Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

PPE > Infection > Flashcards

Infection Flashcards

(188 cards)

Start Studying
0
Q

Give some examples of pathogens using different routes of infection

A

Self - Escherichia coli - Uti
Direct contact - Herpes Simplex Virus - Cold sore
Vector - Plasmodium vivax - malaria
Faeco-oral (food and water) - Clostridium difficile - c diff
Droplet - Influenza - flu
Aerosol - Mycobacterium tuberculosis - TB
Blood - Hepatitis B - hep B
Vertical transmission - cytomegalovirus (placental), Chlamydia trachomatis (delivery)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

Define infection

A

Ann invasion of hosts tissues by microorganisms

Causing disease by microbial multiplication, toxins or host response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Differentiate exo and endo toxins

A

Exo - released by the bacteria usually acting away from the site
Endo - structural components of bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Which types of bacteria are more likely to express endotoxins?

A

Gram -ve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the toxins released by c diff

A

type A create pores in enterocytes

type B are cytotoxic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What pathogen and host factors influence disease severity?

A

Pathogen
Virulence of pathogen
Inoculation size
Antimicrobial resistance

Host
Site
Co morbidities
Age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the two broad categories of investigations for infection?

A

Supportive (e.g. Cxr, fbc)

Specific (e.g. Micorscopy, culture)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What sorts of viruses are effected by alcohol?

A

Enveloped - disrupts their membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Examples of Non enveloped viruses (thus less effected by alcohol)

A 
Paravirus 19 (fifths disease)
HPV (warts)
Enteroviruses (polio)
Noroviruses (D/V)
Rotaviruses (D/V)
Hep A and E
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Give some examples of DNA viruses

A

Herpes viruses
HBV
Paravirus 19
HPV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Counterstain in a gram stain?

A

Safranin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Differentiate the types of fungi

A

Yeast - single cell (e.g. Candida, pneumocystis jiroveci)

Mould - multi cell (e.g. Aspergillus, tinia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Give 3 examples of protazoa and their disease

A

Plasmodium - malaria
Giardia lamblia - giardiasis
Trypanosoma cruzi - chagas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Cause of bilharzia

A

Schistosoma mansoni

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What patient factors influence susceptibility to infection?

A

Age (Stis in teens and 20s, varied levels of immunity to meningococcal meningitis)
Gender (uti and anatomy, suppressed immunity in males)
Physiological state (preggers, puberty/menopause)
Pathological state (immunocompromised, low blood flow)
Drugs (PPIs, steroids)
Social (living cramped, damp)
Time (seasonal infections, incubation)
Place (current - e.g. Hospital, recent - e.g. Travel infections)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the two main categories of infection treatment? What can be done in each?

A

Specific - abx, surgery

Supportive - fluids, o2, pain relief, immunoglobulins, abx against proteins to reduce exotoxin production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the sirs criteria?

A 
2 OF
Temp >38
Pulse >90
Rr >20
WBC 12x10*9
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Give some examples of organ dysfunction seen in severe sepsis

A

Hypotension, confusion, decreased urine output, lactic acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Why does sepsis alter coagulation?

What are the consequences

A

Cytokines initiate thrombin production and inhibit thrombolysis
Endothelial damage exposes TF and impairs prostacyclin production
DIC develops and clots can cause gangrene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the sepsis 6?

A 
Within one hour:
O2
Bloods for culture
Antibiotics administered
Serum lactate
IV fluids up
Urine output monitored
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How is meningococcal meningitis subdivided?

What can we vaccinate against

A

Serogroups a,b, and c

Vaccines for a and c

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What sort of a response does innate immunity provide to the body?

A

Fast and non specific

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the first and second line defences of the innate immune system?

A

First - limits entry and growth

Second - contains and clears

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the four categories of first line innate defences?

A

Physical - eg epithelial barrier, mucus membrane
Physiological - eg d/v coughing, sneezing
Chemical - eg stomach acid, vaginal acid, molecules (lysozymes, IgA, mucous, pepsin)
Biological - normal flora (compete, actively kill)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
How does the stomach act as a chemical barrier to infection?
Acid | Pepsin
25
What is involved in second line innate defences?
Phagocytes Chemicals Inflammation
26
What do phagocytes use to recognise pathogens?
Use pathogen recognition receptors (PRRs) to detect pathogen associated molecular patterns (PAMPs)
27
Examples of PAMPs with associated bacteria
Lipopolysaccerides (gram -ve) Peptidoglycan (gram +ve) Flagellin (flagella bacteria) Mannose rich glycans (mycobacteria)
28
What can enhance recognition of bacteria by PRRs?
Opsinisation with C3b, C4b, IgG, CRP
29
In which bacteria is opsionisation vital?
Encapsulated bacteria - neisseria meningitidis, streptococcus pneumoniae
30
How does phagocytosis occur?
``` PRR recognises PAMP Pseudopods engulph and ingest microbe forming phagosome Phagosome fuses with lysosome Microbe digested leaving residual body Waste discharged from cell ```
31
How do phagocytes kill the microbes..
Oxidative burst | Lysozymes, lactoferrin, proteolytic enzymes
32
What chemical pathways are involved in second line innate immunity?
Compliment | Cytokines
33
How is complement activated?
Classical pathway - antibody antigen complex Alternative pathway - cell surface on microbes (e.g. LPS) Mannose binding lectin - MBL binds to mannose on pathogen
34
What are the active components of compliment? What do they do?
C3a and C5a - chemotaxis C3b and C4b - opsinisation C5-C9 - membrane attack complexes
35
What are the effects of macrophage derived chemical in second line innate immunity?
``` Increase crp Chemotaxis Vasodilation Increase vascular permiability Increase body temperature ```
36
What chemicials do macrophages release?
Tnf alpha Il-1 Il-6
37
In what conditions are second line defences of innate immunity compromised?
``` Asplenia/hyposplenia Decreased neutrophils (leukaemia, chemotherapy) Decreased neutrophil function ```
38
Define a healthcare related infection
An infection arising from a consequence of healthcare both within and out of hospital
39
How are hospital acquired infections differentiated form normal infections?
An infection that was neither present nor incubating at the time of admission (onset of symptoms >48 hrs after admission
40
What are the most common categories of healthcare related infections? What is the in hospital prevalence..
Gi and utis | 8%
41
What can we do to reduced healthcare related infections regarding patient factors?
Screening Prophylactic treatment Optimise physical health Appropriate choice of medications (e.g. Decreased cephalosporins)
42
What can we do to reduced healthcare related infections regarding place factors?
Bed layout with siderooms for high risk patients Pressure isolation rooms Sink and toilets accessible and individual in high risk Sterilisation and decontamination
43
What can we do to reduced healthcare related infections regarding practice factors?
Handwashing Hospital policies (eg. No relative sitting on beds) Leadership up to government level - incentives work Healthcare worker vaccinations Ppe Food hygene
44
What are the subdivisions of streptococcus?
Alpha haemolytic - pneumoniae and viridans Beta haemolytic - pyrogenes Non haemolytic - enterococcus
45
Diseases from strep viridans
Endocarditis | Dental caries
46
Diseases from strep pyogenes
Necrotising fascitis Impertigo Tonsilitis Scarlet fever
47
Diseases from strep pneumoniae
Pneumonia | Meningitis
48
Diseases from staphylococcus
Boils Carbuncles Impertigo Wound infection
49
Treatment options for staphylococcus infection
Flucloxacillin | Co-amoxiclav
50
Treatments for necrotising fasciitis
Initial broad spectrum like tazocin (pipperacillin and tazobactam) Once id as strep pyogenes swich to ben pen Large dose immunoglobulins to neutralise toxins Antiprotein abx like clindamycin to decrease toxins Debridment and amputation
51
Why is travel history important?
``` Different diseases Different strains (resistance change and change in detecting) ```
52
What do you need to know about in a travel hx
``` Where When Via anywhere Doing what Staying where Specific risks (sex, animals, swimming) Preventative measures taken (prophylaxis, vaccinations, bite prevention) ```
53
What should you do with a suspected travel related infection?
Isolate until you know what it is! | Flag as high risk for lab
54
What are the causes of malaria?
P vivax P falciparum P ovale P malariae
55
What is the characteristic fever of malaria? Which subtype differs?
3 day cycling, malariae is 4 day cycling
56
Symptoms of malaria
``` Fever 3 day cycling Headache Cough Fatigue Malaise Arthralgia Myalgia ```
57
What is the usual incubation period for malaria?
1-3 weeks
58
What are the methods of transmission of malaria?
Vector - anaphalies mosquito in endemic region Cryptic - mosi on a plane arriving at non endemic airport Haematogenous Iatrogenic - infected equipment
59
What investigations would you perform in malaria?
``` Blood smear Fbc U and e Lft Glucose ```
60
What are the causative organisms of enteric fever?
Salmonella enterica typhi | Salmonella enterica paratyphi
61
How are Salmonella enterica typhi/paratyphi spread? | How can you reduce your risk?
Faeco oral | Hand hygiene, safe food, vaccination
62
What treatments are effective in enteric fever?
Ceftrioxone | Azithromycin
63
Signs and symptoms of enteric fever
``` Abdo discomfort Cough Constipation or diarrheoa High fever Relative bradycardia Hepatosplenomegally Intestinal haemorrhage and perforation ```
64
Investigations in suspected enteric fever
Fbc Lft Stool and blood cultures
65
How do salmonella enterica typhi/paratyphi cause illness?
Fibriae adhere to epithelium over peyers patches Invasin allows intracellular growth As gram -ve have endotoxins
66
How can salmonella enterica typhi/paratyphi be distinguished in culture from escherichia coli?
They. Are non lactose fermenters | Otherwis both gram neg aerobic bacilli
67
What travel related infection is present in southern Europe?what is the causative organism?
Brucellosis | Brucella abortus/melitensis
68
How does brucellosis spread?
Zoonosis (cattle) Spread via breaks in the skin and via the. Gi tract (e.g. Unpasturised milk) Very rare person to person direct contact spread
69
How does brucellosis present?
``` Non specific flu like febrile illness Bone and joint involvement Epididymitis Weight loss PROLONGED SYMPTOMS Long term complication endocarditis ```
70
How is brucellosis treated?
Doxycycline | Rifampicin
71
What are the two main components of adaptive immunity?
Cellular | Humoural
72
How is mhc adapted to a generalist presenting role?
Co dominant expression giving range of different subgroups | Peptide binding clefts very polymorphic
73
What is the difference in structure of mhc class 1 and class 2?
Class one - three alpha and one beta units Class two - two alpha and two beta units Note that the alpha and beta units are located on separate polypeptide chains.
74
What mhc molecule is active in cellular immunity? Which in humoural immunity?
Cellular - mhc 1 on most cells, both on apcs | Humoural - mhc 2 on apcs
75
How are cytotoxic t cells activated?
CD8 binds to MHC1 on an antigen presenting cell - presenting antigen recognised by t cell receptor T cell binds to antigen on MHC1 on infected cell Costimulation from IL2 produced by activated CD4 TH1 t cells
76
How do activated cd8 t cells kill the cell?
``` Release granzymes (protein digesting enzymes that trigger apoptosis) Release granulysin and perforin (create channels in plasma membrane) ```
77
How does a t cell bind to a antigen presenting cell?
CD4/8 recognises MHC2/1. T cell receptor detects antigen in the MHC
78
How is an antigen attached to MHC1?
``` Sampling of cytosol Proteins broken down by proteasome Fragments released into ER Fragment attached to MHC1 MHC1 moves to cell surface ```
79
How is an antigen attached to MHC2?
Pathogen phagocytosed by APC Pathogen broken down by low pH and proteolysis Vesicle of fragments merges with vesicle containing MHC2 Fragments load onto MHC2 and are moved to cell membrane
80
How are cd4 t cells activated?
Recognise and bind MHC2 on APC | Co stimulated by IL2 from APC
81
What do activated CD4 T cells do once activated?
TH1 - release IL 2 costimulating CD8 cells TH2- costimulate b cells causing them to differentiate into plasma cells. Also activates eosinophils and mast cells TH17 - activate neutrophils
82
What are the different antibodies? | What do they do?
G - opsinisation A - mucosal immunity decreasing aggregation M - initial response to novel antigen E - on mast and basophils involved in allergic reaction/parasites D - B cell receptor
83
What are the main functions of antibodies
Enhancing phagocytosis by opsionisation Neutralisation of toxins Complement activation (classical pathway)
84
In an infection what is the first antibody released? What is released on reinfection? What is different?
IgM | IgG much faster stronger and longer with a higher affinity
85
What are clinical uses of antibodies?
``` Vaccinations Active immunisations (e.g. Rabies) Immunoglobulin therapy Immediate protection (e.g. Post exposure hep b) Diagnostic testing ```
86
What would make a hiv patient a slow progressor?
MHC configured to present antigens of the virus that cannot be altered by the virus, thus the virus cant mutate and avoid being expressed.
87
What is the difference between HLA and MHC
MHC is the protein | HLA is the locus on the genome
88
How can HIV be subclassified generally? What is the epidemiology? Clinical relevance?
Hiv 1 - most common, nearly all western cases Hiv 2 - confined to west africa, more indolent course Different tx
89
How is hiv 1 divided into groups?
M - major N - new O - outlier P
90
How is group M of HIV 1 subclassified!!? | What is the clinical relevance?
A-K - CRF (circulating recombinant forms on co-infection) West mainly B Same tx but different response
91
What is the histological structure of the hiv virus?
Enveloped | SsRNA with reverse transcriptase
92
What is the lifecycle of HiV
Gp120 binds to CD4 Virus fuses with plasma expelling contents Reverse transcriptase converts rna to dna Dna intergrates into host genome Production of viral mrna and proteins Caspid assemble and buds from cell
93
At what point is a hiv infection irreversible?
Once the dna intergrates into the host genome
94
How long is the incubation period for HiV | What happens at the end of it?
2-6 weeks | Seroconversion
95
How does hiv seroconversion present?
Only 25% ill enough to attend hcp | Non specific illness, fever, rash, sore throat, lymphadonopathy, headache
96
How many hiv infected people get seroconversion? What does it mean prognostically?
50-75% | May be at risk of more accelerated disease course.
97
What is the term for the period between seroconversion and symptomatic hiv? What may be present?
Latent period | Lymphadenopathy
98
What may be detectable in a hiv pt undergoing a seroconversion reaction?
Lymphopdnia Low cd4;cd8 ratio Circulating viral rna Viral p24 antigen
99
What causes symptomatic hiv? | How does it present?
Neurotoxins from hiv, cytokine abnormalities, low immunity Aseptic meningitis, dementia, polyneuropathy, puritis, anaemia, anorexia, diarrhoea, weight loss ,
100
What are aids defining illnesses?
``` Candida of lower airways/oesophagus Karposi's sarcoma Tb Pneumocystis jiroveci Cmv retinitis Hiv encephalitis ```
101
What is the hiv core antigen?
P24
102
What blood test will first show hiv? | When?
Viral p24 antigen | 2 to 8 weeks
103
What IgG tests can be used to detect hiv?
IgG to envelope - takes 3 months to build | IgG to core (p24) - detectible after weeks but lost as disease progresses
104
How are hiv antigens detected and assessed?
Elisa followed by western blotting
105
How would you not hiv test a baby of a infected mother?
Using IgG - it crosses the placenta so all babies will be positive
106
What are the general classes of antiretrovirals? | What is the term for the combination used in. hiv?
Reverse transcriptase inhibitors Protease inhibitors Fusion inhibitors
107
What are the subtype of reverse transcriptase inhibitors?
Nucleoside (NRTISs) Nucleotide (NtRTIs) Non-nucleoside (NNRTIs) Highly active antiretroviral therapy (haart)
108
What is a big side effect associated with NRTIs?
Effect mitochondria so lactic acidosis
109
What is the lifecycle of HBV?
Attaches to and enters hepatocyte Looses coat and core enters nucleus Processing of dna with reverse transcriptase New virons enter blood
110
How is hepatic damage caused in hbv?
Immune response against virus
111
What are the immediate outcomes post infection with HBv? What percentage of patients do which?
Acute infections - clear (89%) Acute infection - death (1%) Acute infection - chronic infections (10%
112
What are the symptoms of acute hbv infection?
``` Malaise Jaundice Nausea/vomiting Weight loss Diarrheoa ```
113
What causes death in acute hbv infection?
Fulminant hepatic failure
114
What age group is more likely to develop a chronic hbv infection?
Children (esp infants)
115
How can chronic hbv present?
Progressive - cirrhosis - risk of liver carcinoma | Non-progressive
116
How do hbv antibodies change over the course of a disease with recovery?
Initial rise in HBs antigen and HBc IgG HBs antigen falls HBs IgG rises
117
How do hbv antibodies change in a chronic disease?
Rise and maintainance of HBc IgG and HBc antigen
118
If someone is vaccinated against hbv what antibody would you expect to be high? What would indicate that they had been infected?
HBs IgG If infected HBc antigen and IgG
119
How can HBV be prevented?
Lifestyle changes/PPE HBs antigen vaccination PEP with immunoglobulin
120
Which infection can only occur alongside HBV? In what ways? What is different about the two ways of dual infection?
HDV Coinfection - severe acute disease with low risk of chronic Superinfection - reactivation of HBV with high risk of chronic
121
Why does HDV need HBV?
HDV uses envelope of HBV
122
In what ways can pathogens infect the internal surface of the body or prothesis? Examples of each
Migration - Escherichia coli - UTI Invasion - Streptococcus pyogenes - necrotising fasciitis Haematogenous - streptococcus viridans - infective endocarditis Innoculation - coag -ve staphylococcus - prothesis infection
123
What are the varying causes of infective endocarditis in native and prosthetic valves?
Native and >1 yr prosthetics - Strep. viridans, Staph. aureus, Candida <1 yr prosthetics - coag -ve staphylococcus
124
What are the stages involved in the infection of a prothetic joint? How are bacteria adapted for this?
Adherence - pili/fimbriae Biofilm formation - ecf production, quorum sensing (signalling for neighbours to produce ecf) Invasion and multiplication
125
How do biofilms aid bacteria?
Protection from immune system Protection from abx Nutrients Chemically favourable environment
126
What are the clinical problems regarding biofilms?
Poor abx penetration | Hard to grow as must shake loose first
127
Define hypersensitivity reactions
Antigen specific Immune response Inappropriate or excessive Harm the host
128
What are the four types of hypersensitivity reaction?
Type 1 - antigen interacts with IgE on MAST cells triggering mediators inc. histamine release Type 2 - drug attaches to cell membrane of RBC becoming a hapten then bound by antibodies activating complement causing cell lysis Type 3 - antibody antigen complex not removed from blood by phagocytosis so keeps activating complement causing endothelial damage - can be especially bad if trapped in endothelium Type 4 - activation t cells by hapten protein complex, causes skin inflammation and rash
129
What is the prevalence of allergy? What is the most common? How common is it?
About 50% Peanut 1:50
130
What is the hygiene hypothesis?
Low pathogen exposure (clean living, small family, increased abx, low dirt) Favours increased th2 cd4 t cells which instigate second phase of an allergic reaction
131
What do mast cells release? What do they do?
Histamine - smooth muscle dilation (arterioles) and constriction (bronchioles) Cytokines - stimulate CD4 TH2, promote eosinophils and inflammation Chemokines - attract inflammatory cells Leukotrines - increase vascular permeability
132
How can a diagnosis of allergy be made?
Skin prick testing Blood test for allergen specific IgE Allergy challenge
133
What controls are used in skin prick testing? | Where does it test for reaction
Heparin and saline | Epidermis
134
What are the signs of epidermal allergy, dermis allergy?
Urticaria | Angioedema
135
Management of allergy
``` Allergen avoidance! Education to recognise and get help Epipen Medialert Desensitisation therapy Emergency anaphylaxis tx. ```
136
What levels of disease can transmissable infection cause?
Endemic disease - normal background rate Outbreak - 2 or more cases linked in time and place Epidemic - a rate of infection greater that background rate Pandemic - very high rate of infection across many countries and continents
137
How can we classify if a disease is going to increase in cases, remain constant or decrease in cases?
R0 number - the number of people one case infects If more than 1 then numbers will increase If 1 numbers will be constant If less than 1 numbers will decrease
138
What could lead to an new increase in number of infections?
New pathogens - e.g. Mutation, spread New person - e.g. Migration, newborn baby New practice - e.g. Air conditioning
139
How do the general pattern of cases in epidemics and outbreaks differ?
Epidemics tend to follow a bell curve distribution of incidence against time Outbreaks tend to follow a much more random distribution - they can be large with excellent control or small with non. This can lead to the false belief a certain intervention is effective even when it isn't
140
What is a paradox in polio control regarding immunisation? How can this paradox be applied to a western disease?
Those not immunised are exposed later in life and thus experience more severe disease (increased paralysis) More adult chickenpox and thus increased infertility
141
What are problems with antibiotic resistance generally?
Resistance is irreversible Development has stalled Use causes resistance even if appropriate
142
What are the problems with abx resistance?
Treatment failure More severe treatments required More expensive treatments required Prophylaxis failure
143
What are the different classifications of resistance to abx?
``` Resistant - 1 or more agents in 1or 2 classes Multi drug (MDR) - 1 or more agents in 3 or more classes Extensively drug (XDR) - more than 1 agent in all but 2 classes Pan drug (PDR) - all agents in all classes ```
144
What is the aim of abx stewardship?
``` Improve appropriate abx use Achieve optimal clinical outcome Minimise toxicity Reduce cost Limit resistance ```
145
What clinicians are involved in ABX stewardship?
``` Medical microbiologist Infectious diseases physician Antimicrobial pharmacist Infection control nurse Hospital epidemiologist ```
146
What types of intervention are there for antimicrobial stewardship?
Persuasive - education, consensus between clinicians, reminders, audits, feedback Restrictive - limit abx on susceptability report, restrict formulary, require authorisation, Structural - rapid lab tests to avoid general administration, computerised records
147
What type of abx stewardship intervention is most efficacious?
Initially restrictive but after several months both restrictive and persuasive
148
What are the outcomes seen from abx stewardship?
Non significant reduction in death rate Significant reduction in length of stay Significant increase in readmission (why!)
149
What is the pattern of infection seen in CF patients?
Birth - 3m = haemophillus influenzae 3m - 3y = staphylococcus aureus 3y - teens = pseudomonas aeruginosa teens - 30s = atypical mycobacteria, candida, aspergillus
150
Why are cf patients more at risk of infection?
Lack of mucous clearence Lung damage (bronchiectasis) Steroid treatment
151
Why should cf cf contact be reduced?
Environmental psuedomonas tx is amenable to ABX but given time in a cf pt it develops ability to produce biofilm becoming much harder to treat - this can be spread to other cf patients
152
What pathogens are associated with copd exacerbations?
Haemophilus influenzae, pseudomonas aeruginosa, respiratory syncytial virus, parainfluenza virus, influenza A
153
Why are poorly controlled diabetics more at risk of infection?
Impaired humoural, neutrophil and lymphocyte function Microvascular damage = poor tissue perfusion = damage Neuronal damage = not noticing stimuli = damage Sugar in urine = food for uti
154
What specific infections are associated with diabetes?
Malignant otitis externa Rhinocerebral mucormycosis Utis Ulceration
155
What are risk factors for uti in diabetics?
Increases glucose in urine | Neurogenic bladder that doesn't empty fully
156
What pathogens are prone to infecting diabetic foot ulcers?
``` Staphylococcus aureus Streptococcus pyrogenes (beta haemolytic) ```
157
What is malignant otitis externa?
Otitis externa with psuedomonas aerugenosa that can spread to neighbouring soft tissue and bone
158
What is rhinocerebral mucormycosis?
Mold fungi like aspergillus effecting paranasal sinuses invading blood vessels
159
Does downs syndrome effect risk of infection?
Yes - higher risk of urtis and lrtis due to altered structure of mouth and airways
160
What is an immunodeficiency?
A state in which the immune system is unable to respond appropriately and effectively to infectious microorganisms
161
What immune system deficites (generally) can cause immunodeficiencey
Quantitative | Qualitative
162
What about an infection should make a clinician consider immunodeficiency?
S - severe P - persistent U - unusual R - recurrent
163
Other than infection what are other issues with immunodeficiency?
Linked to autoimmune disease and malignancy
164
What are the categories of primary immunodeficiency? What are each group vulnerable too?
B cell - bacterial infection T cell - viral (and fungal) infection Complement - bacterial infection Phagocyte - bacterial and fungal infection
165
What are the main B cell deficiencies?
``` Common variable immune deficiency IgA deficiency IgG subclass deficiency Bruton's disease ```
166
What is CVID?
Common variable immunodeficiency Inability of B cells to mature into plasma cells Low igg
167
What is brutons disease?
X linked agammagloblinaemia | Impaired b cell development with low igg and iga
168
Hw do b cell deficiencies present?
Recurrent bacterial urti and lrti Gi infections Autoimmune disease Lyphatic and gastric cancers
169
How do you treat b cell deficiencies
Prophylactic ABX Ig replacement Symptomatic management Avoidance of unnecessary radiation due to cancer risk
170
Give two t cell deficiencies
De georges syndrome | Severe combined immunodeficiency (SCID)
171
What are the problems in de georges syndrome
``` C - cardiac abnormalities A - abnormal facies T - thymic hypoplasia C - cleft palate H - hypocalcaemia ```
172
Tx of de georges syndrome
Cardiac surgery Calcium Prophylactic ABX Bone marrow transplant
173
How do SCID diseases present?
Failure to thrive Viral and fungal infections (PCP, CMV, VZV, EBV) Skin and organ abcesses Low t lymphocytes and decreased b activation so low ig
174
How do you treat SCID?
Reverse barrier nursing Abx Bone marrow transplant Gene therapy
175
How do complement deficiencies present?
``` Hereditory angioedema (C1 inhibitor deficiency) Recurrent bacterial infections (C3 deficiency) Neiserria infection (C5-7 deficiency) ```
176
What are the phagocyte deficiencies?
Cyclic neutropenia Leukocyte adhesion deficiency Chronic granulomatous disease Failure of phagosome formation
177
What is chronic granulomatous disease?
Lack of respiratory burst
178
How do phagocyte deficiencies present?
Bacterial and fungal infections of the skin, mucous membranes and lungs
179
How are phagocyte deficiencies treated?
Prophylactic ABX Steroid/interferon gamma (chronic granulomatous disease) Stem cell transplant
180
A young patient presents with a large number of persistent bacterial skin abscesses, what primary immunodeficiencies may he have? What tests would you like?
Phagocyte deficiency T cell deficiency FBC, lymphocyte subset analysis, adhesion molecule expression, neutrophil function tests, IgG levels
181
What can cause primary immunodeficiencies?
Single gene disorders Polygenetic disorders Hla polymorphism
182
What two general categories of secondary immunodeficiency are there? Examples?
Decreased production of immune component - HIV, splenectomy, liver disease, malnutrition Increased loss of immune components - nephropathy, burns, enteropathy
183
What drugs can cause neutropenia?
Pheytoin, alcohol, chemotherapy, immunosuppressants
184
What diseases can cause neutropenia?
HIV, EBV, HBV, vit b deficiency, bone marrow cancer
185
Why might the spleen need removing?
Infarction Trauma Immune haemolytic disease Tumour
186
What disease can cause splenic atrophy?
Coeliac disease
187
What happens after the spleen is removed?
Decreased IgG production Thus decreased opsinisation Thus increased risk of encapsulated bacteria (neiserria meningitidis, haemophillus influenzae, strep. pneumoniae

PPE (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions