Infectious Diseases Flashcards

(196 cards)

1
Q

What is malaria?

A

Infectious disease caused by Plasmodium of protozoan parasites (single-celled organisms)

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2
Q

What is the most severe and dangerous type of malaria?

A

Plasmodium falciparum- Accounts for 80% of malaria causes in the UK

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3
Q

How is malaria transmitted?

A

Through bites from female Anopheles mosquitoes that carry the disease
Not transmitted in the UK- Is associated with travel to areas where malaria is present

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4
Q

List types of malaria

A

Plasmodium falciparum (most common and severe form)
Plasmodium vivax
Plasmodium ovale
Plasmodium malariae
Plasmodium knowlesi

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5
Q

Outline the life cycle of malaria

A

Usually spread at night
Feeding mosquito sucks up infected blood- Parasites reproduce in mosquito’s gut, producing sporozoites
Mosquito bites someone, sporozoites are injected- Travel to liver of newly infected person- P. vivax and P. ovale can lie dormant for months or years before reactivating
Parasites mature in liver into merozoites- Enter blood and infect RBCs- Merozoites reproduce, RBCs rupture, releasing merozoites into blood and causing haemolytic anaemia
In P. vivax and P. ovale- Rupture and release of merozoites occurs every 48h, causing fever spike every other day
P. falciparum- Fever spikes more frequently
P. malariae- Fever spikes every 72h

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6
Q

Outline presentation of malaria

A

Fever (up to 41 degrees C) with sweats and rigors
Fatigue
Myalgia (muscle aches and pains)
Headache
Nausea
Vomiting

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7
Q

What are the signs of malaria on examination?

A

Pallor due to anaemia
Hepatosplenomegaly
Jaundice (bilirubin released during rupture of RBCs)

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8
Q

What is the most characteristic symptom of malaria?

A

Fever which spikes very high every 48h
Exposure can be from several years ago

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9
Q

How is malaria diagnosed?

A

Malaria blood film- Sent in EDTA bottle
3 negative samples taken over 3 consecutive days required to exclude malaria

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10
Q

Outline management of falciparum malaria

A

Admit

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11
Q

Outline oral management of uncomplicated malaria

A

Artemether with lumefantrine (Riamet)- 1st choice
Quinine plus doxycycline
Quinine plus clindamycin
Quinine plus clindamycin
Proguanil with atovaquone (Malarone)
Chloroquine (increasing rates of resistance to chloroquine)
Primaquine (can cause severe haemolysis in patients with G6PD deficiency)

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12
Q

Outline IV management of severe or complicated malaria

A

Admission to HDU or ICU
Artesunate 1st choice (haemolysis common SE)
Quinine dihydrochloride

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13
Q

List complications of P. falciparum malaria

A

Cerebral malaria
Seizures
Reduced consciousness
AKI
Pulmonary oedema
Disseminated intravascular coagulopathy (DIC)
Severe haemolytic anaemia
Multi-organ failure and death

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14
Q

Outline prophylaxis for preventing malaria when travelling to endemic areas

A

No method 100% effective alone
Use mosquito spray (eg: 50% DEET spray)
Use mosquito nets and barriers in sleeping areas
Seek medical advice if symptoms develop
Take antimalarial medication as recommended

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15
Q

What are the main antimalarial medication options?

A

Not 100% effective
Proguanil with atovaquone (malarone)- Take from 2d before until 7d after travel to endemic area
Doxycycline- Taken 2d before until 4wks after travel to endemic area
Mefloquine (risk of psychiatric SEs)- Taken wkly from 2wks before to 4wks after travel to endemic area
Chloroquine with proguanil (less often used due to high resistance)

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16
Q

Outline HIV

A

RNA retrovirus
HIV-1 is most common type
HIV2 mainly found in West Africa
Virus enters and destroys CD4 T-helper cells
Initial seroconversion flu-like illness occurs within few wks of infection- Then asymptomatic until condition progresses to immunodeficiency- May occur yrs after initial infection

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17
Q

Outline transmission of HIV

A

Unprotected anal, vaginal or oral sexual activity
Mother to child- At any stage of pregnancy, birth or breastfeeding- Vertical transmission
Mucous membrane, blood, or open wound exposure to infected blood/bodily fluids- eg: Sharing needles, needle-stick injuries, blood splashed in eye

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18
Q

List AIDS-defining illnesses

A

CD4 count dropped to level that allows for unusual opportunistic infections and malignancies

Kaposi’s sarcoma
Pneumocystis jirovecii pneumonia (PCP)
CMV
Candidiasis (oesophageal or bronchial)
Lymphomas
TB

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19
Q

Outline HIV screening

A

Low threshold for testing
Patients with RFs tested
All patients accessing sexual health/antenatal/substance misuse services offered testing
Verbal consent should be documented

Checks ABs to HIV and p24 antigen
Window period of 45d- Can take up to 45d for +ve test to show
Point of care test- HIV ABs- Give result within mins, have 90d window period
Self-sampling kits- Posted to lab- ABs and p24 antigen

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20
Q

Outline monitoring of HIV

A

Test CD4 count gives number of CD4 cells in blood- Lower count gives higher risk of infection
500-1200 cells/mm3= Normal
<200 cells/mm3= High risk opportunistic infections

Testing for HIV RNA/ml of blood indicates viral load
Undetectable viral load means level below recordable range (20 copies/ml)

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21
Q

Outline treatment of HIV

A

Combination of antiretroviral therapy (ART)- Offered to everyone diagnosed with HIV, irrespective of viral load or CD4 count
Genotypic resistance testing- Establish resistance of each HIV strain to different meds to guide treatment
Aims to achieve normal CD4 count and undetectable viral load

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22
Q

List classes of antiretroviral therapy meds

A

Protease inhibitors (PI)
Integrase inhibitors (II)
Nucleoside reverse transcriptase inhibitors (NRTI)
Non-nucleoside reverse transcriptase inhibitors (NNRTI)
Entry inhibitors (EI)

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23
Q

What is the usual starting regime for antiretroviral therapy?

A

2 NRTIs (eg: Tenofovir plus emtricitabine) plus 3rd agent (eg: Bictegravir)

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24
Q

Outline additional management of HIV

A

PCP- Prophylactic co-trimoxazole given to all HIV +ve patients with CD4 count<200/mm3
Increased risk developing CVD- Monitor blood lipids and consider statins
Yrly cervical smears- Increased risk HPV and cervical cancer
Vaccinations- Yrly influenza, pneumococcal, HPV, Hep A and B- Avoid live vaccines

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25
Outline reproductive health and HIV
Correct use of condoms Effective treatment combined with undetectable viral load can prevent spread of HIV
26
Outline prevention of transmission of HIV during birth
Mother's viral load determines mode of delivery <50 copies/ml- Normal vaginal delivery >50 copies/ml- Consider pre-labour C section >400 copies/ml- Pre-labour C section IV zidovudine infusion during labour and delivery if viral load unknown/>1000 copies/ml Prophylaxis given to baby depending on mother's viral load: <50 copies/ml- Zidovudine for 2-4wks High-risk babies- Zidovudine, lamivudine, nevirapine for 4wks
27
Outline HIV and breastfeeding
Can be transmitted during breastfeeding Risk reduced if mother's viral load undetectable but not eliminated
28
Outline post-exposure prophylaxis (PEP) of HIV
Post-exposure prophylaxis (PEP)- Used after exposure to reduce risk of transmission- Not 100% effective and must be commenced within <72h Combination of ART therapy- Emtricitabine/tenofovir (Truvada) and raltegravir for 28d
29
Outline pre-exposure prophylaxis (PrEP) of HIV
Emtricitabine/tenofovir (Truvada)
30
Outline TB
Caused by mycobacterium TB (rod-shaped acid-fast bacillus)- Require Zeihl-Neelsen stain- Turns bright red against blue background
31
What type of staining is used to diagnose TB?
Require Zeihl-Neelsen stain- Turns bright red against blue background
32
Outline the disease course of TB
Mainly spread by inhaling saliva droplets from infected Several options: - Immediate clearance (most cases) - Primary active TB (active infection after exposure) - Latent TB (Presence of bacteria w/o symptomatic or contagious) - Secondary TB (reactivation of latent TB to active infection)
33
What is miliary TB?
When immune system can't control infection Disseminated and severe disease
34
Outline latent TB
When immune system encapsulates the bacteria and stops progression of the disease No symptoms and can't spread the bacteria Can reactivate, usually due to immunosuppression- Secondary TB
35
Where is the most common site for TB infection?
Lungs
36
List sites of extrapulmonary TB
Lymph nodes Pleura CNS Pericardium GI system GU system Bones and joints Skin (cutaneous TB)
37
What is a cold abscess?
Firm, painless abscess caused by TB, usually in neck No inflammation/redness/pain
38
Outline risk factors for TB
Close contact with active TB Immigrants from areas with high TB prevalence People with relatives/close contacts from countries with high rate TB Immunocompromised (eg: HIV or immunosuppressant meds) Malnutrition, homelessness, drug users, smokers and alcoholics
39
Outline the BCG vaccine
Intradermal injection of live attenuated Mycobacterium bovis Protects against severe and complicated TB, but less against pulmonary TB Tested with Mantoux before vaccine
40
Outline presentation of TB
Chronic, gradually worsening symptoms Most involve pulmonary disease Cough Haemoptysis Lethargy Fever or night sweats Weight loss Lymphadenopathy Erythema nodosum (tender, red nodules on shins caused by inflammation of SC fat) Spinal pain in spinal TB (Pott's disease)
41
Outline investigations of TB
Ziehl-Neelsen stain 2 tests for immune response to TB caused by previous infection/latent TB/active TB- Mantoux test or Interferon-gamma release assay (IGRA) If disease activity suspected- CXR and cultures
42
Outline Mantoux test
Inject tuberculin into intradermal space on forearm Doesn't contain live bacteria Creates a bleb under skin- Read after 72h- >5mm is +ve
43
Outline Interferon-Gamma release Assay (IGRA)
Mixing a blood sample with antigens from M. TB bacteria After previous contact- WBCs become sensitised to bacteria antigens- Will release interferon-gamma on further contact Positive- Interferon-gamma is released during test
44
Outline CXR of TB
Primary TB- Patchy consolidation, pleural effusions and hilar lymphadenopathy Reactivated TB- Patchy or nodular consolidation with cavitation (gas-filled spaces), typically in upper zones Disseminated miliary TB- Millet seeds uniformly distributed across lung fields
45
Outline cultures of TB
Can take several mths Sputum cultures (3 separate collected) Mycobacterium blood cultures Lymph node aspiration or biopsy If not producing enough sputum: Sputum induction with nebulised hypertonic saline Bronchoscopy and bronchoalveolar lavage (saline used to wash airways and collect a sample)
46
Outline Nucleic Acid Amplification Tests (NAAT)
Assesses genetic material of a pathogen Detects TB DNA Faster than traditional culture Used for- Diagnosing TB in patients with HIV or <16y or RFs for multidrug resistance
47
Outline treatment of latent TB
Isoniazid and rifampicin for 3mths Isoniazid for 6mths
48
Outline treatment of active TB
R- Rifampicin for 6mths I- Isoniazid for 6mths P- Pyrazinamide for 2mths E- Ethambutol for 2mths Co-prescribe pyridoxine (Vit B6) to prevent peripheral neuropathy caused by isoniazid
49
What is the main SE of isoniazid and how is this managed?
Peripheral neuropathy Give pyridoxine (Vit B6) Other SE- Hepatotoxicity
50
Outline other management options for TB
Test for other infectious disease (HIV/Hep B/Hep C) Contact tracing Isolate patients with active TB (at least 2wks) Negative pressure rooms in hospitals used to prevent airborne spread
51
What are the SEs of rifampicin?
Red/orange discolouration of secretions- Urine and tears Potent inducer of cytochrome P450 enzymes- Reduces effects of drugs metabolised by this system (eg: combined contraceptive) Hepatotoxicity
52
What are the SEs of Pyrazinamide?
Hyperuricaemia (high uric acid levels)- Results in gout and kidney stones Hepatotoxicity
53
What are the SEs of Ethambutol?
Colour blindness and reduced visual acuity
54
What is meningitis?
Inflammation of meninges usually due to infection Meninges- Lining of brain and spinal cord CSF is contained within meninges (in subarachnoid space)
55
List the causes of bacterial meningitis
Neisseria meningitidis Streptococcus pneumoniae (pneumococcus) Haemophilus influenzae Group B Streptococcus (GBS)- Particularly in neonates Listeria monocytogenes- Particularly in neonates
56
Outline Neisseria meningitidis
Gram-negative diplococcus bacteria Typically known as meningococcus Most common cause of bacterial meningitis
57
Outline Meningococcal meningitis
Bacteria infects meninges and CSF
58
Outline Meningococcal speticaemia
Meningococcus bacterial infection in bloodstream Causes non-blanching rash
59
What are the most common causes of viral meningitis?
Enteroviruses (eg: Coxsackie virus) Herpes simplex virus (HSV) Varicella zoster virus (VZV)
60
How is viral meningitis diagnosed?
Viral PCR testing on CSF sample
61
How is viral meningitis managed?
Aciclovir- Used to treat HSV and VZV
62
Outline presentation of meningitis
Fever Neck stiffness Vomiting Headache Photophobia Altered consciousness Seizures
63
Outline presentation of meningitis in neonates and babies
Non-specific signs and symptoms Hypotonia Poor feeding Lethargy Hypothermia Bulging fontanelle
64
What are the NICE guidelines for investigations of children with suspected sepsis?
Lumbar puncture Under 1mth, presenting with fever 1-3mths and are unwell/have low or high WBC count
65
What are the special tests to perform to look for meningeal irritation?
Kernig's test Brudzinski's test
66
What is Kernig's test?
Lie patient on back, flex one hip and knee to 90 degrees, slowly straighten knee whilst keeping hip flexed at 90 degrees Creates stretch in meninges If meningitis- Produce spinal pain or resistance to movement
67
What is Brudzinski's test
Lie patient flat on back and use hands to lift their head and neck off bed, flexing chin to their chest Positive test for meningitis- Causes patient to flex their hips and knees involuntarily
68
Outline the lumbar puncture result of bacterial meningitis
Cloudy High protein Low glucose High WCC (neutrophils) Bacteria on culture
69
Outline the lumbar puncture result of viral meningitis
Clear Mildly raised/normal protein Normal glucose High WCC (lymphocytes) Negative culture
70
Outline the procedure of a lumbar puncture
Insert needle into L3-L4 or L4/L5 intervertebral space Spinal cord ends at L1-L2
71
Outline management of bacterial meningitis
MEDICAL EMERGENCY Children in primary care with suspected meningitis and non-blanching rash- Urgent benzylpenicillin (IM or IV) Blood cultures and LP before starting ABs- Meningococcal PCR (gives faster result than blood cultures and still positive after treated with ABs) <3mths- Cefotaxime plus amoxicillin >3mths- Ceftriaxone Aciclovir added if viral meningitis suspected Vancomycin added if risk of penicillin-resistant pneumococcal infection (recent foreign travel or prolonged AB exposure) Steroids (dexamethasone) in bacterial meningitis- Reduce frequency and severity of hearing loss and neuro complications
72
What is used to reduce frequency of hearing loss and neurological complications in meningitis?
Dexamethasone
73
List complications of hearing loss
Hearing loss Seizures and epilepsy Cognitive impairment and learning disability Memory loss Focal neurological deficits- Limb weakness or spasticity
74
Outline post-exposure prophylaxis of meningitis
Risk highest with close prolonged contact within 7d before onset of illness Single dose of ciprofloxacin given as soon as possible after diagnosis
75
Outline Clostridium difficile
Gram positive, rod-shaped, anaerobic bacteria Infection associated with repeated use of ABs/PPIs/healthcare settings Spores released in faeces May colonise intestines w/o causing any symptoms or issues Produces Toxin A (enterotoxin) and Toxin B (cytotoxin)
76
List ABs most associated with C. difficile
Clindamycin Ciprofloxacin (and other fluoroquinolones) Cephalosporin Carbapenems (eg: Meropenem)
77
Outline presentation of C. difficile
Colonisation usually asymptomatic Infection- Diarrhoea, nausea and abdo pain Severe infection with colitis- Dehydration, systemic symptoms (eg: Fever, tachycardia, hypotension)
78
Outline diagnosis of C. difficile
Stool tests: C. difficile antigen (specifically glutamate dehydrogenase) A and B toxins (by PCR or enzyme immunoassay)
79
Outline management of C. difficile
Supportive care and oral ABs 1st line- Oral vancomycin 2nd line- Oral fidaxomicin Isolate until 48h after last episode of diarrhoea- High recurrence rate Recurrent cases- Faecal microbiota transplantation
80
List complications of C. difficile
Pseudomembranous colitis Toxic megacolon Bowel perforation Sepsis
81
What is Pseudomembranous colitis?
Inflammation of large intestine Yellow/white plaques form pseudomembranes on inner surface bowel wall Seen during colonoscopy and confirmed on biopsy
82
What is Toxic megacolon?
Complication of severe inflammation in large intestine and involves dilation of colon High risk of bowel rupture
83
List some post-gastroenteritis complications
Lactose intolerance IBS Reactive arthritis Guillain-Barre syndrome HUS
84
Outline general management of Gastroenteritis
Food poisoning- NOTIFIABLE DISEASE Isolate- Barrier nursing and infection control- 48h after symptoms resolve Faeces sample- Microscopy, culture and sensitivities Dehydration- Assess whether need for admission for IV fluids Oral rehydration salt solution Antidiarrhoeal drugs- Avoid Antibiotics- If risk of complications Oral intake tolerated- Light diet with bland foods
85
What is oral rehydration salt solution?
Dioralyte sachets mixed with water Replace losses in risk of dehydration Contains glucose, potassium and sodium
86
Outline giardiasis
Parasite in small intestines of mammals- Releases cysts in faeces- May contaminate food/water Faecal-oral transmission May cause chronic diarrhoea Diagnosis- Stool test (NAAT or EIA) Treat- Tinidazole or metronidazole
87
Outline staphylococcal aureus as a cause of gastroenteritis
Can produce enterotoxins growing on food (eggs/dairy/meat) Cause inflammation in intestines Symptoms- Diarrhoea, vomiting, abdo cramps, fever- Start within hrs of ingestion and settle within 12-24h
88
Outline Yersinia Enterocolitica
Gram negative bacillus Pigs are key carriers (raw pork) and contact with infected humans/animals and faeces Typically affects children- Watery/bloody diarrhoea, abdo pain and fever Incubation 4-7d- Symptoms last >3wks Older children/adults present with R sided abdo pain due to mesenteric lymphadenitis (inflammation in intestinal lymph nodes) and fever- Can impersonate appendicitis
89
Outline Yersinia pestis
Spread through rat flea bites Causes plague
90
Outline Bacillus Cereus
Gram positive rod Spread through contaminated cooked foods- Fried rice/cooked pasta left at room temperature Toxin cereulide causes abdo cramping and vomiting within 5h of ingestion Reheating food can kill bacteria but doesn't destroy the cereulide toxin- Watery diarrhoea Vomiting within 5h, diarrhoea >8h after ingestion- Symptoms resolve within 24h Can also occur with infective endocarditis in IV drug users, where heroin is contaminated
91
What is the most common cause of infective endocarditis in IV drug users?
Staph aureus
92
Outline salmonella
Spread by eating raw eggs/poultry/food contaminated with infected faeces of small animals Incubation 12h-3d- Symptoms resolve within 1wk Symptoms- Watery diarrhoea (may have mucous/blood), abdo pain, vomiting ABs only necessary in severe cases- Guided by stool culture and sensitivities (eg: Ciprofloxacin)
93
Outline Shigella
Spread via faeces Either person-person or through contaminated drinking water/food Incubation period 1-2d- Symptoms resolve within 1wk Symptoms- Bloody diarrhoea, abdo cramps, fever Can produce Shiga toxin- Can cause Haemolytic Uraemic Syndrome Treat severe cases- Azithromycin or ciprofloxacin
94
Outline Campylobacter Jejuni
Traveller's diarrhoea Gram negative bacteria Spread- Raw poultry, untreated water, unpasteurised milk Incubation 2-5d- Symptoms resolve 3-6d Symptoms- Abdo cramps, diarrhoea with blood, vomiting, fever ABs considered if severe symptoms or other RFs (HIV or HF)- Clarithromycin (1st line), azithromycin, ciprofloxacin
95
Outline E. coli
E. coli is normal intestinal bacteria Spread through contact with infected faeces/unwashed salad/contaminated water Produces Shiga toxin- Increased risk HUS- Avoid ABs
96
Outline viral gastroenteritis
Common and highly contagious Rotavirus Norovirus Adenovirus (tends to cause respiratory symptoms)
97
What is acute gastritis?
Stomach inflammation Presents with epigastric discomfort, nausea and vomiting
98
What is enteritis?
Inflammation of intestines Presents with abdo pain and diarrhoea
99
What is gastroenteritis?
Inflammation from stomach to intestines Presents with pain, nausea, vomiting and diarrhoea
100
What is the most common cause of gastroenteritis?
Virus Easily spread Isolate in a healthcare environment
101
What is the prognosis of gastroenteritis?
Most people recover well Can rarely be fatal- Especially in very young or old patients, or those with other health conditions
102
Outline influenza virus
RNA 3 types- A, B, and C A and B most common Outbreaks typically occur in winter
103
Outline influenza vaccination
Yearly required in: >65y Young children Pregnant women Chronic health conditions- Asthma, COPD, HF, diabetes Healthcare workers and carers
104
Outline presentation of influenza
Fever Lethargy and fatigue Anorexia (loss of appetite) Muscle and joint aches Headache Dry cough Sore throat Coryzal symptoms
105
What is the typical difference in features between cold and flu?
Flu- Abrupt onset, fever, 'wiped out' with muscle aches and lethargy Common cold- Gradual onset
106
Outline testing of influenza
Point-of-care tests- Swabs- Detect viral antigens Viral nasal or throat swabs- PCR analysis
107
Outline management of influenza
If risk of complications- Oral oseltamivir (twice daily for 5d), inhaled zanamivir (twice daily for 5d) Treatment needs to be started within 48h of onset of symptoms
108
Outline criteria for receiving post-exposure prophylaxis of influenza
Started within 48h of close contact with influenza Increased risk (eg: Chronic disease or immunosuppression) Not protected by vaccination (eg: <14d since vaccinated)
109
What are the options for post exposure prophylaxis for influenza?
Oral osetamivir 75mg once daily for 10d Inhaled zanamivir 10mg once daily for 10d
110
List complications of influenza
Otitis media, sinusitis and bronchitis Viral pneumonia Secondary bacteria pneumonia Worsening chronic health conditions- COPD and HF Febrile convulsions (young children) Encephalitis
111
What is septic arthritis?
MEDICAL EMERGENCY Infection in joint Can occur in original joint or prosthetic joint replacement
112
Outline presentation of septic arthritis
Usually affects single joint Rapid onset Hot, red, swollen and painful Stiffness and reduced range of motion Systemic symptoms- Fever, lethargy and sepsis
113
What is the most common cause of septic arthritis?
Staph aureus
114
What are the less common causes of septic arthritis?
Neisseria gonorrhoea (gonococcus)- In sexually active individuals- Typically a young patient with single acutely swollen joint- Gram negative diplococcus Group A strep Haemophilus influenza E. coli
115
What is the difference between Septic arthritis and reactive arthritis?
Disclude septic arthritis first Reactive arthritis- Urinary or genital symptoms- Typically triggered by urethritis or gastroenteritis and associated with conjunctivitis
116
What is the difference between Septic arthritis and gout?
Gout- Joint fluid shows urate crystals that are negatively birefringent of polarised light
117
What is the difference between Septic arthritis and pseudogout?
Pseudogout- Joint fluid shows rod-shaped calcium pyrophosphate crystals that are positively birefringent
118
What is the difference between Septic arthritis and haemarthrosis?
Bleeding into joint, usually after trauma
119
Outline management of septic arthritis
Joint aspiration before starting ABs Sample sent for gram staining, crystal microscopy, culture and AB sensitivities- Joint fluid may be purulent (pus) Empirical IV ABs continued for 4-6wks
120
Outline the AB choices for septic arthritis
1st line- Flucloxacillin Penicillin allergy- Clindamycin MRSA suspected- Vancomycin Ceftriaxone- Neisseria gonorrhoea
121
List possible intra-abdominal infections
Acute diverticulitis- Infection in intestinal diverticula Acute cholecystitis- With secondary infection in gallbladder Ascending cholangitis- Infection in bile ducts Appendicitis Spontaneous bacterial peritonitis- Infection in fluid in peritoneal cavity
122
What type of bacteria is E. coli?
Gram-negative
123
What type of bacteria is Klebsiella?
Gram-negative
124
What type of bacteria is Enterocolitis?
Gram-positive
125
What type of bacteria is Streptococcus?
Gram-positive
126
Which bacteria does Co-amoxiclav cover?
Gram +ve Gram -ve Anaerobes
127
Name types of anaerobic bacteria
Bacteroides Clostridium
128
Outline the coverage of amoxicillin plus gentamicin plus metronidazole
Amoxicillin- Gram +ve Gentamicin- Gram -ve Metronidazole- Anaerobes
129
Outline the coverage of ciprofloxacin plus metronidazole
Ciprofloxacin- Gram +ve, Gram -ve Metronidazole- Anaerobes
130
Outline coverage of vancomycin plus gentamicin plus metronidazole
Vancomycin- Gram +ve Gentamicin- Gram -ve Metronidazole- Anaerobes
131
Outline Co-amoxiclav
Covers gram +ve, gram -ve, anaerobes Doesn't cover pseudomonas or atypical bacteria
132
Outline quinolones
Ciprofloxacin and levofloxacin Covers gram +ve, gram -ve, atypical Don't cover anaerobes Usually paired with metronidazole
133
Outline metronidazole
Anaerobic cover Inhibits metronidazole Bactericidal
134
Outline gentamicin
Covers gram -ve bacteria and some gram +ve cover (staph) Bactericidal
135
Outline vancomycin
Gram +ve cover, including MRSA Combine with gentamicin (gram -ve) and metronidazole (anaerobe cover) in patients with penicillin allergy
136
Outline cephalosporins
Broad-spectrum cover against gram +ve and gram -ve bacteria Often avoided due to risk of C. diff infection
137
Outline Piperacillin with tazobactam and meropenem
Cover gram +ve, gram -ve and anaerobic bacteria Don't cover atypical bacteria or MRSA Usually reserved for very unwell patients and those not responding to other ABs
138
What is cellulitis?
Infection of skin and soft tissues underneath May be due to skin trauma, eczema, fungal nail infections or ulcers
139
Outline presentation of cellulitis
Erythema Warm/hot to touch Tense Thickened Oedematous Bullae (fluid filled blisters) Golden-yellow crust indicates Staph aureus May be systemically unwell- Sepsis
140
What are the most common causes of cellulitis?
Staph aureus Group A strep Group C strep MRSA should be considered- Repeated hospital admissions and ABs
141
Outline Eron classification
Severity of cellulitis Class 1- No systemic toxicity or comorbidity Class 2- Systemic toxicity or comorbidity Class 3- Significant systemic toxicity or significant comorbidity Class 4- Sepsis or life-threatening infection
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Outline management of cellulitis
Class 3 and 4 cellulitis requires admission for IV ABs 1st line- Flucloxacillin- Effective against Staph aureus Alternatives- Clarithromycin, clindamycin, Co-amoxiclav (1st line for cellulitis near eyes or nose)
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What are Lower UTIs?
Infection in bladder Causing cystitis (inflammation of bladder)
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What is pyelonephritis?
Inflammation of kidney resulting from bacterial infection Affects kidney tissue (parenchyma) and renal pelvis (ureter joins kidney)
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Outline UTIs
More common in women- Urethra is shorter Primary source is faeces Urinary catheters are a possible source of infection- More challenging to treat
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Outline presentation of Lower UTIs
Dysuria (pain, stinging or burning when passing urine) Suprapubic pain or discomfort Frequency Urgency Incontinence Haematuria Cloudy or foul-smelling urine Confusion- Commonly only symptom in older and frail patients
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Outline presentation of pyelonephritis
Fever Loin or back pain (bilateral or unilateral) Nausea or vomiting Systemic illness Loss of appetite Haematuria Renal angle tenderness
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Outline management of UTIs in pregnancy
7d ABs MSU and MC&S Nitrofurantoin (avoid in 3rd trimester) Amoxicillin (only after sensitivities known) Cefalexin (typical choice)
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Why is nitrofurantoin avoided in 3rd trimester of pregnancy?
Risk of neonatal haemolysis
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Why is trimethoprim avoided in 1st trimester of pregnancy?
Folate antagonist- Folate essential in early pregnancy for normal development of fetus Can cause congenital malformations- Neural tube defects (spina bifida)
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Outline UTIs and pregnancy
Increased risk of pyelonephritis, premature rupture of membranes and pre-term labour
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Outline management of Pyelonephritis
Refer to hospital if features of sepsis 7-10d ABs Cefalexin Co-amoxiclav (if culture results available) Trimethoprim (if culture results available) Ciprofloxacin (keep tendon damage and lower seizure threshold in mind)
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What should you consider if pyelonephritis is not responding to treatment?
Renal abscess Kidney stone obstructing ureter- Causing pyelonephritis
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Outline management of Lower UTIs
Nitrofurantoin- Avoid in patients with eGFR <45 Trimethoprim- Associated with high rates bacterial resistance Alternatives- Pivmecillinam, amoxicillin, cefalexin Typical duration: 3d ABs- Simple lower UTIs in women 5-10d ABs- Immunosuppressed women/abnormal anatomy/impaired kidney function 7d ABs- Men/pregnant women/catheter-related UTIs
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Outline causes of UTIs
E. coli- Most common Klebsiella pneumoniae Enterococcus Pseudomonas aeruginosa Staph saprophyticus Candida albicans (fungal)
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Outline investigations of UTIs
Urine dipstick- Nitrites (bacteria in urine), leukocytes (can be infection), RBCs (microscopic/macroscopic haematuria, common sign of infection/bladder cancer/nephritis) Nitrites better indication of infection than leukocytes UTI- Nitrites or leukocytes plus RBCs Dipstick result less reliable in catheterised patients or women >65y MSU- MC&S
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When is an MSU done?
Pregnant patients Patients with recurrent UTIs Atypical symptoms When symptoms don't improve with ABs
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What is sepsis?
Body launches large immune response to infection, causing systemic inflammation and organ dysfunction
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Outline pathophysiology of sepsis
Macrophages, lymphocytes and mast cells recognise pathogens- Release cytokines (IL and TNF) that activate immune system- Leads to systemic inflammation and release of NO (causing vasodilation) Cytokines cause endothelial lining of blood vessels to become more permeable- Fluid leaks out of blood into ECS, resulting in oedema and reduced intravascular volume- Increased gap between blood and tissues- Reduced amount of oxygen that reaches tissue Activation coagulation system- Deposition of fibrin and formation of thrombi- Compromised organ and tissue perfusion- Consumes platelets and clotting factors- Leads to thrombocytopenia (low platelets) and uncontrolled haemorrhage- DIC Anaerobic respiration- Raised serum lactate and metabolic acidosis
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Outline pathophysiology of disseminated intravascular coagulopathy
Activation of immune system and systemic inflammation Release of cytokines and increased oedema- Reduced O2 reaching tissues Activation of coagulation system- Fibrin deposition- Formation of thrombi- Compromised organ and tissue perfusion Blood clots consume platelets and clotting factors- Thrombocytopenia (low platelets) and uncontrolled haemorrhage
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What is seen on an ABG in sepsis?
Raised serum lactate and metabolic acidosis
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Outline septic shock
Occurs when arterial BP drops despite adequate fluid resuscitation- Results in organ hypoperfusion Anaerobic respiration begins and serum lactate level rises
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Outline diagnosis of septic shock
Low mean arterial pressure (<65 mmHg) despite fluid resuscitation (requiring vasopressors) Raised serum lactate (>2mmol/L)
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How is septic shock managed?
Aggressive treatment with IV fluids to improve BP and tissue perfusion High dependency or intensive care Vasopressors (noradrenaline)- Cause vasoconstriction and increase systemic vascular resistance and MAP- Improves tissue perfusion
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Outline sepsis-related organ failure assessment
Assess severity of organ dysfunction- Takes into account signs of organ dysfunction Hypoxia Increased oxygen requirements Requiring mechanical ventilation Low platelets (thrombocytopenia) Reduce GCS Raised bilirubin Reduce BP Raised creatinine
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List risk factors for sepsis
Any condition causing immune dysfunction/frailty/predisposition to infection Very young/old patients (<1y or >75y) Chronic conditions- COPD and diabetes Chemotherapy, immunosuppressants, steroids Surgery, recent trauma, burns Pregnancy and childbirth Indwelling medical devices, catheters, central lines
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Outline presentation of sepsis
NEWS2 Temperature Heart rate Respiratory rate Oxygen sats Blood pressure Consciousness level Additional signs of infection: Signs of potential sources- Cellulitis, discharge from wound, cough, dysuria Reduced urine output Mottled skin Cyanosis Arrhythmias (new-onset AF) A non-blanching rash (meningococcal septicaemia) Raised RR- Sign of early sepsis Elderly- Non-specific findings- Confusion, drowsiness, 'off legs' Neutropenic/immunocompromised- May have normal obs despite being life-threatening
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Outline investigations of sepsis
FBC- WCC and neutrophils U&Es- Kidney function and AKI LFTs- Liver function and source of infection CRP- Assess for inflammation Blood glucose- Hyperglycaemia and hypoglycaemia Clotting- Assess for DIC Blood cultures- Assess for bacteraemia Blood gas- Lactate, pH, glucose Urine dipstick and culture CXR CT if intra-abdo infection or abscess suspected LP- Meningitis or encephalitis
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Outline management of sepsis
Sepsis protocol and pathway Assess and start treatment within 1h of presenting Sepsis 6
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Outline sepsis 6
Take: Serum lactate Blood cultures Urine output Give: O2- Maintain 94-98% (88-92% in COPD) Empirical broad-spectrum ABs IV fluids
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What is neutropenic sepsis?
Sepsis with neutrophil count <1x10^9/L Usually consequence of anti-cancer or immunosuppressant treatment
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List medications that may cause neutropenia
Chemotherapy Clozapine- Schizophrenia Hydroxychloroquine- RA Methotrexate- RA Sulfasalazine- RA Carbimazole- Hyperthyroidism Quinine- Malaria Infliximab- Monoclonal antibody used for various AI conditions Rituximab- Monoclonal antibody used for various AI conditions and cancers
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Outline management of neutropenic sepsis
Low threshold for suspecting neutropenic sepsis in chemotherapy or meds that may cause neutropenia Any temperature >38 degrees C treated as neutropenic sepsis until proven otherwise Emergency admission Neutropenic sepsis policy Immediate broad-spectrum ABs- Piperacillin with tazobactam
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What is the prognosis of septic arthritis?
Mortality of approx. 10%
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In OSCEs, treating infections which antibiotic would you give?
Antibiotics according to local antibiotic policy
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Which antibiotics inhibit cell wall synthesis?
Antibiotics with beta-lactam ring: Penicillin Carbapenems (meropenem) Cephalosporins Antibiotics w/o beta-lactam ring: Vancomycin Teicoplanin
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Which ABs inhibit folic acid metabolism?
Sulfamethoxazole Trimethoprim Co-trimoxazole (bactericidal)- Combination sulfamethoxazole and trimethoprim (bacteriostatic)
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List ABs that target ribosomes
Inhibit protein synthesis Macrolides (erythromycin, clarithromycin, azithromycin) Clindamycin Tetracyclines (eg: Doxycycline) Gentamicin Chloramphenicol
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Outline nitrofurantoin
Exclusively used to treat lower UTIs Bactericidal Not used to treat pyelonephritis- Only achieves adequate conc. in urine
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Outline coverage of amoxicillin
Gram +ve Strep, listeria, enterococci
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Outline coverage of Co-amoxiclav
Gram +ve, gram -ve, anaerobes Staph, Haemophilus, E. coli
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Outline coverage of clarithromycin
Gram +ve, atypicals
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Outline coverage of clindamycin
Gram +ve, anaerobes
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Outline coverage of gentamicin
Gram -ve
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Outline coverage of ciprofloxacin
Gram -ve, atypicals
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Outline coverage of metronidazole
Anaerobes
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Outline coverage of doxycycline
Gram +ve, Gram -ve, anaerobes, atypicals
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Outline coverage of vancomycin
Gram +ve MRSA
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Outline gram stain
Crystal violet stain- Binds to gram +ve- Turns violet Counterstain- Binds to cell membrane of gram -ve- Turns red/pink
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List gram +ve cocci
Staphylococcus Streptococcus Enterococcus
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List gram +ve rods
Corneybacteria Mycobacteria Listeria Bacillus Nocardia
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List gram +ve anaerobes
Clostridium Lactobacillus Actinomyces Propionibacterium
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List positive gram -ve bacteria
Neisseria meningitidis Neisseria gonorrhoea Haemophilia influenza E. coli Klebsiella Pseudomonas aeruginosa Moraxella catarrhalis
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List 5 causes of atypical pneumonia
Legionella pneumophilia Chlamydia psittaci Mycoplasma pneumoniae Chlamydophila pneumoniae Q fever
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Outline Methicillin-Resistant Staphylococcus Aureus (MRSA)
Staph aureus bacteria resistant to beta-lactam ABs (eg: Penicillin, cephalosporin, carbapenems) Hard to treat Eradication of MRSA on skin- Chlorhexidine ABs used to treat- Doxycycline, clindamycin, vancomycin, teicoplanin, linezolid
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Outline Extended-Spectrum Beta-Lactamase Bacteria
Developed resistance to beta-lactam ABs (penicillins, cephalosporins, carbapenems) Produce beta-lactamase enzymes that destroy beta-lactam ring on AB ESBLs tend to be E. coli or Klebsiella and cause UTIs Can cause other type of infections such as pneumonia and septicaemia Usual treatment: Nitrofurantoin Fosfomycin Carbapenems