Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

ESA 3 > Infection and Immunity > Flashcards

Infection and Immunity Flashcards

1
Q

Give an example of an environmental cause of infection.

A

Ingesting contaminated food eg. Salmonella and cholera (water)

Contaminated air eg. legionella bacteria causing pneumonia (or contacts with surfaces)

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

What is horizontal transmission in disease?

A

Person to person through contact, inhalation or ingestion of contaminants.

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

What is vertical transmission in infection?

A

From mother to child during pregnancy or childbirth.

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

What is the difference between an endotoxin and exotoxin in reference to bacteria?

A

Exotoxin - a chemical produced to elicit an immune response which aids its survival.

Endotoxin - inherent parts of the microorganism causing a host response.

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

Give some examples of supportive diagnostic tests in suspected infection.

A

Full blood count - neutrophils and lymphocytes

C-reactive protein - acute phase protein in inflammation

Blood chemistry - shows liver and kidney function

Imaging - x-ray (lungs), ultrasound (heart), MRI (bowel)

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

What does MCS stand for when identifying bacteria?

A

Microscopy
Culture
Antibiotic susceptibility

(Can also test for antigens and nucleic acids)

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

How are viruses identified?

A

Antigen detection, antibody detection, viral nucleic acid detection

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

What type of bacteria must parasitise cells?

A

Incomplete bacteria

Mycoplasma, chlamydiae, rickettsiae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are bacteriophages?

A

A virus which infects bacteria. Exchanges DNA such as for antibiotic resistance or toxin production

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

What are plasmids?

A

Small circles of DNA with limited bacterial genes, usually antibiotic resistance medicines. Are transferrable between bacteria, including between species.

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

What is the difference between aerobic and anaerobic bacteria?

A

Aerobes survive in the presence of oxygen

Anaerobes survive in the absence of oxygen

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

Give an example of a disease which Staphylococcus aureus typically causes.

A 
Pneumonia
Meningitis
Endocarditis
Toxic shock syndrome
Abcesses
Sinusitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Where can Staphylococcus aureus normally be found without being pathogenic?

A

Respiratory tract and on the skin

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

What is the different between alpha and beta haemolytic streptococci?

A

Alpha use hydrogen peroxide which oxidises haemoglobin, causing incomplete haemolysis.

Beta have streptolysin which causes complete haemolysis.

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

What disease is commonly associated with Listeria monocytogenes?

A

Listeriosis

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

What disease is commonly associated with Bacillus anthracis

A

Anthrax (cutaneous/pulmonary/gastrointestinal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What disease is commonly associated with Bacillus cerus?

A

Food poisoning (vomiting, diarrhoea, nausea)

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

What diseases are commonly associated with Neisseria meningitidis?

A

Meningitis

Meningococcaemia (sepsis)

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

What disease is commonly associated with Neisseria gonorrhoeae?

A

Gonorrhoea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What areas of the body can be affected by Moraxella catarrhalis?

A 
Respiratory system
Middle ear
Eye
CNS
Joints (septic arthritis in conjunction with bacteraemia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What diseases is Kleibsiella pneumoniae associated with?

A 
Pneumonia
Meningitis
UTIs
Bacteraemia 
Septicaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What disease is Salmonella typhi associated with?

A

Typhoid fever (weakness, abdominal pain, constipation, headaches)

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

What serious conditions can be associated with Haemophilus influenzae?

A

Bacteraemia
Pneumonia
Epiglottitis
Acute bacterial meningitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What diseases is Cryptococcus neoformans associated with?

A

Fungal meningitis
Encephalitis
(AIDS defining)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is Pneumocystis jirovecj associated with?

A 
Pneumocystis pneumonia
(AIDS defining)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are dermatophytes?

A

A type of mold which causes infection of the skin, hair and nails, causing inflammation.
E.g. Ringworm and athlete’s foot.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What disease is Plasmodium falciparum

A

Malaria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is microbiota?

A

A collection of microorganisms on the skin and mucosal surfaces. They may normally be harmless or beneficial, but transfer to other sites can be harmful.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Give some factors which affect their susceptibility and response to infectious disease.

A

Age (extremes more susceptible, some diseases more prevalent at specific ages)
Gender (anatomy specific, men in general more susceptible)
Physiological state (pregnancy and stress increase risk)
Pathological state (poorly controlled diabetic, smoker, gestational diabetes)
Social (overcrowded, time in hospital)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Describe what is meant by contiguous spread in infectious disease.

A

Spread of infection along tissue planes or into local blood/lymphatic system i.e. Bacteria aspirated into the lungs from the oropharynx.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Describe what is meant by inoculation in the spread of infectious disease.

A

An injury which introduces a pathogen through the skin, such as a stab wound or scratch.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Describe what is meant by haematogenous spread of infectious disease.

A

When the blood stream transports a pathogen from one location to another, e.g. Superficial Staph aureus transferred to a heart valve, causing endocarditis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Why is debridement important when treating some infectious disease?

A

Dead and dying tissue makes an ideal breeding ground for anaerobic bacteria due to the low oxygen, lack of blood supply, and acidic pH.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Why is it important to remove dead space when preventing infectious disease?

A

The space can fill with serous fluid or blood which supports bacterial growth.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are the ideal features of an antibiotic?

A 
Selective toxicity
Few adverse effects
Reach site of infection
Oral or IV formulation
Long half life (so infrequent dosage)
No interference with other drugs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How does penicillin work?

A

Inhibit penicillin binding enzymes which normally cause cross linking of the cell wall. No linkage means integrity is damaged.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

How does vancomycin work?

A

Binds peptide chains in the cell wall to stop penicillin binding proteins binding.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

How does fluoroquinolone work?

A

Damages the coiling in nucleic acids to reduce synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are the mechanisms of resistance used by bacteria?

A

Drug inactivating enzymes (beta lactamases, aminoglycoside enzymes

Altered target to reduce affinity for antibacterials

Altered uptake - reduced permeability or increased efflux

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Describe the difference between conjugation, transduction and transformation in horizontal gene transfer in bacteria.

A

Conjugation - plasmid transferred from one to another

Transduction - phages infect bacteria and transfer genetic material

Transformation - free DNA enters through pores

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is systemic inflammatory response syndrome (SIRS)?

A

An inflammatory state which affects the whole body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is sepsis?

A

Systemic inflammatory response syndrome with an infection as the cause.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What symptoms/signs must a patient have two of to be diagnosed with sepsis?

A

Unusually high or low temperature
Raised heart rate
Raised respiration rate or low PACO2
White blood cell count is low

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is bacteraemia?

A

Presence of bacteria in the blood, with or without clinical features

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is septicaemia?

A

Clinical term meaning generalised sepsis (clinically unwell)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is septic shock?

A

Severe sepsis with persistent hypotension despite IV fluid resuscitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What type of bacteria is Neisseria meningitis?

A

Diplococcus, gram-negative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What effect do cytokines have on coagulation?

A

Inhibit thrombin production and fibrinolysis so promote coagulation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What issues are caused by the coagulation cascade in sepsis?

A

Microvascular thrombosis leading to organ ischaemia, dysfunction and failure.
Microvascular injury is main cause of shock and multiorgan failure. Seen externally as progressive necrosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What urgent investigations should be carried out in suspected sepsis?

A 
Full blood count, urea and electrolytes for kidney function
Blood PCR or culture to identify
Blood sugar
Liver function tests
C-reactive protein
Clotting studies
Blood gases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Why can you not perform a lumbar puncture with high intracranial pressure?

A

The decreasing pressure in the spinal cord forces the brain down through the foramen magnum (herniation) which can cause instant death.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Describe the differences between the innate and adaptive immune system.

A

Innate - immediate response, lack of specificity, lack of memory, no change in intensity.

Adaptive - slow, long-lasting protection, specificity, immunological memory, changes in intensity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What are the physical defences against pathogens?

A

Skin
Mucous membranes
Cilia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What are some physiological defences against pathogens?

A

Diarrhoea
Vomiting
Coughing
Sneezing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What are some chemical defences against pathogens?

A 
Low pH
Antimicrobial molecules (IgG, lysozyme, mucous, defensins, gastric acid, pepsin)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is the biological defence against pathogens?

A

Normal non-pathogenic flora in strategic positions which out-compete pathogens for attachment sites and resources.

Produce antimicrobial chemicals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What is the function of the spleen?

A

A filter for blood as part of the immune system.
Recycles old red blood cells.
Stores platelets and old white blood cells.
Helps to fight encapsulated bacteria.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is the function of macrophages?

A

Sense harmful non self
Ingest and destroy microbes
Antigen presenting
Produce cytokines and chemokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What is the function of monocytes?

A

Differentiate into macrophages after being recruited by cytokines.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What is the function of neutrophils?

A

Ingest and destroy pyogenic bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What is the function of basophils?

A

Secrete anticoagulants and histamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What is the function of eosinophils?

A

Attack multicellular pathogens (have IgE receptors)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What are the two ways that immune cells are able to recognise pathogens?

A

Toll-like receptors for pathogen-associated molecular patterns (PAMPs)

Opsonisation (C3b, C4b, IgG, IgM, CRP, MBL)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What is the function of C3a and C5a?

A

Recruit phagocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What is the function of C3b and C4b?

A

Opsonise pathogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What is the function of C5-9?

A

Kill pathogens by making holes in the cell membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Describe how phagocytosis kills pathogens?

A

Engulf into phagosome
Fuses with lysosome to form phagolysosome
Forms residual body with the waste inside
Discharge outside the cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What organs do TNF-alpha, IL-1 and IL-6 stimulate, and what do they stimulate them to do?

A

Liver - release opsonins (CRP, MBL)
Bone marrow - increase neutrophil mobilisation
Inflammatory activation - increases vasodilation, vascular permeability, and adhesion molecules
Hypothalamus - increase body temperature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What conditions or drugs can cause neutropenic sepsis?

A

Phenytoin
Leukaemia
Lymphoma
Chemotherapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What is chronic granulomatous disease?

A

When phagocytes struggle to kill some types of bacteria and fungi as they can’t form reactive oxygen compounds.
Granulomas form instead.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What are the principal methods of antibiotic resistance utilised by bacteria?

A

Inactivate the drug
Synthesise modified targets with reduced affinity
Reduce permeability
Actively export drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Give some principles of infection control with relation to the pathogen.

A 
Use antibiotics (to treat and prophylactically)
Disinfectant
Ecological interaction with other bacteria (i.e. use of broad spectrum antibiotics that kill native flora, allowing C. diff to proliferate)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Give some principles of infection control with relation to the patient.

A

Restrict interaction with other patients, healthcare workers, and visitors e.g. with isolation
Optimise patient condition, such as stop smoking, lose/gain weight, optimise diabetic control
Use antimicrobial prophylaxis before surgery to reduce the risk of surgical site infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Give some principles of infection control with relation to the practice in healthcare environments.

A

Policies and their implementation, must be carried out effectively by everyone
General and specific activity of healthcare workers. Ensure everyone washes their hands properly, uses aseptic technique ect.
Healthcare workers remain disease free and vaccinated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Give some principles of infection control with relation to the healthcare environment.

A

Fixed and variable features, such as types of chairs and curtains. Ensuring they are easily cleaned, non-porous
Enough wash basins which are regularly cleaned and used

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What type of bacteria is Clostridium difficile?

A

Gram positive bacillus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What are the symptoms of Clostridium difficile infection?

A

Fever
Diarrhoea
Painful abdominal cramps
Toxic megacolon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What are the treatment and management options for a C. diff infection?

A

Stop other antibiotics if possible along with proton pump inhibitors, immunosuppressants, laxatives and opioids
Refer to an isolation ward
Treat with antibiotics according to severity (vancomycin, metronidazole, fidaxomicin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Why is Staphylococcus aureus commonly seen in hospitals?

A

It is spread by human-to-human contact and respiratory secretions so common with so many people close together and when healthcare workers aren’t cleaning properly or washing their hands before and after patient contact

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Why is S. aureus often resistant to penicillin?

A

Produces beta-lactamases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What antibiotic is MRSA resistant to?

A

Meticillin

* should use vancomycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What type of virus is norovirus?

A

Single stranded RNA, non-enveloped

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What type of bacteria is S. aureus?

A

Gram positive coccus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

How can you reduce the spread of norovirus in a healthcare setting?

A

Minimise patient movement and interaction
Use soap and water for hand hygiene
Use gowns and gloves
Consider ward closure
Routine cleaning and disinfection
Exclude staff from work for a minimum of 48 hours after resolution of symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Why are antigen presenting cells essential?

A

T cells are unable to detect pathogens alone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What are the strategic locations for antigen presenting cells?

A

Skin
Mucus membranes
Lymphoid organs (lymph nodes, spleen)
Blood circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Where are dendritic cells found?

A

Lymph nodes, mucus membranes, blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Where are Langerhan’s cells found?

A

Skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

How do T cells affect macrophages after presentation of an antigen?

A

Enhance the phagocytic action of macrophages

90
Q

How to T cells affect B cells after presentation of an antigen?

A

Stimulate them to produce IgG which is more specific rather than IgM

91
Q

What type of cells are class 1 major histocompatibility complexes on?

A

All nucleated cells

92
Q

What type of microbe do class I MHCs present?

A

Intracellular

93
Q

What type of T cell do class I MHCs present to?

A

CD8+ cytotoxic T lymphocytes

94
Q

What cells are class II MHCs present on?

A

Dendritic cells
Macrophages
B cells

(These also have class I)

95
Q

What type of microbe do class II MHCs detect?

A

Extracellular

96
Q

What type of T cell do type II MHCs present to ?

A

CD4+ T helper cells.

97
Q

What genetic features allow MHCs to be diverse in the same person?

A

Codominant expression so both inherited genotypes are expressed
Polymorphic so have a variable peptide binding cleft

98
Q

Describe the endogenous pathway of antigen presentation.

A

Proteins present in the cytosol cleaved by the proteosome
Fragments transported to the ER where matching MHC forms a complex and transports to the cell surface
Both self and non-self presented to CD8+

99
Q

Describe the exogenous pathway of antigen presentation.

A

Only seen in antigen presenting cells
After phagocytosis, proteins cleaved by the phagolysosome
Fuse with vesicle containing matching MHCII
Complex moves to the cell surface
Both self and non-self presented to CD4+

100
Q

Where do T cells mature?

A

Thymus

101
Q

What is produced by cytotoxic T lymphocytes to kill the host cell?

A

Perforins

Granzymes

102
Q

Describe the function of IgM

A

Activates complement

Fast, strong, long duration, high affinity

103
Q

What is the function of IgG

A

Stimulates Fc-dependent phagocytosis, used for passive immunisation in the short term

104
Q

What is the function of IgE?

A

Immunisation against helminths

Role in mast cell degranulation

105
Q

What is the function of IgA?

A

Important role in mucosal immunity

106
Q

Give some examples of methods of transmission in a travel related infection.

A 
Food/water
Insect/tick bite
Swimming
Sexual contact
Animal bite/contact
Beach/recreation
Mosquitos
107
Q

What tests would you do if you suspected someone who just returned from travelling abroad had an infection?

A 
Full blood count - haemoglobin, platelets, lymphocytes, neutrophils, eosinophils
Urea and electrolytes (kidney function)
Liver function tests
Chest X-ray
Serology and PCR
108
Q

What are the symptoms of malaria infection?

A

Fevers
Chills and sweats

Can then lead to:
Multiorgan failure
Tachycardia
Arrhythmia
Anaemia
Adult respiratory distress syndrome
Renal failure
Anaemia
Disseminated intravascular coagulation
Thrombocytopaemia
Bilirubinaemia 
Diarrhoea
Hypoglycaemia
Metabolic acidosis
109
Q

What is the traditional treatment for malaria?

A

Quinine

110
Q

What organism causes enteric fever?

A

Salmonella enterica (gram negative bacilli)

111
Q

What are the symptoms of enteric fever?

A 
Dry cough
Relative bradycardia
Constipation
Haemorrhage or perforation of the intestine
Moderate anaemia
112
Q

Give some conditions commonly associated with HIV infection.

A 
Candidiasis
Kaposi's sarcoma
Pneumocystis pneumonia
Cryptococcal meningitis
Toxoplasmosis
Cytomegalovirus
HPV infection and cervical cancer
Mycobacterium avium complex
113
Q

What type of virus is HIV?

A

RNA retrovirus

Enveloped

114
Q

What is the mechanism of transmission in HIV?

A 
Sexual
IV drugs use
Vertical - breastfeeding/childbirth
Blood/blood product
Organ donation
Skin grafts
115
Q

How does HIV infect cells?

A

Envelope proteins bind CD4+ receptors on T helper cells, allowing the entry of their contents.
Reverse transcriptase converts RNA to DNA which is inserted into the host genome.

116
Q

What are the 4 stages of HIV infection?

A

Acute - high risk to pass on virus with high viral load. Can have flu-like symptoms. The body mounts a response which isn’t fully effective

Latent - may be totally asymptomatic, struggle to clear the infection

Symptomatic - some serious infections begin to occur such as pneumonia

AIDS - severe infections

117
Q

What is the management of HIV infection?

A

First treat the secondary infections
Test for the HIV antigen/antibody
Begin HAART straight away
Then use three drugs in combination, including two nucleoside reverse transcriptase inhibitors.

118
Q

What are the acute symptoms of HIV infection?

A 
Fever
Weight loss
Malaise
Myalgia
Sores in the mouth
Lymphadenopathy
Rash
Nausea/vomiting
Liver/spleen enlargement
119
Q

What are the steps you should take after diagnosing someone with HIV?

A

Determine the source to reduce spread
Test partners and close family members
Avoid breastfeeding and provide prenatal antiretroviral therapy
PEP for patients with suspected or known exposure
PrEP for patients at high risk

120
Q

What type of virus is hepatitis B?

A

dsDNA virus

121
Q

How is hepatitis B transmitted?

A

Vertical - birth/breastfeeding/pregnancy
Sexual
IV drug use
Needlestick injury

122
Q

How does hepatitis B cause its effects?

A

Viral genomic DNA is inserted into the host cell nucleus to replicate.
Primarily replicates in hepatocytes, and the immune response causes hepatocellular damage and viral clearance, mainly by cytotoxic T lymphocytes.

123
Q

What are the symptoms of an acute hepatitis B infection?

A 
Jaundice
Fatigue
Abdominal pain
Anorexia
Nausea
Vomiting
Arthralgia
124
Q

What are the stages of hepatitis B infection?

A

Surface antigen shows within 6 weeks
Then e-antigen which is the highly infectious stage
IgM - core antibody. First to appear
e-antibody - non infective
surface antibody - recovery, virus cleared
IgG - core antibody which persists for life

125
Q

What is the management of a hepatitis B infection?

A

Early antiviral treatment if the virus is particularly aggressive or if the patient is immunocompromised.
Check the serological status for stage of infection
No drugs to clear the infection but can stop it replicating
Acute infection generally won’t require treatment.

126
Q

Give a common commensal organism of the respiratory tract

A

Neisseria meningitidis
Streptococcus pneumoniae
viridans Streptococci

127
Q

Give a common commensal organism of the intestine

A

Clostridium

Bacterioids

128
Q

Give some examples of prosthetic surfaces which can increase the risk of infection.

A 
IV lines
Peritoneal dialysis catheters
Prosthetic joints
Cardiac valves
Pacing wires
Ventriculoperitoneal shunts
129
Q

What is a vegetation?

A

A clot of platelets, fibrin, white blood cells, clotting factors, and bacteria if present which is able to build if there is damage to the endothelium.
They can embolise and cause damage elsewhere

130
Q

Describe a biofilm.

A

Mucopolysaccharides embedding bacteria onto a surface, aiding them with adherence. This changes metabolism of the bacteria and acts as protection

131
Q

What is quorum sensing?

A

Secretion of autoinducers by bacteria. Its concentration depends on the density of bacteria. This can trigger biofilm formation, sporulation and virulence factor secretion.

132
Q

Describe a type I hypersensitivity reaction.

A

An allergy, occurs within 30 minutes
IgE
Occurs in people prone to them
Caused by environmental, non-infectious antigens

133
Q

Describe a type II hypersensitivity reaction.

A

Antibody mediated 5-12 hours
IgG/IgM
Reaction to tissue or cell components

134
Q

Describe a type III hypersensitivity reaction

A

Reaction to soluble antigens within 3-8 hours
IgG/IgM
Forms an immune complex, triggering the inflammatory process

135
Q

Describe a type IV hypersensitivity reaction

A

Cell mediated within 24-48 hours

Caused by self-antigens or environmental infectious agents

136
Q

What is hypersensitivity?

A

An antigen-specific immune response which is inappropriate or excessive, resulting in harm to the host

137
Q

What are the two phases of hypersensitivity?

A

Sensitisation - first encounter with the antigen. Is clinically silent.

Effector - clinical pathology upon re-exposure to the same antigen

138
Q

What do mast cell granules contain?

A

Histamine
Leukotrienes
Prostaglandins

139
Q

Describe the difference between the first and second exposure to allergens.

A

First - IgE mediated trigger of mast cells

Second - allergen cross-links with IgE on mast cells, directly activating them. Release of histamine, leukotrienes and prostaglandins is triggered. This can cause vasodilation, bronchial constriction, and increased vascular permeability

140
Q

Give some common allergens

A 
Dust mites
Cockroaches
Pollens
Medications
Animals
Latex
Foods
Insect venom
141
Q

Why can there be clinical cross-reactivity between antigens?

A

They may have a strong homology with their proteins, such as peanuts and tree nuts

142
Q

What are the skin manifestations of allergy?

A

Urticaria with erythema due to mast cell activation in the epidermis

143
Q

What are the face manifestations of allergy?

A

Angioedema of the lips, eyes, tongue, and upper respiratory tract due to mast cell activation in the deep dermis

144
Q

What are the systemic manifestations of allergy?

A 
Hypotension
Cardiovascular collapse
Generalised urticaria
Angioedema
Breathing problems

Due to systemic mast cell activation

145
Q

What is the treatment and management for an allergy?

A 
Epinephrine
Antihistamines
Corticosteroids
Anti-IgE IgG
Allergen desensitisation
Avoid substance and high-risk situations
Educate
Medical alert bracelet
146
Q

How does adrenaline help in an allergy?

A

Vasoconstriction to reverse hypotension and oedema
Increased heart muscle contraction
Inhibits mast cell activation
Monitor pulse, blood pressure, ECG and oximetry

147
Q

How do you diagnose an allergy?

A

Clinical history
Blood tests for serum allergen (specific IgE)
Skin prick tests
Allergen challenge

148
Q

What type of bacteria is Neisseria meningitidis?

A

Gram negative

Diplococci

149
Q

What type of bacteria is Staphylococcus aureus?

A

Gram positive

Cocci

150
Q

What type of bacteria is Escherichia coli?

A

Gram negative

Rod

151
Q

Streptococcus pneumoniae

A

Gram positive

Diplococci

152
Q

What type of bacteria is Haemophilus influenzae?

A

Gram negative cocci

153
Q

What type of bacteria is Heliobacter pylori?

A

Gram negative

Rod

154
Q

What does it mean if a disease is endemic?

A

There is a normal background rate

155
Q

What is an outbreak?

A

When two or more cases of disease are linked in time and place

156
Q

What is an epidemic?

A

When the rate of infection is greater than the usual background rate

157
Q

What is a pandemic?

A

When there is a very high rate of infection spreading across many regions, countries and continents

158
Q

What is Ro?

A

The average number of cases that one case generates over the course of the infectious period in an otherwise uninfected, non-immune population.

159
Q

Give some possible reasons for a new outbreak/epidemic/pandemic.

A

New pathogen - altered antigen/virulence factor/antibacterial resistance

New hosts - increased number immunosuppressed, more neonates

New practices - more liberal attitude to sex, not using barriers during sex, more IV drug use, high bed occupancy rates on a ward

New place - people moving to areas not previously colonised

160
Q

What is meant by the term ‘infectious dose’?

A

The number of microorganisms required to cause infection

161
Q

What are some methods of infection intervention at a pathogen level?

A

Reduce or eradicate it (and the vector)

Antibacterial washes
Disinfectant
Decontamination
Sterilisation
Eliminate vector breeding sites
162
Q

What are some methods of infection intervention at a patient level?

A

Nutrition
Medical treatment
Vaccination
IV immunoglobin

163
Q

What are some methods of infection intervention in practice?

A

Use protective clothing
Behaviour changes e.g. Better food and drink prep/hand washing
Geographic - limit where you go

164
Q

What are some methods of infection intervention at a specific location?

A

Safe water and air

Quality of housing

165
Q

Give some consequences of antimicrobial resistance.

A

Treatment failure
Prophylaxis failure
Economic costs

166
Q

What does it mean if a bacteria is multidrug resistant?

A

They aren’t susceptible to at least one agent in more than 3 antimicrobial categories

167
Q

What does it mean if a bacteria is extensively drug resistant?

A

Not susceptible to one agent in two or less antimicrobial categories

168
Q

What does it mean if a bacteria is pan-drug resistant?

A

Not susceptible to all agents in all antimicrobial categories

169
Q

What evidence is there to show that antibacterials cause resistance?

A

Laboratory evidence gives biological plausability
Ecological studies relate community use to levels of resistance
Individual level data relates prior antimicrobial use to subsequent presence of antibiotic resistance

170
Q

What are the principles of antimicrobial stewardship?

A

Appropriate use of antimicrobials
Optimal clinical outcomes
Minimise toxicity and other adverse effects
Reduce the cost of healthcare for infections
Limit selection for antimicrobial resistant strains

171
Q

What are some persuasive methods of antimicrobial stewardship.

A 
Education
Consensus
Opinion leaders
Reminders
Audit
Feedback
172
Q

What are some restrictive methods of antimicrobial stewardship?

A

Restrictive susceptibility reporting
Formulary restriction
Prior authorisation
Automatic stop orders

173
Q

What are some structural methods of antimicrobial stewardship?

A

Computerised records
Rapid lab tests
Expert systems
Quality monitoring

174
Q

How can you measure the outcome of antimicrobial stewardship?

A

Patient outcome
Emergence of resistance
Clostridium difficile infection rate

175
Q

How can chronic disease affect infection?

A

It changes the structure and function of affected tissues/organs which may alter the interaction between patient and microorganism

This may be affected by altered presence of microbes and their treatment

176
Q

What is the progression of organisms which colonise people with cystic fibrosis?

A

Haemophilus influenzae
Staphylococcus aureus
Pseudomonas aeruginosa/Burkholderia
Atypical Mycobacteria/Candida albicans

177
Q

What should you do with someone who has cystic fibrosis to reduce the risk of serious infection?

A

Physiotherapy
Antibiotics
Improve nutrition

178
Q

What is significant about the mucoid strains of Pseudomonas aeruginosa?

A

They produce mucopolysaccharides for a biofilm.

179
Q

What damage does COPD cause?

A

Breakdown of lung tissue
Small airway disease
Acute mucus production
Damaged cilia

180
Q

What organisms commonly colonise the respiratory tract In COPD patients?

A 
Streptococcus pneumoniae
Haemophilus influenzae
Moraxella catarrhalis
Pseudomonas aeruginosa
Escherichia coli
181
Q

How does having diabetes increase infection risk?

A

Hyperglycaemia/acidaemia impair humoral immunity and polymorphonuclear leukocyte/lymphocyte function.
Micro/macrovascular disease reduces tissue perfusion, increasing infection risk
Diabetic neuropathy causing diminished sensation, resulting in unnoticed skin breaks

182
Q

Describe malignant otitis externa in the context of diabetes

A

It starts externally, then spreads to soft tissue, cartilage, and bone
Severe ear pain and otorrhoea
Pseudomonas aeruginosa
Virtually exclusive to diabetes

183
Q

Describe rhinocerebral mucormycosis in relation to diabetes.

A

Prevalent in poorly controlled diabetes, especially with diabetic ketoacidosis.
Colonise the nose and paranasal sinuses. Invade blood vessels, causing soft tissue necrosis and bony erosion

184
Q

Why can people with diabetes mellitis be prone to urinary tract infections?

A

Neurogenic bladder defects prevent full emptying, holding bacteria in it.

185
Q

What urinary tract infections are common in diabetes?

A

Pseudomonas aeuruginosa

Enterobacteriaecea

186
Q

Describe common variable immunodeficiency.

A

Inability of B cells to mature to plasma cells

187
Q

What is the presentation of common variable immunodeficiency?

A

Upper and lower respiratory tract infections (can cause bronchiectasis)
GI complications (giardiasis)
Arthropathies (Mycoplasma/Ureaplasma)
Increased incidence of autoimmune disease (thrombocytopaenia)
Increased risk of lymphoma and gastric carcinoma

188
Q

What is the management for common variable immunodeficiency?

A

Immunoglobin replacement therapy
Manage respiratory function
Avoid unnecessary exposure to radiation
Prophylactic antibodies

189
Q

What are the manifestations of phagocyte defects?

A 
Skin and mucus infections (ulcers)
Osteomyelitis
Deep abcesses
Catalase positive Staphylococcus infections
Invasive Aspergillosis (e.g. Pulmonary)
Inflammatory problems (granuloma)
190
Q

Give an example of a phagocyte defect.

A

Cyclic neutropaenia
Leukocyte adherence deficiency
Chronic granulomatous disease
Chediak-Higashi syndrome

191
Q

What is the management for phagocyte defects?

A 
Prophylactic antibiotics/antifungals
Stem cell transplantation
Immunisation
Surgical management
Steroids (CGD)
192
Q

Give an example of a T cell deficiency.

A

DiGeorge syndrome

Severe combined immunodeficiency (SCID)

193
Q

What is the presentation of severe combined immunodeficiency?

A

Failure to thrive
Deep skin and organ abcesses
Low lymphocyte count
High susceptibility to bacterial, fungal and viral infections

194
Q

What is the management of severe combined immunodeficiency?

A

No live vaccines
Irradiated blood products
Aggressively treat infections
Bone marrow/stem cell transplantations before 3 months old

195
Q

Give some causes of secondary immunodeficiency.

A 
Malnutrition
Infection (HIV)
Liver disease
Lymphoproliferative diseases (cancer)
Splenectomy
196
Q

What are some reasons for a splenectomy?

A 
Infarction e.g. Sickle cell, coeliac
Trauma
Autoimmune haemolytic disease
Infiltration e.g. Cancer
Congenital
197
Q

Why is the spleen essential?

A

Detects bloodborne pathogens, especially encapsulated bacteria, to opsonise them
Antibody production
Splenic macrophages remove opsonised microbes and immune complexes

198
Q

What is the presentation in an asplenic patient?

A

Increased susceptibility to encapsulated bacteria

OPSI

199
Q

What is the management of asplenic patients?

A

Penicillin prophylaxis
Immunisation
Medic alert bracelet

200
Q

How do beta-lactam antibiotics work?

A

They inhibit the action of penicillin binding proteins by directly binding to them.

201
Q

What type of bacteria are penicillin antibiotics particularly active against?

A

Gram positive

202
Q

Give an example of a penicillin antibiotic.

A

Penicillin

Flucloxacillin

203
Q

Give two classes of beta lactam antibiotics other than penicillins. How is their action different?

A

Cephalosporins
Carbapenems
They are active against gram negative organisms

204
Q

How do glycopeptides work as antibiotics?

A

Bind to the cell wall to prevent penicillin binding proteins having action.

205
Q

Give an example of a glycopeptide antibiotic.

A

Vancomycin

206
Q

What type of bacteria are glycopeptide active against?

A

Gram positive

207
Q

How do quinolones act as antibiotics?

A

Inhibit DNA gyrase to stop DNA synthesis

208
Q

What type of bacteria are quinolones active against?

A

Gram negative

Atypical

209
Q

Give an example of a quinolone antibiotic.

A

Ciprofloxacin

Fluoroquinolone

210
Q

How do tetracyclines exhibit antibiotic action?

A

Inhibits tRNA binding to the A site of ribosomes

211
Q

Give an example of a tetracycline.

A

Doxacycline

212
Q

How do aminoglycosides exhibit antibiotic action?

A

Inhibiting protein synthesis by binding to the 30S ribosome

213
Q

What type of bacteria are aminoglycosides active against?

A

Gram negative

214
Q

Give an example of and aminoglycoside antibiotic.

A

Gentamycin

215
Q

How do macrolides exhibit antibiotic action?

A

Binds to the 50S subunit of ribosomes to inhibit protein synthesis.

216
Q

Give an example of a macrolide antibiotic.

A

Erythromycin

217
Q

How does trimethoprim exhibit antibiotic action?

A

Inhibits folic acid synthesis

218
Q

What type of virus is norovirus?

A

ssRNA non-enveloped

219
Q

What type of bacteria is Clostridium difficile?

A

Gram positive bacillus
Spore forming
Obligate anaerobe

220
Q

What type of bacteria is Salmonella enterica?

A

Gram negative bacillus

221
Q

What type of virus is hepatitis B?

A

Partially dsDNA

222
Q

What type of bacteria is Pseudomonas aeruginosa?

A

Gram negative bacillus

ESA 3 (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions