GEP (Life Protection) Week 3 Flashcards

1
Q

What are the 2 main types of adaptive immunity

A

Part of adaptive immunity, which has two branches
Humoral immunity (mediated by B-cells)
Cellular immunity (mediated by T-cells)

Part of the immune response carried out by a cell, not by a molecule they release
T-cells involved: 2 main types:
T helper (CD4+)
Cytotoxic T (killer) cell (CD8+)

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2
Q

What are antigen presenting cells and how are they involved in immune response

A

APCs are cells that are able to phagocytose pathogenic material and transport it to lymphatics
From here, they are able to present that antigen to naive T cells in order to activate an adaptive immune response
APCs present Ag on special proteins called Major Histocompatibility Complexes, which can match to specific T cell receptors (TcRs) and bind to them, causing activation of T cells

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3
Q

How does APC interact with T cells during an immune response

A

Antigen Presenting Cells (APCs) will convert antigenic material into an Ag peptide, that is bound to a Major Histocompatibility Complex (MHC), and transported onto the cell surface
APC will then travel to secondary lymph organs (spleen and nodes) and present to naive T cells
Depending on the type of MHC the Ag is presented on, it will cause differentiation into a specific T cell

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4
Q

What is MHC and the different type of classes

A

MHC is Major Histocompatibility Complexes

  • There are two types of MHC, class 1 and class 2
  • MHCI: Present Ag peptides to CD8+ T cells
    Are expressed by all nucleated cells, which expresses a self-antigen to tell the body it is a native cell
  • MHCII: Present Ag peptides to to CD4+ T cells
    Are expressed by APCs only, to tell T cells that foreign/damaged cells are present
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5
Q

Describe the activation of T cells

A

Step 1: Activation. Binding of Ag-MHC complex to TcR and CD. TcR binds to receptor and CD binds to MHC (this acts as complimentary anchor, preventing binding of self cells)

Step 2: Survival. More signals are required to activate the cell. CD28 (from T cell) is expressed, and binds to B7.1&2 (aka CD80&86), which are overexpressed when Ag is detected by APC. This leads to the rapid proliferation of the T cell. This process is highly regulated by other receptors that bind to B7s, to ensure there isn’t overstimulation/unwarranted stimulation
These steps together are called Co-stimulation

Step 3: Differentiation. Signal 1&2 together initiate expression of cytokines to differentiate the T cell into the specific cell it needs for the appropriate response
IL-2 (produced by T cell to increase gene expression)
IL-12 (produced by APC to stim Th1 cell)
IL-4 (produced by APC to stim Th2 cell)

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6
Q

What are the roles Th1 and Th2 and CTL (cytotoxic T cell).

A

Th1 cells: Produces IFNy, which induces activation of phagocytes (mainly macrophages) to increase destruction of intracellular pathogens
also stimulate production of IgG to increase phagocytosis (complement)

Th2 cells: Helps in destruction of Helminths.
Produces IL-4 and IL-13, which recruits B cells to produce Ab to opsonise helminths so that eosinophils and mast cells are recruited for its destruction

CTL: Role in destruciton of viruses and mircobes that escape from phagosome (TB and malaria)
Also important in immunity to tumours and rejection of organ transplants
Deliver the ‘kiss of death’ by attaching and releasing cytolytic proteins into cell, triggering apoptosis
Peforins open pores in membrane, granzymes infiltration and initiate apoptosis

Depending on the varying signals, different T cells are produced with different roles:

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7
Q

What are viruses

A
  • Simply defined as an obligate intracellular parasite
  • Consists of:
    Viral genome (ss/ds RNA/DNA)
    Protein coat (capsid)- shape varies
    Can be enveloped or non-enveloped
  • Can vary greatly
  • Capable of replication only within the living cells of bacteria, animals or plants
  • Very small 20-400nm
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8
Q

How are viruses classified

A

Classification is dependent on characteristics of viral particles:
-Type of Nucleic Acid (DNA/RNA, ss or ds)
-Capsid shape
-Presence or absence of envelope
-Process of replication
-Host organisms
-Type of disease caused

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9
Q

How do Viruses replicate

A
  • Can only replicate by infecting a host cell and utilising the cell’s replicating systems (ribosomes, enzymes, ATP etc)
  • This process can vary also:
    RNA translated directly into viral proteins in ribosomes of host cell
    DNA transcribed into viral mRNA first
  • This proteins then form new virions, which eventually cause lysis of cell wall so they can spread around host
  • Some viruses can ‘live’ in a dormant state inside the body. This is called latency. They wait for an opportune moment to reactive and replicate, causing illness once again
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10
Q

How do viruses cause disease and damage

A

Viruses cause many human diseases, ranging from mild to fatal
Diseases occurs due to:
Viruses causing host cells to burst open and die
Disrupting homeostasis of host cells

Characteristics of the illness depend on where they enter the body and what host cells they infect (and ultimately destroy)
e.g HIV affects immune cells, so when destroyed in high number, leads to immunodeficiency

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11
Q

Give an overview of Herpes Simplex Virus (HSV)

A

Symptoms :
HSV-1:
cold sore on lips
painful scab
can spread further on face in immunosuppressed
HSV-2:
pain/itching around scabs
small bumps/blisters around genitals
painful urination
discharge

Spreads through cutaneous exposure

Is diagnosed through combination of symptoms, swab (HSV-2) and Nucleic Acid Amplification Test (NAAT)

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12
Q

Give and overview Varicella Zoster Virus and what they cause

A

Chickenpox
itching fluid filled blisters covering body
eventall turn into scabs
fever
headache
swollen glands
Shingles
pain, burning or tingling
red rash with fluid filled blisters
fever
Headache

Spreads through direct with blisters, salvia or mucus of infected

Diagnosed by symptoms and swabs of ulcer (PCR)

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13
Q

Give an overview of cytomegalovirus (CMV)

A

Symptoms:
* In adults is often asymptomatic or flu like
* In neonates:
Rash
Jaundice
Microcephaly
Retinitis
Seizures
Hepatosplenomegaly
Low birth weight

Spreads congenitally, or through close contact and bodily fluids

Diagnosed via a urine sample from babies ideally, or can test saliva or blood

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14
Q

Give an overview of the Epstein-Barr Virus (EBV)

A
  • Often asymptomatic in children, particularly under 5 years old. But can cause:
    fatigue
    fever
    inflamed throat
    swollen lymph nodes in neck
    hepatosplenomegaly
    rash
    post infection chronic fatigue syndrome
  • Spreads via saliva, and can be sexually transmitted
  • Diagnosed by Hx and age, physical examination, heterophile Ab and serological tests
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15
Q

Give an overview of the adenovirus

A

Symptoms:
cough (croup, barking like)
runny nose
ear pain/infection
diarrhoea/vomiting
UTI
Conjunctivitis

Transmitted by droplets (coughs and sneezes) or the faecal/oral route

Diagnosed with Ag detection, PCR, virus isolation and serology

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16
Q

Give an overview of Human papillomavirus (HPV)

A

Presents as warts (oral or genital, depending on how it has been spread)

Is sexually transmitted

Can be diagnosed with cervical screening and scab tests

Those with HPV have a increased risk of many different cancers (penile, vulval, anal, cervical)

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17
Q

Give an overview of measles

A

Presents with:
Total body skin rash
Flu like symptoms
small white spots inside mouth (Koplik’s spots)

Is an airborne pathogen

Diagnosed by symptoms and lab testing:
positive measles IgM Ab
detection of viral RNA

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18
Q

Give an overview of Mumps

A

Presents with:
Swelling of parotid glands
Fever
Headache
Dry mouth
Abdo pain
Loss of appetite
Fatigue

Spreads via droplets of saliva

Diagnosed by symptoms, RT-PCR and IgM serology

19
Q

Give an overview of Rubella

A

Presents with:
Rash
Swollen lymph nodes (neck and behind ears)
Fever
Headache
Sore, red eyes
Aching fingers, wrists and knees

Spreads via droplets of saliva

Diagnosed via Serology and ELISA

20
Q

Give an overview of parvovirus (Slapped cheek Virus)

A

Presents with:
Facial rash (particularly cheeks)
Painful or swollen joints
Anaemia (more so adults)
Fatigue
Low grade fever

Spreads through droplets and can be passed on to a foetus

Diagnosed by serology and symptoms

21
Q

Give an overview of the rotavirus

A

Presents with diarrhoea, which left untreated can lead to severe dehydration

Spreads via the faecal oral route

Diagnosed by symptoms and PCR (viral NA and Ag detecting test)

22
Q

Give an overview of heamorrahagic Fever (Lassa Fever)

A

Presents as:
Weakness
Malaise
Headache
Sore throat
Muscle pain
Vomiting/diarrhoea
Abdo pain
Unexplained bleeding/bruising

Spread by coming into contact with food or items contaminated with rodent urine/faeces

Diagnosed by blood PCR

23
Q

Give an overview of Ebola (type of haemorrahgic fever)

A

Presents with:
Fever
Headache
Diarrhoea
Vomiting
Stomach pain
Muscle pain
Unexplained bleeding or bruising

Spreads through direct contact its blood or bodily fluids

Diagnosed by blood PCR

24
Q

Give an overview on rabies

A

Presents with:
Weakness
Fever
Headache
Cerebral dysfunction
Anxiety
Confusion
Agitation

Spreads through contact with saliva, or bite from infected animals (bats, dogs etc)

Diagnosed by PCR of CSf or Nuchal skin biopsy

25
Q

Give an overview of HIV (human immunodeficiency virus)

A

Presents with:
Fever
Headache
Muscle aches and pains
Rash
Sore throat and painful mouth sores
Swollen lymph nodes
Weight loss
Diarrhoea
Sexuallty transmitted, as well as contact with bodily fluids
Diagnosed via blood test
Is an enveloped virus with protein

26
Q

Give an overview of Rhinovirus (Common cold)

A

Is the predominant cause of the common cold

Is airborne, and diagnosis is based on symptoms

27
Q

Give an overview of Influenza

A

Causes ‘the flu’:
Headache
Cough
Sore throat
Loss of appetite
Joint pain/ aches
Fever
Fatigue

Is airborne

Diagnosed based on symptoms, RT-PCR, Viral culture and immunofluorescence assay

28
Q

Give an overview on Poxvirus

A

Presents with:
Fever
Headache
Muscle aches
Backache
Swollen glands
Exhaustion
Joint pain
Rash that spreads from the face to the entire body (raised spots that turn into blisters, similar to chicken pox)
Spreads through:
close contact with blisters
cough/sneezes
contact with items used by patients

Diagnosed by swab from the rash

29
Q

Give an overview on the STI: Chlamydia (Chlamydia Trachomatis)

A

Atypical gram negative bacteria
* SIGNS/SYMPTOMS:
Asymptomatic
Vaginal/Penile discharge (white/yellow)
Abdominal pain
Post coital bleeding (women)
Intermenstural bleeding
Dysuria

  • ONSET:
    Few weeks after exposure
    Usually picked up in screening from 2 weeks post exposure
  • COMPLICATIONS:
    Pelvic inflammatory disease (PID)
    Epididymitis or orchitis
    Infertility
    Ectopic pregnancy & pregnancy complications
    Sexually acquired reactive arthritis (SARA)
  • MANAGEMENT:
    Antibiotics: azithromycin or doxycycline

PID occurs in 16% of women with untreated chlamydia
Pregnancy: Increased PROM, premature delivery, low birthweight.
Infections of the eyes, lungs, nasopharynx, and genitals in the neonate, due to exposure in the birth canal during delivery

30
Q

What are the screening programme for chlamydia

A

National Chlamydia Screening Programme
(NCSP)

Public health initiative to reduce the prevalence of chlamydia
Primarily targets age 15-24 (highest risk group)
Normalise regular sexual health screening

Involves:
Free testing (SH clinics, GP’s, Online)
Sexual health education
Access to treatment: prompt treatment and free of charge
Confidentiality

31
Q

Give an overview of the STI: Gonorrhoea (Neisseria Gonorrhoea)

A

Gram Negative Bacteria
* SIGNS/SYMPTOMS:
Asymptomatic (1:10 men; 1:2 women)
Vaginal/Penile discharge, thin and watery (green/yellow)
Pelvic pain (women)
Intermenstrual bleeding
Dysuria
Inflammation of the foreskin/testicles
Rectal infection
Pain/discomfort
Discharge
Throat infection
Asymptomatic
Sore throat

  • ONSET:
    ~2 weeks post exposure
  • COMPLICATIONS:
    PID
    Epididymitis, orchitis or prostatitis
    Infertility (men & women)
    Disseminated gonorrhea
  • MANAGEMENT:
    IM injection ceftriaxone
    Sometimes dual therapy is used due to antibiotic resistance or co-infection with chlamydia:
    IM ceftriaxone
    PO azithromycin/doxycycline

PID occurs in up to 30% of women with untreated gonorrhoea infections
Pregnancy complications similar to chlamydia
Disseminated gonorrhea: 0.5–3% of untreated gonorrhoea cases. It occurs with bacteraemia and spreads, leading to septic arthritis, polyarthralgia, tenosynovitis, petechial/pustular skin lesions, or, on rare occasions, endocarditis, or meningitis

32
Q

Give an overview of the STI: Syhilis (Treponema pallidum)

A

Atypical gram negative bacteria

  • SIGNS/SYMPTOMS:
    Primary (1-3 weeks)
    Chancre (painless ulcer)
    Secondary (6-12 weeks)
    Skin rashes- particularly palms/soles (reddish brown)
    Mucous membrane lesions (mouth/genitals)
    Fever
    Fatigue
    Swollen lymph nodes
    Latent
    No symptoms
    Tertiary (years after initial infection)
    Neurosyphilis
    Cardiovascular syphilis
    Gummatous syphilis
    Systemic infection/symptoms
  • ONSET:
    10-90 days
  • COMPLICATIONS:
    Cardiac: AA, angina, heart failure
    Neuro: dementia, seizures, personality changes, paralysis
    Nerve pain
    Joint pain
    Systemic complications: liver, skin, bones, eyes, testicles, etc!
  • MANAGEMENT:
    Number of doses determined by stage
    Primary/Secondary: 1 dose IM penicillin G
    Tertiary: 3 doses IM penicillin G over 3 weeks
    Penicillin allergy: use either doxycycline, erythromycin or azithromycin (all oral)

PID occurs in up to 30% of women with untreated gonorrhoea infections
Pregnancy complications similar to chlamydia
Disseminated gonorrhea: 0.5–3% of untreated gonorrhoea cases. It occurs with bacteraemia and spreads, leading to septic arthritis, polyarthralgia, tenosynovitis, petechial/pustular skin lesions, or, on rare occasions, endocarditis, or meningitis

33
Q

Give an overview of the STI: Trichomoniasis (Treponema pallidum)

A

Protozoan (parasite)

  • SIGNS/SYMPTOMS:
    Asymptomatic (particularly in men)
    Genital itching/swelling
    Vaginal discharge, foul smelling (green, frothy)
    Penile discharge (white and thin)
    Dysuria
    Pain with sex (dyspareunia)
    Pain with ejaculation
  • ONSET:
    5- 28 days
  • COMPLICATIONS:
    Rare for complications
    Increased risk of other STIs including HIV
    PID
    Complications if pregnant
    Low birth weight
    Premature delivery
  • MANAGEMENT:
    Oral metronidazole
34
Q

Give an overview of Genital Herpes Background, risk facros and epidemiology

A
  • BACKGROUND:
    Can be caused by both HSV1 & HSV2, although more often by HSV2
    Both are members of the Herpesviridae family
    Enveloped virus, with double stranded linear DNA
    Cutaneous exposure
    Can be spread through oral, vaginal or anal sex
  • RISK FACTORS:
    Sex with multiple partners
    Anonymous sexual partner
    Presence of another STI
    Female
  • EPIDEMIOLOGY:
    HSV1: 7 in 10; HSV2: 1 in 10 (UK)
    6% of all newly diagnosed STIs in the UK
    HSV2 more common in women than men
35
Q

What are the clinical features of Genital Herpes

A

Small bumps/blisters around genitals, anus, thighs or bottom
Pain/itching around scabs
Dysuria
Discharge

Infections are recurrent
Can self resolve
Reactivation often triggered by event:
Stress (physical/emotional)
Immunocompromised state
Trauma to genitals
Menstruation
Hormonal changes
UV light exposure
Prodrome of pain 2 hours - 2 days prior in recurrent infections

36
Q

What is the pathophysiology of Genital Herpes

A
37
Q

What is the main differences between HSV1 and 2

A

HSV1 (Oral Herpes) : Trigeminal ganglia
HSV2 (Genital Herpes) : Sacral ganglia

38
Q

What are the investigations for Genital Herpes

A

Symptoms:
Swab of ulcer
Nucleic acid amplification test (NAAT)
Polymerase chain reaction (PCR)
Antibody testing:
IgM: primary infection
IgG: recurrent infection

REMEMBER!
IgM : Modern (new infection)
IgG : Geriatric (old infection)

39
Q

What is the management of Genital herpes management

A

Patient education
Usually self resolving
Self management
Saline baths
Analgesia
Petroleum jelly
Antivirals: Acyclovir

40
Q

What is the MICRA for Acyclovir

A

M
Converted to acyclovir triphosphate:
-Inhibits viral DNA replication
I
Most species of Herpesviridae family:
-HSV1/2, VZV, EBV
C
-Hypersensitivity
-Caution in hepatic/renal failure
-Safe in pregnancy
R
Oral (tablet or liquid)
IV
A
Nausea, vomiting, diarrhoea, headache
Nephrotoxicity (acyclovir crystals in kidneys)

41
Q

What are the prognosis for gentital herpes

A

Lifelong infection, no cure but active infections can be managed
Recurrent infections tend to improve and become less frequent over time
Few complications in healthy people

Immunocompromised individuals may experience:
Severe active infections
Further spread of ulcers
Increased frequency of active infections

42
Q

Give an overview of pregnancy and transmission of infections such as syphillis etc.

A

Best way to remember is STORCHH
S
-Syphilis
-Transplacental
T
Toxoplasmosis
Transplacental
O
Other-
-Viruses: VZV, parvovirus, zika, Influenza, covid-19
-Bacteria: Group A Strep, GBS

VZV - transplacental
Parvo - transplacental
Zika - transplacental
Influenza - transplacental
Covid - transplacental
GBS - perinatal

R
-Rubella
-Transplacental
C
CMV
Transplacental, Postnatal (breastmilk)
H
-HSV
-Perinatal
H
-HIV
-Perinatal

43
Q

Give an overview of Neonatal HSV

A

Neonatal Herpes is a potentially life threatening disease, contracted during delivery
Mothers from 36 weeks with known HSV2 should have prophylactic acyclovir
Viral shedding can occur without active infection
Primary HSV2 infection of the mother during the third trimester or within 6 weeks of delivery = highest risk of neonatal herpes

Disease can be classified in 3 ways:
Skin, eye and mouth (SEM) disease
Central nervous system (CNS) disease
Disseminated disease - 30% mortality with treatment
Neonates that survive may experience serious morbidities

Management:
~14 days of IV Acyclovir with SEM disease
21 days of IV Acyclovir with CNS or disseminated disease