Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Infectious Diseases > ID I > Flashcards

ID I Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How is HIV transmitted

A

Blood
Sexual
Vertical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Treatment aim of HIV

A

CD4 > 400cells/mm3

Viral load = 0

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What make up AIDS related complex

A 
Pyrexia
Night sweats 
Diarrhoea
Weight loss 
- oral hairy leukoplakia
- oral candida
- herpes zoster
- herpes simplex
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

List AIDS defining illnesses

A 
PCP
CMV
TB
Sentinel tumours (Kaposi's sarcoma, lymphoma)
HIV becomes AIDS in 5-10 years
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Name and state the side effects of NRTI

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Name and state the side effects of NNRTI

A

Nevirapine
Rash
Liver toxicity
Drug interactions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Name and state the side effects of PI

A

Lopinavir
GI disturbance
Diarrhoea
Peripheral neuropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Barriers to compliance with HIV

A

Social Ecconomic class
Social support
Stigma of HIV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Name the types of malaria

A 
P.Falciparum 
P.Vivax
P.Ovale
P.Malariae
P.Knowlesi
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Outline the pathology associated with Malaria

A
  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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Primary prevention in Malaria

A 
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Malaria symptoms

A 
Fever paroxysms 
Chill and rigors followed by fever and sweats 
Headache 
Weakness
Myalgia
Arthralgia
Anorexia 
Diarrhoea
Jaundice 
HSM
Pallor
Tacycardia
Hypotension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Investigations in Malaria

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Management of Malaria

A

Primaquine single dose

Falciparum

  • Chloroquine (sensitive)
  • Artesunate + mefloquine
  • Quinine sulfate + doxycycline

IV Severe Infection
- Artesunate + fluid management + airway support

Ovale/Vivax

  • Choroquine
  • Hydroxychloroquine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Complication of Malaria

A 
Acute renal failure 
Hypoglycaemia 
Metabolic acidosis 
Seizure 
Acute resp distress syndrome due to pulmonary oedema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What organism causes syphilis

A

Spirochaete treponema pallidum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Classify syphilis

A
  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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Investigations for syphilis

A

Dark ground microscopy of swab: coiled spirochaete
Serum T pallidum particle agglutination (+ve lifelong)
LP/CSF analysis
CXR (widened aortic root)
ECHO (aortic regurgitation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Treatment of syphilis

A

IM benzylpenicillin + prednisolone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What causes viral haemorrhagic fevers

A 
5 types of RNA virus 
Filovirus: Ebola and Marburg 
Flavivirus:
- Yellow fever
- Zika virus 
- Japanese encephalitis 
- Tick borne encephalitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Pathology of viral haemorrhagic fevers

A 
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Warning signs of a potential viral haemorrhagic fever

A

Febrile illness
Foreign travel or contact
Exposure to rodents, bats, insects
Flu-like symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Presentation of a viral haemorrhagic fever

A 
Sudden headache 
Pleuritic pain 
Backache 
Myalgia 
Conjunctivitis 
Dehydration 
Facial flushing 
High temperature 
Bleeding 
Renal failure 
Encephalitis 
Coma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Investigations for viral haemorrhagic fever

A 
FBC 
- leukopenia
- thrombocytopenia 
LFT
- elevated transaminases

Coagulation screen

  • PTT
  • INR
  • clotting times prolonged
  • evidence of DIC (high D dimer and fibrinogen low)

PT-PCR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Signs of altered vascular permeability

A 
Coagulopathy 
Haemorrhagic complications (hepatic damage) 
Myocarditis 
Encephalitis 
Multi-system organ failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Management of viral haemorrhagic fevers

A 
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What organism causes Dengue fever and how is it spread

A

Arbovirus

Spread by the aides mosquitp

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Classify the different types of Dengue fever

A

Primary infection
- Benign in nature

Secondary infection

  • Dengue haemorrhagic fever
  • Dengue shock syndrome
  • Vascular leak (hypoalbuminaemia and pleural effusions, ascites)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Presentation of Dengue fever

A

Flu-like illness (>40 degree)
Rash (maculopapular)
Flushing
Retro-orbital pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Presentation of Dengue haemorrhage fever

A

Widespread effusions

  • pleuritis CP
  • Dyspnoea
  • Cough

DIC

Hepatomegaly

Can cause circulatory collapse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Investigations of Dengue fever

A

FBC

  • Elevated HCT
  • Leukopenia
  • Thrombocytopenia

LFT

  • Deranged (high)
  • Albumin (low)

Serology

  • +ve IgM
  • +ve IgG
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Treatment of Dengue fever

A 
Oral/ IV fluids 
Supportive care 
Antipyretics 
Notification 
Beware of fluid overload
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Exclusion criteria for Dengue

A

Symptoms start > 2 weeks post leaving a Dengue area

Fever lasts > 2 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What causes Leishmaniasis

A

Sandflies

51
Q

Classify the types of Leishmaniasis

A

Cutaneous

  • Skin ulcers
  • Chiclero’s ulcer

Mucocutaneous

  • Respiratory system (Upper)
  • Cause scarring

Visceral

  • Black sickness
  • Deadly disease
  • Spread via lymphatics
  • Leishman-Donovan bodies
52
Q

Presentation of Leishmaniasis

A 
Prolonged fever 
Wt loss and night sweats 
Ulcerative lesions
Skin nodules (warty)
Mucosal infiltration 
Hyperpigmentation 
Pancytopenia
53
Q

Investigations to confirm Leishmaniasis

A

Microscopy biopsy/aspirate
- amastigote

Leishmania skin test
- >5mm

rK39 Dipstick
- antibodies against rK39

54
Q

Management of Leishmaniasis

A

Cutaneous: Sodium stibogluconate

Visceral: Amphotericin B

55
Q

Name the types of trypanosomiasis

A

African

  • T Brucei
  • Sleeping sickness

South American

  • T cruzi
  • Chagas disease
  • Incurable
56
Q

Outline the stages of African trypanosomiasis

A

Stage I: Haemolymphatic

  • Rash
  • Fever
  • Flu like illness
  • Painless chancre
  • Lymphadenopathy
  • Winterbottom’s sign

Stage II: Meningoencephalitis

  • Headahce
  • Drowsiness
  • Convulsions
  • Coma
57
Q

Presentation of South American Trypanosomiasis

A 
Local sore
Orbital/ Generlaised oedema 
Heart 
- Cardiomegaly 
- CCF
- Arhythmia 
Megaoesohagus 
Megacolon

Destruction of the enteric nerves

58
Q

Investigations of Trypanosomiasis

A

Giemsa statin on blood film
FBC
- pancytopenia

ESR
- elevated

Serum immunoglobulins elevated (Chagas IgG ELISA)

Rapid diagnostic tests
- presence of specific antibodies

59
Q

Treatment of sleeping sickness

A

Seek expert help
Treat anaemia and infections first
EARLY
- IV suramin

Late
- Melarsopol

Chagas

  • no cure
  • symptomatic
60
Q

What causes schistosomiasis

A

Schistoma
Blood flukes
Transmitted from contaminated fresh water

61
Q

Types of schistosomiasis

A

S. Haematobium (GU symptoms)
S.Japonicum (intestinal and portal hypertension symptoms)
S.Mansoni (as above)

62
Q

Diagnosis of schistosomiasis

A

Microscopic visualisation of eggs in stool or urine

63
Q

Treatment of schistosomiasis

A

Praziquantel

Anti-helminthic

64
Q

Outline the pathology of schistosomiasis

A
  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

  1. Hypersensitivity reaction
    - Eosinophilia
  2. Chronic infection
    - Anaemia
    - Malnutrition
    - Obstructive uropathy
    - portal HTN

Fibrosis, obstruction, granulomas

65
Q

Outline the signs seen in chronic schistosomiasis

A 
Haematuria 
Dysuria 
Frequency 
HSM
Chronic bowel disease 
Blood stained stool
66
Q

Investigations in schistosomiasis

A

Stool or urine microscopy
- visualisation of the eggs

Tissue biopsy
- granulomas sure eggs

Urinanalysis
- haematuria

FBC
- eosinophillia

Thickening of the bladder wall

67
Q

Treatment of schistosomiasis

A

Praziquantel

Corticosteriods

68
Q

What organism is responsible for amoebiasis

A

Entamoeba histolytica
Tropics
Spreads through ingestion of cysts in faecally contaminated food and water

69
Q

Presentation of amoebiasis

A 
Diarrhoea 
Dysentery (blood + mucus)
Abdo tenderness
Weight loss
Sweating 
Fever 
Cough due to phrenic nerve irritation
70
Q

Pathology of amoebiasis cess (E whistle

A 
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
Q

Investigations in amoebiasis

A

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
Q

Treatment of amoebiasis

A

Nitromidazole
(metronidazole + luminal agenet
If abscess must aspirate

73
Q

What organism causes Giardiasis

A 
Giardia lambia (flagellated protozoan 
Tropical
74
Q

How is giardiasis transmitted

A

Oral ingestion of cyst via faec-oral route
Swallowing water from swimming
Tap water
Eating lettuce

75
Q

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?

A

Giardiasis

76
Q

What investigations would you order in a case of suspected giardiasis

A

Stool microscopy (x3) cysts and trophozoites
Stool antigen tests (ELISA) +ve cell wall
String test (mucus examined for trophozoites
Baseline FBC

77
Q

Treatment of giardiasis

A

Metronidazole

Tinidazole

78
Q

List the presenting symptoms of typhoid

A 
High fever 
Dull frontal headache 
Dry cough 
Malaise 
Prostration 
Diarrhoea
79
Q

Outline the investigations you would order in cases of suspected Typhoid

A 
FBC: mild anaemia
LFt: transaminase x2/3
Blood culture +ve
Stool culture +ve
Bone marrow culture+ve
80
Q

List the potential complications of Typhoid fever

A

Chronic biliary carriage
Typhoid hepatitis
Bowel perforation

81
Q

Treatment of Typhoid

A

ABX: Ceftriaxone and azithromycin
Fluids
Antipyretics

82
Q

Complications of malaria

A 
Acute renal failure 
Hypoglycaemia 
Metabolic acidosis 
Seizure 
Acute respiratory distress ssyndrome
83
Q

What diseases are linked to bats

A

Histoplasmosis
Leptospirosis
VHF
Rabies

84
Q

What is MRSA

A

Methicillin Resistant staphylococcus aureus

Resistant to beta lactams

85
Q

What do you treat MRSA with

A

Vancomycin

Teicoplanin

86
Q

What antibiotics cause C.diff

A 
Ciprofloxacin 
Co-amoxiclav
Carbepenems 
Clindamycin 
Cephalosporins 
Also caused by PPI change in gut flora
87
Q

What is the organism that cause glandular fever

A 
EBV
Mononucleosis syndrome (CMV, HIV, HSV, HBV,HCV, VZV)
88
Q

Presentation of glandular fever

A 
Fever 
Pharyngitis 
Lymphadenopathy 
Atypical lymphocytosis 
Fever
Fatigue 
Depression 
Splenomegaly
89
Q

Diagnostic test for glandular fever

A

Blood film: Lymphocytosis
Heterophil antibody test (Monospot test): +ve at three weeks
Serology for EBV
IgM and IgG

90
Q

Complications of glandular fever

A

Thromboytopenia
Haemolytic anaemia
Fulminant hepatitis
Acute renal failure

91
Q

Pathology of EBV

A

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
Q

Management of glandular fever

A
  1. Supportive care

2. Do not give ampicillin or amoxicillin

93
Q

Outline the manifestations of primary herpes simplex virus

A
  1. Genital herpes (HSV-2)
  2. Ginivostomatitis
  3. Eczema herpeticum
  4. Herpes simplex encephalitis
  5. HSV keratitis
94
Q

Presentation of genital herpes

A

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
Q

Management of genital herpes

A

Aciclovir

If immunocompromised
Famiciclovir

96
Q

What causes chickenpox

A

Varicella zooster virus

Contagious febrile illness with crops of blisters at various stages

97
Q

Outline the natural history of chickenpox

A

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
Q

VZV can remain dormant in the dorsal root ganglion for years prior to reactivation. What is this condition called and how does it present?

A

Shingles
Pain in a dermatomal distribution
Malaise
Fever

99
Q

Treatment of Shingles

A

Acute zoster: acyclovir 800mg 5 times/d PO 7 days
Post shingles pain
- Amitriptyline

100
Q

Where is affected in ophthalmic shingles

A

CN V branch 1

101
Q

Presentation of ophthalmic shingles

A 
Pain 
Keratitis 
Iritis 
Hutchinson's sign
- Nose tip involvement 
Blistering rash
102
Q

Treatment of ophthalmic shingles

A

3% aciclovir ointment

103
Q

What is the mode of transmission of CMV

A

Direct contact
Blood transfusion
Organ transplantation

104
Q

Diagnostic tests for CMV

A

Serology: specific IgM (acute infection)

CMV PCR

105
Q

Treatment of CMV

A

Supportive care
Serious infection (immunocompromised)
- Ganciclovir

106
Q

How is CMV prevented post transplant

A

Weekly PCR to detect CMV antigens
or
Pre emptive ganciclovir

107
Q

Name the types of TB infection

A

Pulmonary Tb

  • Active
  • Latent

Extra Pulmonary TB

108
Q

Outline the pathophysiology of TB

A

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
Q

Diagnostic tests in HIV

A

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
Q

Presentation of pulmonary TB

A 
Cough 
Sputum 
Malaise 
Fever 
Haemotypsis 
Pleural effusion
111
Q

Discuss the systems affected in extra pulmonary TB

A 
Meningitis 
GU
Bone (Potts)
Lymph nodes 
Skin 
Peritoneal
112
Q

Management of TB

A
  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
Q

Discuss the side effects associated with the TB drugs in turn

A

RIFAMPACIN

  • Hepatitis ( increase LFT)
  • Orange discolouration of the urine and tears

ISONIAZID

  • Hepatitis
  • Low WCC
  • Peripheral neuropathy

PYRAZINAMIDE

  • Hepatitis
  • Arthalgia

ETHANUTAMOL
- Optic neuritis

114
Q

What type of virus is Hep A and how is it spread

A

RNA virus

Faeco-oral route

115
Q

In a patient infected with HepA what would their blood work show

A 
HAV IgM
HAV IgG
LFT
- ALT: AST (2:1 ratio)
- Raised bilirubin
116
Q

What type of virus is Hep E and how is it spread

A

RNA

Faeco-oral route

117
Q

In a patient infected with HepE what would their blood work show

A

HEV IgM
HEV IgM
Viral PCR

118
Q

How is Hep C spread

A

Blood or bodily fluid
IVDU
Needle stick injury

119
Q

What investigations would you do in a patient suspected of having HepC

A

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
Q

Management of Hepatits C

A
  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
Q

How is Hep B spread

A

DNA virus
Blood and bodily fluids
Vertical transmission
Sexual contact

122
Q

Outline the relation of the following components to the Hep B virus

  • HBsAg
  • Anti-HBs
  • HBcAG
  • Anti-HBc
  • HBeAG
  • Anti-HBe
A

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
Q

Presentation of Hep B

A

Acute

  • prodromal
  • VANFAM

Hepatic

  • can become fulminate, watch INR
  • hepatomegaly
  • jaundice
  • RUQ pain

Chronic

  • > 6months
  • Fibrosis
  • Cirrohosis
  • HCC
124
Q

Management of Hep B

A

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

Infectious Diseases (1 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions