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Year 3 > Week 6 and 7 Micro > Flashcards

Week 6 and 7 Micro Flashcards

1
Q

Types of antibiotic use (Guided vs Empirical vs prophylactic)

A

Guided: Based on identifying cause of infection, choosing antibiotic based on selectivity testing

Empirical: Best (educated) guess, based on clinical/epidiemological acumen

Prophylactic: preventing before it starts

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2
Q

Narrow vs Broad spectrum

A

Spectrum: range of bacterial species that an antibiotic can effectively treat

Narrow: Effective against a limited range of bacteria. Useful when infection is known. Limited effect on colonising bacteria

Broad: Effective against wide range bacteria. Treat most causes of infection. But, marked effect on colonising bacteria

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3
Q

Antibiotic action

A

Bactericial: Sterilises site of infection. Lysis bacteria can lead to toxin release and inflammation

Bacteriostatic: Suppresses growth of bacteria but does not sterilise site of infection. Requires additional factors to clear bacteria.

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4
Q

Antibiotics safe and unsafe in pregnancy

A

Considered safe:

Most B-lactams

Macrolides

Anti-tuberculants

Unsafe:

Trimethoprim: neural tube defects in 1st trimester Nitrofurantoin: haemolytic anaemia in 3rd trimester Aminoglycisides: ototoxicity in 2/3rd trimester Tetracyclines: bone/teeth abnormalities Quinolones: bone/joint abnormalities

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5
Q

Inherent vs. Acquired resistance

A

Inherent: bacteria naturally lack a pathway or target which the drug can interact with

Acquired: antibiotic that was previously sensitive not anymore, as bacteria become resistance by inheriting genetic information

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6
Q

4 mechanisms bacteria can use to be resistant to antibiotics

A
  1. Produce enzymes e.g. B-lactams
  2. Change drug target e.g methylation of 23S ribosomal subunit (resistant to erthyromycin)
  3. Decrease cell permeability (downregulate porins)
  4. Export drug out from inside cell (pseudomonas produces efflux pump)
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7
Q

4 ways bacteria gain resistance

A
  1. Chromosomal mutation
  2. Gain mobile piece of DNA (plasmid, integron which contains resistance)
  3. Transformation: bacteria gains genetic information from environment
  4. Transduction: pieces of DNA transferred between bacteria from virus
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8
Q

Gene transfer

A

Vertical transfer: parent bacteria passes on genetic information to progeny by binary fission

  • spontaneous mutation - occurs less often than transfer of mobile pieces of DNA

Horizontal transfer: mobile pieces of DNA transferred other than traditional reproduction

  • Conjugation: requires cell-cell contact between bacteria, and plasmids (circular, double stranded DNA) transferred (which contain information for resistance). Most important horizontal transfer.
  • Transduction: pieces of DNA transferred by virus (bacteriophages - viruses which infect bacteria)
  • Transformation - when bacteria die, can release DNA. Some bacteria can take up DNA and insert it into their chromosome.
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9
Q

Fitness cost

A

Antibiotics attack the biological function of the bacteria, so bacteria develop mutations but can lead to a slower growth rate - fitness cost. In a non-selective environment, slower-growing bacteria can be outgrown by wild-type bacteria and die. However, in a selective pressure environment e.g. hospital, the importance of these mutations outweighs the drawback of the slower growth rate, so these bacteria will survive, So increase selection pressure can lead to increased resistance

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10
Q

MRSA

A

Bacteria strains which resistant to all B-lactams. MecA gene encodes for a variant of the normal penicillin binding protein (allows crosslinking of peptidoglycans in cell wall) which have a decreased affinity for methicillin. So, these bacteria still produce a cell wall, even in presence of B-lactams

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11
Q
A

Gram -ve bacilli (pink)

E.g. E.Coli, pseudomomas

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12
Q

B-lactamase inhibitors

A

Clavulanate

Tazobactam

Bind to B-lactamses, allowing B-lactam drugs to work

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13
Q

Coliforms

A

Gut commensals - Gram -ve bacilli which live in gut e.g. E.coli, Klebsiella, Enterobacter

Also cause UTI, HAP, intra-abdominal sepsis

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14
Q

Extended Spectrum Beta Lactamses

A
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15
Q

Pseudomonas

A

Has modifying enzymes and porin down regulation

4 efflux pumps, which one is always expresses so more resistant to antiobiotics than other gram -ves

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16
Q

ESBLs (extended spectrum beta lactamases)

A

Plasmid encoded resistant, so can hydrolyse Beta -lactam ring in penicillins and cephalosporins

Treatment: Ciprofloxacin, Gentamicin, Meropenem,

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17
Q

Carbapenemases

A

Hydrolydse meropenems via enzyme, AmpC, and causes porin loss

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18
Q

Ways to reduce resistance

A

Use narrow spectrum antibiotics

Follow emperical guidelines

Short courses e.g. UTI - 3 days

Infection control for patients who are infected

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19
Q

Non-genetic mechanisms of resistance

A
  • Abscess formation
  • Bacteria in resting stage e.g. TB
  • Foreign body e.g. biofilms - bacteria in close proximity so can transfer genetic material which contain resistance
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20
Q

Which bacteria has developed resistance to Carbapenems?

A

Klebsiella pneumoniae

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21
Q

Antibiotic pescribing steps

A

Is it required?

Which one?

How should it be administered?

How long?

Adjunctive measures?

Review

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22
Q

When not to give antibiotics

A

Viral

Self-limiting respiratory tract infections

Uncomplicated UTI

Ingrown toe nails

Systemic inflammatory response e.g. cancer

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23
Q

Symptoms of infection

A

General:

Fever, sweats, rigors

Localising:

Dysuria

Cough+green/brown sputum, creps

Erythema, heat, swollen

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24
Q

Antibiotics for uncomplicated UTI, lower respiratory tract infections (LRTI), mild cellulitis

A

Uncomplicated UTI: trimethoprim, nitrofurantoin

LRTI: Amoxillin, doxycycline

Mild cellulitis: flucoxacillin, doxycyline

Severe:

IV combination e.g. B-lactam + gentamicin

<1hr admin

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25
Q

Antibiotics which especially cause C.diff

A

Cephalosporins

Co-amoxiclav

Clindamycin

Carbapenems

Ciprofloxacin

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26
Q

Systemic inflammatory repsonse

A

Fever/hypothermia (>38/<36)

RR (>20/min)

HR (>90bpm)

low/high WBC ( < 4 or >12)

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27
Q

Sepsis

A

Life-threatning organ dysfunction (defined using q-sofa score) due to infection

>2 of:

Altered mental status (GCS <15)

RR >22/min

BP systolic < 100mmHg

Can lead to septic shock: Sepsis induced hypotension, requiring ionotropic support, or hypotension not respdoning to fluid resus

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28
Q

Collateral damage with antibiotic use

A

Unintended consequences

Anitbiotic resistance

Drug interactions

Diarrhoea

Vasuclar site infection (S. auerus bacteraemia)

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29
Q

Guidlines for systemic inflammatory response (if unknown)

A

Blood cultures and IV antibiotics within 1 hr

Review anatomical systems

CXR

Add cover for S.aureus (if healthcare assoc.)

Add cover for MRSA (if previous infection, recent carrier)

Add cover for Streptococcal (if pharyngitis, erythoderma, hypotension)

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30
Q

Guidlines for sepsis (unknown)

A

IV amoxcillin + IV gentamicin

If suspected S.aureus

Add IV flucoxacillin

If suspected MRSA

Add IV vacomycin

If suspected Streptococcal

Add IV clindamycin

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31
Q

Which antibiotics for COPD exacerbation with green sputum

A

IV amoxicillin or doxycyline

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32
Q

Organisms which cause fever in travellers

A

Bacteria: Enterotoxigenic or Enteroaggregrative E.coi

Shigella

Salmonella

Campylobacter

Viruses: Norovirus, Rotavirus

Parasites: Giardia (takes weeks to present)

Symptoms: Fever, watery diarrhoea, nausea/vomiting

Management:

Fluids

Antibiotics e.g. Quinolones (only if have co-morbidities)

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33
Q

Types of mosquitoes which spead typhoid and malaria

A

Malaria: Anopheline mosquito. Evening biter

Typhoid: Aedes mosquito. Day biter.

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34
Q

Malaria

A

Most common cause of fever in subsaharan Africa

Organisms:

P.falciparum (worldwide. main cause)

P.vivax (Commonly Asia. Chloroquine resistant. Persistent liver infection)

P.ovale (West Africa. Persistet liver infection)

P.malariae (worldwide)

Symptoms:

Fever, malaise, myalgia, jaundice, cerebral malaria

Treatment: artemether, quinine+doxycyline

Prevention: Nets, DEET, clothing, doxycycline (can cause photosensitisation), malarone (expensive)

Diagnosis: Blood film - thick (haemolysed RBCs, sensitive) thin (monlayer red cells, not as sensitive)

Antigen test - detects malarial antigens. Not as sensitive as thick blood film. Differentiates P.falciparum and non P.falciparum

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35
Q

Typhoid

A

Organisms: S.typhi and S.paratyphi can cause enteric fever

Human to human, contaminated water

Clinical features: Fever, abdo pain, constipation/diarrhoea, neuro symptoms e.g. headache, enteric encelopathy, septic shock

Treatment: Quinolones (best)

Cephalorsporins (emperical)

Diagnosis: blood culture

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36
Q

Dengue fever

A

Clinical features: “breakbone fever” - fever, myalgia, arthalgia, headache, rash

Laboratory features: leucopenia, thrombocytopenia

Management: symptomatic

Diangosis: PCR

<1% infections lead to Dengue haemorrhagic fever

  • Increased vascular permeability, fever, thrombocytopenia, bleeding
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37
Q

Viral haemorrhagic fever

A

Ebola, yellow fever

Can take up to 21 days to present

Treatment: Supportive, Ribavirin

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38
Q

Chain of infection

A

Infectious agents

  • Staph. coccus
  • Streptococci

Resevoir

Enovironment, animals, humans

Portal of Exit

TB: Respiratory tract

Norovirus: vomit

Modes of Transmission

Direct e.g. contact

Indirect e.g. airborne

Portal of Entry

Resp tract, mucous membranes

Susceptible hosts

Elderly, immunocompromised

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39
Q

Strageties for healthcare assoc infections

A

Isolation, screening, standard and transmission based precautions, antibiotic stewardship

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40
Q

Aseptic technique

A

Reduce activity in area

Keep exposure to susceptible site to minimum

Check sterile pack for damage

Hand washing prior

Gloves

Waste disposal

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41
Q

Chronic granulomatous disease

A

X-linked

Defect in NADPH oxidase

Deficiency in production of oygen radicals, and intracellular killing

Increased risk of bacterial and fungal infections leading to lung, skin abscesses

Wide spread granuloma formation

Pulmonary infections e.g. staph. aureus (as catalse detroys hydrogen peroxide), Aspergillus

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42
Q

Cellular immunity supressed by:

A

Primary: Di George syndrome

Secondary: Lymphoma, chemo, drugs e.g. corticosteroids, rituximab

Increased risk of viral, fungal, protazoa infections

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43
Q

Humoral immunity suppressed by:

A

Primary: Bruton’s agammaglobulinaemia

Multiple myeloma, chemo, radiotherapy

Increased risk of Strep.pneumoniae, H. Influenzae, Nisseria meningitidis

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44
Q

Splenic function

A

Splenic macrophages phagocytose encapsulated bacteria

Site of primary immuniglobulin response

Increased risk of strep.pneumoniae, haemophilus influenzae, nisseria meningitidis

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45
Q

Physical barriers

A

Skin

Conjunctivae

Mucosa - GI, resp

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46
Q

Mucosal barrier injury

A

Chemo/radiotherapy affects cells with high mitotic index including mucosa

Leads to mucositis - pain, dysphagia - impairs GI function - alteres nutritional status

PPIs, antiobitcs - alters microbiome

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47
Q

Severe nutritional deficiency

A

<75% total body weight or rapid weight loss + hypoalbuminaemia

Anorexia, nausea, vomiting, mucositis

Leads to impaired host defese

Iron deficiency leads to reduced neutrophil and T cell function

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48
Q

Organ dysfunction

A

Tumours can lead to obstruction and infection esp. in lung

49
Q

Infection in solid organ transplant

A

Causes are diverse:

  • community acquired e.g pneumococcus,
  • opportunistic infections e.g. pneumocystis jirovecii, aspergillus
  • donor derived e.g. TB, E.coli, HSV

Pulmonary infections rapidly progress

Inflammatory repsonses impaired

  • symptoms are diminished

Diagnosis difficult

50
Q

Febrile neutropenia

A

Febrile neutropenia = infection until proven otherwise

Also caused by

  • malignancies e.g. 100% haemotological malignancies, 50% solid tumours
  • Chemo
  • Antibiotics
51
Q

Common pathogens in neutropenic cancer patients

A

Gram postive

  • Coagulase negative staphylococci
  • Staph aureus

Gram neg

  • E.coli

Anaerobes

  • Clostridium

Viruses:

  • HSV

Fungal

  • Candida
52
Q

Neutropenic sepsis

A

Neutrophil count <0.5, or <1 if recent chemo

+

Fever/hypothermia (>38/<36) OR SIRS OR sepsis/septic shock

SIRS: sweat, chills, rigors, malaise

<36/>38, RR > 20, HR > 90, WC <4/ > 12

Sepsis: evidence of infection and organ dysfunction (2 or more of qSOFA: GCS < 15, BP <100, RR > 22)

Septic shock: Sepsis induced hypotension, requiring ionotropes or hypotension unrepsonive to fluid resusication.

53
Q

Clinical management neutropenic sepsis

A

Medical emergency

Assess within 15 mins of presentation

Assess sepsis severity with NEWS

Sepsis 6 in one hour

  • High flow O2
  • Blood cultures
  • IV antibiotics
  • IV fluids
  • Lactate/FBC
  • Urine output
54
Q

Antibiotics for neutropenic sepsis

A

Standard risk (NEWS <6)

- IV tazocin

High risk (NEWS >7, septic shock)

- IV tazocin + IV gentamicin

If penicillin allergy:

- IV vancomycin + IV ciprofloxacin

If soft tissue infection add vancomycin (in case of MRSA)

If susepct atypical pneumoinia add clarithromycin

55
Q

What is the most important risk factor for infection?

A

Neutropenia

Can be caused by chemo/radiotherapy - decreased haemopoietic progenitors - depletes marrow reserves

56
Q
A
57
Q

3 factors to consider in positive blood result for endocarditis

A

Is it a contaminant?

Coagulase negative Staphylococci most common

If not, what if the source?

What antibiotic to use?

58
Q

How to take blood cultures for bacterial endocarditis

A

3 sets blood cultures (First and last one hour apart)

10ml each

From peripheral veins (as central has increased risk of contamination)

Sterile technique

Prior to antibiotics

59
Q

Treatment streptococcal endocarditis

A

Benzylpenicillin 4 wks, and gentamicin for 2 wks

Need to monitor renal function

60
Q

Organisms which cause biliary sepsis

A

Enteric flora -

Gram neg: E.coli, Klebsiella, Enterobacter

Gram positive: Enterococci

Anaerobes e.g. Clostridia

Treatment:

Gent + Amox + Metranidazole

Needs to be referred to surgical team (to identify obstruction)

61
Q

4 classes of Necrotising fascitiis

A

Type I: synergistic infection with aerobes (e.g. Streptococci) and anaerobes (e.g. bacteriodes)

More common in elderly diabetics

Type II: Group A Strep - Streptococcus pyogenes via toxin production

Type III: vibrio vulnificus

Type IV: fungal

62
Q

Antibiotics for Nec fas

A

IV benzylpenicillin (streptococcus)

IV flucoxacillin (staphylococcus)

IV gentamicin (gram neg)

IV metranidazole (anaerobes)

IV clindamycin (anaerobes/toxin production)

IV vancomycin (MRSA)

63
Q

Bacterial GI infections can cause illness in two ways

A

Infectious: bacterial pathogens develop in gut after ingestion e.g. salmonella

Intoxication: bacterial pathogens grow on food produce exotoxins e.g. Staph aureus

64
Q
A

TB

Central casseous granuloma

Epitheloid cells surrouding granuloma

Lymphocytes (outer)

Langerhans giant cell

65
Q

Why does strong cell mediated immunity fail to clear TB?

A

Granuloma

66
Q
A
67
Q

Dysentery

A

Inflammatory disease of large bowel

Pain, bloody stool, fever

68
Q

Transmission of GI infections

A

Faecal-oral

Food, fluids, fingers

Person-person

69
Q

Lab diagnosis of GI infection

A

Enrichment broth - nutrients promotes growth of certain pathogen

Selective media - supresses growth of background flora, while allowing growth of pathogen

Differential media - distinguishes mixed microorganisms on same plate.

  • Salmonella and Shigella are non-lactose fermenters
  • Salmonella: black
  • Shigella: pink
70
Q

Risk factors for C.diff

A

Over 65

Recent hospitilisation

Recent course of antibiotics

71
Q

When to give antibiotics for diarrohea

A

Signs of sepsis

C. Diff infection

Significant co-morbidity

72
Q

How does HIV cause illness?

A

Infect cells which carry CD4 receptors e.g. T helper cells, macrophages, dendritic cells

Cause depletion of CD4 T helper cells by:

  • direct viral killing of cells
  • apoptosis of uninfected cells
  • CD8 cytotoxic T cells killing infected CD4 cells

Impairs B cell activation and antibody production

Impairs cytotoxic T cell immunity

Once CD4 count below 350: symptomatic (require anti-retovirals)

<200: increased risk of opportunistic infections e.g. thrush, oral hairy leokoplakia, TB, pneumocystis jirovecii

<100: serious infections e.g. CMV, mycoplasma

73
Q

HIV (symptoms, investigations)

A

Single stranded RNa retrovirus

Needs to transcribe itself into double stranded RNA so make lots of errors - mutations in HIV genome common

Symptoms:

Fever, weight loss, maculopapular rash, lymphadenopathy, oral thrush

Investigations:

HIV antibody via ELISA, confirmed by Western blot

HIV p24 antigen

74
Q

Drug targets

A

NRTI/NNRTI (non/nucleotide reverse transcriptase inhibitors) - stops transcription

Fusion inhibitor - stops CD4 binding, stopping internalisation of virus

Protease inhibitor - stops cleavage of protein to make new viral proteins

Integrase inhibitor - stops enzyme (integrase) from inserting HIV genome into host cell DNA

75
Q

HIV latency

A

Period between initial infection and advanced HIV (AIDS)

76
Q

HIV resistance

A

HIV can still mutate and develop, when whilst on medication which leads to drug resistance HIV strains

So adherence of medication every day, is essential

77
Q

HIV clinical markers

A

CD4 cell count: no. of CD4 T helper cells

600-1200 normal

<200 risk of opportunistic infections

HIV-1 plasma RNA (viral load): measures HIV RNA in plasma

Less than 40 copies/ml - undetectable

78
Q

Differential diagnosis primary HIV

A

Infectious mononucleosis

Secondary Syphillis

Drug rash

Viral - Cytomegalovirus

79
Q

HIV Treatments

A

HAART (highly active antiretroviral treatment) - triple therapy (cART)

  • 2 NRTIs+ 1 non-nucleotide reverse transcriptase inhibitor or protease inhibitor)

Started when CD4 count <350, or symptomatic

Disadvantages:

Requires good adherece

Short term toxicity - rash, CNS symptoms

Long term toxicity - renal, hepatic toxicity

Drug interactions - mediated by CYP450. Can interact with statins, PPIs

Long term mortality affected by: CD4 count, viral load at diagnosis, individuals with an AIDs illness, poor adherence to HAART

Prophylaxis: 2NRTI + PI within 72 hrs

80
Q

AIDS

A

Group of life-threatning conditions that are caused by damage to immune system by HIV

Viral: CMV

Bacterial: TB

Fungal: Candidiasis

Protazoal: Cryptosporidium

Malignancies: Kapsoi’s sarcoma (human herpes virus 8)

Other: dementia

81
Q

Non-infectious causes of diarrohea

A

IBD - Young people. Bloody stool. May have weight loss

Bowel cancer - Older people. Altered bowel habits. Marked weight loss

Diverticular disease - Older people. Alternating diarrohoea and constipation. May have diverticulitis - diverticulae becomes impacted with faeces leading to infection

Chornic pancreatitis - alcohol

Ischaemic bowel disease - Older people. History of vascular disease or AF

HIV - Enterocytes infected with HIV. Oral thrush, shingles, weight loss, thrombocytopenia

Sepsis

82
Q

Viruses causing gastroenteritis

A

Norovirus and sappovirus - Calciviridae family

Affects healthy individuals

Rotavirus/Adenovirus/Astrovirus - affects under 2s, elderly, immunocompromised

83
Q

Norovirus

A

SS RNA virus

GII-4 most common in UK

Transmission: Person-person (faecal oral), food borne, water

Vomiting, diarrhoea

Treatment: IV/oral fluids, analgesics

84
Q

Rotavirus

A

DS RNA virus

G1 accounts for 70% infections

Clinical features: low infectious dose, person-person

Clinical features: watery diarrhoea, loss of electrolytes leads to dehydration

1st infection after 3 months most severe

Vaccination: Rotarix

85
Q

Adenovirus 40/41

A

DS DNA virus

Clinical features: Fever, watery diarrhoea

Treatment: Supportive

86
Q

Astrovirus

A

SS RNA virus

Causes less severe gastroenteritis than other viruses

87
Q

Nisseria gonorrhoea

A

Gram neg cocci

Presents with purulent discharge and urethritis

Diagnosis:

Urethral gram film

NAAT (nucleic acid amplification test):

  • male urine +/- rectal/throat swab
  • vulvovaginal swab

Confirm positive NAAT with gonococcal culture

Complications: disseminated gonorrhoea - arthritis, pustules on digits

Treatment: Ceftriaxone, azithromycin

Partner notification

Resistance to penicillins, tetracyclines, quinolones as easily acquire plasmids

88
Q

Chlamydia trachomatis

A

Clinical features: asymptomatic

Complications: tubal damage, inflammatory pelvic disease

Treatment: Doxycylcine, Azrithromycin

Lymphogranuloma venereum

Lymphotropic chlamydia

Severe proctitis (inflammation of lining of rectum) - constipation, bleeding

inguinal “bubos” (enlarged LN in groin area)

89
Q
A

Nissseria gonorrhae

Gram neg diplococci

90
Q

Triponeum Pallodium

A

Syphillis

Primary (chancre (painless ulcer)) - Secondary (rash, flu-like illness) - Tertiary - Gumma (granulotamous lesion), Cardio - aortic regurg, Neuro - meningitis

Treatment: penicillin

91
Q

Viral STIs

A

Herpes simplex virus

HSV2 - causes gential herpes

Symptoms: asymptomatic, shallow, painful ulcers

Fever, bilateral lymphadenopathy

Treatment: Aciclovir

Molloscum contagiosum

Pox virus

Pearl-like smooth papules

Pubic area

If extensive/on face - can indicate immunosuppression

Treatment: Self limiting

Human papilloma virus

HPV 6, 11 - genital warts

Warts on genitalia in females, and on penile shaft and urethra in males

Treatment: Imiquimod, Cryotherapy

92
Q

Natural history HIV

A

Primary infection - CD4 depleted, symptoms: fever, maculopapular rash, weight loss

Body has immune repsonse against HIV, CD4 count increases

Clinical latency:

Symptoms don’t occur for years

CD4 count slowly decreases

Consitutional symptoms: fever, malaise, swollen LNs

Opportunictic infections: oral thrush, pneumocystic jirovecii

93
Q

Types of vaccinations

A

Live attenuated

Promotes full immune repsonse after 1 or 2 doses

Virus is weakened/attenuated

MMR, VZV

Not given to immunocompromised

Inactivated - either whole or part of virus/bacterium

Subtypes:

Toxin mediated - Diptheria

Bacteria mediated (polysaccharide based) - pneumococcal

94
Q

Conjugate vaccines

A

Plain polysaccharide antigens don’t stimulate immune system as broadly as protein antigens e.g. diptheria

So polysaccharise vaccines enhanced by conjugation of protein antigens e.g. MenC

95
Q

Septic arthritis

A

Joint infection. Medical emergency. Can lead to OA and septic shock

Organisms:

  • Gram positive: MSSA, MRSA, streptococci pyogenes
  • Gram negative: H. influenzae

Clinical features: fever, single hot joint (hip, knee), loss of movement, pain

Investigations

Bloods - FBC, CRP, blood cultures

Joint aspirate - gram stain, microscopy for culture

Imaging

Treatment: IV antibiotics

96
Q

Prosthetic joint infections

A

Pathogens: Staph aureus, Coag negative staphylococci

Low virulence - coag neg

High virulence - MSSA, MRSA

Clinical presentation:

Pain, effusion, warm joint, fever

Spread:

Local spread - 80% infections, organisms from skin surface

Haematogenous spread - 20% infections. Presents later. Can be any organism

Pathogenesis:

Prosthetics need fewer bacteria to cause sepsis

Avascular surface protects bacteria from immune system, antibiotics

Cement can inhibit phagocytosis

Treatment

Antibiotic prophylaxis - Cephalosporins

DAIR - (debride, antitiobitcs, implant retained)

  • If prosthesis acute (<30 days), debride, wash joint, IV antibiotics can keep it in (IV Gent+IV Vanc)

If infection over 30 days - remove: Girdlestone procedure (no joint), one/two stage revision

97
Q

Osteomyelitis

A

Progressive infection of bone characterised by death of bone and formation of sequestra (piece of bone separated by surrounding bone due to necrosis)

Spread: Haematogenous, contiguous (actual contact)

Pathogens: MSSA, MRSA, Anaerobes

Treatment: Surgery to debulk infection, IV antibiotics

98
Q

Vertebral discitis

A

Infection of a disc space and adjacent vertebral end plates

Can cause deformity, SC compression, paraplegia

Organisms: MSSA, MRSA, TB

99
Q

Investigations and treatments for STIs

A

Examination:

Genital, anal, proctoscopic exam (exams anal cavity)

Mouth - candida, oral hairy leukoplakia

Investigations:

Bloods - HIV, syphillis, Hep B

NAAT - gonorrhoea, chlamydia

Rectal swab - for gram stain

HSV/syphillis PCR

Treatment:

Gonorrhoea - Ceftriaxone (resistant to penicillin, tetra, quinolones)

Chlamydia - Doxycycline or azithromycin

Syphillis - Pencillin

HSV - Aciclovir

HIV - HAART

100
Q

VZV

A

Itchy vesicular rash, fever

Starts on face, chest and spreads to rest of body - centripetal distribution

Reactivation - herpes zoster (shingles) - reactivation of VZV from latency in dorsal root ganglia

Complications: bacterial infection, haemorrhagic varicella

Risk factors: adults, neonates, immunucompromised (risk of disseminated infection - haemorrhagic varicella)

Transmission:

Contagious 48 hours before onset of rash, up to when lesions are crusted over

Respiratory transmission, contact with vesicle fluid

Treatment

Aciclovir - Converted to aciclovir triphosphate, nucleic acid analogue, inhibits viral DNA polymerase, inhibits viral replication

Side effects: nephrotoxicity, NandV

101
Q

Enterovirus

A

Hand, food and mouth disease

Common cold-like symptoms, fever

Non-itchy vesicular rash on palms and soles

Painful mouth ulcers

Herpangina - oropharyngeal vesicular rash. Commonly due to coxsackievirus A16, B

Most common enterovirus: coxsackie virus A16, 6

102
Q

Differentials for vesicular rash

A

HSV

VZV

Enterovirus

103
Q

Investigations for VZV, HSV, Enterovirus

A

Chicken pox - clinical diagnosis

VZV, HSV, Enterovirus - PCR via vesicle swab

104
Q

Immunocompromised patients

A

Primary immunodeficiency - SCID (severe combined immunodeficiency)

Chemo/radiotherapy

Pts who recieved solid organ transplant and on immunosuppressive treatment

Pts on high-dose steroids

Immunosuppresive drugs e.g. methotrexate

105
Q

VZV prophylaxis

A

Varizellar zoster immunoglobulin

Indicated for:

Significant exposure to chicken pox/herpes zoster

Immunocompromised

No antibodies to VZV

Not indicated for immnunosuppressed with antibodies

106
Q

Strep pneumoniae

A

Symptoms: chest symptoms - cough, purulent sputum, pleuritic chest pain

Treatment: Amoxcillin

If severe (3 or more CURB65): IV Clarithromycin + IV amoxcillin

Atypicals: Clarithromycin or Doxycycline

Can cause pleural effusions - parapneumonic effusions (usually self limiting).

However, bacteria can enter fluid and cause infection - complicated pleural effusion.

Can lead to empyema (pus in pleural space)

Treatment: chest drain, IV amox

107
Q

TB (symptoms, pathophy, investigations, treatment)

A

Mycobacterium tuberculosis

Others: M.bovis, avium

Symptoms:

weight loss, night sweats, fever

Differential: bronchial carcinoma, CAP

Pathophysiology:

Inhaled TB into lungs, taken up into alveolar macrophages, which are not phagocytosed. Kill macrophages and are released, activating immune response

Leads to primary disease, or more commonly latent disease

Latent TB:

Containment of TB depends on T helper cell mediated immunity. T cella and macrophages forms necrotising (casseous) granuloma, with mostly lymphocytes and macrophages at periphery

Active usually occurs by re-activation from latent TB. HIV, immunosuppressants, corticosteroids can increase risk

Investigations:

Sputum culture: Ziehl-Nielsan stain showing acid-fast bacilli

CXR (exclude bronchail neoplasm, or active TB - Ghon complex (calcified granuloma). When assoc with hilar lymph node - Ranke complex

Sceondary (re-activated) TB - lung apices

Pleural fluid

Pleural biopsy - show necrotising granuloma

Alwayas test for HIV

Treatment:

RIPE

Pyrazinamide - little acitivity agianst slow growing bacilli so stopped after 2 months

Ethambutol stopped if sesitivities known

Isoniazid can lead to peripheral neuropathy as anatagonises pyridoxine. Pyridoxine used as prophylaxis

R, I, P = hepatotoxic

Rifampicin induces hepatic CYP450

Ethambutol = visual problems

Complications TB:

Milary TB - disseminated TB in lung

Nodal TB: cervical

Osteomylitis: esp. bones of vertebral column

CNS TB: Cerebral TB or meningtis TB

108
Q

Pneumocystis jirovecii

A

Opportunisitc infection

Fungal

Causes progressive SOB, dry cough

Perihilar interstitial shadowing on CXR

Can lead to pneumothorax

Treatment: Co-trimoxazole and steroids

109
Q

HIV diagnosis

A

HIV antibody test: ELISA, confirm with Western blot - gel electrophoresis to detect HIV protein

p24 antigen test

110
Q

HIV treatment

A

HAART

2 NRTI and 1 other e.g. NNRTI or PI

Started when CD4 count less than 350

111
Q

Risk factors for immunocompromised patients

A

Neutropenia: < 0.5

Risk of gram positive: staph. aureus

neg: E.coli

Damaged skin due to IV lines: staph. aureus

Oral mucositis: strep. viridans

Damaged gut mucosa: E.coli

Impaired cellular immunity: viral, protazoal

Impaired humoral immunity: strep. pneumoniae

Hyosplenism: strep. pneumoniae

Malnutrition

112
Q
A

Candida

Candida endophthalmitis

Commonly disseminates to eye

Treatment:

Amphotericin

(Fluconazole in an immunocompetent patient)

113
Q

PCOS

A

Symptoms: Annovulation (ammenorhoea), hyperandrogenism (hirsutism, acne)

Present at adolescence

Raised testosterone and LH

Patho

Gonadotrophins

Increased LH (increased LH receptors, supports ovarian theca cells - increased androgens), decreased FSH (decreased conversion of androgens to oestrogen)

Increased androgen biosynthesis

  • Increased androgen production from theca cells
  • Decreased steroid hormone binding globulin (binds testosterone. Only free testosterone is active)

Increased insulin resistance

  • increased insulin secretion - reduces SHBG, increased circulating androgens

Investigations

Testosterone

SHBG

LH/FSH

TMD2

Treatment:

Metformin: not effective for infertility, hirsutism but could be useful for diabetes

COCP: ovarian androgen supppression

Corticosteroids: adrenal androgen suppression

Spironolactone: androgen receptor antagonist

114
Q

Causes of ammenorrhoea

A

Primary:

Rokitasnky syndrome

Turner’s syndrome

Kallman’s syndrome

Secondary:

Asherman’s syndrome

PCOS

Prolactinoma

Others:

Pregnancy, OCP, Cushing’s

115
Q

Hirsutism

A

Excess hair growth in male pattern due to increased androgens

Causes:

PCOS

Androgen secreting tumour

116
Q

Adrenal cortex

A

Glomerulosa: Aldosterone

Fasciculata: Cortisol

Reticularis: Androgens

Adrenal medulla: Catecholamines

117
Q

p. jirovecii

A

Opportunistic fungal infection

Causes interstitial plasma cell pneumonia, with foamy exudates in alveoli

CXR: interstitial peri-hilar shadowing

Symptoms: progressive SOB, dry cough, fever and failure to respond to usual antibiotics

Complications: resp failure

Treatment: co-trimoxazole, and steroids

118
Q

Bacterial Meningitis

A

Reduced GCS and febrile pt indicates CNS infection and BM

Symptoms: nuchal rigidity, headache, confusion, fever

Causes: strep. pneumoniae, nisseria meningitidis

Complications: CN palsies e.g. sensorineural hearing loss, seizures (more common in pneumococcal)

Risk factors for pneumococcal; >60, alcohol dependence, immunosuppressed, middle ear disease, previous head trauma

119
Q

Resp viruses

A

Common cold: Rhinovirus, coronavirus

Pharyngitis: Adenovirus

  • sore throat, pharyngeal inflammation

Croup: parainfluezna

  • distinctive cough

Acute bronchitis: RSV

Bronchiolitis: RSV

  • lower resp tract of young children
  • wheeezing, tacycardia, persistent cough

Pneumonia: Influenza, RSV

Common complications: otitis media, sinusitis

Uncommon complications: Reye syndrome

Year 3 (15 decks)

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