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3B Specialties > Infectious Diseases > Flashcards

Infectious Diseases Flashcards

1
Q

Routes of Transmission

HEP B

A

Vertical
Horizontal
–> Sexual (very common- more infectious than HIV or HCV)
–> Blood transfusion and procedures (dialysis/ operations)
–> Needles or sharps- re-use or injury
–> Household transmission - use of shared razors or toothbrushes

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2
Q

Etiological agent of Hep B

A

enveloped DNA virus of hepadnaviridae family

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3
Q

Antigens of Hep B

A
  • surface antigen (HBsAg)
  • envelope antigen (HBeAg)
  • core antigen
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4
Q

HBsAG (hep b surface antigen)

A

protein found in blood or serum of patients with current infection

  • used as diagnostic confirmation of infection
  • genetically producable –> used a vaccine
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5
Q

HBeAg (Envelope antigen)

A

allows for assessment of phase of infection

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6
Q

HBsAb (surface antibody)

A

indicates immunity to hep B following immunisation or infection

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7
Q

HBeAB (envelope antibody)

A

appears in the later phase of the disease in acute and chronic infection

evidence of immune response

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8
Q

HBcAb (core antibody)

A

found in most people exposed to HBV
- tested as total (IgG and IgM)
- doesn’t discriminate between acute/chronic/past infections
- not found after immunisation
IgM routine test on new diagnosis - identifies acute infection

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9
Q

HBV DNA

A

measured and quantified by nucleic acid testing like PCR

- determines grade of replication and activity of the virus

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10
Q

Acute or Chronic?

Hep B

A

host characteristics determines if the virus is cleared within 6 months - age, immune status

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11
Q

Acute hep B management

A

usually self limiting
no indication for treatment
occasionally fulminant hepatitis can cause liver failure (indicated by rising INR) –> requires a liver transplant

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12
Q

Chronic Hep B

A
  • lasting longer than 6 months
  • if acquired at birth may last decades (90% of cases chronic)
  • 5% of adults with Hep B have chronic disease
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13
Q

Chronic Hep B

Prevention

A

immunisation
immunoglobulin post exposure administration
- both used in highly infectious mothers at the end of pregnancy

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14
Q

Hep B diagnosis

A

usually asymptomatic

serological testing

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15
Q

Chronic Hep B complications

A

cirrhosis
hepatocellular carcinoma
considered an oncogenic virus

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16
Q

Chronic Hep B management

A
  • identifying phase of the infection
  • control viral replication
  • reduce inflammation
  • pegylated interferon alpha (weekly injections 48/52)
  • ## Tenofovir or Entecavir daily (long term)
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17
Q

Hep C

A

hepacivirus from Flaviviridae family
160,000 chronically infected in the UK
3rd largest cause of end stage liver disease

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18
Q

Hep C modes of transmission

A
  • parenteral
  • common in former IVDUs
  • small number of pts from infected transfusions
  • needle stick injuries and tattooing
  • low risk of household transmission unless sharing razors or toothbrushes
  • sexual transmission is rare
  • vertical transmission in 6% of positive mothers
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19
Q

Response to infection

Hep C

A
  • most asymptomatic or symptoms that require medical attention
  • 15% - malaise, nausea, RUQ pain and jaundice
  • if symptomatic more likely to clear the disease
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20
Q

Symptoms of Chronic Hep C

A 
non-specific 
usually asymptomatic but may have:
- malaise
- fatigue 
- intermittent RUQpain
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21
Q

Extra-hepatic manifestations of Hep C

common associations

A
  • essential mixed cryoglobulinaemia (abnormal proteins in blood that clump together in cold temps)
  • membranoproliferative glomerulonephritis
  • porphyria cutanea tarda (photosensitivity)
  • autoimmune thyroid disease (women)
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22
Q

Extra-hepatic manifestations of Hep C

rare associations

A
  • lichen planus
  • Sjogren’s syndrome
  • B-cell lymphoma
  • interstitial lung disease
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23
Q

Diagnosis of Hep C

A

primarily serological
enzyme immunoassay followed by confirmatory testing with an immunoblot assay
positive serology –> HCV RNA testing with PCR to confirm current infection

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24
Q

HCV genotypes

A

6 with different geological distributions
most common in the UK are genotypes 1 & 2/3
Genotype 4 common in Africa/ Middle East
Genotype 5 common in South Africa
Genotype 6 common in SE Asia

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25
Q

Hep C and ESLD

A

chronic infection –> 1/3 chance of ESLD in 25 years
further 1/3 will develop ESLD after 25 years
- risk increased/ accelarated by :
HIV
African- Americans

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26
Q

Clinical Assessment of Hep C

A

Fibro-scan for fibrosis baseline
Potentially need a liver biopsy

advanced fibrosis (Metavir F3) or cirrhosis (Metavir F4) –> screening for HCC 6/12 AFP (alpha fetoprotein) and liver USS

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27
Q

Treatment of Hep C

A

Aim is curative (undetectable HCV RNA 12/52 after finishing treatment)

  • direct acting anti-retroviral drugs
  • higher cure rates, shorter treatment durations and less side affects than pegylated interferon alpha and ribavarin dual therapy
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28
Q

Direct Acting Anti-Retrovirals

A
  • act on specific HCV enzymes, analogous to ART for HIV
  • NS3/4A protease inhibitors (-previr) (CI in decompensated cirrhosis)
  • NS5A inhibitors (-asvir)
  • NS5B inhibitors (buvir)

combination of 2 agents

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29
Q

Re-Treatment regime for Hep C

A 
3 agents (CI in decompensated cirrhosis)
Sofosbuvir/ Velpatasvir and ribavirin (funded for pts with decompensated cirrhosis)
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30
Q

What causes infectious mononucleosis?

glandular fever

A

Epstein- Barr

spread by saliva or droplets

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31
Q

EBV- demographics

A
  • early childhood few symptoms
  • adolescents/ young adults - infectious mononucleosis
  • associated with cancers - stomach/nasal/lymphoma
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32
Q

EBV facts

A
  • DNA herpesvirus
  • predilection for B-lymphocytes and causes
  • causes proliferation of T-cells which are cytotoxic to EBV, can proliferate like immunoblastic lymphoma
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33
Q

Signs and Symptoms of EBV

A
  • sore throat, temp, anorexia, malaise, lymphadenopathy, palatal petechiae, splenomegaly, fatigue, low mood
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34
Q

severe chronic active EBV infection

A
  • anaemia
  • low platelets
  • hepatosplenomegaly
  • fatigue
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35
Q

Severe complications of EBV

A 
meningoencephalitis
cerebellitis
Guillan- Barré
myeloradiculitis
cranial nerve lesions
fulminant hepatitis 
RDS (respiratory distress syndrome)
severe thrombocytopeania/ aplastic anaemia
acute renal failure
Myocarditis
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36
Q

EBV Blood Film

A

lymphocytosis

atypical lymphocytes - large irregular nuclei

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37
Q

Differential Diagnosis for EBV

A 
Streptococci
CMV
Viral hepatitis
HIV seroconversion
Toxoplasmosis
Leukaemia
DIptheria
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38
Q

Management of EBV

A

none
manage chronic fatigue- avoid vigorous sports - splenic rupture
Steroids +/- aciclovir for severe symptoms

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39
Q

EBV oncogenicity

A

Lymphoma
Nasopharyngeal cancer
Leiomyosarcoma
Oral hairy leucoplakia

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40
Q

CMV

A

Direct transmission
Becomes latent after acute infection but may reactivate at times of stress or immunocompromise
may be indistinguishable from glandular fever or acute hepatitis

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41
Q

CMV post transplant

A

fever> pneumonitis> colitis> hepatitis> retinitis

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42
Q

CMV &HIV

A

retinitis> colitis >CNS disease

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43
Q

CMV diagnosis

A

IgM acute infection (unreliable if HIV +ve)

CMV PCR of blood/CSF/ bronchoalveolar lavage

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44
Q

CMV treatment

A

only if serious infection

- ganciclovir IV or valganciclovir, foscarnet, cidofovir

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45
Q

Post-transplant prevention for CMV

A
  • weekly PCR 14/52

- treat if positive

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46
Q

Congenital CMV

A

jaundice
hepatosplenomegaly
purpura
Chronic defects –> low IQ, cerebral palsy, epilepsy, deafness and eye problems

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47
Q

Tetanus

A

Tetanospasmin - exotoxin of Clostridium tetani

Causes muscle spasm, rigidity, cardinal features of tetanus

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48
Q

Pathogenesis of Tetanus

A

C. tetani spores live in soil, faeces, dust and on instruments
Diabetics at increased risk
Exotoxin travels up peripheral nerves and interferes with inhibitory synapses

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49
Q

Signs of Tetanus

A

Prodrome –> fever, malaise, headache
Classic features –> trismus (lock jaw), risus sardonicus (grin), opisthonus (neck hyperextension), spasm, autonomic dysfunction

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50
Q

Differential diagnosis for tetanus

A

dental abscess
rabies
phenothiazine toxicity
strychnine poisoning

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51
Q

Poor prognosis in tetanus

A 
incubation <1 week 
trismus --> spasm in < 48hrs 
Neonates/elderly
Post-infective
Post-partum
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52
Q

Tetanus treatment

A

ITU

  • may need tracheostomy and ventilation
  • Human tetanus immunoglobulin
  • sedation but rousable
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53
Q

Tetanus prevention

A

Neonatal/ maternal vaccination
Vaccinate if uncertain vaccination history,
Severe wound - give vaccine and tetanus immunoglobulin

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54
Q

Necrotising Fascitis

A

Rapidly progressing infection of the deep fascia causing necrosis of subcutaneous tissues
- intense pain over affected skin and underlying muscle
Group A Beta-Haemolytic Streptococci, but often polymicrobial

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55
Q

Fournier’s gangrene

A

necrotising fascitis localised to the scrotum and the pernieum

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56
Q

Management of nec fasc

A

radical debridement +/- amputation

IV abx - benzylpenicillin and clincamycin

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57
Q

Herpes zoster

A

varicella = chicken pox

contagious febrile illness with crops of blisters

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58
Q

Comlications of of h.zoster

A

purpura fulminans/ DIC (may need heparin)
pneumonitis
ataxia
–> commoner in pregnancy and adults than children

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59
Q

H. zoster incubation

A

11-21 days

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60
Q

H. zoster infectivity

A

4 days before rash until all lesions are scabbed (~1 week)

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61
Q

Shingles

A

reactivation of h. zoster

pain in dermatological distribution preceding malaise and fever

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62
Q

Shingles treatment

A

aciclovir (SE decreased GFR, vomiting, encephalopathy, urticaria)

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63
Q

post-herpetic neuralgia

A

affected dermatomes can last years- try amitriptyline, topical lidocaine

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64
Q

Genital Herpes

A

flu-like prodrome
grouped vesicles/papules develop around genitals, anus or throat
pupules burst and form shallow ulcers
–> give anti-virals (aciclovir)

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65
Q

herpes simplex encephalitis

A

spreads from cranial nerve ganglia to frontal and temporal lobes

  • Fever
  • Fits
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66
Q

Osteomyelitis

- causative organisms

A

staphylococcus aureus
psuedomonas
e. coli
streptococci

others: salmonella (sickle cell)
mycobacteria
funghi

67
Q

osteomyelitis categorisation

A

acute haematogenous
secondary to contiguous local infection (+/- vascular disease)
direct inoculation from trauma/ surgery

68
Q

Clinical features of osteomyelitis

A

cancellous bone - vertebrae (IVDU) and feet (DM)
in children - vascular bones (long bone metaphyses- distal femur/ upper tibia)
Infection leads to cortex erosion (cloacae)
exudation of pus lifts up periosteum and disrupts blood supply to underlying bone –> necrosis

69
Q

Signs and symptoms of osteomyelitits

A

pain of gradual onset
unwillingness to move
tenderness, warmth, erythema and slight effusion in neighbouring joints

70
Q

HIV facts

A

retrovrius

  • binds via gp120 to CD4 receptors on t-lymphocytes, monocytes, macrophages and neural cells
  • CD4 +ve cells migrate to the lymphoid tissue where the virus replicates
  • infection progresses –> depletion or impaired function of CD4 +ve cells and decreasing immune function
71
Q

HIV virology

A

9 subtypes (clades)
viral reverse transcriptase makes a DNA copy of the RNA genome
-viral integrase integrates this into the host DNA
- viral protease cuts up polypeptide blocks
- completed virions are released by budding

72
Q

HIV seroconversion

A

primary infection

  • accompanied by transient illness 2-6 weeks after infection
  • fever, malaise, myalgia, pharyngitis, maculopapular rash or meningoencephalitis
  • followed by asymptomatic infection (30% have persistent generalised lymphadenopathy)
73
Q

Persistent generalised lymphadenopathy

A

nodes >1cm diameter at >/ extra-inguinal sites for 3+ months

74
Q

Later constitutional symptoms of HIV

AIDS-related Complex

Prodrome to AIDS

A 
Temp
Night sweats
Diarrhoea
Weight loss
\+/- minor opportunistic infections - oral candida, oral hairy leukoplakia, herpes zoster, seborrhoeic dermatitis, tinea
75
Q

AIDS

A

HIV + indicator disease

e.g. TB, pnuemocystis jiroveci, aspergillosis, cryptococcus, histoplasma
Kaposi’s sarcoma, lymphoma, lymphoid interstitial pneuomonitis
CMV- retinitis/pneunomitis
Toxoplasmosis
Candida
Chronic HIV-associated neurocognitive diseorder

76
Q

HIV diagnosis

A
  • serum/salivary HIV-Ab by ELISA (may be -ve 1-3 weeks post exposure)
  • HIV RNA or core p24 antigen in plasma
77
Q

HIV prevention

A

blood screening
disposable equipment
antenatal anti-retrovirals if HIV +ve +/- C-section +/- bottle feeding

78
Q

Anti-retrovirals

Protease inhibitors

A

slow cell-to-cell spread
and lengthen the time to the first clinical event
often given with low-dose ritonavir
metabolised by cytochrome p450 so increases concentrations of certain drugs by competitive inhibition of their metabolism
can cause dyslipidaemia, hyperglycaemia/ insulin resistance

79
Q

Non-nucleoside reverse transcriptase inhibitors

A

may also interact with drugs metabolised

80
Q

Non-nucleoside reverse transcriptase inhibitors

A

may also interact with drugs metabolised by cytochrome p450

81
Q

Integrase strand transfer inhibitors

InSTIs

A

SE: GI upset, insomnia

maybe combined with tenofovir lamivudine

82
Q

CCR% antagonists

A

CC-chemokine recepotr 5

83
Q

Egs of HAART regime

A

efavirenz (NNRTI) + 2 NRTIs
Monitor U&Es
use at least 3 agents to reduce resistance

84
Q

TB Diagnosis (latent)

A

Mantoux test

Interferon- gamma testing (Quantiferon or T-spot TB)

85
Q

TB Diagnosis (active) (pulmonary)

A 
sputum sample (3+) for MC&amp;S for acid fast bacilli Zeihl  Neelsen
May need bronchoscopy and lavage
86
Q

TB diagnosis (active) (non-pulmonary)

A

sputum/ pleura/ pleural fluid/ urine/ pus /ascites/ peritoneal/ bone marrow or CSF samples for culture
CXR
Incubate samples for 12 weeks on Lowenstein-Jensen medium

87
Q

TB diagnosis (further tests

A

PCR- look for rifampicin resistance
Histology - caseating granuloma
CXR - consolidation, cavitation, fibrosis and calcification

88
Q

Immunological evidence of TB

A

Tuberculin skin test - indicates immunity- previous exposure, BCG. False negatives in immunospupression

89
Q

Treating pulmonary TB

A
  • test colour vision (Ishihara test) (ethanbutmbutol may cause reversible ocular toxicity)
  • inital phase 8 weeks: Rifampicin, Isoniazid, Pryazinamide, ethambutol
  • Continuation phase 16 weeks: rifampicin and isoniazid. Continue pyridoxine
  • Consider steroids if meningeal or pericardial TB
90
Q

TB treatment SE

Rifampicin

A 
- raised LFTs, stop if bilirubin increases, 
decreased platelets, 
orange discolouration, 
inactivation of the Pill, 
flu symptoms.
91
Q

TB treatment SE

Isoniazid

A
  • raised LFTs
  • low WCC
  • stop if neuropathy and give pyridoxine
92
Q

TB treatment SE

Ethambutaol

A

Optic neuritis (colour vision first to deteriorate)

93
Q

TB treatment SE

Pyrazinamide

A

heptatitis

arthralgia (CI acute gout or porphyria)

94
Q

Chemoprophylaxis for asymptomatic TB

A

one or two anti-TB drugs for 3 or 6 months

adults with documented recent tuberculin convrsion and some young immigrants with t-spot TB /mantoux +ve

95
Q

Clinical features TB

Pulmonary

A
  • silent
  • cough
  • sputum
  • malaise
  • weight loss
  • night sweats
  • pleurisy
  • haemoptysis
  • pleural effusion
  • super-imposed pulmonary infection
96
Q

Clinical features TB

Miliary

A 
haematogenous dissemination 
may be non-specific or overwhelming
-CXR
- may be retinal TB
Biopsy - lung/liver/lymph nodes or marrow
97
Q

Clinical features TB

Genitourinary

A

-dysuria
- frequency
- loin/ back pain
- haematuria
- sterile pyuria
Renal TB may spread to bladder, seminal vesicles, epididymis or fallopian tubes

98
Q

Clinical features TB

Peritoneal

A

Abdominal pain
GI upset
Ascites
may need laparotomy

99
Q

Clinical features TB

Bone

A

vertebral collapse

Potts vertebrae

100
Q

Clinical features TB

Skin

A

lupus vulgaris

jelly like nodules

101
Q

Clinical features TB

Acute TB pericarditis

A

exudative allergy lesion

102
Q

Clinical features TB

Chronic pericardial effusion and constrictive pericarditis

A
  • fibrosis/ calcification
  • may spread to myocardium
  • steroids for 11 weeksk
103
Q

Clinical features TB

Meningitis

Prodrome

A 
30% mortality
- fever 
- headache
- vomiting
- abdo pain
- drowsiness
meningism 
- delirium 
worsening over weeks +/- seizures
104
Q

Clinical features TB

Meningitis

CNS signs

A

tremor
papilloedema
cranial nerve palsies

105
Q

Clinical features TB

Meningitis

Diagnosis

A

LP
TB PCR
MRI + enhancement

106
Q

Cholera

cause

A

vibrio cholerae gram negative curved flagellated motile vibrating rod

107
Q

Cholera

INcubation

A

hours to days

108
Q

Cholera

Spread

A

faecal-oral

109
Q

Cholera

Signs

A

Profuse, watery ‘Rice-water’ Stools
fever
vomiting
rapid dehydration –> cause of death with associated metabolic acidosis

110
Q

Cholera

Diagnosis

A

stool microscopy and culture

111
Q

Cholera

Treatment

A

strict barrier nursing

  • prompt oral rehydration
  • IVI of 0.9% saline +KCl
112
Q

Cholera

Prevention

A

Education

Good hygiene & waste disposal

113
Q

Diptheria

A

Corynebacterium diphtheriae toxin
Signs: tonsillitis +/- pseudomembrane over the fauces +/- lymphadenopathy
Rx- erthyromycin

114
Q

Thrush (candida albicans)

A

discharge described as white curds
Vulva & vagina - red, fissuredand sore
RF: pregnancy, immunodeficency, DM, the Pill and abx
Rx: imidazole vaginal pessary - clotrimzaole

115
Q

Malaria biology

A

Plasmodium protozoa injected by female anopheles mosquitos multiply in RBCs –> haemolysis, RBC sequestration and cytokine release

116
Q

Malaria fever paroxysms

A

synchronous release of flocks merozoites from mature schizonts

  1. Shivering
  2. Hot stage- T =41, flushed, dry skin, N&V, headache
  3. Sweats. T falls.
117
Q

malaria protective factors

A
  • GDP6 deficiency
  • sickle cell trait
  • melanesian ovalocytosis (oval shaped erythrocytes)
  • HLA B53
118
Q

Falciparum malaria

A

Mortality = 20% (higher in < 3/ pregnancy)
present within 1/12 of infection
plasmodium falciparum

119
Q

Falciparum Malaria symptoms

A

prodromal headache
Malaise
myalgia
anorexia before first fever paroxysm (+/- faints)

120
Q

Falciparum Malaria signa

A

anaemia
jaundice
hepatosplenomegaly - no rash or lymphadenopathy

121
Q

Falciparum Malaria complications

A

anaemia

thrombocytopenia

122
Q

Falciparum Malaria

5 grim signs

A
  1. decreased conciousness/ coma (cerebral malaria)
  2. convulsions
  3. co-exisiting chronic illness
  4. Acidosis (esp. HCO3 <15)
  5. Renal failure (acute tubular necrosis)
123
Q

Falciparum Malaria

Diagnosis

A

serial thick and thin blood films
% parasitaemia
Rapid stick testss
FBC (anaemia/ TCP), clotting, ABG, U&E, urinalysis, blood cultures

124
Q

Falciparum Malaria

Treatment (medicines)

A

use different drugs to prophylaxis

  • most resistent to chloroquine
  • uncomplicated:
  • -> Artemether-lumefantrine
  • -> artesunate-amodiaaquine
  • -> Dihydroartemisinin-napthoquine
  • -> cholorquinine + doxycycline + clindamycin
125
Q

Falciparum Malaria

Treatment (other)

A
  • tepid sponging
  • paracetamol
  • transfusion if anaemic
126
Q

Malaria travel prophylaxis

A
  • proguanil (low chloroquine resisitance)

- chloroquine resistance –> mefloquine, doxycyline or atovaquone + proguanil (Malarone)

127
Q

Chloroquine SE

A

Headache
psychosis
Retinopathy (chronic use)

128
Q

Malarone SE

A

Abdo pain
nausea
Headache
Dizzinessxx

129
Q

Rabies

A

rhabdovirus spread by infected animal bites

- slight risk from scratches, licks to cuts/mouth/eyes

130
Q

Rabies patients

A

present 9-90 days incubation

Prodrome: headache, malaise, odd behaviour, agitation, fever and itch around bite site.

131
Q

Furious rabies

A

e.g. water provoked muscle spasms accompanied by hydrophobia

132
Q

Dumb rabies

A

flaccid paralysis in the bitten limb

133
Q

UTI classification

Uncomplicated

A

NOrmla renal tract adn function

134
Q

UTI classification

Complicated

A

Abnormal renal/GU tract
decreased host defence (immunosuppression/ DM)
urinary tract obstruction - stones/catheter/malformation

135
Q

UTI organism

A

E. Coli
Proteus mirabilis and klebsiella pneumoniae
Staphylococcus saprophyticus

136
Q

Acute pyelonephritis symptoms

A 
high fever,
 rigors, 
vomiting
loin pain
tenderness
oliguria (AKI)
137
Q

Cystits

A 
frequency
Dysuria
Urgency 
Haematuria
Suprapubic pain
138
Q

Prostatitis symptoms

A

flu-like symptoms
low back ache
few urinary symptoms
swollen or tender prostate

139
Q

Signs of UTI

A 
fever
abdominal or loin tenderness
foul smelling urine
occasionally 
--> distended bladder or enlarged prostate
140
Q

Causes of sterile pyuria

A 
Treated UTI <2 weeks ago 
Inadequately treated UTI 
Appendicitis 
Calculi, prostatitis 
Bladder tumour 
UTI with fastidious culture requirements
Papillary necrosis 
Tubulinterstitial nephritis
Polycystic kidneys
Chemical cystitis
141
Q

Causes of CAP

A
  • streptococcus pneumoniae
  • haemophilus influenzae
    -mycoplasma pneumoniae
    (-staphylococcus aureus)
142
Q

Causes of Hospital acquired pneumonia

A

commonly gram-negative enterobacteria or staph. aureus

Pseudomonas, Klebsiella, Bacteroides and clostridia

143
Q

Causes of aspiration pneumonia

A 
stroke
myasthenia
bulbar palsies
decreased conciousness
oesphageal disease
poor dental hygiene
144
Q

Causes of pneumonia in the immunocompromised patient

A
  • strep pneumoniae
  • H. influenzae
  • staph. aureus
  • M. catarrhalis
    M. pneumoniae
    Gram -ve bacilli and pneumocystis jiroveci
    Fungi
    Viruses - CMV, HSV
    Mycobacteria
145
Q

Symptoms of pneumonia

A 
fever
Rigors
anorexia 
Dyspnoea
cough
purulent sputum 
Haemoptysis 
Pleuritic pain
146
Q

Signs of Pneumonia

A 
Pyrexia
Cyanosis 
Confusion 
tachypnoea
Tachycardia
Hypotension
Signs of consolidation
Pleural Rub
147
Q

Signs of consolidation

A

diminished expansion
Dull percussion note
Increased vocal femitus/resonance
Bronchial breathing

148
Q

Pneumonia tests

A

ABG
CXR
FBC, U&Es, LFTs, CRP, Blood cultures
Sputum cultures

149
Q

Pneumonia severity

A

CURB-65

  • Confusion
  • Urea >7mmol/L
  • Resp rate >/ 30/min
  • BP <90 systolic
  • Age >65

0-1 –> Home
2–> hospital therapy
3> severe- mortality 15-40% consider ITU

150
Q

Penumonia Management

A 
Abx --> typically co-amoxiclav/ amoxicillian or clarythromycin or doxycyline
Oxygen --> keep PaO2 >8.0
IV fluids 
VTE prophylaxis
Analgesia if pleurisy
151
Q

Complications of pneumonia

A 
pleural effusion 
empyema
lung abscess
respiratory failure
septicaemia 
brain abscess 
pericarditis
myocarditis
cholestatic jaundice
152
Q

Lung abscess

A

cavitating area of localised, suppurative infection within the lung

153
Q

Lung abscess causes

A
  • inadequately treated pneumonia
  • aspiration
  • bronchial obstruction
  • pulmonary infarction
  • septic emboli
  • subphrenic or hepatic abscess
154
Q

Clincial features of lung abscesses

A 
swinging fever 
cough 
purulent, foul smelling sputum 
pleuritic chest pain, 
haemoptysis 
malaise
weight loss

–> finger clubbing, anaemia, crepitations

155
Q

Lung abscess tests

A

FBC- anaemia & neutrophilia, ESR, CRP, blood cultures
Sputum microscopy and cultures and cytology
CXR

156
Q

Meningitis organisms

A

meningococcus or pneumococcus

Less commonly haemophilus influenzea, listeria monocytogenes, CMV, cryptococcus or TB

157
Q

Meningitis differentials

A 
malaria
encephalitis 
septicaemia 
subarachnoid haemorrhage
dengue
tentanus
158
Q

Early features of meningitis

A

headache
leg pains
cold hands and feet
abnormal skin colour

159
Q

Later features of meningitis

A

Meningism - neck stiffness, photophobia, Kernig’s sign (pain and resistance on passive knee extension with fully flexed hips)
- decreased conciousness, coma
- seizures +/- focal CNS +/- opisthotonus
-petechial rash
Galloping sepsis - slow cap refill, DIC, low BP, temp, high or normal pulse

160
Q

Meningitis management

A

start abx asap –> cefotaxime

rifampicin for close contacts or ciprofloxacin

161
Q

Meningitis investigations

A

U&E, FBC, LFTs, glucose, coagulation screen
Blood cultures, throat swabs, rectal swab, serology (EBV)
LP- after CT or if GCS 15 with no focal neurology

162
Q

LP results in Meningitis

Bacterial

A
  • often turbid
  • predominantly polymorphic cells
  • cell count 90-1000
  • glucose - low/normal (<1/2)
  • protein - >1.5
  • bacteria in smear and culture
163
Q

LP results in Meningitis

TB

A
  • fibrin web
  • mononuclear cells
  • cell count - 10-1000
  • <1/2 plasma glucose
  • protein high (1-5)
  • no bacteria in smear
164
Q

LP results in Meningitis

Viral

A

Usually clear appearance

  • mononuclear cells
  • cell count 50-1000
  • glucose >1/2 plasma
  • low protein
  • no bacteria on culture

3B Specialties (7 decks)

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