Infection (viral Infection) Flashcards

1
Q

AZT – zidovudine
Side effects?

A

Nausea
bone marrow suppression
myopathy

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2
Q

3TC – lamivudine
Side effects?

A

peripheral neuropathy
pancreatitis

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3
Q

There are five classes of antiretroviral drugs:

A

• Nucleoside (and nucleotide) reverse transcriptase inhibitors (NRTIs)
• Non-nucleoside reverse transcriptase inhibitors (NNRTIs)
• Protease inhibitors
• Intergrase inhibitors
• CCR5 receptor blockers

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4
Q

HAART regim

A

💜children aged <2 years should be started on treatment regardless of CD4 count

💜children aged 2–5 years require treatment if CD4 count <25% or absolute count <750 cells/mm3

💜children aged >5 years with CD4 count <350 cells/mm3 require treatment

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5
Q

HIV encephalopathy

A

HIV encephalopathy
• May present with
🔺regression of milestones 🔺behavioural difficulties
🔺acquired microcephaly
🔺motor signs, e.g. spastic diplegia, ataxia, pseudobulbar palsy
• Exclude CNS infections and lymphoma
• Treatment: HAART

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6
Q

What causes infectious mononucleosis (glandular fever)?

A

EBV infects pharyngeal epithelial cells and then B lymphocytes

EBV stands for Epstein-Barr Virus.

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7
Q

How is infectious mononucleosis transmitted?

A

Saliva, aerosol

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8
Q

What is the incubation period for infectious mononucleosis?

A

30–50 days

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9
Q

List common clinical presentations of infectious mononucleosis.

A
  • Fever
  • Sore throat
  • Lymphadenopathy
  • Palatal petechiae
  • Malaise
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10
Q

What is the incidence of hepatitis in infectious mononucleosis?

A

80%

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11
Q

What is the percentage of patients that experience clinical jaundice with infectious mononucleosis?

A

5%

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12
Q

What are some hematological complications associated with infectious mononucleosis?

A
  • Thrombocytopenia
  • Haemolytic anaemia
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13
Q

What percentage of patients of infectious mononucleosis develop a maculopapular rash when given ampicillin?

A

90%

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14
Q

What are key diagnostic features for infectious mononucleosis?

A
  • Atypical lymphocytosis
  • Positive Paul–Bunnell test or Monospot test (often negative in young children)
  • Serology
  • Heterophile antibodies
  • PCR
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15
Q

What is the primary treatment approach for infectious mononucleosis?

A

Supportive care, steroids for severe inflammatory processes

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16
Q

CYTOMEGALOVIRUS in immunocompermized patient?

A

severe disease may occur with pneumonitis
retinitis
encephalitis
hepatitis and GI disturbance

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17
Q

How to diagnose CMV??

A

🔺immunofluorescence
🔺 intranuclear inclusions in biopsy specimens
culture
🔺detection of early antigen fluorescence foci (DEAFF) test
🔺PCR

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18
Q

What is most common congenital infection?

A

CMV

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19
Q

When should zidovudine (AZT, azidothymidine) be started for a baby?

A

Within 12 hours of birth

Zidovudine is used for the prevention of HIV transmission from mother to child.

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20
Q

How long should zidovudine treatment continue for the baby?

A

4 weeks

This treatment duration is crucial for reducing the risk of HIV infection.

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21
Q

What is the timing for the first HIV PCR test after birth?

A

24–48 hours

The PCR test helps in early detection of HIV in the newborn.

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22
Q

When should the second HIV PCR test be conducted?

A

6 weeks

This is also when Septrin prophylaxis should be started.

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23
Q

What should be done if all three HIV PCR tests are negative?

A

95% not infected

Stop Septrin

Follow HIV antibodies till they cleared

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24
Q

Fill in the blank: The third HIV PCR test should be repeated at _______.

A

3–4 months

This timing helps confirm the absence of HIV infection.

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25
Q

HIV Clinical stage 1

A

• Asymptomatic
• Persistent generalized lymphadenopathy

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26
Q

HIV Clinical stage 1

A

• Asymptomatic
• Persistent generalized lymphadenopathy

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27
Q

HIV Clinical stage 2

A

• Unexplained persistent hepatosplenomegaly
• Unexplained persistent parotid enlargement
• Papular pruritic eruptions
• Extensive wart virus infection
• Extensive molluscum contagiosum
• Herpes zoster
• Fungal nail infections
• Recurrent oral ulcerations
• Lineal gingival erythema
• Recurrent or chronic upper respiratory tract infections (otitis media, otorrhoea, sinusitis, tonsillitis)

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28
Q

What is prophylaxis for Herpis zoster ?

A

ZIG is given if high risk (e.g. immunodeficiency, immunosuppressive treatment)

ZIG helps prevent chickenpox in high-risk individuals.

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29
Q

When should a neonate receive zoster immunoglobulin (ZIG)?

A

If the mother develops chickenpox within 5 days before to 2 days after delivery

This is crucial to protect the neonate from chickenpox.

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30
Q

What treatment is administered if a baby develops chickenpox?

A

Intravenous aciclovir

Aciclovir is an antiviral medication used to treat infections caused by certain types of viruses.

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31
Q

What is the effect of zoster immunoglobulin (ZIG) on the incubation period in children?

A

The incubation period is extended to 28 days

This means that children who received ZIG may show symptoms of chickenpox later than usual.

32
Q

Parvovirus B19

A

erythema infectiosum
slapped cheek

33
Q

HHV-6

A

Roseola infantum
exanthem subitum

34
Q

HHV-6

A

Roseola infantum
exanthem subitum

35
Q

Roseola infantum

A

🔺sudden onset of high fever (up to 41°C) with absence of clinical localizing signs
🔺at days 3–4 fever abruptly stops and macular/papular rash appears which lasts from <24 h to a few days

🧶This is one of the most common causes of febrile convulsions in the 6- to 18-month age group

36
Q

Red cells production in the embrue?

A

🔺In the human fetus clusters of stem cells (called blood islands) ➡️in the yolk sac ♂️3rd week
🔺these cells migrate to the liver ♂️ 3 months

🔺The bone marrow gradually takes over synthesis ♂️ 5 months and by birth almost all red cells are made in the bone marrow.

37
Q

Causes of bone marrow failure

A

associated with a low reticulocyte count.
🔺marrow infiltration(e.g.acute lymphoblastic leukaemia or neuroblastoma)
🔺aplastic anaemia.

38
Q

Aplastic anaemia causes?

A

The pluripotent stem cells are affected with reduction in all cell lines.
♂️About 20% are inherited, with Fanconi anaemia being the mostcommon Inherited aplastic anaemia.
♂️ acquired forms, many are
🔺 idiopathic
🔺viral infections (CMV, Non-A, non-B hepatitis, HIV, EBV),
🔺drugs (acetazolamide,chloramphenicol,chemotherapy)
🔺whole body irradiation.

39
Q

Aplastic anaemia management

A

🔺supportivetreatment with blood and platelet transfusions and treatment of infections.
🔺 If an HLA-matched donor isavailable,bone marrow transplant is often the treatment of choice.
If a suitable donor is not available,
🔺immune suppression with antithymocyte globulin (ATG) and cyclosporin can be used.

40
Q

What type of bone marrow failure Parvovirus B19?

A

🚀 erythroid progenitor cells🚀 resulting in isolated red cell aplasia.

41
Q

Hereditary spherocytosis

A

The genetic abnormality results in defects in proteins of the red cell cytoskeleton. Spectrin defect is the most common abnormality but ankyrin, band 3 and band 4.2 defects are also known.

42
Q

Spherocytes RBC

A

♂️spheroidal, less deformable
♂️ have a life span of only 28 days.

43
Q

Spherocytes RBC

A

♂️spheroidal, less deformable
♂️ have a life span of only 28 days.

44
Q

What are the types of infections in immunodeficiency?

A

Antibody : BVP
Cellular : BVPF
Neutrophils: BF
Complement : B

45
Q

What are the causes of encephalitis?

A

is predominantly viral in origin.
Common viral causes include:
🕳️ Enteroviruses ❤️
🕳️Herpes simplex virus (HSV)-1 and HSV-2
🕳️Varicella-zoster virus
🕳️Measles
🕳️Mumps
🕳️ Influenza

Rare causes include:
• Adenoviruses, rubella virus, Epstein–Barr virus (EBV), arenaviruses (e.g. Japanese B encephalitis), rabies virus and Mycoplasma spp., West Nile virus

46
Q

When the peak incidence of viral encephalitis??

A

is in the first 6 months of life with 1 or 2 cases per 1000 children.

47
Q
A

peak incidence of viral encephalitis is in the first 6 months of life with 1 or 2 cases per 1000 children.

48
Q

What is most common cause of bacterial meningitis??

A

Neisseria meningitidis
✔️ most cases being N. meningitidis B since the introduction of the conjugate meningococcal C vaccine.

49
Q
A

Neisseria meningitidis is the most common cause of community-acquired bacterial meningitis in the UK, with most cases being N. meningitidis B since the introduction of the conjugate meningococcal C vaccine.

50
Q
A

Specific contraindications to lumbar puncture include:
• Signs of raised intracranial pressure with changing level of consciousness, focal neurological signs or severe mental impairment
• Cardiovascular compromise with impaired peripheral perfusion or hypotension • Respiratory compromise with tachypnoea, an abnormal breathing pattern or hypoxia • Thrombocytopenia or a coagulopathy

51
Q
A

bacterial meningitis, the CSF glucose level is usually low with a CSF:blood ratio <0.5, and the protein level is frequently raised to >0.4 g/l.

52
Q
A

bacterial meningitis, the CSF glucose level is usually low with a CSF:blood ratio <0.5, and the protein level is frequently raised to >0.4 g/l.

53
Q
A

The most common long-term complication of meningitis is sensorineural deafness. The overall rate of deafness after meningitis is less than 5%. Hearing impairment is higher in cases of pneumococcal meningitis than in meningococcal infections

54
Q

Incubation period for varicella zoster?

A

10-21 days
2-3 weeks

55
Q

What time for IG to peak and for how long

A

IgM= 7-10 d / few weeks
IgG= 4-6 w /for life

56
Q

What function of IgD?

A

Signalling activation of B cell

57
Q

Describe clinical manifestation in chickenpox?

A

1-2 d fever and malaise
Pruritic erythematous rash - vesciular rash

58
Q

What are the types of infections in antibody difficiency?

A

🔹Bacterial : Staphylococcus😑 Streptocous 😑Haemophilus infleunze
🔹Viruses : Enteroviruses
🔹Protozoa: Giardia spp

59
Q

What are the types of infection in cellular immunodeficiency??

A

🔹Bacteria :Mycobacterium spp 😑 Listeria spp.
🔹Virus : Cytomegalovirus(CMV)😐herpesvirus 😐Measles 😕RSV😔Adenoviruses
🔹Fungi : candida 😞aspergillus
🔹Protozoa: pneumocystis spp

60
Q

How much it takes for hypothalmic - pituitary axis to recover after steroid administration??

A

full recovery of the HPA may take several months even
after cessation of treatment

61
Q

What endocrine abnormalities after long term steroid use ??

A

🔹⬇️Cortisol
🔹⬇️ACTH
🔹⬇️CRH

62
Q

What is the appropriate stress response for patients taking long term steroid??

A

®️ Standard practice is to double
or treble the current steroid dose. If no vomiting, it is appropriate to prescribe
the double steroid dose by the oral route . In the case of surgery, steroids may
be provided by an intravenous infusion.

®️ It is also important to pay close attention to hydration, electrolyte
balance and blood glucose

63
Q

Hydronephrosis The main causes of hydronephrosis are as follows:
• VUR – see Section 12.1 • Pelviureteric junction (PUJ) obstruction • Usually detected on antenatal ultrasonography • Occasionally detected during investigation of UTI or abdominal pain • Main aspects of assessment are: • ultrasonography – degree of renal pelvic dilatation measured in the anteroposterior diameter: 5–10 mm mild; 11–15 mm moderate; >15 mm severe • MAG-3 renogram – findings that suggest significant obstruction are poor drainage despite furosemide given during scan and impaired function, e.g. <40% on hydronephrotic side • follow-up in the first 2 years after birth is based around ultrasonography every 4 months, withMAG-3 scan undertaken if hydronephrosis is severe initially, or progressively worsens over time
• surgical correction is by pyeloplasty • Usual when MAG-3 indicates obstruction and/or ultrasonography shows progressive increase in hydronephrosis • When dilatation is >30 mm, surgery is likely • Surgery is also considered if hydronephrosis is complicated by a proven UTI
• Vesicoureteric junction obstruction • Usually detected in the same ways as for PUJ obstruction • Ultrasonography shows renal pelvic and ureteric dilatation • Interventions include stenting the vesicoureteric junction (temporary measure) and surgical reimplantation

64
Q

Hydronephrosis The main causes of hydronephrosis are as follows:
• VUR – see Section 12.1 • Pelviureteric junction (PUJ) obstruction • Usually detected on antenatal ultrasonography • Occasionally detected during investigation of UTI or abdominal pain • Main aspects of assessment are: • ultrasonography – degree of renal pelvic dilatation measured in the anteroposterior diameter: 5–10 mm mild; 11–15 mm moderate; >15 mm severe • MAG-3 renogram – findings that suggest significant obstruction are poor drainage despite furosemide given during scan and impaired function, e.g. <40% on hydronephrotic side • follow-up in the first 2 years after birth is based around ultrasonography every 4 months, withMAG-3 scan undertaken if hydronephrosis is severe initially, or progressively worsens over time
• surgical correction is by pyeloplasty • Usual when MAG-3 indicates obstruction and/or ultrasonography shows progressive increase in hydronephrosis • When dilatation is >30 mm, surgery is likely • Surgery is also considered if hydronephrosis is complicated by a proven UTI
• Vesicoureteric junction obstruction • Usually detected in the same ways as for PUJ obstruction • Ultrasonography shows renal pelvic and ureteric dilatation • Interventions include stenting the vesicoureteric junction (temporary measure) and surgical reimplantation

65
Q

Duplex kidney
• Often detected on antenatal ultrasonography or during investigation of UTI • Two ureters drain from two separate pelvicalyceal systems; ureters sometimes join before common entry into the bladder, but more commonly have separate entries, with the upper pole ureter inserting below the lower pole ureter
• Common complications associated with duplex systems are: • Obstructed hydronephrotic upper moiety and ureter, often poorly functioning, associated with bladder ureterocele • Dilatation and swelling of submucosal portion of ureter just proximal to stenotic ureteric orifice can be seen within bladder on ultrasonography and as a filling defect on MCUG
• Ectopically inserted upper pole ureter, entering urethra or vagina; clue to this from history is true continual incontinence with no dry periods at all, as ectopic ureter bypasses bladder • VUR into lower pole ureter, sometimes causing infection and scarring of this pole

66
Q

Multicystic dysplastic kidney
• Irregular cysts of variable size from small to several centimetres; no normal parenchyma • Dysplastic atretic ureter • No function on MAG-3 or DMSA scan • Commonly involute over time • No indication for routine surgical removal • Follow-up with ultrasonography at 3 months, then 12 months, 2 years and 5 years
• At the 5-year visit, if ultrasonography shows normal contralateral kidney with compensatory hypertrophy of this kidney, and the child has a normal BP, no proteinuria and normal plasma creatinine, then reasonable to discharge from long-term hospital follow-up • 20–40% incidence of VUR into contralateral normal kidney

67
Q

Horseshoe kidney
• Two renal segments fused across midline at lower poles in 95%, upper poles in 5% • Isthmus usually lies low, at the level of the fourth lumbar vertebra immediately below the origin of the inferior mesenteric artery
• Associations include Turner syndrome, Laurence–Moon–Biedl syndrome • Usually asymptomatic but increased incidence of PUJ obstruction and VUR, so may develop a UTI

68
Q

Hypospadias
• Opening of urethral meatus is on the ventral surface of penis, at any point from the glans to base of penis or even perineum
• Meatus may be stenotic and require meatotomy as initial intervention • Foreskin is absent ventrally; it is used in surgical reconstruction of a deficient urethra so circumcision should not be performed
• Usual best age for surgical correction is around 12 months • Chordee is the associated ventral curvature of the penis, seen especially during erection, and this also requires surgical correction; caused by fibrous tissue distal to the meatus along the ventral surface of penis

69
Q

Impalpable testes
• May be intra-abdominal, inguinal or pre-scrotal • Main aim of diagnosis and management is: • to preserve fertility • to reduce risk of malignancy and to enable early detection of malignant change if it occurs
• Infants should be referred to paediatric surgeon or urologist by age 6 months • Ultrasonography may detect inguinal testis, but is of limited use for intra-abdominal testis; MRI may be better, but usually requires general anaesthetic for infant; laparoscopy may be final method for localising testis
• Surgical orchidopexy has 95% success rate; hormonal therapy with human chorionic gonadotrophin (hCG) <15% success and so surgery is preferred option
• Optimum age for surgery is 9–12 months; usually combined with repair of the associated inguinal hernia; may require two-stage procedure for intra-abdominal testis

70
Q

Impalpable testes
• May be intra-abdominal, inguinal or pre-scrotal • Main aim of diagnosis and management is: • to preserve fertility • to reduce risk of malignancy and to enable early detection of malignant change if it occurs
• Infants should be referred to paediatric surgeon or urologist by age 6 months • Ultrasonography may detect inguinal testis, but is of limited use for intra-abdominal testis; MRI may be better, but usually requires general anaesthetic for infant; laparoscopy may be final method for localising testis
• Surgical orchidopexy has 95% success rate; hormonal therapy with human chorionic gonadotrophin (hCG) <15% success and so surgery is preferred option
• Optimum age for surgery is 9–12 months; usually combined with repair of the associated inguinal hernia; may require two-stage procedure for intra-abdominal testis

71
Q

Boys presenting with scrotal pain will often need to be assessed by a paediatric surgeon • History and examination are the most important components of assessment • Ultrasonography with colour Doppler to assess testicular blood flow may contribute • Torsion of testicle: • Acute abrupt onset of often severe pain • Early puberty • Swelling of testis and hemiscrotum, often with erythema/discoloration of scrotal skin • Diffuse tenderness of testis • Negative urinalysis • Treatment is surgical exploration
• Torsion of appendix of epididymis: • More common than torsion of testicle • Subacute onset of pain over hours • Pre-pubertal • Tenderness localized to the upper pole of testis • Negative urinalysis • If confident of diagnosis may be managed conservatively; however, may be difficult to distinguish from torsion of testicle so may require surgical exploration
• Epididymitis: • Gradual insidious onset of discomfort or pain • Adolescence • Epididymal tenderness • Urinalysis often positive (although may be negative) • May have low-grade fever; raised C-reactive protein (CRP) • Treatment with antibiotics (e.g. co-amoxiclav, cefalexin) if urinalysis suggestive of infection
• Trauma: • History usually informative • Trauma may cause a haematocele or testicular haematoma
• Hernia or hydrocele: • Not usually acutely painful • Swelling in scrotum, extending into inguinal canal if hernia • No erythema or discoloration of overlying scrotal skin • Hydrocele will transilluminate with pen torch

72
Q

Bladder extrophy and epispadias
• Rare disorder; more common in boys • Bladder mucosa is exposed (and with exposure and infection becomes friable), bladder muscle becomes fibrotic and non-compliant
• Anus anteriorly displaced • Boys – penis has epispadias (dorsal opening urethra) and dorsal groove on glans, with dorsal chordee and upturning; scrotum is shallow and testes are often undescended • Girls – female epispadias with bifid clitoris, widely separated labia• Pubic bones separated • Requires surgical reconstruction; long-term urinary incontinence is common

73
Q

ACID–BASE, FLUID AND ELECTROLYTES 6.1 Metabolic acidosis A primary decrease in plasma bicarbonate and a decrease in plasma pH as a result of:
• Bicarbonate loss, e.g. • Gastrointestinal loss in severe diarrhoea • Renal loss in proximal (type 2) renal tubular acidosis (RTA)
• Reduced hydrogen ion excretion, e.g. • Distal (type 1) RTA • Acute and chronic renal failure
• Increased hydrogen ion load, e.g. • ↑ endogenous load: • inborn errors of metabolism, e.g. maple syrup urine disease, propionic acidaemia • lactic acidosis, e.g. cardiovascular shock • ketoacidosis, e.g. diabetic ketoacidosis (DKA) • ↑ exogenous load, e.g. salicylate poisoning

74
Q

Anion gap
• A classification of metabolic acidosis involves assessing the anion gap – the ‘gap’ between anions and cations made up by unmeasured anions, e.g. ketoacids, lactic acid
• Measured as [Na+ + K+] – [HCO3 – + Cl–]; thus normal anion gap is [140 + 4] – [24 + 100] = 20
• Acidosis may be a normal anion gap, when Cl– will be raised, i.e. hyperchloraemic • May be an increased anion gap, when Cl– will be normal, i.e. normochloraemic
Examples:
• Normal anion gap, hyperchloraemia, acidosis – RTA • Na+ 140, K+ 4, Cl– 110, HCO3
– 14, anion gap = 20
• Increased anion gap, normochloraemia, acidosis – DKA • Na+ 140, K+ 4, Cl– 100, HCO3
– 15, anion gap = 30