Infectious diseases Flashcards

1
Q

Which bacteria causes TB?

A

mycobacterium tuberculosis (acid fast, rod shaped bacillus)

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2
Q

What is the difference between primary and secondary TB?

A

primary = non immune host exposed to m.tuberculosis can develop a primary infection of the lungs

secondary = if the host is immunocompromised, the initial infection can reactivate (usually in the apex of the lungs and then spreads to distal sites)

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3
Q

Describe the pathology of TB?

A
  1. inhaled m. tuberculosis bacteria is engulfed by alveolar macrophages
  2. T helper cells secrete INF gamma which activates macrophages into epithelioid histiocytes
  3. these aggregate into granulomas
  4. these have caseous necrosis In the centre
  5. migrate to the lymph nodes
  6. inflammatory response is mediated by a type 4 hypersensitivity reaction
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4
Q

How does pulmonary TB present?

A
cough with sputum, haemoptysis 
dyspnoea 
malaise
weight loss
night sweats
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5
Q

How does extra pulmonary TB present?

A

GENITOURINARY - dysuria, increased frequency, loin/back pain, haematuria

BONE - Potts disease, vertebral collapse

SKIN - lupus vulgaris

PERITONEAL- abdo pain, GI upset

TB MENINGITIS - confusion

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6
Q

How does TB meningitis present and how is it treated?

A

for 1-3 weeks: fever, headache, vomiting, drowsiness, delirium seizures

CNS signs: tremor, papilloedema, cranial nerve palsies

Rx: treat for 12 months with RIPE

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7
Q

What is used to screen for latent TB?

A

MANTOUX TEST
inject antigen of the mycobacterium into the skin -> read result 2-3 days later

if rash <6mm = negative result
if rash 6-15 mm= positive (could be due to previous TB or BCG)
if rash >15mm = strongly positive (suggests TB infection)

(interferon gamma blood test also been introduced, used when Mantoux test positive)

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8
Q

If found to have a positive Mantoux test, which investigations should be done next?

A
  1. sputum sample x3 (one should be early morning)- cultured in MGIT and send for MCandS for acid fast bacilli in ziehl nielson staining
  2. Chest x-ray - shows patchy consolidation, cavitation fibrosis, calcification , Ghon focus (= calcified granuloma)
  3. PCR - rapid identification of species and drug resistance
  4. histology - necrotising caseating granulomatous inflammation
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9
Q

how is TB treated?

A

6 months of:

  1. RIFAMPICIN
  2. ISONIAZID

+ 2 months of:

  1. PYRAZINAMIDE
  2. ETHAMBUTOL
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10
Q

if suspicious patient won’t comply for TB treatment, what can be implemented?

A

Directly Observed Therapy (DOTS)

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11
Q

What are the side effects of rifampicin?

A

orange secretions (in tears, urine)
hepatitis
flu symptoms

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12
Q

What are the side effects of isoniazid?

A

peripheral neuropathy
hepatitis
PALLAGRA (vit B3 deficiency) - diarrhoea, dementia, dermatitis

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13
Q

What are the side effects of pyrazinamide?

A

gout (hyperuricaemia)
hepatitis, liver toxicity
arthralgia

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14
Q

What are the side effects of ethambutol?

A

optic neuritis (should have baseline eye check before starting treatment)

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15
Q

How is latent TB treated?

A

3 months of rifampicin and isoniazid (in order to prevent active TB)

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16
Q

How does multidrug resistant tB occur and how is it treated?

A

TB that is resistant to rifampicin and isoniazid is due to poor management of TB with failure to comply to medication or incomplete courses of treatment leading to resistance

should be treated with 5-8 different drugs for up to 2 years

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17
Q

What kind of virus is hIV?

A

Human Immunodeficiency virus is an enveloped RNA RETROVIRUS* virus

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18
Q

list the risk factors for transmission of HIV?

A

unprotected sex
contaminated needles in IVDU
breast milk (bottle feeding recommended)
transmission from mother to baby (C section if viral load >50)

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19
Q

Describe the pathology of HIV infection

A
  1. HIV binds via its GP120 receptor to CD4 receptors on T helper lymphocytes, monocytes, macrophages and neural cells
  2. it makes a copy of the cells RNA genome and uses integrate to integrate this new copy into the host DNA
  3. virus replicates to produce billions of new virions - infecting further CD4 cells
  4. depletion of CD4 +ve cells
  5. decreased immune function
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20
Q

How is HIV diagnosed?

A
  1. serum HIV antibodies after 4 weeks of exposure -> by ELISA and western blot
  2. HIV RNA PCR / core p24 antigen in the plasma *= confirms diagnosis
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21
Q

How does a patient initially present 3-12 weeks after first infected with HIV?

A
malaise
fever
weight loss
lymphadenopathy 
myalgia 
maculopapular rash
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22
Q

Describe the stages of HIV infection and the symptoms of each

A
  1. SEROCONVERSION
    “flu like illness” e.g. malaise, fever, lymphadenopathy, myalgia
  2. LATENT PHASE
    asymptomatic but PERSISTENT GENERALISED LYMPHADENOPATHY
    nodes >1cm diameter in >2 extra inguinal nodes for >3 months
  3. CONSTITUTIONAL SYMPTOMS
    diarrhoea **, fever, weight loss, night sweats
    + minor opportunistic infections e.g. oral candida, herpes zoster, capos sarcoma, seborrheic dermatitis
  4. AIDS
    HIV + AIDS defining illness + CD4 < 200 x 10^6/L
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23
Q

List possible AIDS defining illnesses

A

CD4 200-500 - shingles, hairy leukoplakia, oral thrush, Kaposi sarcoma (purple papules on skin)

CD4 100-200 - cryptosporidiosis, cerebral toxoplasmosis, PML, pneumocytic jurivecci pneumonia (dry cough, desaturations, Rx- co-trimoxazole), HIV dementia

CD4 50-100 - aspergillosis, oesophageal candidiasis, cryptococcal meningitis, primary CNS lymphoma

CD4 <50 - Mycobacterium avium infection, CMV retinitis

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24
Q

What is used to establish how advanced a patients disease is and monitor their response to treatment/ PROGNOSIS?

A
  1. CD4 COUNT
    normal range= 450-600
    low (AIDS) and at risk of opportunistic infections = <200
    at risk of MAI and CMV = <50
  2. VIRAL LOAD**
    uncontrolled hIV = >500,000
    well controlled hIV = undetectable = untrasmissable
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25
List the complications of HIV?
PULMONARY pneumocystitis jiroveci pneumonia (Rx: cotrimoxazole) Kaposi sarcoma (purple papules on skin with ulceration) M. avian intracellular Non hodgkin lymphoma ``` GI candidiasis infection - of oesophagus, mouth ulcers (Rx: fluconazole) viral hepatitis mycobacterium avian infection chronic diarrhoea cervical cancer ``` EYE CMV retinitis CNS meningitis/ encephalitis toxoplasma gondii CNS lymphoma
26
How is HIV managed?
HAART (highly anti retroviral therapy) = 2 x NRTI + 1 x NNRTI / protease inhibitors / integrase inhibitors
27
Name HIV drug classes and examples of each
Nucleoside Reverse Transcriptase Inhibitors e.g. zidovudine, abacavir SE: peripheral neuropathy, haemolytic anaemia Non Nucleoside Revserse Transciptase Inhibitors e.g. efavirenz, etravirine Protease inhibitors e.g. indinavir, atazanavir SE: GI upset Integrase inhibitors e.g. raltagravir
28
What is given to prevent opportunistic infections in AIDS?
co-trimoxazole
29
What can be used for prophylaxis for hIV?
Pre exposure Prophylaxis (PrEP) Truvada (tenofovir + emtricitabine) taken daily available on the NHS in Scotland and Wales and can be bought online
30
define cellulitus
bacterial infection of the dermis layer of the skin and deeper subcutaneous tissue
31
how is cellulitis caused and by which organisms?
infection usually due to a BREAK/PUNCTURE in the skin which allows bacteria to enter organisms: staphylococcus aureus and streptococcus pyogenes
32
List the risk factors for cellulitis
``` diabetes insect bites obesity elderly immunosuppression skin conditions IVDU previous cellulitis ```
33
how does cellulitis commonly present?
unilateral red hot swollen painful area of the skin, spreads quickly +/- fever, malaise, rigors
34
How does orbital and periorbital cellulitis present?
PERI ORBITAL - red, swollen painful eye with acute onset ORBITAL - red, swollen eye, severe ocular pain, visual disturbance
35
How is orbital cellulitis managed?
1. refer to ophthalmology immediately - MEDICAL EMERGENCY | 2. IV antibiotics
36
What are the possible complications of cellulitis?
``` abscess formation sepsis osteomyelitis necrotising fasciitis persistent leg ulceration chronic lymphedema ```
37
How is cellulitis managed?
1. clinically diagnose 2. use the Eron classification 3. analgesia 4. elevate legs 5. uncomplicated/ community: PO flucloxacillin QDS for 7 days (clarithromycin in penicillin allergic) 6. admit to hospital if facial cellulitis, immunocompromised, elderly/ v young, severe deteriorating cellulitis for IV flucloxacillin
38
Which organism causes malaria?
parasitic infection of the RBC by protozoa plasmodium 5 different species of the plasmodium mosquito: 1. P. falciparum ** - most dangerous 2. P. vivax (most common benign malaria) 3. P. ovale 4. P. malariae 5. P. knowlesi
39
Describe the pathology of malaria
1. infected female anopheles mosquito bites human and infects with the parasite 2. they enter hepatocytes which rupture 3. infected protozoa enters bloodstream and infects RBC causing RBC to rupture and release toxins
40
What are the risk factors for malaria?
``` endemic area e.g. sub sahara africa, SE asia no chemoprophylaxis absence of bed net pregnancy immunocompromised older ```
41
How does malaria infection present?
symptoms present within 1 month of mosquito event non specific: prodromal headache, malaise, myalgia, anorexia, fever spikes, nausea, confusion, anaemia , jaundice, hapatomegaly
42
if a person comes back from an endemic malarial area with a fever/ unwell, how are they investigated?
GIEMSA STAINED BLOOD FILM*** thick (locates presence) and thin (identify species) x 3 samples parasitised red cells (>2% parasiteaemia = complicated malaria) RAPID DIAGNOSTIC TEST ``` FBC -> anaemia, low platelets U&E -> renal failure blood culture -> rule out sepsis clotting -> check for DIC urine dip -> haemoglobulinaemia LDH ABG glucose ```
43
How is a patient diagnosed with malaria treated?
1. refer to infectious diseases 2. if >2% parasiteaemia = IV artersunate ** + plasma exchange >10% parasites 3. if <2% parasiteaemia = artemisinin combination therapy
44
How would you monitor response to malaria treatment?
parasite count daily
45
What are the complications of malaria?
``` anaemia AKI - blackwater fever - dark red urine liver damage cerebral malaria hypoglycaemia metabolic acidosis DIC ARDS severe haemolytic anaemia ```
46
Define sepsis
dysregulated immune host response to bacteria in the blood causing organ dysfunction
47
What is in the septic 6?
patients scoring SHEWS >3 should be screened for sepsis within 1 hour B- Blood cultures U- urine output (<0.5 ml/kg for 2 hours) F - fluids (0.9% normal saline 500ml fluid bolus) A- antibiotics (tazocin) L - lactate (>2) O- oxygen (high flow via non rebreathe mask)
48
Which tests are in the septic screen?
``` FBC U&E CRP ABG (lactate) blood cultures clotting screen + urine dipstick, CXR ```
49
How is sepsis managed?
AIRWAY make sure airway patent and open BREATHING measure RR, oxygen sats give high flow oxygen via non rebreathe mask ausculate the chest - signs of consolidation, crackles ABG -> order CXR if necessary CIRCULATION measure cap refill, pulse, BP obtain IV access with canula and get blood cultures and bloods needed fluid bolus 500ml 0.9% saline ECG ring blood bank to cross match and group and save catheterise and measure urine output DISABILITY check blood glucose GCS score EXPOSURE full body examination, ring reg for support or ITU if necessary
50
How is MRSA prevented?
nasal / wound swab all patients that come into hospital wash hands isolate patients with suspected MRSA/ previous MRSA use gowns/ gloves when dealing with infected patients
51
How is MRSA treated?
vancomycin (ask microbiologist)
52
What is clostridium difficile infection?
a gram +ve superbug infection whose spores are v contagious caused by use of broad spectrum antibiotics e.g. clindamycin, 3rd gen cephalosporins
53
What are the signs of c.diff infection?
increased temp colic mild diarrhoea / bloody diarrhoea pseudomembranous colitis
54
how is c.diff infection confirmed?
C. difficile stool culture - confirmed by ELISA or PCR
55
How is c.diff infection managed?
1. stop causative antibiotic (commonly 3rd gen cephalosporins and clindamycin) 2. metronidazole/ vancomycin for 10 days
56
How does hepatitis A and E spread?
faecal -oral
57
How does hepatitis A/E present?
``` incubation period 2-6 weeks fever malaise anorexia nausea arthralgia jaundice hepato-splenomegaly ```
58
How is hep A/E managed?
supportive, self limiting infection avoid alcohol Hep A has vaccination = Havrix monodies
59
How does hepatitis B spread?
BLOOD BORNE products e.g. blood transfusions, needles sexual* vertical transmission* IVDU
60
How does hep B present?
incubation 1-6 months | fever, malaise, jaundice, arthralgia, anorexia
61
what are the complications of hep B?
Fulminant hepatic failure cholangiocarcinoma chronic hepatitis - ground glass hepatocytes hepatocellular carcinoma
62
Which antigens in hepatitis B are of clinical importance?
CORE ANTIGEN (HBcAg) - not used diagnostically ENVELOPE ANTIGEN (HBeAg) * - allows assessment of phase of infection SURFACE ANTIGEN (HBsAg) * - current infection
63
How are the antibodies which the antigens trigger of clinical importance in hep B?
CORE ANTIBODY - immunity from previous exposure IgM initially rises in acute phase and then IgG rises and longer lasting -> IgM core antibody ** tested to identify new infection ENVELOPE ANTIBODY - later phase of disease SURFACE ANTIBODY - immunity to hep b
64
When is chronic hepatitis B diagnosed and when does this normally occur?
if surface antibody has not been produced within 6 months of infection, they have CHRONIC HEPATITIS (core antibody +ve, surface antigen +ve, surface antibody -ve) commonly caused when acquired at birth or in childhood,
65
Why is chronic hepatitis important to diagnose?
increases risk of complications e.g. cirrhosis, liver cancer 6 monthly fibroscan and AFP
66
How is hepatitis B managed?
avoid alcohol immunise sexual contacts self limting if ALT >30 iu/L, then need anti virals (entecavir)
67
How does hepatitis C spread?
IVDU ** | blood - transfusions , tattoo, needle stick injury
68
How does hepatic C present?
Early infection: mild, asymptomatic 85% develop silent chronic infection 25% develop cirrhosis 4% develop HCC
69
How is hep C diagnosed?
anti HCV antibodies (2-3 months after exposure) HCV PCR - confirms ongoing infection liver biopsy and LFTs
70
How is hep c managed?
non structural 2 serine protease inhibitors e.g. boceprevir | avoid alcohol
71
How does autoimmune hepatitis present?
acute hepatitis (fever, jaundice) or chronic liver disease amenorrhoea usually occurs in females
72
How is autoimmune hepatitis diagnosed and managed?
1. raised IgG 2. ANA antibodies 3. liver biopsy 4. steroids +/- liver transplant
73
How is HIV managed in pregnancy?
screen all women with blood test anyone with HIV should have HAART begin zidovudine infusion during 4hrs before C section neonate given oral zidovudine do NOT breastfeed
74
What is used for malaria prophylaxis?
chloroquine (1 week before travel) - SE: headaches, psychosis, retinopathy doxycycline mefloquine + DEET containing mosquito spray, net around bed, long sleeved tops and full length trousers
75
which questions are important to ask in a patient with potential hepatitis?
recent travel needle/ IVDU sexual contacts alcohol - alcohol hepatitis?
76
Which tests are done for viral hepatitis ?
hepatitis antigens and antibodies Non invasive liver screen USS Coagulation
77
What is found on serology of an acute infection of Hep B?
core antibody +ve ** envelope antigen +ve in early infection, envelope antibody +ve in later phase of infection surface antigen +ve **
78
what is found on serology of someone who is immunised against Hep B?
surface antibody +ve
79
what is found on serology of someone who was previously infected with Hep B but now cleared?
core antibody +ve surface antigen -ve surface antibody +ve
80
list the differentials for cellulitis?
DVT necrotising fasciitis abscess compartment syndrome
81
Other than medical management, what else must you do in tB?
notify public health as notifiable disease (call within 24 hrs or form within 3 days)
82
Which tests should be done before commencing treatment for TB?
LFTs | ophthalmology screening with snellen chart
83
Which antibiotics can cause c.difficle?
``` 5 C's C- clindamycin C - cephalosporin C - co amoxiclav C - ciprofloxacin C - Carbapenems e.g. meropenem ```
84
Which symptoms would indicate legionnaires as a cause of pneumonia?
``` dry cough + fever + flu like confusion recently been on holiday e.g. air conditioning, Spain hyponatraemia pleural effusion ```
85
how is legionnaires diagnosed?
urinary antigen for legionella
86
How is legionnaires managed?
1. erythromycin | 2. notify public health
87
differentials for malaria?
``` typhoid hepatitis dengue fever influenza HIV meningitis viral haemorrhage fever ```
88
How is TB managed at home/ protecting family?
contagious for 2-3 weeks don't share bed with someone else, open windows, stay away from work, throw away tissues contact tracing - do Mantoux test and Chest x ray on close contacts offer BCG vaccination if <35 y/o inform public health England