Session 8 Flashcards

(31 cards)

1
Q

What is the immunocompromised host?

A

State in which he immune system is unable to respond appropriately and effectively to infectious microorganism

Due to a defect in one or more components of the immune system e.g B cells, neutrophils, T cells, complement proteins

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2
Q

Why is a host immunocompromised?

A

Primary immunodeficiency
- congenital

Secondary immunodeficiency

  • acquired
  • underlying disease/treatment
  • get decrease function/production of immune components
  • loss or catabolism of immune components
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3
Q

Why suspect immune defieicny?

A
SPUR 
S - severe infection
P - persistent, don’t respond to meds quick
U - unusual site of infection
R - recurrent, keeps coming back
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4
Q

What are some warning signs of PID in children?

A
  • four or more ear infections in 1 year
  • 2+ months on antibiotics with little effect
  • failure to gain weight/ grow normally
  • persistent thrush in mouth or fungal skin infection
  • need IV antibiotics to clear infection
  • 2 or more pneumonia’s in 1 year
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5
Q

What are the warning signs of PID in adults?

A
  • 2+ ear infections in 1 year
  • family history (25% chance)
  • recurrent viral infections
  • chronic diarrhoea and weight loss
  • pneumonia ever year for more than 1 year
  • deep abscesses of skin/internal organs
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6
Q

What are the limitations of these warning signs of PID?

A
  • lack of population based evidence
  • PID patients with deferent defects/presentations
  • PID patients with non infectious manifestation
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7
Q

How does onset of PID suggest the type?

A

Onset before 6 months = T cell/phagocyte deficiency

Onset between 6 months - 5yrs = B cell/antibody or phagocyte deficiency

Onset more than 5 years = B cells/ antibody or SID

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8
Q

How will people with complement deficiency present?

A

Pyrogenic infections
Meningitis/sepsis/arthritis
Angioedema

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9
Q

How will people with phagocytic defects present?

A
  • Skin/mucous infections
  • Deep seated infections
  • Invasive fungal infections
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10
Q

How will people with antibody deficiency’s present?

A
  • sinorespiratory infections
  • arthropthies
  • GI infections
  • malignancies
  • autoimmunity
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11
Q

How will people with T cell defects present?

A
  • death if not treated
  • deep skin tissue and abscesses
  • opportunistic infections
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12
Q

How do you manage PIDs?

A

Supportive

  • prophylaxis
  • treat infections promptly
  • nutritional support for vitamins

Specific

  • regular immunoglobulin therapy
  • haematopoietic stem cell therapy

Comorbidities

  • autoimmunity and malignancies
  • organ damages
  • avoid non essential exposure to radiation
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13
Q

What causes SID?

A
  • malnutrition
  • infection
  • liver disease
  • lymphoproliferative diseases
  • splenectomy: causes are - infarction (e.g sickle cell anaemia), trauma, autoimmune haemolytic disease, infiltration, coeliac disease, congenital
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14
Q

What is the spleens immune role?

A
  • Gets rid of blood borne pathogens
  • Antibody production - acute IgM and one term IgG production
  • splenic macrophages
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15
Q

How would the asplenic patient Present and whats the management?

A

Presentation

  • increased susceptibility to encapsulated bacteria
  • overwhelming post splenectomy infection

Management

  • penicillin prophylaxis
  • immunisation against encapsulated bacteria
  • medic alert bracelet
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16
Q

How will patients with haemoatological malignancy be more prone to infection?

A

May have chemotherapy induced neutropenia or damage to mucosal barriers.

Treat suspected neutropenic sepsis ASAP

17
Q

What kind of deficiency’s will viral, fungal and bacterial infections be prevalent in?

A

Virus and fungi = T cell deficiency

Bacteria and fungi = B cell/granulocyte deficiency

18
Q

What hepatitis?

A

Inflammation of the liver

Viruses replicate specifically in hepatocytes and thus cause their destruction

19
Q

What types if hepatitis are chronic?

20
Q

How is bilirubin excreted and how does hepatitis prevent this?

A

RBC break down in spleen and bilirubin is transported to the liver for coagulation before being excreted as bile.

Hepatitis prevents conjugation in liver.

21
Q

What does a liver function test detect?

A
  • Bilirubin
  • Liver transaminases (ALT) and (AST) excreted in large amounts in hepatocytes if damaged.
  • alkaline phosphatase secreted in biliary tract damage
  • albumin levels
  • test of coagulations as clotting factors are synthesised in liver
22
Q

Whose at risk of hepatitis B?

A
  • vertical transmission
  • sexual contact
  • IV drug users
  • close household contacts
  • healthworkers via needlestick injuries
23
Q

What are the symptoms of HepB?

A
Jaundice
Fatigue
Abdominal pain
Anorexia
Nausea
Vomiting 
Arthralgia ( joint pain)
24
Q

How long is the incubation period for acute hepB?

A

6 wks/6 months
Clear infections within 6 months
Becomes chronic in 10% of cases

25
What is chronic Hep B?
The presence of HBsAg after 6 months | May lead to cirrhosis and carcinomas
26
What’s the treatment of HepB?
No cure Life long anti virals to suppress viral replication Not required for everyone e.g inactive carrier
27
What’s the vaccination for HepB?
3 doses and a booster Genetically engineered surface antigen HBsAg If you have the surface antibody = infection almost/ is cleared
28
Whose at risk of Hep c?
- IV druggies - sexual contact - infants born to HCV positive mums - blood transfusions prior to 1991 - needlestick injuries
29
How does hep c progress?
``` 80% become chronic Get liver cirrhosis/chronic liver disease - decompensated liver disease - hepatocellular carcinoma - transplant - death ```
30
What are the symptoms of HepC?
``` Most are asymptomatic Vague symptoms include - fatigue - anorexia - nausea - abdominal pain ```
31
What’s the treatment for HepC?
Cure - directly acting antiviral combo However u can get reinfected