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Y3 > Infection & Immunology > Flashcards

Infection & Immunology Flashcards

1
Q

What is an abscess?

A

Mass of necrotic tissue, with dead and viable neutrophils suspended in tissue breakdown products (pus), surrounded by inflammatory exudate

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2
Q

What causes an abscess?

A

Tissue barrier disrupted by injury/infection/migration of normal flora to sterile areas
Becomes walled off in an attempt to limit further spread of infection
Common bacteria - Staph, Strep, Enteric (E Coli)

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3
Q

What kind of abscesses does TB cause?

A

COLD - no inflammation

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4
Q

What are the risk factors for abscesses?

A

Local: tissue necrosis, under perfusion, foreign body
Systemic: diabetes, immunosuppression

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5
Q

What are the symptoms of an abscess?

A

Local pain, swelling, heat, redness, impaired function of area
Systemic - fever, malaise

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6
Q

What are the signs of an abscess O/E?

A

Acute inflammation
If in organ -> localising signs
Swinging fever (periodic release of microbes/cytokines into systemic circulation) –> initiate search for infected collection

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7
Q

Where is an abscess often found if you can’t find one anywhere?

A

Under diaphragm

Subphrenic abscess

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8
Q

How are abscesses investigated?

A
  1. Bloods - neutrophilia
  2. Imaging - USS, CT, MRI to search for site
  3. Aspiration - pus = low glucose, acidic, culture pus for organisms/AB sensitivity
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9
Q

How are abscesses managed?

A
  1. Prevention - prophylactic ABx (during ops) if given early during infection, not effective once abscess formed
    2/ General - drainage, removal of necrotic tissue, correction of predisposing cause
  2. Surgery - drain by incision w packing/drains
  3. Interventional radiology - US/CT to localise and aspirate
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10
Q

What are the complications of abscesses?

A
  • Spread > cellulitis / bacteraemia w systemic sepsis
  • Chronic abscess
  • Discharging sinus/fistula
  • Destruction of normal underlying tissue
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11
Q

What is the prognosis for an abscess?

A

Good if drained and predisposing factor removed
Untreated - tend to point to nearest epithelial surface and discharge contents
Deep abscesses may become chronic

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12
Q

Which tissues does candida usually invade?

A

Tissues normally resistant to infection

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13
Q

What causes candidiasis most commonly?

A

Candida albicans

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14
Q

What does candidiasis look like?

A

Erythematous
Peeling edges
Moist
Rugged

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15
Q

How is candidiasis investigated?

A

Superficial smear of lesion for microscopy - +ve for Candida

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16
Q

What is cellulitis?

A

Acute, non-purulent spreading infection of the SC tissue, causing overlying skin inflammation

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17
Q

What causes cellulitis?

A
  • Penetrating injury (cannulation)
  • Local lesions (bites, seb cysts surgery)
  • Fissuring (anal, toe web spaces)
    All allow pathogenic bacteria to enter skin
  • Rarely arises spontaneously from blood-borne sources (septicaemia)
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18
Q

What are the risk factors for cellulitis?

A

Skin break
Poor hygiene
Poor vascularisation of tissue - DM

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19
Q

How do cellulitis and erysipelas differ?

A

Both - erythema, oedema, warm, tender

Cellulitis - not raised, indistinct margins

Erysipelas - characteristic raised, indurated border

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20
Q

What are the signs of cellulitis O/E

A

Lesion
No fluid thrill, fluctuation

Periorbital - swollen eyelids, conjunctival infection
Orbital - proptosis, impaired acuity, eye movement

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21
Q

How is cellulitis investigated?

A
  1. Bloods - high WCC
  2. If next to wound/pustular focus - CULTURE and molecular diagnostic procedures - growth of common pathogen, e.g. S. aureus
  3. CT/MRI if abscess suspected/orbital - assess posterior spread of infection
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22
Q

How is cellulitis managed?

A

Medical -

  • Flucloxacillin/co-amoxiclav PO
  • Hospitals - IV vancomycin (MRSA cover) + ceftazidime (Pseudomonas cover for immunocompromised)
  • Penicillin/macrolide prophylaxis if recurrent

Surgical - orbital decompression

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23
Q

What causes HSV?

A

dsDNA
Transmitted via close contact with individual shedding the virus
Kissing
Sexual intercourse

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24
Q

What are the symptoms of HSV?

A

HSV1: primary infection often asymptomatic, but possibly pharyngitis, painful eating, herpetic whitlow (finger abscess)

Recurrent infection/reactivation: prodrome (6h), peri-oral tingling and burning, vesicles appear (48h), ulcerate, crust over, heal in 8-10d

HSV2: very painful blisters and rash in genital, perigenital and anal area, dysuria, fever, malaise

HSV encephalitis - HSV1
HSV keratoconjunctivitis - epiphoria (watering eyes), photophobia

25
Q

What are the signs of HSV1 primary infection?

A

Tender cervical lymphadenopathy
Erythematous/oedematous pharynx
Oral ulcers filled with yellow slough (gingivostomatitis)
Digital blisters/papules (herpetic whitlow)

26
Q

What are the signs of HSV2 infection?

A 
Maculopapular rash
Vesicles
Ulcers
Inguinal lymphadenopathy
Pyrexia
27
Q

How is HIV transmitted?

A
  1. Sexual transmission
  2. Blood (+other bodily fluids) - mother to child (intrauterine, childbirth, breastfeeding), needles (IVDU, healthcare workers), blood product transfusion, organ transplantation
28
Q

What are the symptoms of HIV?

A

1 - Seroconversion (4-8w post-infection)
Self-limiting: fever, night sweats, lymphadenopathy, sore throat, oral ulcers, rash, myalgia, headache, encephalitis, diarrhoea

  1. Early/asymptomatic (18m-5y+)
    Persistent lymphadenopathy (>1cm nodes at 2+ extrainguinal sites for >3m)
    Progressive minor symptoms - rash, oral thrush, WL, malaise
  2. AIDS
    Syndrome of secondary diseases - severe immunodeficiency/direct effect of HIV infection
    - CD4<200
29
Q

What are the direct effects of HIV infection?

A

Neuro: polyneuropathy, myelopathy, dementia
Lung: lymphocytic interstitial pneumonia
Heart: cardiomegaly, myocarditis
Haem: anaemia, thrombocytopaenia
GI: anorexia, HIV enteropathy (malabsorption, diarrhoea), severe wasting
Eyes: cotton wool spots

30
Q

What are the common secondary infections in AIDS?

A 
Bacterial: Mycobacterium TB - lungs, GI, skin
Staphylococci - skin
Salmonella
Strep pneumoniae
Haemophilus influenza
Viral: CMV - retinitis, colitis, encephalitis
HSV - encephalitis
VSV - recurrent shingles
HPV
EBV

Fungal: PCP, cryptococcus (meningitis), Candida, aspergillosis

31
Q

What tumours are related to HIV/AIDS?

A

Kaposi’s sarcoma
Squamous cell carcinoma
Non-Hodgkin’s/Hodgkin’s lymphoma

32
Q

How is HIV investigated?

A
  1. Serum HIV ELISA followed by Western Blot to confirm (expensive)
  2. Serum HIV rapid test
  3. Serum p24 antigen - high
  4. Serum HIV DNA PCR
  5. CD4 count - staging >500 asymp, <350 substantial immunosuppression, <200 AIDS
  6. Viral load
33
Q

What causes infectious mononucleosis and how is it transmitted?

A
  • EBV
  • Transmitted by close contact
  • Humoral and cellular immune response - IL2 production
  • Despite IR, EBV is latent in lymphocytes
34
Q

When is infectious mononucleosis most common?

A

2 peaks
1-6y asymptomatic
14-20y

35
Q

How does infectious mononucleosis present?

A
  • Incubation period of 4-8w with abrupt onset

- Sore throat, fever, fatigue, headache, malaise, anorexia, sweating, abdo pain

36
Q

What are the signs of infectious mononucleosis O/E?

A 
Pyrexia
Oedema, erythema of pharynx/soft palate
White exudate on tonsils - confluent after 1-2d
Palatal petechiae
Cervical lymphadenopathy
Splenomegaly 50%
Hepatomegaly 10%
Jaundice 5%
Maculopapular rash in pts who have received ampicillin
37
Q

How is infectious mononucleosis investigated?

A
  1. Bloods: FBC = leucocytosis / LFT = raised aminotransferases
  2. Blood film: lymphocytosis (>20% atypical lymphocytes)
  3. Paul-Bunnell/Monospot test: presence of heterophile antibodies produced in response to EBV
  4. Throat swab to exclude strep tonsils
38
Q

How is infectious mononucleosis managed?

A

CONSERVATIVE: rest, no contact sports for 2w due to increased risk of splenic rupture

MEDICAL:
Paracetamol, NSAIDs for fever, throat discomfort, malaise
Corticosteroids in severe cases - haemolytic anaemia, tonsillar swelling, obstructive pharyngitis

39
Q

When do patients with mono develop a widespread maculopapular rash?

A

Amoxicillin

Ampicillin

40
Q

What are the complications of infectious mononucleosis?

A
  • Lethargy for months
  • Airway obstruction
  • Haemolytic/aplastic anaemia, thrombocytopaenia
  • Splenic rupture, fulminant hepatitis, pancreatitis, renal failure
  • GBS, encephalitis, viral meningitis
41
Q

What is malaria?

A

Infection with the protozoa Plasmodium (P. falciparum - most serious and potentially fatal, P. vivax, P. ovale, P. malariae)

42
Q

What causes malaria?

A

Transmitted through bite of female Anopheles mosquito

Protozoa infect RBC and grow intracellularly

43
Q

Which populations have some innate immunity to malaria?

A

Sickle cell trait
G6PD deficiency
Pyruvate kinase deficiency
Thalassaemia

44
Q

How does malaria usually present?

A

Non-specific: headache, weakness, myalgia, arthralgia, anorexia, diarrhoea

Peak temperatures every 48h
Cerebral malaria - headache, disorientation, coma

45
Q

What are the signs of malaria O/E?

A

Pyrexia
Rigors
Anaemia
Hepatosplenomegaly

46
Q

How is malaria investigated?

A
  1. Giemsa-stained thick and thin blood smears - detection of asexual or sexual forms of the parasites inside erythrocytes
  2. Rapid diagnostic tests - show visible band after 15m
3. Bloods:
FBC - thrombocytopaenia, mild anaemia
U/E
LFT - high UC BR, aminotransferases
ABG - metabolic/lactic acidosis
Glucose - hyper or hypo
  1. Clotting profile - prolonged PT
  2. Urinanalysis - protein, urobilinogen, BR
47
Q

How is VSV transmitted?

A

Highly contagious
Aerosol inhalation
Direct contact with vesicular secretions

48
Q

How does chickenpox present?

A

Prodromal malaise
Mild pyrexia
Sudden appearance of intensly itchy spreading rash on face+trunk>extremities, oropharynx, conjunctivae + genitourinary tract
As vesicles weep and crust over, new vesicles appear
Contagious from 48h before rash and until all vesicles crust over (7-10d)

49
Q

How does shingles present?

A

May occur after period of stress
Tingling/hyperparasthesiae in dermatomal distribution
Followed by painful skin lesions
Recovery in 10-14 days

50
Q

What are the signs of chickenpox O/E?

A

Maculopapular rash evolving into crops of vesicles with areas of weeping (exudate) and crusting (vesicles, macules, papules, crusts may all be present at one time)

Skin excorations

Mild pyrexia

51
Q

What are the signs of shingles O/E?

A

Vesicular maculopapular rash in dermatomal distribution

Skin excoriation

52
Q

How is chickenpox managed?

A

Kids - treat symptoms - chamomile lotion, analgesia, antihistamines

Adults - consider acyclovir, valaciclovir or famciclovir if within 24h of rash onset, esp in elderly, smoker, immunocompromised or pregnant

53
Q

How is shingles managed?

A

Consider acyclovir, valaciclovir or famciclovir if within 24h of rash onset, esp in elderly, smoker, immunocompromised or pregnant

Low dose amitriptyline

Simple analgesia - paracetamol

54
Q

What are the complications of chickenpox?

A 
Secondary infection
Scarring
Pneumonia
Encephalitis
Cerebellar snydrome
Congenital varicella syndrome
55
Q

What are the complications of shingles?

A

Post-herpetic neuralgia
Zoster opthalmicus (rash involves ophthalmic division of CNV)
Ramsay-Hunt syndrome
Sacral zoster –> urinary retention
Motor zoster - muscle weakness of myotome at similar level to affected dermatome

56
Q

Which organism most commonly causes orbital cellulitis?

A

Haem. influenzae

57
Q

Which organisms commonly cause cellulitis?

A

Strep. pyogenes

Staph. aureus (MRSA not common)

58
Q

What is erysipelas?

A

A distinct form of superficial cellulitis with a raised, sharply demarcated edge distinguishing it from uninvolved skin

59
Q

When may EBV reactivation occur?

A

Period of stress

Immunosuppression

Y3 (20 decks)

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