?
Muscarine and atropine opposes it and nicotinic receptors and curare
94
What are the sympathetic ganglia like?
They occur close to the spinal cord and have long post ganglionic neurons
95
What do the post-synaptic nerve fibres of parasympathetic use as a transmiter?
Acetylcholine that affects muscarinic receptors
96
What do the post synaptic nerve fibres of sypathetic nervous system use as neurotransimttters?
alpha/beta adrenergic receptors activated by noradrenaline
97
Which organs are innervated by only sympathetic nervous system?
sweat glands and blood vessels
98
Which organs are only parasympathetic innervation?
Bronchial smooth muscle
99
What are the things to interfere with pharmacologically in the autonomic nervous system?
Acetylecholine used in both, noradrenaline used in sympathetic
100
At which stage is the same neurotransmitter released in both systems?
they both release acetylcholine in the first junction
101
What is released in post-ganglionic parasympathetic fibres?
acetylcholine that acts on muscarinic receptors
102
What is released at the sympathetic post ganglionic fibre end?
noradrenaline acting on alpha and beta adrenoreceptors although sweat glands it is Ach and muscarinic
103
What are other pathways?
Non-adrenergic, non-cholinergic autonomic transmitters such as NO vasoactive intestinal eptide or ATP and neuropeptide Y
104
What does nicotine stimulate?
Nicotine stimulates all autonomic ganglia by nicotinic receptors
105
Where does muscarine act?
Activates the muscarinic receptors of the parasympathetic nervous system
106
What type of receptor are muscarinic receptors?
7 transmembrane protein g coupled receptor with Trimeric g proteins
107
Where are the 5 muscarinic types of receptor found?
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
108
What are some muscarinic agonists?
Pilocarpine stimulates salivation, contracts iris smooth muscle to treat glaucoma but it can slow the heart
109
What are some muscarinice antagonists?
Atropine can block parasympathetic hyoscine, local delivery can give specificity
110
What is the use of a muscarinic antagonist?
To prevent bradycardia and BP drop and dry sectetions or to treat excessive betablockers
111
What drugs are used for treatment of bronchoconstriction?
anti-muscarines like ipratropium bromide short acting and tiotropium (mainly blocks M3 receptors) glycopyrrhonium
112
What is the use of anticholinergics in palliative care?
In stopping painful spasms of the GI tract
113
where is Ach used outside of the autonomic system?
In memory formation tends to treat nausea and used in sceletal muscle nicotinic receptors
114
What are common side effects of anticholinergics?
memory loss and confusion constipation dryng of the mouth and tachycardia and
115
What are cholinergic side effects?
muscle twitching and paralysis, salivation and confusion
116
What is the difference between noradrenaline and adrenaline?
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
117
Where are alpha 1 receptors found?
blood vessels but not brain lung and heart
118
Where are alpha 2 receptors?
In nose
119
Beta 2 receptors?
in the lungs smooth muscle
120
Where are beta 1 receptors?
increase in heart rate
121
Why are beta 2 agonists good?
They cause bronchial smooth muscles to relaxi and can affect the heart as well
122
What do beta blockers do?
they slow heartrate reduce tremmors but can casuse a wheeze, can lower blood pressure,
123
What is clearance?
The amount of blood cleared of the drug completely per unit of time
124
Why is clearance important?
If you want a constant effect from the drug you need to be able to calculate what the repeated drug dose should be.
125
How many half lives does it take to reach 95% f steady state concentration?
4-5 half lives
126
How can steady state be calculated?
Rate of infusion/Clearance
127
What is involved in oral dosing calculations?
bioavailability the dose and clearance rate and the dosing interval
128
What is a loading dose?
Give a large dose to begin with to load the system to speed up getting to steady state.
129
What is an allergy?
Abnormal response to a harmless foreign material
130
What does Atopy mean?
Tendancy to develop allergies
131
Which allergies are not allergies?
intolerances such as lactose
132
What are some allergic disease?
anaphallaxis, allergic asthma, food allergies, dermatitis
133
What immunoglobulins can be used in allergic reactions?
IgE, IgG4 and IgA occasionall
134
What causes allergy?
Genetic factors and mast cells
135
Which are the main cells involved with allergic response?
Mast cells eosinophils and basophils
136
How strongly does IgE interact with its receptor?
It is quite high and has short half life because it bnds to receptors so hard
137
What is the low affinity IgE receptor?
it is involved with IgE production
138
which is the most importance cell for allergic reaction?
Mast cells variable around the body and involved in many disease proceses and involved in many disease processes
139
What are found in the mast cell granules?
histamine, chemotactic factors proteases cytokines tryptase chymase and proteoglycans, also release over longer time they leukotrieinds
140
What are the effects of mast cells?
Eosinophil attraction and activation, capillary leakage bronchochonstriction
141
How can mast cells be activated?
IgE receptor mediated, by an allergen perhaps, bacterial/viral antigens,
142
What cells are involved in allergy?
Lymphocytes, dendritic cells, neurons, epithelial cells fibriblasts
143
Why are some antigens allergenic?
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
144
What happens in anaphylaxis?
ABCDE very rapid reaction
145
How can you diagnose anaphalaxis serologically?
IgE or direct activation serum tryptase histamine elevated
146
What are the risk factors for anaphalaxis?
Young female drugs fods diagnostic agents
147
What are the main trestment stratergies of allergies?
Avoid allergens, desensitisation, prevent IgE interaction and production
148
What is desensitisation?
Introduce antigen to the skin, in increasing doses but is very dangerous and isn't that effective in asthma
149
How can IgE production be done?
Get Th1 route activated, give Th1 cytokines antagonise IL4 for Th2 Activation
150
what can reduces mast cell activation?
Beta 2 agonists, glucocorticoids and others
151
How does an epipen work?
epinephrine has
152
What is the importance of being aware of adverse drug reactions?
5% of hospital admissions, 10-20 percent of cases in hospitals
153
what are the types of adverse drug reactions?
Toxic effects beyond therpeutic range, collaterl effecs in the range and hypersusceptibilit effects below the therapeutic range
154
Why might you get toxic effects of a drug?
If its not removed as fast as it could be by kidney, interaction with other drugs.
155
What are some collateral effects?
Beta blockers cause bronchoconstriction, antibiotics causin c difficile and pseudomembranous colitis
156
What are hypersuceptibility reactions?
Anaphalyaxis and penicillin
157
What are time independent reactions?
Ones that take place at any time during treatment
158
What are the types of time dependant reactions/
Rapid reactions, first dose reactions, early reactions, intermediate reactions, late reactions and delayed reactions
159
What are the classifications of adverse drug reactions?
Augmented pharmacological Type A B bizarre or idiosyncratic, Chronic delayed end of treatment or failure of therapy
160
What does DoTS system mean?
Dose relatedness, timing eg fast infusions hearing loss patient susceptibility
161
What is a type A reaction?
augmented the intended effect is too much, more than would be expected
162
What is type B reactions?
Not predictble not dose dependant and can't be reversed easily, usually lifethreatening
163
What is a type C reaction?
Uncommon cumulative dose reaction, nephropathy from overuse of drugs
164
What is type D?
Uncommon can be very delayed, eratogenesis, carcinogenic
165
What is type F?
failure to have the required response
166
What are most common anaphalactic causing drugs?
Antibiotics anti cancer, NSAIDS CNS drugs
167
What are the most common systems to be affected?
GI, renal, metabolic, deratologic, endocrine, haemorrhagic
168
What is MHRA?
Medicines and healthcare products regulatory agency
169
What is the yellow card scheme?
Collects adverse drug reactions, and records them
170
Why should we report adverse drug reactions?
to help point out things missed in safety testing
171
What is a black triangle?
Undergoing additional surveillance
172
What goes on a yellow card?
The drug involved the reaction, patient's details and reporter details
173
What is required for an allergic reaction to drugs?
need an exposure then a re-exposure, doesn't have to be serious
174
What is important when a patient says they are allergic?
are they allergic or intollerant how serious
175
What are the two types of drug hypersenstivity?
Anaphalaxis from immunological or non-immuological cause
176
What mediates type 1 hyperensiticity?
IgE mediated
177
What happens in type 1 hypersensitivity?
IgE mediated after exposure then causes mast cell degranulate and repease substances causing a response
178
What happens in anaphalaxis?
vasodilation increased vascular permeability, bronchoconstriction, urticaria, angio-oedema swelling of face and mouth
179
What is a type 2 reaction?
Antibody dependant cytotoxicity, IgG or IgM and antibodies activate complement
180
What are the main features of anaphalaxis?
Immediate response(tablet within hour) rash not always, swelling of lips and face, wheeze, hypotension cardiac arrest
181
What is the management of anaphalaxis?
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
182
What does adrenaline do to affect anaphalaxiss?
Vasoconstriction Beta 1 adenoreceptors for heart, reduces oedema bronchodilates and attenuates mediators
183
Is IgE involved with complement?
no
184
Which cells respond to lots of IgE?
Mast cells Eosinophils and basophils
185
Which type of immunity are mast cells involved with?
both
186
How can Th2 response be suppressed?
IL-12-18 redices IgE production in mice. Anti-IgE therapy with monoclonal antibodies anticytokine antibodies
187
What is a commensal organism?
one that can colonise the hostwith normal circumstances
188
What is an opportunist pathogen?
Only causes disease if defences are compromised
189
How are bacteria names?
Genus then species
190
What are the shapes of bacteria?
Coccus round or bacillus rod,
191
What are the morphologies of bacteria?
Diplococcus, streptococcus(long chain), staphylococcus clusters. chain of rods curves rods vibrio, spiral rod spirochaete
192
What makes a bacterium gram negative or positive?
2 membranes gram negative one membrane gram positive
193
What is the outermost layer of a bacteriu?
Capsule
194
What are Ziehl-neelsen stain used for
Mycobacteria acid-fast bacilla
195
What is the bacterial cell envelope like of gram positive?
Cell membrane with peptidoglycan on the outised with a capsule occasionally
196
What is the bacterial cell envelope like for gram negative bacteria?
inner membrane then lipoprotein and peptidoglycan layer then an outer membrane with lipopolysaccharide layer which is endotoxin
197
What are bacterial spores?
They can protect the bacteria from heat because it holds their DNA
198
What can bacteria live in?
large range of temperature pH.
199
What is doubling time of most viruses?
less than an hour
200
Why is it slow to diagnose mycobacteria?
Their doubling time is very long
201
Which type of bacteria have endotoxins?
Gram negative bacteria
202
What is an exotoxin?
Secreted by bacteria
203
What is the difference between endotoxins and exotoxins?
Protein endotoxins vs lipopolysaccaride xotoxis are specific heat labile strong antigenicity produced by both and can bec converted to toxoid
204
What is bacterial conjugation?
Transfer of genetic material between two of them by sex pilli
205
How can bacteria be classified?
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
What are the sages of gram staining?
Crystal-violet staining then washing with alcohol and then another stain to be able to see gram negative
207
What is the structure of the outer membrane of gram-negtive bacteria/
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
What is the envelope structure of mycobacteria?
They ajve am iter lipit bilayer with mycolic acids they have no proteoglycans
209
Which are importang gram negative phyla of bacteria?
Proteobacteria, chlamydiae, spirochaetae and bacteroidetes
210
Which are the important positive bacteris?
Actinobacteria, firmicutes, tenericutes
211
What is virulence determinants?
An aspect that contributes to pathogenicity of an organism
212
What are some factors of virulance?
Adhesisns, invasins nutrient aquisition defence against the host and toxins that usually secrete protein substances
213
What are enterobacteria?
Most motile and are rod shaped, anaerobic but can be aerobically ssome colonise the intestinal tract
214
What is Shigella flexnei?
Causes GI infections not motile. cannot use lactose
215
What is Escherichia coli?
Can use lactose unlike salmonella and is motile causes GI infections
216
How is the use of Macconky-actose agar useful?
has pH indicator if Lactose is used as substrate it produces lactic acid changing colour of the pH so must be E. coli
217
How can flagella and other structures be detected?
Using antibodies to detect structures
218
What are serovars?
Organisms of the same species but with different strains as they have different surface antigens
219
What is often an infection caused by E.Coli?
Wound infections, UTI, gastroenteritis, traveller's diarrhoea, bacteraemia sepsis syndrome, meningitis occasionally
220
What makes some E.coli pathogenic?
Have a commonDNA sequences but cna aquire a pathogenic variant of new genes from other bacteria from lateral gene transfer causing pathogenicity islands
221
What do enterotoxigenic E.coli do?
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
How do EHEC and EPEC wor?
Inect a protein into the cell and then attach itself usin that receptor to attach itelf
223
What are Enetoinvasive bacteria?
they don't release a toxin
224
What are symptoms of shigella?
Blood in diarrhoea and frequent stool passage
225
How does Shigella get to the enterocytes?
They enter thrugh M cell to destroy undrlying macrophage and then pass through the cells disctroying gut epithelium
226
What toxin does shigella do?
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
What are three main types of salmonella poisoning?
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
How is gastroenteritis mediated?
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
What happens in enteric fever?
The infection spreads in macrophages around the body causing systemic infection
230
What does proteas mirabilis do?
It travels and can swim it breaks down urea and cause kidney stones long term
231
What is vibrio cholerae?
causes pandemics, from salt water environments, from contaminated water by shell fish
232
How does cholera spread?
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
How is the cholera pathogenic?
It adheres to the TCP pilli cholera toxin which goes into cells and activates CFTR again to give diarrhoea
234
What does Pseudomonsa aeruginosa do?
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
What happens in P. aeruginosa in CF patients?
It mutates in their lungs during chronic infection and leads to mucous producing bacteria that make F worse
236
How many fungi are pathogenic to mammals?
150
237
How common is an invasive disease of fungi?
1%
238
How dangerous are fungal infections?
They kill more globally than breast cancer
239
What type of infections are fungal ones normally?
oportunistic
240
What is endemic mycoses?
fungal diseases that are often only found in tropical regions
241
What forms do fungal infections take?
Skin infections including keratitis, mucosal infection mild but occasionally debilitating, invasive infection that is very likely to cause death
242
What are the natural reservoir of fungal infection/
animal vectors, commensal they live just on the body, most are environmental organisms
243
Why are fungal infections more common in fish than animals?
They don't survive well at our body temperature
244
Where do most fungal infections go?
into the upper layers of the skin onlyand feed of keratin
245
What is fungal eye keratitis?
Ulceratve corneal infection, common cause of blindness.
246
What are fungal wound infections like?
Traumatic injury rare complication of chronic wounds they are devastating
247
What are the major fungal disease?
Candida oral thrush, three main species with one new one which is resistant to anti microbial agents
248
What is aspergillosis?
in the environment found in warmer temperatures like compost heaps, conidial fungus with spores.
249
What disease can aspergillosis cause?
causes invasive disease in immunocompromised allergic response, chronic pulmonary can happen with compromised immunity
250
What is pneumocystis pneumonia?
Parasite of the lung only not sure how it transmitted mild or subclinical infection lots of uncontrolled HIV
251
What is cryptococcus?
in a ring and have a capsule cause meningitis, found in the environment
252
What is the theory behind treating fungal disease?
Selective toxicity, kill fungi or inhibit more than standard cells
253
Why is it hard to target fungi?
DNA/RNA synthesis is similar they are more similar to us than bacterial cells
254
What do antifungals work on?
Echinocandins to attack the cell wall, amphotericin, azoles, terbinafine that dammage ergosterol the human cell membrane
255
How can the cell membrane be attacked?
Polyenes form a pore in the membrane to allow he contents to leave the fungal cell
Ergosterol synthetic pathway inhibitors
256
What do Azoles do?
Stop formation of ergosterol, originally for candida but can act in other organisms
257
What are the side effects of azoles?
GI symptoms can have reversible visual disturbances photosensitivity CYP450 interaction depending on relative affinity of drugs for individual enzymes
258
What are problems with echinocandins stop cell wall synthesis?
Not too many but generally not too many interactions, fungicidal, susceptible to yeasts fungistatic to moulds. IV only. type 1 hypersensitivity only sometimes
259
What is febrile?
Feverish
260
Why is it hard to diagnose fungal disease/
the tequniques in blood culture etc is quite hard to diagnose fungal compared to bacteria
261
What is the best way to detect fungal infection?
using aspirated or biopsy
262
What is the most common fungal infection?
Fungal nail disease, dont tend to cause infection systemically from too high temperature, sometimes caused by non dermatophytes
263
What are differentials for nail infection?
psoriasis lichen planus trauma eczema yellow nail syndrome, lamellar onychoshizia, periungual squamous cell malignant meanoma alopecia areata
264
What is Onychomycosis?
Nail fungal infection, poor treatment outcomes take a long time to act due to nail growth being slow
265
What usually causes osteomyelitis?
staphylcoccus aureus
266
How can staphylococcus be further divided?
Into coagulase positive or negative that can protect the bacteria from phagocytosis
267
How are staphylcoccus aureus spread?
Carriers and shedders, coughing and sneasing
268
What is MRSA?
resistant to beta lactams, gentamicin erythromicin tetracycline.
269
How is staph. aureus virulent?
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
What are the three types of conditions associated with staph aureus?
Pyogenic, Toxin mediated, Coagulase negative
271
What are virulence factors for coagulase negative staphylcocci?
opportunistic in catheters, ability to form persistent biofilms some can produce kidney stones
272
What is beta haemolytic?
destry RBC completely
273
What is alpha haemolysis?
it splits haemaglobin by release of H2O2
274
What are the ways you can group streptococci?
Haemolysis, Lancefield typing and biochemical properties
275
What is special about haemophilus influenzae?
Causes meningitis sinuses, bronchopneumonia bacteraemia, pneumonia
276
Which plate can show factor Y?
Chocolate agar
277
What are the benefits to a bacterium having a capsule?
Can penetrate the nasopharengeal epithelium and resistance to phagocytosis and complement system
278
What does haemopholus influenza LPS do?
Avoids activation of complement, inflammation
279
What are sources of Legionella pneumophila?
warm man made aquatic environments
280
What does leigonella do to the macrophages?
It lives in it and protects itself in the phagosome and then go back to individual form then leave macrophage
281
What does fastidious organism mean?
Need nutrient rich environment
282
What toxins do pertussis produce?
pertussis toxin, and a shiga-like toxin that stops adenylate
283
What are neisseria?
Diplococci, gonorrhoea and meningitidis
284
Where are you likely to find outbreaks of meningitis?
In person to person transmision in areas of high population
285
What is the pathogenesis of Neisseria meningitidis?
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
What are the virulence determinants of meningitis?
Capsule has anti-phagocytic properties, LPS causes cytokine cascade and sepsis
287
What are the properties of gonorrhoea?
Person to person only, higly asymptomatic, can infect genitalia and also eye occasionally non-capsulated
288
What are campylobacter?
Spiral rods, they are unipolar or bipolar flagella. cause a lot of food poisoning low infective dose can shed for 3 weeks
289
What is helicobacter pylori?
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
What are bacteroides?
They are commensals of the large intestine can cause opportunistic tissue injury
291
What are chlamydia and chlamydophila?
They are very small bacteria and non-motile and obligate intracellular parasites. often live asymptomatically in symbiotic organisms cannot culture them
292
What is the lifecycle of chalmidia?
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
What are the types of chlamydia?
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
What are spirochaetes?
Long spiral bacteria often free living and non-pathogenic 3 are pathogenic
295
What the purposes of endoflagellum?
Good for moving through viscous fluids
296
What are important spirochetes?
Lymes disease, borrelia burgdorferi, leptospira interrogans, leptospirosis Weil's disease, siphyllis
297
What are stages of syphilis?
primary wount ulcer, secondary lyph infection and teriary where dammage is not reversible
298
What shape are mycobacteria?
Rods
299
What damage can mycobacteria produce?
Ulcers bone destruction, nodule, deforming
300
How big is the burden of TB?
very big much more than other diseases as it has been around a long time?
301
How do you treat TB?
Treatment of Antibiotics for 2 months and then others for 4 months and can have hepatotoxicity and neuropathy
302
What is the problem with TB?
It is becoming drug resistant there are some totally drug resistant strains
303
How does TB infect the body?
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
How does TB infect the body?
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
What does the TB do to the lungs?
Granulomas around bacilli that settle in the apex of the lung with more air with less blood flow
306
What is the primary complex?
Granuloma, lymphatics, lymph nodes
307
What are the common tissues TB infects?
Meningits, bone and joints, kidney etc
308
Where does mycobacteria sit?
Technically gram positive but it doesnt stain neeed to use Ziehl-Neelsen stain acid fast positive
309
How is TB usually detected?
augumented staining
310
What is different about the cell envelope of mycobacteria?
waxy coating outside the other layers
311
How long does it take for mycobacteria to replicate?
15-20hours making hard to target replication in antibiotic treatment
312
What does the body do to respond to mycobacteria/
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
What is a granuloma?
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
What can destabilise a granuloma?
TNF alpha depletion, HIV,
315
Which diseases cause granulomas?
Leprocy and TB
316
What are the forms of leprosy?
Tuberculoid leprosy, lepromatous leprosy.
317
How can TB be diagnoses?
Solid or liquid culture but takes a lot of time as selective antibiotics to remove others takes weeks, Nucleic acid detection PCR detection
318
How can latent TB be detected?
T cell response use tuberculin skin test SC derivatives of TB that can give skin swelling and redness if you already have it
319
How can TB be studied?
in animal models like mouse Guinea pig and rabbit also zebrafish, and Primates
320
What are some serious virus?
Flu viral stomach infection HIV/AIDS
321
What are some globally important viruses?
Spanish flu, Ebola MERS
322
What are the importance viral problems for the uk?
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
Why are immunosuppressed patients problems?
They can get CMV or EBV can reactivate afterwards
324
What is a virus?
An infectious obligate intracellular parasie and has DNA or RNA surrounded by a coat and or a membrane
325
What are the shapes of viruses?
Helical icosahedral, complex
326
What size are viruses?
They are much smaller than bacteria but they have a large size variation
327
How do viruses replicate?
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
How do viruses cause destructio of cells?
Infects a cell population and splits the ell after the viruus has replicated
329
How do viruses cause change to host cells?
They can cause chages in the cells eg atrophy of villi causing problems with the functioning of the cells
330
How can viruses cause immine issues?
Heapatitis attacks the cells and displays its viral antigen on the cell and then the immune system attacks the cells
331
How do viruses cause proliferation?
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
How do viruses evade host defences/
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
What is secondary infection
When a latent virus can come back up an eg chicken pox can cause shingles
334
How else can host defence be evaded?
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
How can viruses be detected?
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
What is the most important staphylococcus?
It is gram positive, Saureus is coagulase positive it is found in the nose and skin
337
How is staph.aureus spread?
aerosol and touch
338
What are characteristics of streptococcus pyogenes?
beta haemolytic facultatively anaerobic penicillin sensitive
339
How are streptococi classified?
Haemolysis and lancefield typing (for coag negative)
340
What is anti SLO test?
To look at antibodies for SLO to test for streptococcal antibodies
341
What are the virulence factors for S pyogenese?
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
Which bacteria form draughtsman colonies?
Strep pneumonia,
343
What can S.pneumoniae cause?
pneumonia, otitis media, sinusitis, meningitis
344
What are the virulence factors for strep pneumoniae?
polysaccharide capsule, inflammatory wall constituent teichoic acid and peptidoglycan and it produces pneumolysin a cytotoxin
345
What are the most virulent viridans streptococci?
milleri group s intermedius s angiosus and s constellatus
346
What are protozoa?
One celled animals, 5 main groups
347
What are the main classifications of protozoa?
Flagellates, amoebae, microsporidia, sporozoa and cilliates
348
Which disease is sleeping sickness?
African Trypanosomaisis,
349
What is african trypanosomaisis?
From tsetse fly bite, causes flu like symptoms, CNS involvement, coma and death diagnoses with blood sample
350
What is American trypanosomaisis?
Chagas disease flu like symptoms can cais cardiomyopathy megaoesophagus and megacolon long term
351
What is Giardiasis?
faeco-oral spread, diarrhoesa bloating flatulance with history of recent travel cysts or trophozoites seen in the stol treat with metroidazole
352
What symptoms can amoeba cause?
Dysentry colitis liver and lung abscesses
353
When do you worry about malaria?
Recent travel and fever? anaemia jaundice hepatosplenomegaly
354
What is Entamoeba hystolytica?
causes sever dysentry, more in tropical areas and sanitation one of the bad amoeba in the gut
355
How is Amaoebosis treated?
Metronisazol
356
What is romana's sign?
a swelling of the eyelid
357
What are the 3 types of leishmaniais?
Cutaneous mucocutaneous and visceral
358
What is Trichomonas vaginalis?
STI sores in genital areas, more in woamen that men,
359
Which form of malaria lies dormant in the liver?
Plasmodium vivax and ovale
360
How does plasmodium get into humans?
Sporosites are injected by mosquito and travel toliver and infect the cells then become Shizonts
361
What hapens in the liver to schizonts?
They rupture and release merozoites into the blood, merozoites go into RBC, enter ring stage trophozoite
362
What hapens after entering the ring stage of malaria?
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
How is malaria transmitted?
The gametocytes mature in mosquito over 9 days
364
what causes symptoms in malaria/
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
What is bad about Pfalciparum?
Causes cytoadherance. rosetting to be protected and swquestration. can cause clots
366
What are haemotalogical changes in malaria/
haemolytic anaemia, haemoglobin uria and jaudice reduced platelets from all the clotting factors
367
Where can malaria cause complications?
Cerebral malaria, renal failure, ARDS, Bleeding and shock
368
How is malaria diagnosed?
using thick and thin films
369
What is the treatment for complicated malaria?
IV artesunate
370
What is split into coagulase positive and negative?
Staphylococci, S aureus is positive
371
Why are coagulase positive dangerous?
They can coagulase blood and can cause a worse infection
372
What is a biofilm?
When bacteria stick togethr to form a community that can work together and share immunity and protects against attacks
373
What attacks bacteria?
IgA, AB C3b Complement and Antibodies toneutralise toxins
374
What cell mediated substance can cause fever?
TNF alpha
375
How do worms evade host defences?
They can establish hyporesponsiveness in the host so that it can't respond to the infection
376
What kind of infections can be caused by staphylococcus aureus?
Wound infectons abcesses, impetigo, septicaemia osteomyelitis pneumonia, endocarditis
377
What are virulence factors for S.pyogenes?
Hyaluronidase to help with spreading streptokinase to break clots C5a peptidase reduces chemotaxis
378
What are Beta-lactams?
Cell wall killers break down peptidoglycan walls
379
What are some beta lactams?
Cefuroxime ceftriaxone cefotaxime, piperacillim-tazobactam penicillins and cephalosporins
380
What is different about cephalosporins?
Good for penecillin allergy better for ressistant bugs get into other parts of the body
381
Why do gram negative bacteria need a different typ of antibiotic?
They are thincell walled and a different structure to gram positive
382
What can you attack using antibiotics?
The cell walls, inibit protein synthesis, inhibit nucleic acid synthesis, anti-metabolites, inhibitors of membrane function
383
What are macrolides?
They inhibit protein synthesis and work on gram positives and atypical pneumonia pathogens
384
What to tetracyclines do?
They inhibit protein syntheis doxycycline, Broad spectrum mainly positive can be used in cellulitis and chest infections
385
What does lincosamides do?
for grampisttves and can turn of toxins made by gram positives
386
What is used or gram negatives?
Ciproflocain, nitrofurantoin and trimethroprime
387
What are antibiotics?
a molecule produced by an organism that kills others
388
What do beta lactams do?
break down the cell wall
389
Which drugs are beta lactams?
Penicillins cephalosporins carbapenems and monobactams, vancomycin also
390
What do beta lactams do?
They disrupt peptidoglycn production by binding covalently and irreversibly to the PBP casuing lysis
391
How could the patient have resistant bacteria?
If they have been on antibiotics in the last few weeks
392
Why might people not be able to take antibiotics?
Pregnancy breast milk, drug interatcions, renal and liver function, age, side effects allergy anaphylaxis risk of C. difficile
393
What are betalactamases?
they are drugs that break down beta lactams to stop them working
394
What is special about amoxicillin-clavulanate piperacillin-tazobactam meropenem and cephalosporins?
They inhibit beta lactamase or dont get broken down it. cephalosporins are not bad for penicillin allergies and get into different parts.
395
What do you use for skin and soft tisue S. aurius?
Flucloxacillin, becasue lots can break down penacillins
396
What is the limitation of penicillin V?
It oly gets enough in the throat if orally so only for throught symptoms
397
Why can penicillin be used in strep throat?
there is no resistance to it
398
What are glycopeptides?
Vancomycin and teicoplanin IV they only do gram positive, they are cell wall weapons
399
What are glycopeptides?
Vancomycin and teicoplanin IV they only do gram positive, they are cell wall weapons
400
What are gram negative rods that are lactose fermentingg?
Keibmosis, E. coli
401
What is gentamicin used for?
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
What is quinolones of?
DNA synthesis oral or IV affects gram negative, usually used in penicillin and UTI and intra-abdominal infections
403
What is the problem with nitrofurantoin?
It is only good in Lower UTI doesn't get to other parts
404
What are beta lactams most effective against?
rapidly multiplying organisms
405
What does metronidazole do?
Nucleic acid synthsis
406
What antibiotics target ribsimes?
Tetracyclines macrolides, lincosamids, aminoglycosides
407
What are we trying to achieve in antibiotics?
Kill bacteria or stop them being hostile
408
What are bacteriostatic antibiotics?
They inhibit replication, but do effectively kill them somewhat
409
What is Minimum bactericidal concentration?
Lowest concentration that required to give a bacteriocidal level
410
When are bacterocidal antibiotics most important?
In time sensitive ones like meningitis
411
WWhy might a baceriostatic antibacterial work better?
Redce toin production, less of an endotoxin surg and reducsed repease of bacterial components
412
Which antibiotics are time dependant?
beta lactams, clindamycin macrolides and oxazolodonones
413
What is a time dependant antibiotic?
One that needs extra time to work on the bacteria
414
What is a concentration dependant drug?
One that simply requires high levels of the drug to wor not a long time
415
What are the phases pf HIV infection?
1 acute primary infection can have acute seroconversion illness then asymtomatic phase and early symptomatic HIV finally AIDS when CD4<200
416
What happens to viral levels and CD4 in primary infection?
viral load increases rapidly and CD4 drops and then recovers viral load can drop again
417
WWhat happens when AIDS starts?
CD4 has dropped below 200 and virus increases rapidly
418
What are examples of AIDS related conditins?
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
What is likely to occur in Primary HIV infection?
2-4 weeks get abrupt onset of non-specific symptoms, fever weight loss lethargy depression aseptic meningitis and oportunistic infections but unlikely
420
What are early symptomatic HIv symptoms?
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
When should you consider testing for HIV?
recurrant shingles, candidaisis especially if with risk factors for HIV
422
Where do HIV drugs act?
Fusion inhibitors reverse transcriptase inhibitors and protease inhibitors
423
If a patient has TB what should test for as well?
HIV
424
What is HAART?
Highly active antiretroviral therapy
425
How does HIV develop resisstance?
Non-adherence, Drug-Drug interactions lanzoprazol,
426
What type of virus is HIV?
Retrovirus and a lentivirus
427
What are the types of HIV?
Main Outlyin and New, there are lots of types A-K B is predominant in europe
428
What are the stages of virus replication for HIV?
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
What is the function of reverse transcriptase?
It turns RNA into singlestranded DNA then into doublestranded DNA
430
Which cells can HIV infect?
CD4+ cells like t cells, macrophages and maybe dendritic cells
431
What is the bodys humoral immunity to HIV?
Poor slow to develop antibodies the glycoprotein on HIV is poorly immunogenic
432
What is the bodys cell mediated response to HIV?
CD8 cells initially do have an effect but are not produced in high enough concentrationt to remove the virus,
433
Why is an HIV vaccine not already around?
Not identified a protective immune response against HIV so can't expect to sensitise the body to it
434
What are long term non-progressors in HIV?
Hetrogenous indivduals who dont get AIDS, genetic factors and high CTL responses and MHC HLA difference may be the cause
435
What are the consequences on the immune system on HIV?
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
What are the 3 type of genes in HIV?
Structural regulatory and accessory
437
What is CCR5?
chemokine receptor that HIV uses to bind after CD4
438
What is the error-prone replication?
HIV has at least 1 error per replication
439
What is a key driving force for HIV infection?
The immune response
440
What makes HIV-1 hard for immune system to respond to?
Has human like sugars, the key parts of envelope cover the antigenic parts of the virus, there are very few docking parts
441
Why is treated HIV life expectancy lower?
The immune systems response
442
Which countries are increasing in HIV infections?
Eastern europe from IV drug use, africa
443
When are viral infections most dangerous?
in the first few days of getting symptoms
444
Which groups can viral infections affect the most?
immunocompromised patients, pregnant women, smokers, infants
445
What are the stages of VZV rashes?
Macule then raisted spot, fluid filld spots, puss filled spots then crust over and fall off
446
How can chicken pox be distinguished from other viral infection?
rash distribution is over the hot areas of the body. Cropping where lesions are at different stages
447
Where are the small pox rashes?
The extremities
448
How can you test for chicken pox?
green viral swab, prick vesicle and swab it
449
What are some complications of chicken pox?
Dehydration, haemorragic change, cerebellar ataxia, encephalitis pneumonia, soft tissue infections more happen in adults
450
What is foetal varicella syndrome?
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
How can mother be protected from foetal varicella syndrome?
Test for immunity
452
What is hutchinsons sign?
skin on nose has shingles as can affect the eye
453
What is enteroviruses?
hand foot and mouth pustules, can cause cardiomyopathy
454
What gives lesions on palm?
Secondary Syphilis, enterovirus
455
What is parvovirus B19?
slapped cheeks rash body more affected in adults. reticular virus. Can cause haemolytic anaemia from destroying reticulocytes
456
What does herpes simplex look like?
Vesicles occur on the mucosa of lips and skin. can have antiviral therapy
457
What do you see in Primary CMV?
can have rash and lymphadenopathy, CMV can cause end organ failure
458
What is the problem with measals?
Morbilliform rash, sparing on pressure points, coplic spots on throat. R is very high. needs reporting to PHE
459
What is dengue shock syndrome?
When the tourniquet put on get a lot of bruising
460
What are the groups of worms?
Nematodes (round worms)
Trematodes (flatworms of flukes)
Cestodes (tapeworms)
461
What is worm like in UK?
Rare in UK, adult worms cannot usually reproduce without a period outside the body. produce a lot of larvae
462
What is pre-patent period?
The time between infection and the eggs exiting body
463
What are intestinal nematodes?
Soil-transmitted varieties, all are transmitted human to human via eggs
464
What are ascariasis?
20-30cm worms round worm can get through meatloop through lung mucosa then get swallowed again
465
What are the signs and symptoms of roundowrms?
Loeffler's sydrome from lungs couch fever CXR infiltrates, wheeze eosinophilia, can cause obstructions
466
How are roundworms treated?
oyrantel mebendozole vert treatable
467
What are hookworm?
Very thin worms very small but 40-100 days before see eggs coming out, crawl through the skin pulmonary symptoms
468
What is commonest reason for anaemia?
hookworms
469
What is the most common worm in UK?
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
What are the clinical symptoms of pinworms?
Puritis ani affects whole families,
471
What are whipworms?
Quite large 3cm. straining to the toilet, can cause bowel prolapse 1,000 cases a year in UK 70-90 day incubation
472
What is an example of way to diagnose worms?
Eosinophils high
473
What is Toxicaris cannis?
Comes from dog poo and infects children, can infect the eye, hepatomegaly, splenomegaly.
474
What is Anisakiasis?
From eating raw fish
475
What are dracunculus, medinensis?
1 meter long. guinaeworm. comes out of skin when ready erupts whilst showering. comes from fresh water from a crustacean.
476
What is filaria?
Insect born, commonest cause of elephantiatis, Ear blood sample.DEC and ivermectin
477
What is Loa loa?
eyeball worm west africa
478
What are tapeworm like?
Live in beef, some take as weight loss, can be not too bad
