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ESA 3 steven > Infection > Flashcards

Infection Flashcards

0
Q

Give some examples of ways a patient could get an infection

A 
STI
Vector
Airborne droplets
Contaminated food or water
From another part of the patient
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1
Q

What is an infection and how does it cause disease?

A

Invasion of a hosts tissue by microorganisms.

Disease caused by microbial multiplication, toxin production and host response

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2
Q

What is the difference between horizontal and vertical transmission?

A

Horizontal is via contact/inhalation/ingestion

Vertical is mother to child before or after birth

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3
Q

What are the stages of disease?

A

Exposure, adherence, invasion, multiplication, dissemination

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4
Q

What are some determinants of disease?

A

Pathogen - virulence factor, inoculum size and anti microbial resistance
Patient - site and co morbidities

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5
Q

How do we know if a patient has an infection?

A

History - symptoms/exposure
Examination - organ dysfunction
Investigation - full blood count, C-reactive protein, imaging

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6
Q

What are the 4 types of microbe?

A

Virus, bacteria, fungi and parasites

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7
Q

What are the different types of virus?

A

DNA/RNA, Single/double strand, enveloped/non enveloped

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8
Q

What are some different types of bacteria?

A

Crocus, spirillus, bacillus

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9
Q

Give some examples of types of parasites and fungi

A

Parasite - Protozoa/worms

Fungi - yeast/molds

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10
Q

Outline an infection model

A

A patient and pathogen come together and an infection occurs. It is then managed before an outcome is reached

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11
Q

How could we class antibacterial drugs?

A

Bactericidal/bacteriostatic
Broad/narrow spectrum
Target side
Chemical structure

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12
Q

What would be the ideal features of an anti microbial?

A

Selective toxicity, few side effects, reaches site of infection, can be given orally or IV, long half life and doesn’t interfere with other drugs

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13
Q

What are the main classes of antibiotic and give an example of each

A

Cell wall synthesis - B lactam/glycopeptide
Protein synthesis - tetracycline, aminoglycoside, macrolide
Cell membrane function - polymixin
Nucleic acid synthesis - quinolones

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14
Q

Outline the mechanism of action for penicillin

A

Inhibit the penicillin binding proteins which stops the catalysing of cross links in bacterial cell walls

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15
Q

How can antibiotic resistance develop?

A

Drug inactivating enzymes produced
Target altered
Uptake altered - decrease permeability/increase efflux

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16
Q

What is SIRS?

A 
Systemic inflammatory response syndrome
Any two of: Temperature 38
Heart rate >90/min
Respiratory rate >20/min
WBC 12x10^9
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17
Q

What is bacteraemia?

A

Presence of bacteria in the blood

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18
Q

What is sepsis?

A

Systemic response to infection - SIRS + documented/suspected infection

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19
Q

What is severe sepsis and septic shock?

A

SIRS + organ dysfunction/hypoperfusion

Sepsis + low BP despite receiving IVF

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20
Q

Outline the inflammatory cascade

A

Endotoxins stimulates local production of cytokines to start inflammatory response and promote wound repair. They enter the circulation and stimulate GF, macrophages and playelets to try and restore homeostasis.
SIRS - homeostasis not restored

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21
Q

How is coagulation caused in SIRS and what are the potential consequences?

A

Cytokines initiate thrombin production and inhibit fibrinolysis. Causes microvascular thrombosis and therefore ischaemia, dysfunction and failure

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22
Q

What other investigations should be done to confirm sepsis?

A

FBC, PCR, CRP, blood sugar, liver function, blood gas

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23
Q

What are the sepsis six?

A 
High O2 flow
Blood cultures
IV antibiotics
Serum lactate
IVF resuscitation
Urine output measurement
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24
Q

What are some potential complications of sepsis?

A 
Irreversible hypotension
Respiratory failure
Renal failure
Increased inter cranial pressure
Ischaemic necrosis
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25
Q

What are some methods of preventing sepsis?

A

Vaccine

Antibiotic prophylaxis

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26
Q

What is the immune system?

A

Cells and organs that contribute to immune defences against infectious and non infectious conditions

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27
Q

What is an infectious disease?

A

When a pathogen succeeds in evading and/or overwhelming a hosts immune defences

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28
Q

What are the roles of the immune system?

A

Recognise pathogens
Contain/eliminate infection
Regulate itself
Remember pathogens

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29
Q

What are the differences between the innate and the adaptive immune system?

A

Innate: fast, recognises groups of pathogens, no memory, no intensity change
Adaptive: slow, recognises one pathogen, immunological memory, increasing intensity

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30
Q

What is the first line of defence?

A

Barriers - physical (skin), physiological (vomiting), chemical (low pH), biological (normal flora)

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31
Q

What is the second line of defence?

A

Phagocytes, chemicals and inflammation

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32
Q

Outline the steps involved in destroying a bacteria

A

Adherence of microbe to phagosome
Ingestion by phagocyte forming a phagosome
Fuse phagosome with lysosome
Digest with enzymes
Residue put in body and removed from cell

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33
Q

What are healthcare infections?

A

Infections that arise as a consequence of health care

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34
Q

What are things that can be done to the patient to prevent healthcare infections?

A

Optimise their condition
Antimicrobial prophylaxis
Physical barriers - isolate/protect

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35
Q

What are some things that can be done for healthcare workers and the environment to prevent healthcare infections?

A

Make sure workers are healthy and vaccinated

Clean the surfaces and medical equipment. Good food hygiene

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36
Q

What is the importance of taking a travel history?

A

Imported diseases
Different strains
Infection prevention

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37
Q

What are the causative organisms and the transmission route for malaria?

A

Plasmodium falciparum, vivax, ovale and malariae

Female mosquito

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38
Q

What are some signs and symptoms a malaria patient will present with?

A

1-3 week incubation
Headache, cough, malaise, arthalgia, myalgia, fatigue
Fever, sweats and chills in a 3-4 day cycle
Few signs +- splenomegaly

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39
Q

What investigations should be done if you suspect malaria?

A

Blood smear, FBC, LFT, U+E, glucose

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40
Q

How do you treat malaria?

A

Falciparum - quinine/artemisinin

Others - chloroquine +- primaquine

41
Q

How can malaria be prevented?

A

Assess risk
Bite prevention
Chemoprophylaxis

42
Q

What is main causative organism for enteric/typhoid fever and what is the transmission route?

A

Salmonella enterica - gram -ve cocci

Foecal oral from food/water

43
Q

What signs and symptoms do you expect to see in a patient suffering from typhoid fever?

A

Fever, headache, abdominal discomfort, constipation, dry mouth, rash, hepatsplenomegaly
7-14 day incubation

44
Q

What investigations should be done for typhoid fever?

A

Anaemia, lymphopenia, LFT, blood and faecal culture

45
Q

How would you treat typhoid fever? And prevent it?

A

Azuthromycin or ceftriaxone

Food/water hygiene and vaccine

46
Q

Describe the HIV virology

A

Enveloped, single stranded, RNA retrovirus

47
Q

Describe the pathogenesis of HIV

A

The viral RNA is transcribed to ssDNA and integrated into the host cell genome

48
Q

How is HIV diagnosed?

A

Presence of virus antibodies in the blood

PCR on a genome

49
Q

What are the types of drugs used to treat HIV?

A

Fusion inhibitor, entry inhibitor, reverse transcriptase inhibitor and integrate inhibitor

50
Q

Describe the virology of Hep B

A

Enveloped DNA virus

51
Q

How can hep B be transmitted?

A

Mother to infant, sexual, percutaneous

52
Q

Describe the change in incidence of symptomatic and chronic infections as age changes

A

More likely to get symptoms as you get older (from <10% up to 50%) but less likely to get a chronic infection (from 90% down to 3%)

53
Q

How is Hep B prevented?

A

Vaccine

54
Q

Describe the virology of Hep C

A

Enveloped, ssRNA virus

55
Q

How is Hep C transmitted?

A

Mainly blood borne

Occasionally vertical or sexual

56
Q

How is Hep C treated?

A

With the aim of curing - antivirals, interferons and ribavarin

57
Q

What is CRP?

A

An acute phase protein produced by the liver

58
Q

How does presence of a pathogen lead to acute phase proteins production?

A

Pathogen –> macrophage/monocytes –> cytokines (IL-6) –> liver –> acute phase proteins

59
Q

What is the function of CRP?

A

Opsonisation - enhance binding

60
Q

What is CRPs clinical use?

A

Rapidly produced and easy to measure in response to infection, trauma, surgery, burns, infarction, inflammation and cancer

61
Q

What are microbiota?

A

Micro-organisms carried on skin and mucosal surfaces that are normally harmless or beneficial

62
Q

How can a patient infect themselves? Give an example of each route

A

Invasion - strep pyogenes - pharyngitis
Migration - E. coli - UTI
Inoculation - coag negative staphylococcus - joint infection
Haematogenous - viridans strep - endocarditis

63
Q

Give examples of external and internal infections

A

Cellulitis, pharyngitis, conjunctivitis

Endocarditis, osteomyelitis

64
Q

Give examples of prosthetic infections and the causative organism

A

Prosthetic valve endocarditis - coag -ve staphylococci
Joint infections - coag -ve staph and staph aureus
Pacing wire - coag -ve staph and staph aureus

65
Q

Explain the pathogenesis of a surface infection

A

Adhere to host cells/prosthetic surface using pili or fimbriae
Biofilm formation
Invade and multiply
Host response - pyogenic or granulomatous

66
Q

What is the problem with bio films?

A

Difficulty in removing bacteria

67
Q

How do you diagnose surface infections and what are some challenges?

A

Blood culture
May need sonication
They adhere and may be low numbers

68
Q

How do you treat surface infections and what are some challenges?

A

Sterilise or remove the surface

Poor penetration due to biofilm and the risks of surgery

69
Q

How do you prevent surface infections?

A

Maintain surface integrity, prevent/remove colonisation

70
Q

Define hypersensitivity

A

Antigen specific immune responses that are inappropriate/excessive and result in harm to the host

71
Q

Explain the two phases of hypersensitivity reactions

A

Sensitisation phase - first exposure

Effector phase - clinical pathology upon re-exposure

72
Q

What type of hypersensitivity is an allergy?

A

Type 1

73
Q

Name some common allergens

A

Mites, pets, pollen, insect venom, medication and food

74
Q

Outline the pathway leading to an allergic response

A

Plasma cells produce IgE and this along with irritants stimulate mast cells to produce histamine, cytokines, leukotrienes and prostaglandins which cause an increase in vascular permeability, vasodilation and bronchial contraction

75
Q

How is an allergic reaction diagnosed?

A

History and testing blood for mast cell products

Skin prick and challenge tests

76
Q

What are some visible allergic reactions?

A

Wheel and flare
Urticaria
Angioedema
Wheezing

77
Q

How does an epipen work?

A

reverse vasodilation and airway obstruction and inhibit mast cells

78
Q

How do you manage allergic reactions?

A

Remove allergen
Educate - epipen use, symptom recognition
Medic alert bracelet
Drugs - antihistamine, corticosteroids, anti IgE, epipen
Allergen desensitisation

79
Q

Give examples of source - person, person - person and vector - person conditions

A

Food - food poisoning, environment - legionella, animals - rabies
Influenza, norovirus
Mosquito - malaria/dengue, tick - Lyme disease

80
Q

Define endemic rate, outbreak, epidemic and pandemic

A

Background rate
2+ cases linked by time and place
Rate of infection greater than the background rate
Very high rate of infection spanning countries and continent

81
Q

What is R0?

A

Average number of cases one case generates in uninfected, non immune population

82
Q

What are some reasons behind outbreaks?

A

New pathogen - new antigens/antibiotic resistance
New host - none immune
New practise

83
Q

What interventions can be done to prevent outbreaks?

A

Remove pathogen - decontaminate/sterilise or kill vector
Improve patient health - nutrition, medication, vaccination
Improve practise - protective clothing, behaviour (safe sex and needles)
Environment - clean water and air

84
Q

What are the consequences of Antimicrobial resistance?

A

Treatment and prophylaxis failure

Economic costs

85
Q

What methods to achieve Antimicrobial stewardship are in place?

A

Persuasive - educate and remind
Restrictive - formulary restriction and authorisation
Structural - computer records and expert advice

86
Q

What microbes cause disease in cystic fibrosis and the order they occur in?

A

H influenza
Staph aureus
Burkholderia cepacia

87
Q

Explain cystic fibrosis

A

Autosomal recessive defect in the CFTR protein causing less chloride to move into the mucus and therefore making it thicker. This blocks ducts and gets colonised

88
Q

How does diabetes increase risk of infections?

A

Hyperglycaemia and acidaemia - reduce humoral immunity and lymphocyte/leukocyte function.
Micro/macrovascular - causes poor perfusion and infection
Neuropathy - less sensation so ulcers and skin infections. Incomplete bladder emptying cause UTIs

89
Q

Define immunodeficiency

A

State in which the immune system is unable to respond appropriately and effectively to infectious microorganisms

90
Q

What are the criteria for diagnosing immunodeficiency?

A

Spur

Severe, persistent, unusual, recurrent infections

91
Q

What are the types of primary immunodeficiencies in order of commonness?

A

B cell - 50%
T cell - 30%
Phagocyte - 18%
Complement 2%

92
Q

Give some examples of B cell problems

A

Common variable immunodeficiency - B cells don’t mature to plasma
IgA deficiency - B cells don’t become IgA
Bruton’s disease - impaired B cells
Hyper IgM

93
Q

How might a patient with immunoglobulin deficits present? How are they managed?

A

Recurrent respiratory infections and GI problems

Prophylactic antibiotics, immunoglobulin replacement therapy, manage respiratory function

94
Q

Give some examples of phagocyte deficiencies

A

Leukocyte adhesion deficient

Chronic granulomatous disease - no respiratory burst

95
Q

How might a patient with phagocyte deficiency present? How are they managed?

A

Recurrent infections - ulcers, abscesses, invasive aspergillosis
Antibiotics, antifungals, immunise, surgery, stem cells
Chronic granulomatous disease - interferon and steroids

96
Q

Give examples of T cell deficient conditions

A

Di George - no thymus

Severe combined immunodeficiency

97
Q

How is Di George diagnosed and managed?

A

Catch 22 - cardiac abnormalities, abnormal facies, thymol hypoplasia, cleft palate, hypocalcaemia, 22 chromosome
Neonatal cardiac surgery, give Ca2+ supplements, bone marrow and antibiotics

98
Q

Give an example of a complement deficiency

A

C1 inhibitor deficient

Hereditary angio oedema

99
Q

Give some causes of secondary immunodeficiencies

A

Reduced immune components - malnutrition, infection, liver, neutropenia, splenectomy
Increased loss or catabolism - burns and protein losing conditions

100
Q

What is the spleens function?

A

Kill encapsulated pathogens - H influenza, strep pneumoniae, neiserria meningitidis
Produce IgM and IgG
Remove opsonised microbes and immune complexes

ESA 3 steven (5 decks)

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