renal/gu 2*
List Alpha Herpesviruses (3)
1) HHV-1, Type 1 Herpes Simplex Virus
2) HHV-2, Type 2 Herpes Simplex Virus
3) HHV-3, Varicella Zoster Virus
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Where do Alpha Herpesviruses infect
Epidermal/Neuronal Viruses with a Wide Host Range
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What sort of infections does HHV-1 cause
Oral Infections
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What sort of infections does HHV-2 commonly cause
Genital Infections
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What sort of infections does Varicella Zoster Virus cause (HHV-3)
Infection of Epidermal and Neuronal Tissues
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What are Beta Herpes-viruses
Slow Growing Viruses infecting T Cells and Leukocytes
including
Cytomegalovirus (HCMV or HHV-5), Human Herpesvirus 6 (HHV-6) and Human Herpesvirus 7 (HHV-7)
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What are Gamma Herpesviruses
Viruses that infect primarily B Lymphocytes including Epstein Barr Virus (EBV or HHV-4) and Human Herpesvirus 8 (HHV-8)
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What disease does Varicella-Zoster Virus (HHV-3) cause
Chicken Pox (Varicella)
Shingles (Zoster)
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What infections does Epstein Barr Virus cause (HHV-4)
3 Marks
1) Infectious Mononucleosis (Glandular Fever)
2) Burkitt's Lymphoma
3) Nasopharyngeal Carcinoma
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What are Early Phase Genes
Genes associated with the replication of viral DNA efficiently
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What are Early Genes Translated into. How does this act on Human Polymerase.
Early Genes are translated into Viral Protein and associate with Human Polymerase. This changes the affinity of Human Polymerase so that it binds more readily to Viral DNA.
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What are Late Phase Genes
Genes associated with structural proteins like the capsid and proteins associated with plasma membrane
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What is the Primary Infection of HHV-1
Herpetic Gingivostomatitis
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What is the Secondary Infection of HHV-1
Herpes Labialis
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How does HHV-1 become latent?
Virus enters the trigeminal sensory neurones and migrates to the Trigeminal Ganglion where it hides until it is reactivated to cause secondary infection
In 50% of cases it remains dormant in the trigeminal ganglion
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What happens when HHV-1 is reactivated
When reactivated it moves back to the area where there was initial infection. For HHV-1 this is the vermillion border of the lips.
Virus then reinfects the epithelial cells and viral particles are shefd.
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What causes the reactivation of HHV-1 (4)
1) UV Light
2) Stress
3) Illness
4) Immuno-suppression
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What happens to the virus after Secondary Infection
Even after secondary infection, the virus can still remain dormant in the Trigeminal Ganglion and cause further reinfection and reactivation
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True or False
Most Primary Infections of HSV-1 are Asymptomatic
TRUE.
90-99% of HSV-1 Primary Infections are Asymptomatic.
1-10% are Symptomatic.
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What are the Signs of Herpetic Gingivostomatitis (4)
1) Multiple Oral Vesicles which may rupture to form extensive sloughing ulcers
2) Gingivitis with Erythema and Sloughing
3) Lymphadenopathy
4) Hyperkeratosis
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What tests are done to confirm the diagnosis of Herpetic Gingivostomatitis
1) Rising Antibody Titre, Presence of IgM antibodies
2) Viral Culture or PCR
However Lab Tests are not normally done. Typical Clinical Appearance is usually enough to make the diagnosis
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Describe the Basic Method of PCR
1) Denature DNA to single Strands
2) Annealing of specific primers to DNA
3) Extension by Polymerase
4) Repeat 30-35 times.
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What is the Treatment and Management for Herpetic Gingivostomatitis
- Acyclovir (200mg 5x daily for 5 days)
- Fluids and Soft Diet
- Analgesics/Antipyretics
- Cross Infection Control
- Local Antiseptics (Chlorhexidine)
- Topical Analgesics (Difflam)
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How does Acyclovir work
The Structure of Acyclovir is similar to Guanosine.
Guanosine makes GTP which is used make DNA
Human Thymidine Kinase (TK) phosphorylates guanosine when HSV DNA replicates
However Human TK cannot phosphorylate Acyclovir as well.
In HSV infected Cells, Acyclovir is phosphorylated by Viral TK enzyme to form ACV-P
ACV-P then inhibits virus replication
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How does ACV-P inhibit Virus Replication (2)
1) It Gets incorporated into replicating viral DNA but further bases cannot be added as ACV-P lack a terminal hydroxyl group therefore is a Chain Terminator.
2) ACV-P acts on the virus DNA complex and inhibits the activity of one or more of these enzymes, so Viral DNA manufacture is slower.
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What are the Clinical Features of Herpes Labialis (5)
1) Prodromal Irritation
2) Vesicles at or Near Mucocutaneous Junction of Lip
3) Crusting Lesions lasting 7-10 days
5) Usually Occurs at the Same site of Primary Infection
4) May occur Intra-orally, in nose or elsewhere on skin but this is Rare.
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Explain why Prophylatic Treatment in the Management of Herpes Labialis is rarely justified
Prophylactic Acyclovir will prevent lesions in the immunocompromised or those susceptible to erythema multiforme
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Describe the Value of Acyclovir in Herpes Labialis using Evidence
Prophylactic Oral Acyclovir (600-1000mg/day in 2 doses) is effective
- Reduces Duration of Pain by 1.4days
- Reduces time to lesion crusting by 2.1 days
- Reduces occurrence of new lesions by at least 50%
- Increases mean time to next recurrence from 46 to 118 days
- Reduces mean number of recurrences over a 4 month observation period
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What is Herpetic Whitlow
This is a Herpetic Infection of the Fingers from Handling the Oral Tissues of Someone with Active Primary or Secondary Herpes Simplex Lesions
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What is HSV Encephalitis
a rare neurological disorder characterized by inflammation of the brain caused by HSV-1
It affects the frontal lobes of the brain
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Which Groups of People are Affected by HSV-Encephalitis
People >50years (HSV-1) and Neonates (HSV-2) are affected.
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What are the symptoms of HSV Encephalitis (HSV-1) in Adults
1) Headache and Behavioural Changes over Several Days
2) Fever
Only 11% of cases have a history of recurrent HSV infections
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What are the symptoms of HSV Encephalitis in Neonates (HSV-2)
5 Marks
1) Skin Rash, Lesions and CNS Symptoms
2) Virus is present in the Liver, Lung and Adrenal Glands
3) Respiratory Distress
4) Fits and Convulsions
5) Raised Intracranial Pressure
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What is the Primary Infection of Varicella Zoster Virus (HHV-3)
Chicken Pox (Varicella)
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What is the Secondary Infection of Varicella Zoster Virus (HHV-3)
Herpes Zoster (Shingles)
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Where does HHV-3 remain Latent
In the Dorsal Root/ Trigeminal Ganglia
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What factors cause Reactivation of HHV-3 (4)
1) Age (70% >50years)
2) Stress
3) Illness
4) Immunosuppression)
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Where does Shingles more commonly affect and why
Chest and Back Regions
HHV-3 goes latent in the Dorsal Root
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Herpes Zoster can also result in Oral Disease. It commonly affects one of the divisions of the Trigeminal Nerve.
What are the 3 Phases
1) Pre-herpetic Neuralgia
2) Rash
3) Post-Herpetic Neuralgia
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What occurs in the Pre-Herpetic Neuralgia phase of Herpes Zoster
This phase is before a lesion is seen or observed
There is pain in the distribution of the affected division of the trigeminal nerve. Prior to development of the rash.
This pain may mimic dental pain
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What occurs in the Rash Phase of Herpes Zoster
Depending on which nerve branch the virus comes down will depend on which areas of the face you see the viral pathology.
Unilateral Vesicles break down to form Ulcers in the Mucosa or Crusting Lesions on the skin which last 2-3 weeks.
Unilateral is Characteristic of Oral Herpes Zoster
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What eye problems may Herpes Zoster cause (4)
- Glaucoma
- Cataract
- Double Vision
- Scaring of the Cornea
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What is the Management and Treatment of Herpes Zoster (HHV-3) caused.
- Acyclovir (800mg 5 times daily for 7 days)
- Analgesics
- Ophthalmic Referral if eye is involved
- Avoid contact with children
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What occurs in the Post-Herpetic Neuralgia phase of Herpes Zoster
10% of patients go on to develop extremely unpleasant intractable burning pain in the distribution of the affected nerve.
This is more common in the elderly
Effective early treatment of Zoster may decrease the risk of Neuralgia
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What happens in the Primary Infection of HHV-4/EBV
Primary Infection replicates in the Oro-Pharyngeal Epithelial Cells
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Where does EBV/HHV-4 become latent
Establishes Latency in B-Lymphocytes
EBV Latent Infection of B-Lymphocytes is necessary for virus persistence, subsequent replication in epithelial cells and release of infectious virus into saliva.
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How is HHV-4 different from other Human Herpesviruses
Human Herpesviruses infect Keratinocytes but HHV-4 infects Oro-pharyngeal Cells
HHV-4 establishes latency in B Lymphocytes instead of Nervous System.
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What is Infectious Mononucleosis
EBV infection that causes Glandular Fever.
Most infections are asymptomatic.
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Although most infections of Infectious Mononucleosis are Asymptomatic, if Symptomatic, what are the symptoms.
1) sore Throat
2) Swollen Cervical Lymph Nodes
3) Mild Fever
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What is the Clinical Presentation of Infectious Mononucleosis (Oral)
1) Petechiae on Soft Palate
2) Creamy Exudates on Fauces
3) Cervical Lymphadenopathy
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What is Burkitt's Lymphoma
A malignant B Cell Lymphoma of high prevalence in Children in Tropical Africa.
Severe Clinical EBV infections in early childhood predispose an individual to Burkitt's Lymphoma
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What is the Treatment of Burkitt's Lymphoma
Cyclophosphamide (Chemo)
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What does HHV-5 (Cytomegalovirus) cause in Healthy Individuals
- Glandular Fever-Like illness
- Salivary Gland Swelling
Both are Rare
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What does HHV-5 (Cytomegalovirus) cause in Immunocompromised Individuals
1) Large Ragged Oral Mucosal Ulcers
2) Salivary Gland Swelling
3) Retinitis
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What is Hepatitis
Inflammation of the Liver
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What are the general signs and symptoms of Hepatitis (4)
1) Malaise
2) Jaundice
3) Dark Urine
4) Pale Fatty Stools
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How can you differentiate between the different Serotypes of Hepatitis
Serum & Urine Tests. PCR to look for certain proteins, antibodies, antigens etc.
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What are the 5 Major Types Of Viral Hepatitis
Hepatitis A - E
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Which Hepatitis Viruses are Non Enveloped
Hepatitis A & E
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Which Hepatitis Viruses are spread through Faecal Oral Routes
Hepatitis A & E
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What type of Virus is Hepatitis A
RNA virus
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What are the Genotypes of Hepatitis A
Genotypes I - VII
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Which Genotypes of Hepatitis A is associated with Human Disease (4)
Genotypes I, II, III and VII
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Which Genotype of Hepatitis A causes majority of Human Diseases
Genotype I (80%)
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What is the Incubation Period, Prodrome and Recovery Period of Hepatitis A
2 Week Incubation
4 to 10 day Prodrome and Few Weeks for Recovery.
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What is the treatment of Hepatitis A
Managed at home
Bed rest followed by gradual ambulation
Teaching: regarding sanitation and hygiene
Diet: Small frequent meals, IV glucose
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What is the prevention for Hepatitis A
Formalin-Killed Virus Vaccine
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What is the correlation of Hepatitis A with Age
The severity of Hepatitis A increases with Age.
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Which Immunoglobulin is produced the first time a Host is exposed to an antigen
IgM
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When levels of IgM decrease after primary exposure, Which Immunoglobulin is produced
IgG
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The Incubation Period for Hepatitis A is 2 Weeks. The virus however can be detected before the Prodrome.
Explain How.
Virus is detectable in Liver Biopsy and Faeces before the Prodrome, before any symptoms start. It is also detectable in the blood before the Prodrome.
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What sort of Virus is Hepatitis B
DNA Virus (Double Stranded DNA - dsDNA)
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How does Hepatitis B spread
Parenteral Route of Transmission
spread through saliva, blood, semen, menses, vaginal secretions.
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Where does Hepatitis B reside once inside host.
Resides and Multiples in Hepatocytes. Propagates in Liver Cells
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2-5% of Infected Hepatitis B Patients develop Chronic Carrier State.
What are the two types of Chronic Carrier State
- Chronic Persistent Hepatitis (Healthy Carrier)
- Chronic Active Hepatitis, which spread Hepatitis quite easily
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Describe the Structure of the Hepatitis B Virion (4)
1) dsDNA
2) DNA polymerase enzyme
3) HBcAg
4) HBsAg
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During Active Hepatitis Infection HBcAg breaksdown
When HBcAg breaksdown, what does it produce
HBeAg which is a soluble marker of Active Infection detectable in Serum
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Hepatitis B is formed of dsDNA
What does the dsDNA code for (4)
The dsDNA codes for 4 genes (S, C, P and X)
1) S = Surface Antigen (HBsAg)
2) C = Core Protein (HBcAg)
3) P = DNA Polymerase
4) X = Regulatory
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What is Hepatitis D
Defective RNA Virus which coexists with Hepatitis B
It cannot exist on its Own.
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What is Hepatitis C
A small enveloped single stranded RNA virus (ssRNA)
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How Many Genes does Hepatitis C contain
10 Genes transcribed as a Polyprotein
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What percentage of Hepatitis C cases become Chronic
50-85% become chronic
of which 5% develop Hepatocellular Cancers within 30 years and 25% develop Cirrhosis within 20 Years.
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What is the Treatment of Hepatitis C
Interferon Alpha and Ribavirin
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What does Ribavarin do
Synthetic Guanosine Nucleoside Antiviral Agent that interferes with the synthetic of viral mRNA
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Which Age Groups does Hepatitis E commonly affect
Young-Middle Aged Adults mostly in developing countries due to sanitation, food and water hygiene.
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What are the symptoms of Hepatitis E
Mild Disease which usually clears by itself but can lead to persistent immunosuppression leading to liver damage
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What topic is covered in the Conventional History when suspecting Infectious Disease
Epidemiological History including recent travel, vaccines, prophylaxis history, occupation, food & drink, recreational, sexual, animal contact and special medical procedures.
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A patient visits your dental practice for a routine assessment. They have recently just returned from a tropical country after travelling. They present with a high fever.
What infectious do you first suspect
Malaria until proven otherwise
Other differential diagnoses may include: Typhoid, Dengue, Viral Hemorrhagic Fever
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Which infectious disease can be prevented via Prophylaxis Treatment
Malaria
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Which Infectious Diseases can be prevented via Vaccines
1) Hepatitis A
2) Typhoid
3) Neisseria
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Your Occupation can put you at risk of getting infectious disease. List Occupations at Risk (6)
1) Farmers
- Blood Borne Viruses
- Diarrhoea
2) Farmers
- Leptospirosis
- Coxiella
3) Sewage Workers
- Leptospirosis (Weil's Disease)
- Hep A
- Gastroenteritis
4) Sexual Workers
- HIV
- Hep B
- HSV
- Gonococcus
- Syphilis
- Chlamydia
5) Pet Shop Owners
- Psittacosis
6) Military Workers
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Playing certain sports can put you at risk of Infectious Disease. List Sports that increase the risk of Infectious Diseases
1) Canoeing
- Leptospirosis
- Gastroenteritis
2) Cavers
- Histoplasmosis
- Marbung
3) Trekkers
- Lyme Disease
- Tick-Borne Diseases
4) Rugby
- HSV
- Fungal Infections
5) Swimming
- Fungal Infections
- Pox Virus
- Leptospirosis
- Gastroenteritis
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What infectious diseases can an Alcohol dependant patient develop
1) TB
2) Pneumonia
3) HIV
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What infectious diseases can a Cannabis user develop
1) Pneumonia
2) early COPD
3) Lung Abscess
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Use of Immunosuppression increases the risk of which infectious diseases?
- CMV (Cytomegalovirus)
- VZV (Varicella Zoster Virus)
- PCP (Pneumocystis Pneumonia)
- Neutropenic Sepsis
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Which infectious diseases can be developed through Intrauterine Contraceptive Devices
- Actinomycosis
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What are systemic signs of infectious disease (5)
1) Fever/Malaise
2) Vital Signs
3) C-Reactive Protein Test
4) White Blood Cell Count
5) Rashes
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List Sterile Sites from where a Pathogen can be isolated from (4)
1) Blood
2) CSF
3) Urine
4) Bone/Joint
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Which Age groups is HIV more prevalent in
HIV transferred during Sexual Activity therefore active during 25 to 64 year olds
HIV has a long period of clinical inapparent disease, some people will develop later on in life i.e. >64 even though they are not sexually active later on in life.
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What is HIV
Human immunodeficiency virus.
Immune system becomes weaker, certain opportunistic diseases are more likely to occur. CD4 cell count decreases.
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What are the Risk Factors for Shingles (2)
1) Age
2) Immunocompromised
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What are 4th Generation Tests
Using ELISA to test for Antigen and Antibody Complexes.
Looks for Antibody to HIV and Separates Antigen from Virus.
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List 4 other methods of testing for HIV other than Serological Tests
1) Point of Care Tests
- Finger Prick, Mouth Swab, Saliva
2) Antibody Only Tests
3) Antigen Only Tests
4) HIV RNA PCR
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Patients with Advanced HIV can have Skin & Oral Manifestations of Kaposi's Sarcoma
What is Kaposi's Sarcoma
a type of cancer that can form masses in the skin, lymph nodes, or other organs.
Human herpesvirus 8 (HHV8) is found in the lesions of all those who are affected
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How does Kaposi Sarcoma Present
1. Purple patches, plaques, and nodules on the skin (would not blanche because it is not a complete blood vessel)
2. May involve visceral organs
Usually Linked to HIV
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What is the presentation of Kaposi's Sarcoma on Biopsy
Spindle Cells
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How does Oral Hairy Leukoplakia Present
White Patches that cannot be scraped off.
Linked with HIV, Smoking & Immunosuppression
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How is HIV Managed
HAART (Highly Active Anti-Retroviral Therapy)
The use of 3 anti-retroviral drugs to get good efficacy
All 3 drugs act on different points in the HIV replication cycle to suppress the virus.
Note this is not a cure but a lifelong therapy.
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Where in the HIV Cell Cycle can Anti-Retroviral Drugs act on?
Anti-Retrovirals can be Fusion Inhibitors, Reverse Transcriptase Inhibitors, Integrase Inhibitors, Protease Inhibitors.
Using 3 Drugs, 2 of the same class with inhibit Viral Mutations
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Why does HIV become Resistant to Drugs
Resistance occurs due to HIV lacking proofreading enzymes to correct errors during reverse transcription and its rapid production rate is prone to a higher error rate.
However as long as all 3 drugs are in the system, resistance will not occur.
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What changes can occur in Drug Levels that lead to Resistance
1) Non-Adherence
- If Monotherapy or Dual Therapy is done then this will lead to resistance. All 3 Drugs in HAART must be taken
2) Drug-Drug Interactions (Many Drugs interact with Anti-Retrovirals, therefore cause subtherapeutic levels)
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What does HIV cause
AIDS (acquired immunodeficiency syndrome)
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HIV are part of a group called Lentiviruses. What are Lentiviruses
Slow Growing Retroviruses which integrate into the host chromosome
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How is HIV Transmitted? (5)
1) Sexual Contact
- Mucosal Surface Contact, Exchange of Fluid
2) Blood-Blood Contact
- IV Drug Use, Open Wound to Open Wound
3) Infected Blood Products, routine Infected Blood Transfusion
4) In Utero
5) Breast Milk (Vertical Transmission)
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There are Two Types of HIV, 1 & 2. Which is most common
HIV 1 is most common.
HIV 2 is less easily transmitted and less pathogenic.
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Why is it difficult to create an Immune Response against HIV
HIV mutates readily and Reverse Transcriptase does not proofread. Different Base Pairings go unrecognised.
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What are the 3 main groups of HIV 1
1) Main (M-Pandemic Strains)
2) New (N)
3) Outlier (O)
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Where did HIV 1 Originate
Cameroonian Chimps, Spread to Congo further spread by urbanisation
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What are the two major Glycoproteins found on the Envelope of HIV
GP41 and GP120.
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How does HIV attach to CD4 cells initially
Initial Attachment is via GP120
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How does HIV Progress
Initially T Cells manage to remove the virus however the Number of T Cells begin to decrease to the point where there are not enough T Cells to cope with the virus. This is the IMMUNE CRISIS.
In the beginning you may get flu like symptoms, as the disease progresses you get higher chance of getting opportunistic infections
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What Bacterial Opportunistic Infections may occur during HIV & AIDs (3)
- Mycobacterium Tuberculosis
- Salmonella
- Haemophilus, Streptococcus, Pneumococcus, Pyogenic Infections
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How does HIV progress to AIDs
10% of Untreated HIV cases progress within 2-3 years
5-10% are clinically asymptomatic after 10 years.
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What do Protease Inhibitors do
Prevents Virus from converting GP120 to GP41 to make new virus
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What is the First Line Regimen for HAART
Use 2 NRTIs
i.e. Zidovudine, Lamivudine, Emtricitabine, Stavudine
AND
1 NNRTI
i.e. Efavirens, nevirapine
OR
A Protease Inhibitor.
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What are the side effects of NNRTIs
- Stevens Johnson Syndrome, a severe disorder of mucous membranes
- Teratogenicity
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How is HIV Tested
ELISA Based Blood Test, detects HIV Antibodies in the Blood.
Antibody takes 6-12 weeks to develop,
Most reliable testing at 3 months.
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