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ESA 3 steven > Infection > Flashcards

Infection Flashcards

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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
What are some potential complications of sepsis?
``` Irreversible hypotension Respiratory failure Renal failure Increased inter cranial pressure Ischaemic necrosis ```
25
What are some methods of preventing sepsis?
Vaccine | Antibiotic prophylaxis
26
What is the immune system?
Cells and organs that contribute to immune defences against infectious and non infectious conditions
27
What is an infectious disease?
When a pathogen succeeds in evading and/or overwhelming a hosts immune defences
28
What are the roles of the immune system?
Recognise pathogens Contain/eliminate infection Regulate itself Remember pathogens
29
What are the differences between the innate and the adaptive immune system?
Innate: fast, recognises groups of pathogens, no memory, no intensity change Adaptive: slow, recognises one pathogen, immunological memory, increasing intensity
30
What is the first line of defence?
Barriers - physical (skin), physiological (vomiting), chemical (low pH), biological (normal flora)
31
What is the second line of defence?
Phagocytes, chemicals and inflammation
32
Outline the steps involved in destroying a bacteria
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
33
What are healthcare infections?
Infections that arise as a consequence of health care
34
What are things that can be done to the patient to prevent healthcare infections?
Optimise their condition Antimicrobial prophylaxis Physical barriers - isolate/protect
35
What are some things that can be done for healthcare workers and the environment to prevent healthcare infections?
Make sure workers are healthy and vaccinated | Clean the surfaces and medical equipment. Good food hygiene
36
What is the importance of taking a travel history?
Imported diseases Different strains Infection prevention
37
What are the causative organisms and the transmission route for malaria?
Plasmodium falciparum, vivax, ovale and malariae | Female mosquito
38
What are some signs and symptoms a malaria patient will present with?
1-3 week incubation Headache, cough, malaise, arthalgia, myalgia, fatigue Fever, sweats and chills in a 3-4 day cycle Few signs +- splenomegaly
39
What investigations should be done if you suspect malaria?
Blood smear, FBC, LFT, U+E, glucose
40
How do you treat malaria?
Falciparum - quinine/artemisinin | Others - chloroquine +- primaquine
41
How can malaria be prevented?
Assess risk Bite prevention Chemoprophylaxis
42
What is main causative organism for enteric/typhoid fever and what is the transmission route?
Salmonella enterica - gram -ve cocci | Foecal oral from food/water
43
What signs and symptoms do you expect to see in a patient suffering from typhoid fever?
Fever, headache, abdominal discomfort, constipation, dry mouth, rash, hepatsplenomegaly 7-14 day incubation
44
What investigations should be done for typhoid fever?
Anaemia, lymphopenia, LFT, blood and faecal culture
45
How would you treat typhoid fever? And prevent it?
Azuthromycin or ceftriaxone | Food/water hygiene and vaccine
46
Describe the HIV virology
Enveloped, single stranded, RNA retrovirus
47
Describe the pathogenesis of HIV
The viral RNA is transcribed to ssDNA and integrated into the host cell genome
48
How is HIV diagnosed?
Presence of virus antibodies in the blood | PCR on a genome
49
What are the types of drugs used to treat HIV?
Fusion inhibitor, entry inhibitor, reverse transcriptase inhibitor and integrate inhibitor
50
Describe the virology of Hep B
Enveloped DNA virus
51
How can hep B be transmitted?
Mother to infant, sexual, percutaneous
52
Describe the change in incidence of symptomatic and chronic infections as age changes
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
How is Hep B prevented?
Vaccine
54
Describe the virology of Hep C
Enveloped, ssRNA virus
55
How is Hep C transmitted?
Mainly blood borne | Occasionally vertical or sexual
56
How is Hep C treated?
With the aim of curing - antivirals, interferons and ribavarin
57
What is CRP?
An acute phase protein produced by the liver
58
How does presence of a pathogen lead to acute phase proteins production?
Pathogen --> macrophage/monocytes --> cytokines (IL-6) --> liver --> acute phase proteins
59
What is the function of CRP?
Opsonisation - enhance binding
60
What is CRPs clinical use?
Rapidly produced and easy to measure in response to infection, trauma, surgery, burns, infarction, inflammation and cancer
61
What are microbiota?
Micro-organisms carried on skin and mucosal surfaces that are normally harmless or beneficial
62
How can a patient infect themselves? Give an example of each route
Invasion - strep pyogenes - pharyngitis Migration - E. coli - UTI Inoculation - coag negative staphylococcus - joint infection Haematogenous - viridans strep - endocarditis
63
Give examples of external and internal infections
Cellulitis, pharyngitis, conjunctivitis | Endocarditis, osteomyelitis
64
Give examples of prosthetic infections and the causative organism
Prosthetic valve endocarditis - coag -ve staphylococci Joint infections - coag -ve staph and staph aureus Pacing wire - coag -ve staph and staph aureus
65
Explain the pathogenesis of a surface infection
Adhere to host cells/prosthetic surface using pili or fimbriae Biofilm formation Invade and multiply Host response - pyogenic or granulomatous
66
What is the problem with bio films?
Difficulty in removing bacteria
67
How do you diagnose surface infections and what are some challenges?
Blood culture May need sonication They adhere and may be low numbers
68
How do you treat surface infections and what are some challenges?
Sterilise or remove the surface | Poor penetration due to biofilm and the risks of surgery
69
How do you prevent surface infections?
Maintain surface integrity, prevent/remove colonisation
70
Define hypersensitivity
Antigen specific immune responses that are inappropriate/excessive and result in harm to the host
71
Explain the two phases of hypersensitivity reactions
Sensitisation phase - first exposure | Effector phase - clinical pathology upon re-exposure
72
What type of hypersensitivity is an allergy?
Type 1
73
Name some common allergens
Mites, pets, pollen, insect venom, medication and food
74
Outline the pathway leading to an allergic response
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
How is an allergic reaction diagnosed?
History and testing blood for mast cell products | Skin prick and challenge tests
76
What are some visible allergic reactions?
Wheel and flare Urticaria Angioedema Wheezing
77
How does an epipen work?
reverse vasodilation and airway obstruction and inhibit mast cells
78
How do you manage allergic reactions?
Remove allergen Educate - epipen use, symptom recognition Medic alert bracelet Drugs - antihistamine, corticosteroids, anti IgE, epipen Allergen desensitisation
79
Give examples of source - person, person - person and vector - person conditions
Food - food poisoning, environment - legionella, animals - rabies Influenza, norovirus Mosquito - malaria/dengue, tick - Lyme disease
80
Define endemic rate, outbreak, epidemic and pandemic
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
What is R0?
Average number of cases one case generates in uninfected, non immune population
82
What are some reasons behind outbreaks?
New pathogen - new antigens/antibiotic resistance New host - none immune New practise
83
What interventions can be done to prevent outbreaks?
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
What are the consequences of Antimicrobial resistance?
Treatment and prophylaxis failure | Economic costs
85
What methods to achieve Antimicrobial stewardship are in place?
Persuasive - educate and remind Restrictive - formulary restriction and authorisation Structural - computer records and expert advice
86
What microbes cause disease in cystic fibrosis and the order they occur in?
H influenza Staph aureus Burkholderia cepacia
87
Explain cystic fibrosis
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
How does diabetes increase risk of infections?
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
Define immunodeficiency
State in which the immune system is unable to respond appropriately and effectively to infectious microorganisms
90
What are the criteria for diagnosing immunodeficiency?
Spur | Severe, persistent, unusual, recurrent infections
91
What are the types of primary immunodeficiencies in order of commonness?
B cell - 50% T cell - 30% Phagocyte - 18% Complement 2%
92
Give some examples of B cell problems
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
How might a patient with immunoglobulin deficits present? How are they managed?
Recurrent respiratory infections and GI problems | Prophylactic antibiotics, immunoglobulin replacement therapy, manage respiratory function
94
Give some examples of phagocyte deficiencies
Leukocyte adhesion deficient | Chronic granulomatous disease - no respiratory burst
95
How might a patient with phagocyte deficiency present? How are they managed?
Recurrent infections - ulcers, abscesses, invasive aspergillosis Antibiotics, antifungals, immunise, surgery, stem cells Chronic granulomatous disease - interferon and steroids
96
Give examples of T cell deficient conditions
Di George - no thymus | Severe combined immunodeficiency
97
How is Di George diagnosed and managed?
Catch 22 - cardiac abnormalities, abnormal facies, thymol hypoplasia, cleft palate, hypocalcaemia, 22 chromosome Neonatal cardiac surgery, give Ca2+ supplements, bone marrow and antibiotics
98
Give an example of a complement deficiency
C1 inhibitor deficient | Hereditary angio oedema
99
Give some causes of secondary immunodeficiencies
Reduced immune components - malnutrition, infection, liver, neutropenia, splenectomy Increased loss or catabolism - burns and protein losing conditions
100
What is the spleens function?
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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