ID I Flashcards

(124 cards)

1
Q

Define HIV

A

Retrovirus that destory CD4 T cells
Acquired immunodeficiency syndrome (AIDS)
The virus is capable of reverse transcription
Incorporated into host cells
Two types exist
HIV I is the global epidemic

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2
Q

Pathophysiology of HIV

A
  1. HIV enters cells through binding of the viral envelope glycoprotein (GP120)
    Links to specific receptors on the cells (CD4 present on T helper cellsm MP and glial cells)
  2. Conformatational change in GP120
  3. CD4 cells migrate to lymphoid tissue. Viral replication. New virons to new T cells
  4. Depletion or impaired function CD4 cells. Decreased immune function
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3
Q

Discuss how new virons are generated

A
Attachment 
Entry 
Uncoating 
Reverse transcription 
Genomic integration (integrase)
Transcription viral mRNA
Splicing of mRNA and translation into proteins (GAG)
New virons = budding
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4
Q

Outline the reasons the body struggles to develop an immune response towards to virus

A

Neutralising antibodies of low magnitude
Envelope glycoprotein is poorly immunogenic
Mutation (error prone): viral escape

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5
Q

Where are the reservoirs of HIV replication

A

CNS (glial)
Testes (genital tract)
Macrophage (long lived cell population)
Resting CD4 T Cells (latently infected

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6
Q

How is HIV transmitted

A

Blood
Sexual
Vertical

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7
Q

Certain symptoms should make you suspicious of a possible HIV dx. List the symptoms

A
Generalised lymphadenopathy 
Acute generalised rash 
Flu like illness/ Glandular fever
Prolonged herpes simplex 
Frequent candidiasis
Odd looking mouth lesions
Unexplained night sweats, weight loss
Recurrent bacterial infection
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8
Q

Discuss the investigations involved in the dx of HIV

A
  1. Simple serology:
    - detect antibodies and antigens of the virus
    - pre and post testing counselling
    - negative results will require re testing in the window period
    - positive result can be reactive will require re testing
  2. ELISA
    - can give false negatives
    - +ve result western blot
  3. Western blot
    - Confirmation
  4. Serum p24 antigen: present during high viral replication
  5. Serum CD4 count, serum HIV RNA (PCR) for viral load
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9
Q

What other investigations might you like to consider in a patient recently tested +ve for HIV

A
Pregnancy test
Serum Hep B serology 
Serum Hep C serology 
TB  skin test
CXR
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10
Q

Who should be contacted in the case of a HIV +ve result

A

Partner notification
Criminally liable if know status and transmit infection
May disclose to partner if known risk and unaware

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11
Q

Discuss the monitoring of HIV

A

CD4 and viral load are used as parameters to determine how advanced the disease is

Monitor treatment response

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12
Q

Treatment aim of HIV

A

CD4 > 400cells/mm3

Viral load = 0

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13
Q

Discuss the natural history of HIV

A

SEROCONVERSION/PRIMARY HIV

  • Short illness, flu like post infection
  • highly infective
  • blotchy red rash
  • mouth ulcers

ASYMPTOMATIC HIV INFECTION

  • last several years
  • generalised lymphadenopathy

SYMPTOMATIC HIV INFECTION

  • Opportunistic infection
  • Certain cancers

LATE STAGE HIV INFECTION

  • Opportunistic infection
  • AIDS related complex
  • CD4<200
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14
Q

What make up AIDS related complex

A
Pyrexia
Night sweats 
Diarrhoea
Weight loss 
- oral hairy leukoplakia
- oral candida
- herpes zoster
- herpes simplex
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15
Q

List AIDS defining illnesses

A
PCP
CMV
TB
Sentinel tumours (Kaposi's sarcoma, lymphoma)
HIV becomes AIDS in 5-10 years
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16
Q

AIDS is associated with many opportunistic infections. List some of them

A
Tuberculosis
Pneumocystic jirovecci pneumonia (BAL)
Candidiasis: candidia albicans
Cryptococcal meningitis: cryptococcus neoformans
Toxoplasmosis: Toxoplasma gondii
CMV
Mycobacterium avium complex
HSV/VZV at multiple dermatomes
Kaposi sarcoma (HHV8)
Oral hairy leukoplakia
Burkitt's lymphoma
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17
Q

HIV is now a treatable disease. List the treatment available for HIV +ve people

A

Nucleoside reverse transcriptase inhibitors (NRTI): Prevent elongation of DNA chain from the RNA template

Non nucleoside reverse transcriptase (NNRT): Act near site of reverse transcriptase to block viral replication

Protease inhibitors: Block cleavage of active proteins from polyprotein formed by viral transcription

Fusion inhibitors (FI): Block virus entering the CD4 cells

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18
Q

Outline the treatment regimens that are generally offered to people that are HIV +Ve

A

Used at least 3 different antiretroviral drugs

1 NNRTI + 2 NRTI

2 NNRTI + 1 PI

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19
Q

Name and state the side effects of NRTI

A

Lamivudine (AZT): Haemolytic anaemia
Zidovudine (AZT): Haemolytic anaemia
Tenofovir: Renal impairment

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20
Q

Name and state the side effects of NNRTI

A

Nevirapine
Rash
Liver toxicity
Drug interactions

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21
Q

Name and state the side effects of PI

A

Lopinavir
GI disturbance
Diarrhoea
Peripheral neuropathy

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22
Q

What is given as prophylaxis exposure for HIV

A

4 week course
Tenofovir
Emtricitabine
Raltegravir

Must be given between 1hr and 3 days

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23
Q

Barriers to compliance with HIV

A

Social Ecconomic class
Social support
Stigma of HIV

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24
Q

How is vertical transmission of HIV reduced

A

Can be transmitted via delivery or breast milk
Antenatal antiretroviral therapy from the end of T1
HAART
Zidovudine monotherapy

VL<50 can be vaginal delivery

Postnatal: zidovudine monotherapy for 4W
Exclusively forumla fed

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25
Name the types of malaria
``` P.Falciparum P.Vivax P.Ovale P.Malariae P.Knowlesi ```
26
Outline the pathology associated with Malaria
1. Infected female anopheles inject: SPOROZITES 2. Sporozoites enter hepatocytes 3. Reproduce to form shizonts (asexual). Remain asymptomatic until this 4. Many merozoites released into the blood to penetrate erythrocytes. Pre-patent period 5. Merozoites undergo schizonts. They rupture to produce merozoites. Invasion of new erythrocytes 6. Fever paroxysms occurs 7. Rupture of erythrocytes. Release toxins that induce CK release from MP.
27
Primary prevention in Malaria
``` Avoid outdoor after sunset Insect repellent Long sleeves Insecticide treated bed nets Antimalarial chemoprophylaxis ``` P.Falciparum - Chloroquine or hydroxychloroquine 1 week prior, during, 4 weeks post If resistant to the above - Doxycycline - Atovaquone/proguanil
28
Malaria symptoms
``` Fever paroxysms Chill and rigors followed by fever and sweats Headache Weakness Myalgia Arthralgia Anorexia Diarrhoea Jaundice HSM Pallor Tacycardia Hypotension ```
29
Investigations in Malaria
1. Giemsa stained thick (parasite number) and thin blood films (species) - trophozoites in RBC - gametocytes in RBC 2. Rapid dx test - detection of parasite antigen or enzymes 3. FBC (pancytopenia) 4. Blood sugar as treatment can drop this
30
Management of Malaria
Primaquine single dose Falciparum - Chloroquine (sensitive) - Artesunate + mefloquine - Quinine sulfate + doxycycline IV Severe Infection - Artesunate + fluid management + airway support Ovale/Vivax - Choroquine - Hydroxychloroquine
31
Complication of Malaria
``` Acute renal failure Hypoglycaemia Metabolic acidosis Seizure Acute resp distress syndrome due to pulmonary oedema ```
32
What organism causes syphilis
Spirochaete treponema pallidum
33
Classify syphilis
1. Primary syphilis - Local macule/ papule/ulcer - chancre at 14-21 days - lymphadenopathy (rubbery) 2. Secondary syphilis - 4-8 weeks characterised by spirochetemia and dissemination to skin - Diffuse rash on palms of hands and soles of feet - trunk with mucous membrane involvement - Alopecia - Condylomata lata (warty) 3. Tertiary syphilis - chronic end organ complications years after the infection - CVS, neuro, gummatous - Memory impairment, dementia, argyll-robertson pupil, ataxia, rombergs, visual disturbances - Diastolic murmur due to aortic regurgitation (aortic root affected)
34
Investigations for syphilis
Dark ground microscopy of swab: coiled spirochaete Serum T pallidum particle agglutination (+ve lifelong) LP/CSF analysis CXR (widened aortic root) ECHO (aortic regurgitation)
35
Treatment of syphilis
IM benzylpenicillin + prednisolone
36
What causes viral haemorrhagic fevers
``` 5 types of RNA virus Filovirus: Ebola and Marburg Flavivirus: - Yellow fever - Zika virus - Japanese encephalitis - Tick borne encephalitis ```
37
Pathology of viral haemorrhagic fevers
``` Ebola and Marburg = Spread from BATS 2-21 days incubation Vascular affects - Flushing - Conjunctival injection - Petechial haemorrhage - Fever - Myalgia ``` Central pathological process leading to increased vascular permeability Mucous membrane haemorrhage Hypovolaemia with hypotension Shock and circulatory collapse
38
Warning signs of a potential viral haemorrhagic fever
Febrile illness Foreign travel or contact Exposure to rodents, bats, insects Flu-like symptoms
39
Presentation of a viral haemorrhagic fever
``` Sudden headache Pleuritic pain Backache Myalgia Conjunctivitis Dehydration Facial flushing High temperature Bleeding Renal failure Encephalitis Coma ```
40
Investigations for viral haemorrhagic fever
``` FBC - leukopenia - thrombocytopenia LFT - elevated transaminases ``` Coagulation screen - PTT - INR - clotting times prolonged - evidence of DIC (high D dimer and fibrinogen low) PT-PCR
41
Signs of altered vascular permeability
``` Coagulopathy Haemorrhagic complications (hepatic damage) Myocarditis Encephalitis Multi-system organ failure ```
42
Management of viral haemorrhagic fevers
``` Notify public health and proper officer Seek advice on prevention transmission Barrier nursing and vistor restriction Supportive management - Blood volume - Clotting - Care of major organs Antivirals - Ribavirin not for ebola ```
43
What organism causes Dengue fever and how is it spread
Arbovirus | Spread by the aides mosquitp
44
Classify the different types of Dengue fever
Primary infection - Benign in nature Secondary infection - Dengue haemorrhagic fever - Dengue shock syndrome - Vascular leak (hypoalbuminaemia and pleural effusions, ascites)
45
Presentation of Dengue fever
Flu-like illness (>40 degree) Rash (maculopapular) Flushing Retro-orbital pain
46
Presentation of Dengue haemorrhage fever
Widespread effusions - pleuritis CP - Dyspnoea - Cough DIC Hepatomegaly Can cause circulatory collapse
47
Investigations of Dengue fever
FBC - Elevated HCT - Leukopenia - Thrombocytopenia LFT - Deranged (high) - Albumin (low) Serology - +ve IgM - +ve IgG
48
Treatment of Dengue fever
``` Oral/ IV fluids Supportive care Antipyretics Notification Beware of fluid overload ```
49
Exclusion criteria for Dengue
Symptoms start > 2 weeks post leaving a Dengue area | Fever lasts > 2 weeks
50
What causes Leishmaniasis
Sandflies
51
Classify the types of Leishmaniasis
Cutaneous - Skin ulcers - Chiclero's ulcer Mucocutaneous - Respiratory system (Upper) - Cause scarring Visceral - Black sickness - Deadly disease - Spread via lymphatics - Leishman-Donovan bodies
52
Presentation of Leishmaniasis
``` Prolonged fever Wt loss and night sweats Ulcerative lesions Skin nodules (warty) Mucosal infiltration Hyperpigmentation Pancytopenia ```
53
Investigations to confirm Leishmaniasis
Microscopy biopsy/aspirate - amastigote Leishmania skin test - >5mm rK39 Dipstick - antibodies against rK39
54
Management of Leishmaniasis
Cutaneous: Sodium stibogluconate Visceral: Amphotericin B
55
Name the types of trypanosomiasis
African - T Brucei - Sleeping sickness South American - T cruzi - Chagas disease - Incurable
56
Outline the stages of African trypanosomiasis
Stage I: Haemolymphatic - Rash - Fever - Flu like illness - Painless chancre - Lymphadenopathy - Winterbottom's sign Stage II: Meningoencephalitis - Headahce - Drowsiness - Convulsions - Coma
57
Presentation of South American Trypanosomiasis
``` Local sore Orbital/ Generlaised oedema Heart - Cardiomegaly - CCF - Arhythmia Megaoesohagus Megacolon ``` Destruction of the enteric nerves
58
Investigations of Trypanosomiasis
Giemsa statin on blood film FBC - pancytopenia ESR - elevated Serum immunoglobulins elevated (Chagas IgG ELISA) Rapid diagnostic tests - presence of specific antibodies
59
Treatment of sleeping sickness
Seek expert help Treat anaemia and infections first EARLY - IV suramin Late - Melarsopol Chagas - no cure - symptomatic
60
What causes schistosomiasis
Schistoma Blood flukes Transmitted from contaminated fresh water
61
Types of schistosomiasis
S. Haematobium (GU symptoms) S.Japonicum (intestinal and portal hypertension symptoms) S.Mansoni (as above)
62
Diagnosis of schistosomiasis
Microscopic visualisation of eggs in stool or urine
63
Treatment of schistosomiasis
Praziquantel | Anti-helminthic
64
Outline the pathology of schistosomiasis
1. Contaminated water and skin contact 2. Penetrate skin - cercarial dermatitis - swimmer's itch 3.Migration to the blood stream - flu like symptoms - abdo pain eggs laid in tissues 4. Hypersensitivity reaction - Eosinophilia 5. Chronic infection - Anaemia - Malnutrition - Obstructive uropathy - portal HTN Fibrosis, obstruction, granulomas
65
Outline the signs seen in chronic schistosomiasis
``` Haematuria Dysuria Frequency HSM Chronic bowel disease Blood stained stool ```
66
Investigations in schistosomiasis
Stool or urine microscopy - visualisation of the eggs Tissue biopsy - granulomas sure eggs Urinanalysis - haematuria FBC - eosinophillia Thickening of the bladder wall
67
Treatment of schistosomiasis
Praziquantel | Corticosteriods
68
What organism is responsible for amoebiasis
Entamoeba histolytica Tropics Spreads through ingestion of cysts in faecally contaminated food and water
69
Presentation of amoebiasis
``` Diarrhoea Dysentery (blood + mucus) Abdo tenderness Weight loss Sweating Fever Cough due to phrenic nerve irritation ```
70
Pathology of amoebiasis cess (E whistle
``` Cyst passes to small intestine Excyst to invasive trophozoite Cellular damage at the invasion site Intestinal epithelium is invaded Extra intestinal spread to the peritoneum and liver Haematogenous dissemination via portal venous system Amoebic liver abscess and brain ```
71
Investigations in amoebiasis
Stool antigen detection PCR stool or liver abscess (E histolytica DNA) Serum antibody test Stool microscopy (x3) - trophozoite and cyst with 4 nuclei - motile amoeba Liver USS - hypo echoic round lesion CXR - oval lesion
72
Treatment of amoebiasis
Nitromidazole (metronidazole + luminal agenet If abscess must aspirate
73
What organism causes Giardiasis
``` Giardia lambia (flagellated protozoan Tropical ```
74
How is giardiasis transmitted
Oral ingestion of cyst via faec-oral route Swallowing water from swimming Tap water Eating lettuce
75
A patient presents with diarrhoea which they describe as greasy and foul smelling. They also complain of frequent belching , ado bloating and pain. What do you suspect as the diagnosis?
Giardiasis
76
What investigations would you order in a case of suspected giardiasis
Stool microscopy (x3) cysts and trophozoites Stool antigen tests (ELISA) +ve cell wall String test (mucus examined for trophozoites Baseline FBC
77
Treatment of giardiasis
Metronidazole | Tinidazole
78
List the presenting symptoms of typhoid
``` High fever Dull frontal headache Dry cough Malaise Prostration Diarrhoea ```
79
Outline the investigations you would order in cases of suspected Typhoid
``` FBC: mild anaemia LFt: transaminase x2/3 Blood culture +ve Stool culture +ve Bone marrow culture+ve ```
80
List the potential complications of Typhoid fever
Chronic biliary carriage Typhoid hepatitis Bowel perforation
81
Treatment of Typhoid
ABX: Ceftriaxone and azithromycin Fluids Antipyretics
82
Complications of malaria
``` Acute renal failure Hypoglycaemia Metabolic acidosis Seizure Acute respiratory distress ssyndrome ```
83
What diseases are linked to bats
Histoplasmosis Leptospirosis VHF Rabies
84
What is MRSA
Methicillin Resistant staphylococcus aureus | Resistant to beta lactams
85
What do you treat MRSA with
Vancomycin | Teicoplanin
86
What antibiotics cause C.diff
``` Ciprofloxacin Co-amoxiclav Carbepenems Clindamycin Cephalosporins Also caused by PPI change in gut flora ```
87
What is the organism that cause glandular fever
``` EBV Mononucleosis syndrome (CMV, HIV, HSV, HBV,HCV, VZV) ```
88
Presentation of glandular fever
``` Fever Pharyngitis Lymphadenopathy Atypical lymphocytosis Fever Fatigue Depression Splenomegaly ```
89
Diagnostic test for glandular fever
Blood film: Lymphocytosis Heterophil antibody test (Monospot test): +ve at three weeks Serology for EBV IgM and IgG
90
Complications of glandular fever
Thromboytopenia Haemolytic anaemia Fulminant hepatitis Acute renal failure
91
Pathology of EBV
DNA herpes virus Predilection for B lymphocytes in the tonsils B cells spread the infection to the liver and the spleen Antibodies are produced Rapid response to T cells (atypical mononuclear cells)
92
Management of glandular fever
1. Supportive care | 2. Do not give ampicillin or amoxicillin
93
Outline the manifestations of primary herpes simplex virus
1. Genital herpes (HSV-2) 2. Ginivostomatitis 3. Eczema herpeticum 4. Herpes simplex encephalitis 5. HSV keratitis
94
Presentation of genital herpes
Flu-like prodrome Grouped vesicles and papillose around the genitals and anus Shallow ulcers (generally clear in 3 weeks) Urethral discharge Dysuria (females) Urinary retention
95
Management of genital herpes
Aciclovir If immunocompromised Famiciclovir
96
What causes chickenpox
Varicella zooster virus | Contagious febrile illness with crops of blisters at various stages
97
Outline the natural history of chickenpox
Incubation prior: 11-21d Infectivity: 4d before the rash appears and lasts until all the lesions are scabbed over (~1 week) Post infection the virus remains dormant in the dorsal root ganglion
98
VZV can remain dormant in the dorsal root ganglion for years prior to reactivation. What is this condition called and how does it present?
Shingles Pain in a dermatomal distribution Malaise Fever
99
Treatment of Shingles
Acute zoster: acyclovir 800mg 5 times/d PO 7 days Post shingles pain - Amitriptyline
100
Where is affected in ophthalmic shingles
CN V branch 1
101
Presentation of ophthalmic shingles
``` Pain Keratitis Iritis Hutchinson's sign - Nose tip involvement Blistering rash ```
102
Treatment of ophthalmic shingles
3% aciclovir ointment
103
What is the mode of transmission of CMV
Direct contact Blood transfusion Organ transplantation
104
Diagnostic tests for CMV
Serology: specific IgM (acute infection) | CMV PCR
105
Treatment of CMV
Supportive care Serious infection (immunocompromised) - Ganciclovir
106
How is CMV prevented post transplant
Weekly PCR to detect CMV antigens or Pre emptive ganciclovir
107
Name the types of TB infection
Pulmonary Tb - Active - Latent Extra Pulmonary TB
108
Outline the pathophysiology of TB
Primary TB - Naive infection with TB - Organisms multiple = GHON FOCUS - Macrophages take TB to LNS - Node + lung lesion = GHON COMPLEX - Cell mediated immunity = RANKE COMPLEX Primary Progressive TB - Appears like acute bacterial pneumonia - Mid and lower lobe consolidation - Hilar lymphadenopathy - Lymphogematgenous spread: extra pul and milary TB Latent TB - Infected but no X-ray or clinical signs Secondary TB - Reactivation of latent TB - Reduced host immunity - @ upper lobes - Casating granulomas due to hypersensitivity
109
Diagnostic tests in HIV
Latent TB - Mantoux test - cell mediated response 48-72hrs Active TB - CXR: Consolidation, Cavitation, Calcification and Fibrosis - BAL: Ziehl nielson stain, Lowstein-Jensen culture Quantiferon TB Gold - IFN gamma if previously exposed
110
Presentation of pulmonary TB
``` Cough Sputum Malaise Fever Haemotypsis Pleural effusion ```
111
Discuss the systems affected in extra pulmonary TB
``` Meningitis GU Bone (Potts) Lymph nodes Skin Peritoneal ```
112
Management of TB
1. Check colour vision, FBC, U&Es and LFT's prior to starting treatment 2. Initial phase - 8 wks 4 drugs - Rifampacin - Isoniazid - Pyrazinamide - Ethabutamol 3. Continuation phase - 16 wks 2 drugs - Rifampacin - Isoniazid DOTS
113
Discuss the side effects associated with the TB drugs in turn
RIFAMPACIN - Hepatitis ( increase LFT) - Orange discolouration of the urine and tears ISONIAZID - Hepatitis - Low WCC - Peripheral neuropathy PYRAZINAMIDE - Hepatitis - Arthalgia ETHANUTAMOL - Optic neuritis
114
What type of virus is Hep A and how is it spread
RNA virus | Faeco-oral route
115
In a patient infected with HepA what would their blood work show
``` HAV IgM HAV IgG LFT - ALT: AST (2:1 ratio) - Raised bilirubin ```
116
What type of virus is Hep E and how is it spread
RNA | Faeco-oral route
117
In a patient infected with HepE what would their blood work show
HEV IgM HEV IgM Viral PCR
118
How is Hep C spread
Blood or bodily fluid IVDU Needle stick injury
119
What investigations would you do in a patient suspected of having HepC
HCV serology - anti HCV ab - HCV IgM - HCV IgG PCR HCV RNA: treat if still detectable at >2 months LFTs - Raised AST - Rasied ALT (ratio will be greater than 1) Biopsy of the liver: degree of inflammation
120
Management of Hepatits C
1. Prevention of needle exchange programme. Alcohol avoidance 2. Screen for HCC 3. Dual therapy: pegylated IFN alpha and Ribavrin 4. Direct acting antiretrovirals Leading cause of a liver transplant in the UK
121
How is Hep B spread
DNA virus Blood and bodily fluids Vertical transmission Sexual contact
122
Outline the relation of the following components to the Hep B virus - HBsAg - Anti-HBs - HBcAG - Anti-HBc - HBeAG - Anti-HBe
HBsAg - Surface antigen - Current infection Anti-HBs - Surface antibody - indicate immunity from post exposure or immunisation HBcAg - core antigen - not used HBeAg - Envelope antigen - assessment of phase of infection Anti-HBe - evidence of immune response
123
Presentation of Hep B
Acute - prodromal - VANFAM Hepatic - can become fulminate, watch INR - hepatomegaly - jaundice - RUQ pain Chronic - >6months - Fibrosis - Cirrohosis - HCC
124
Management of Hep B
Some people clear the acute infection. Chronic infection requires treatment. It is treated to control the disease not to cure . 1. Prevention - Blood screening - Safe sex - Partner notification 2. Acute - Supportive - Notify proper officer 3. Chronic - 48 wks IFN alpha (can also give tenofovir) - 6 monthly screen for HCC