Brainscape's Knowledge GenomeTM

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


See full index

ID Review > HIV Diagnostics and Non-Infectious Complications > Flashcards

HIV Diagnostics and Non-Infectious Complications Flashcards

1
Q

What type of virus is HIV?

A

Lentivirus genus belonging to the family Retroviridae.

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

What is the difference between HIV-1 and HIV-2?

A

HIV-1 is responsible for the majority of infections globally. HIV-2 has a lower virulence and infectivity and is largely confined to West Africa.

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

What cells does HIV target? [3]

A
  1. CD4
  2. Dendritic cells
  3. Macrophages
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How does HIV fuse to cells?

A

gp120 with co-receptor CCR5 or CXCR4 bind to CD4

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

What increases the likelihood of HIV transmission? [3]

A

High viral load [most important]
Presence of other sexually transmitted infections (STIs) (especially those causing genital ulcerations).
High risk behaviors

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

Risk of HIV spread [NOTE]

A 
Mother-to-child transmission (without breastfeeding)	30.
Breastfeeding for 18 months 15.
Needle-sharing injection-drug use 0.67
Receptive anal intercourse	0.5
Percutaneous needlestick	0.3
Insertive anal intercourse	0.065
Insertive penile–vaginal intercourse	0.05
Receptive oral intercourse	0.01
Insertive oral intercourse	0.005
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Symptoms of acute/early HIV infection?

A

fever, malaise, myalgia, night sweats, weight loss.
Lymphadenopathy, particularly axillary, cervical, and occipital
Persistent generalized lymphadenopathy
sore throat, painful mucocutaneous ulcers
Generalized Skin Rash
Nausea, diarrhea, anorexia, weight loss.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is Persistent generalized lymphadenopathy?

A

Lymphadenopathy in at least two areas for at least 3 months.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Common neurologic presentation of acute HIV?

A

HA is the most common symptom

Aseptic meningitis, acute inflammatory demyelinating polyneuropathy, or mononeuritis multiplex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is a long term non-progressor in HIV?

A

HIV-infected individuals whose CD4+ count remains >500 cells/μL with a viral load <5000 copies/mL for at least 8 years despite not commencing ART.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is an elite controller in HIV?

A

Maintain an undetectable viral load (i.e., plasma HIV-RNA remains <50 copies/mL) without commencing ART.

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

What diagnosis prompts universal HIV testing? [7]

A 
HCV
TB
HBV
Lymphoma
Pregnancy
IVDU
STI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are Fiebig stages?

A

This is the classification of serologic events associated with acute HIV infection.

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

List the Fiebig stages

A

I RNA + [day 3-8]
II p24 Ag + [day 7-14]
III Elisa IgM + [day 10-17]
IV Western Blot +/- [Day 15-23]
V Western Blot + to p24 core and env [antibody production], no antibody to p31/32 integrase [day 47-130]
VI Same as 5 but p31/32 integrase is now positive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the first line HIV test assay?

A

ELISA testing for both HIV-1/HIV-2 antibodies as well as the p24 antigen (a capsid protein of the virus).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

If the HIV screen is positive, what is the next test in testing

A

Differentiation between HIV 1 and 2 with antibodies specific to each of the viruses.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is both HIV 1 and 2 antibody differentiation testing is negative?

A

PCR [NAT] should be done for HIV 1 and 2

If negative it is likely a false positive screen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Recommendation for breast feeding in an HIV infected mother?

A

AVOID

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

What is HIV-associated neurocognitive disorders (HAND syndrome)?

A

changes in memory, concentration, attention, and motor skills that cannot be attributed to an alternative cause

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

What are the three levels of impairment in HAND?

A

(1) asymptomatic neurocognitive impairment
(2) mild neurocognitive disorder
(3) HIV-associated dementia (HAD)

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

How dos HAD present?

A

Symptoms that wax and wane over time, including cognitive deficits, behavioral and mood changes as well as motor symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How does the mild neuroconitive disorder in HIV present?

A

Primarily memory problems and generalized slowing in processing information. Overall, cognitive deficits may be described as mental slowing with impairment in higher executive functions leading to decreased ability to perform instrumental activities of daily living (IADLs)

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

Motor signs in HAND? [4]

A

Slowness in movement, hyperreflexia, frontal release signs, and dysdiadochokinesia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Diagnosis of HAND?

A

Exclusion

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

HAND work up? [7]

A

Progressive multifocal leukoencephalopathy, malignancy, nutritional deficiencies (vitamin B12 deficiency), endocrine disorders (thyroid or adrenal dysfunction), substance abuse, psychiatric disorders or other dementia syndromes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

HAD MRI findings?

A

Symmetric, periventricular hyperintense lesions on T2-weighted sequences

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

What is CNS viral escape syndrome

A

HIV replication in the CNS leading to neurocognitive symptoms in patents who are virally suppressed on ART. Most patients have viral drug resistance in the CSF.

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

Work up and mgmt for CNS viral escape syndrome?

A

CSF HIV RNA must be evaluated for resistance with regimen based on results.
–> Typically efavirenz is avoided.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is Distal symmetric peripheral neuropathies (DSPN)?

A

Symmetric, bilateral pattern of diminished sensation and reflexes typically starting in the toes spreading proximally in the lower extremities.

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

Drugs associated with DSPN? [8]

A

didanosine and stavudine, dapsone, isoniazid, ethambutol, nevirapine, thalidomide, and vincristine

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

Risk factors for DSPN? [4]

A

Poorly controlled HIV, age >50 years, metabolic syndrome, and substance abuse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

DSPN presentation?

A

numbness and tingling in the lower extremities, decreased sensation in a stocking distribution and reduced deep tendon reflexes in the lower extremities

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

DSPN diagnosis?

A

Clinical

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

What is Vascular myelopathy

A

Vacuolization of the lateral and posterior columns of the thoracic spine leading to a spastic paraparesis, loss of sensation, and urinary incontinence.

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

Describe the relationship between ART and stroke?

A

Long term ART use may also lead to increased risk of stroke due to endothelial toxicity and vascular dysfunction.

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

Describe the rash of acute HIV exanthem and enanthem

A

non-pruritic rash involving the upper trunk, proximal limbs, and potentially the palms and soles. It can be seen in up to half of patients with acute infection. It typically resolves in 1–2 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is eosinophilic folliculitis?

A

Typically described in patients with advanced disease and is a pruritic skin eruption of follicular papules or pustules, predominantly located on the scalp, face, neck, and upper chest

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

Pathogenesis of eosinophilic folliculitis?

A

Infection (with bacteria, Pityrosporum yeast, or Demodex mites) or an autoimmune reaction to sebocytes.

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

Presentation of eosinophilic folliculitis?

A

Recurrent, pruritic, erythematous follicular papules and rare pustules (3–5 mm diameter) on locations of the body with more sebaceous glands.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Diagnosis of eosinophilic folliculitis?

A

Labs: High IgE and eosinophil levels
Dx: Punch biopsy

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

Treatment of HIV associated eosinophilic folliculitis? [3]

A

ART (resulting in resolution for most) and symptomatic management with topical corticosteroids and oral antihistamines.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Important endocrine side effect of ritonavir?

A

Cushing syndrome in patients also given any steroid; even a steroid as mild as nasal or inhaled fluticasone.

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

How might HIV lead to graves?

A

Consequence of IRIS 1-2 years following ART initation

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

What comorbid conditions with HIV are a/w low testosterone levels? [3]

A

advanced disease, protease inhibitors (PIs), co-infection with hepatitis C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Work up of suspected testosterone def in HIV patient?

A
  1. AM testosterone
  2. Free testosterone
  3. LH and FSH levels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

How will primary and secondary hypogonadism look on labs

A

Primary: LH and FSH are high
Secondary: LH and FSH are low or inappropriately normal

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

Work up of primary hypogonadism in HIV patient [3]

A

prolactin level, iron studies, and evaluation of other hormones that reflect anterior pituitary dysfunction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Work up of secondary hypogonadism in HIV patient

A

OI

Scrotal US

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Mgmgt of hypogonadism

A
  1. ART

if no improvement testosterone

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

How does HIV lead to bone-mineral dysfunction

A
  1. HIV infection which is independently associated with lower bone mineral densities due to proinflammatory cytokines increasing osteoclastic activity.
  2. ART [specifically TDF]
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What HIV medication is a/w vit D def?

A

efavirenz

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

In PLWH who should get DEXA scans?

A

all HIV-infected postmenopausal women and men >50 years of age.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Work up if you find OA or osteopenia? [5]

A

testosterone levels, PTH, TSH, 25-OH-vitamin D, and 24-hour urine calcium.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Risk factors for HIV osteonecrosis? [5]

A

White race, male, CD4 count <200 cells/μL, prior osteonecrosis, prior fracture, and having an AIDS-defining illness, prior PI use, EtOH, steroid use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Osteonecrosis diagnosis?

A

MRI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

How does osteonecrosis present?

A

Joint pain. Classically in the hip but all joints may be effected.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What is AIDS wasting syndrome?

A

Weight loss over 3 months of more than 10% body weight with a disproportionate loss of lean body mass and sparing of body fat. Predictor of poor outcomes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What lab is present with AIDS wasting syndrome?

A

Elevated triglycerides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Treatment of AIDs wasting syndrome?

A

ART.

60
Q

What is lipoatrophy?

A

Loss of subcutaneous fat in the face (buccal and/or temporal fat pads), arms, legs, abdomen, and/or buttocks. However, lean tissue mass is typically spared

61
Q

HIV medications that cause lipoatrophy? [5]

A

Older medications; stavudine and zidovidine

efavirenz, rilpivirine, and PIs may increase risk

62
Q

Treatment of lipoatrophy?

A
  1. Change ART

2. In DM addition of thiazolidinediones

63
Q

What is fat accumulation in HIV?

A

Excess of visceral adipose fat with normal subcutaneous fat resulting in increased abdominal girth. May also occur around the dorsocervical area (i.e., “Buffalo hump”), trunk, and upper chest. This can also be seen in visceral organs like the liver.

64
Q

Diagnosis of fat accumulation?

A

physical exam findings (abdominal circumference in men >102 cm and women >88 cm).

65
Q

Tx of fat accumulation?

A

Treatment consists of diet, exercise, and treatment of type 2 diabetes mellitus. Metformin

66
Q

What condition in HIV might metformin make worse?

A

Lipoatrophy

67
Q

Infections in HIV that lead to hypoplastic anemia? [2]

A

Parvo

MAC

68
Q

HIV medication that causes macrocytic anemia?

A

zidovudine

69
Q

HIV associated medications that can lead to neutropenia? [4]

A

zidovudine, TMP–SMX, ganciclovir, and hydroxyurea

70
Q

Infections in HIV that lead to neutropenia? [2]

A

EBV, B19

71
Q

How might HIV reduce platelet counts? [2]

A
  1. HIV infects megakaryocytes

2. IgG cross reactivity between platelet glycoprotein complex (GP)IIb/IIIa and HIV envelope glycoproteins GP 120/120.

72
Q

Diagnosis of HIV associated thrombocytopenia?

A

Exclusion

73
Q

Treatment of HIV associated thrombocytopenia? [8]

A
  1. ART
  2. steroids
  3. Intravenous immune globulin, and anti-D immune globulin.
    Refractory cases: dapsone, interferon alfa, vincristine, and splenectomy.
74
Q

Who gets HIV associated TTP

A

Advanced HIV, often co-infected with Hep C

75
Q

Etiology of HIV associated TTP

A

HIV infection of endothelial cells leading to vWF release and depletion of ADAMTS13

76
Q

Diagnosis of HIV associated TTP?

A

Exclusion

Shigella and E.coli ruled out

77
Q

Treatment of HIV associated TTP?

A

ART

Plasma exchange

78
Q

What is HIVAN?

A

HIV-associated nephropathy
Collapsing form of segmental glomerulosclerosis and can be seen after seroconversion and throughout disease progression, but is more common in patients with advanced disease. More common in African Americans

79
Q

Presentation of HIVAN?

A

nephrotic range proteinuria

rapid decline in kidney function

80
Q

Diagnosis of HIVAN?

A

Kidney biopsy

81
Q

Treatment of HIVAN

A
  1. ART
  2. ACE/ARB
  3. Nephro referral
82
Q

What is fanconi syndrome

A

Loss of the following in the urine..

  1. Protein
  2. Glucose
  3. Potassium
  4. Phos
  5. Aminoacids
  6. Bicarbonate

NOTE: NOT ALL MAY BE PRESENT AT ONCE [may be only a few]

83
Q

What HIV medications increase risk for cardiovascular events?

A

lopinavir–ritonavir and indinavir

84
Q

Etiology of pericarditis in HIV?

A
  1. Bacteria
  2. Fungal
  3. Cancer
85
Q

What is HIV-associated pulmonary hypertension?

A

Result in part from vascular changes resulting in remodeling of the media and adventitia of the arterial pulmonary tree, the extracellular matrix and plexiform lesions induced by infection with HIV-1.

86
Q

Treatment of HIV-associated pulmonary hypertension?

A

epoprostenol, inhaled prostacyclin, inhaled iloprost, bosentan, and sildenafil in addition to initiation of ART.

87
Q

What is Nonspecific interstitial pneumonitis in HIV?

A

Seen in PLWH with CD4 <200

Prevalence and etiology is not known

88
Q

Diagnosis of nonspecific interstitial pneumonitis in HIV?

A

Exclusion of other infections

89
Q

Clinical manifestations of Lymphocytic interstitial pneumonitis in HIV patients?

A

diffuse lymphadenopathy
peripheral CD8+ T lymphocytosis
Imaging findings vary in chest radiographs from normal to diffuse alveolar, nodular, or interstitial infiltration.

90
Q

Diagnosis of Lymphocytic interstitial pneumonitis?

A

Exclusion of a pathogen on biopsy. Typically lymphocytic infiltration is seen and plasma cells. Septal infiltration differentiates LIP from NIP.

91
Q

Treatment of LIP?

A

ART

92
Q

Treatment of COP?

A

ART, steroids

93
Q

What is HIV enteropathy?

A

HIV infection of enterocytes, leading to loss of gastrointestinal mucosa and increased permeability. Also, faster intestinal transit times may result from HIV directly damaging the autonomic nerves of the intestine

94
Q

Diagnosis of HIV enteropathy?

A

Exclusion, exclude infections

95
Q

NOTE:

A

ART may cause diarrhea that is self limiting over 8-12 weeks

96
Q

Cause of salivary gland enlargement in HIV patient?

A

Cysts or lymphocytic process that is different than sjogrens

97
Q

Treatment of salivary gland disease and xerostomia in HIV?

A

Salivary gland stimulation

98
Q

What is Diffuse interstitial lymphocytosis syndrome (DILS)?

A

characterized by CD8+ T-cell infiltration of multiple organs can manifest with bilateral parotid gland. lung infiltration as a lymphocytic interstitial pneumonia may occur, other organ systems that may be affected include nervous system, liver, kidneys, and digestive tract.

99
Q

Treatment of DILS?

A

ART

Steroids as 2nd line

100
Q

Cause of acalculous cholecystitis in HIV pt?

A

Associated with infection with CMV or Cryptosporidium.

101
Q

What is AIDS cholangiopathy?

A

Dilated intra- and extrahepatic biliary ducts and presents with right upper quadrant pain, icteric sclera, and elevated alkaline phosphatase.

102
Q

Cause of AIDS cholangiopathy?

A

Advanced AIDs

CMV or cryptosporidium less commonly

103
Q

Presentation of Kaposi sarcoma?

A

Cutaneous disease appears as red or violet macules, papules, or nodules in various sizes up to several centimeters in diameter. Extracutaneous involvement can be respiratory, mucosal, or GI. Oral involvement most commonly involves the palate or gingiva and is present in about a third of PLWH with KS.

104
Q

Diagnosis of KS?

A

Biopsy, CXR and stool for occult blood to r/out lung and GI involvement.

105
Q

Treatment of KS?

A

ART

liposomal doxorubicin or liposomal daunorubicin if progressive or visceral disease

106
Q

What is Multicentric Castleman’s disease?

A

Lymphoproliferative disorder characterized by angiofollicular lymph node hyperplasia associated with HIV and human herpesvirus 8 (HHV-8) infection as well as other malignancies including concomitant KS.

107
Q

Presentation of Multicentric Castleman’s disease?

A

Fever, fatigue, generalized lymphadenopathy, hepatosplenomegaly, and pancytopenia. Usually non-white men age 50-65 with CD4 >200

108
Q

Diagnosis of Castleman’s?

A

Biopsy

109
Q

Treatment of Castleman

A

Steroids

Rituximab if refectory

110
Q

What infections with HIV puts you at risk for Non-Hodgkin lymphoma?

A

HHV-8, EBV

111
Q

Risk factors for PLWH to develop Non-Hodgkin lymphoma [5]

A 
CD4 counts <100 cells/μL 
high HIV viral loads
family history
Not being on ART. 
co-infected with hepatitis B or C
112
Q

Treatment of Non-Hodgkin lymphoma?

A

cyclophosphamide, doxorubicin, vincristine (Oncovin), and prednisone (CHOP) or CHOP–rituximab (CHOP-R) with concurrent initiation of ART.

113
Q

What is Primary effusion lymphoma?

A

Rare type of NHL that occurs exclusively in PLWH
A/w HHV-8
Grows in body cavities (pleural, pericardial, and peritoneal) as lymphomatous effusions that are not associated with a mass.

114
Q

Diagnosis of primary effusion lymphoma?

A

cytology of the pleural fluid.

115
Q

What are the AIDS related lyphomas? [4]

A

Diffuse large B cell lymphoma
Burkitt’s lymphoma
Plasmablastic lymphoma
Hodgkin lymphoma

116
Q

Describe the pathology of Diffuse large B cell lymphoma

A

large, atypical lymphoid patterns that express pan-B cell antigens.

117
Q

Describe the pathology of Burkitt’s lymphoma

A

starry-sky” pattern with prominent cytoplasmic vacuoles in monomorphic, medium-sized cells with multiple nuclei.

118
Q

Presentation of Plasmablastic lymphoma

A

presents in the oral cavity and is driven by HHV-8 infection. They are very aggressive and have a poor prognosis.

119
Q

Describe the pathology of Hodgkin lymphoma

A

Reed–Sternberg cells seen

120
Q

Presentation of Primary central nervous system lymphoma

A

confusion, memory loss, focal neurologic deficits, and seizures as well as B symptoms

121
Q

What will imaging show with a primary CNS lymphoma?

A

solitary or multiple mass lesions may be seen, Lesions also may be ring enhancing or have enhancement that is irregular or patchy.

122
Q

How does primary CNS lymphoma differ from toxo on imaging? [3]

A
  1. Toxo will have multiple lesions, CNS lymphoma is typically single.
  2. CNS lymphoma is large [typically >4cm]
  3. CNS lymphoma is typically NOT in the posterior fossa
123
Q

Diagnosis of primary CNS lymphoma?

A

LP if no mass effect [only helpful in 15% of cases]

Brain biopsy is gold standard

124
Q

Treatment of primary CNS lymphoma?

A

Methotrexate

125
Q

Presentation of anal cancer?

A

itching, rectal bleeding or discharge, and tenesmus; however, most patients are asymptomatic.

126
Q

Anal cancer screening in PLWH? [3]

A

Anal cytology among the following risk groups:
MSM
women with history of anal intercourse or abnormal cervical Pap smears,
those with genital warts.

127
Q

Treatment for anal cancer if small?

A

<1cm base: topical therapy with trichloroacetic acid and imiquimod

128
Q

Treatment for anal cancer if larger?

A

infrared coagulation and anoscopy-directed lesion ablation

129
Q

What is ragged red fiber disease?

A

This is ZDV induced myopathy [nucleoside induced myopathy]. Rare now, used to be due to pts being iatrogenically overdosed with ZDV

130
Q

Treatment of methhemoglobinemia?

A

Stop offending drug [often dapsone]

Methylene blue if methemoglobin level is >30%

131
Q

In whom does methylene blue not work?

A

Those with G6PD def

132
Q

How might early treatment of acute retroviral syndrome complicate HIV testing?

A

Early treatment may blunt humoral immune response and confirmatory assay may become unreliable.

133
Q

How is HIV-2 different from HIV 1?

A

HIV-2 is..

  1. Less pathogenic
  2. Less likely to transmit to baby
  3. Less likely to have kaposi sarcoma
  4. Instrinsically resistant to NNRTI and fusion drugs
134
Q

Where is HTLV-1 prevelant?

A

Japan and South East Asia [30-50%]
Indigenous tribes in Australia [up to 40%]
Caribbean

135
Q

How is HTLV-1 transmitted? [4]

A

Sex
Breastfeeding
IVDU
Drug transfusion

136
Q

How is HTLV-1 diagnosed?

A

Blood serology

ELISA with confirmatory western blot

137
Q

What disease does HTLV-2 cause?

A

NONE!

It is a distractor.

138
Q

How might HTLV-1 present

A 
95% asymptomatic
In a patient from the right endemic area..
Recurrent pneumonia with bronchiectasis
TB, MAC, leprosy
PCP
Recurrent strongyloides
Scabies, Norwegian scabies
Hypercalcemia + lytic bone lesions
Uveitis
Lymphocytic pneumonitis
139
Q

What malignancy may complication HTLV-1?

A

Acute T-cell leukemia

140
Q

Treatment of Acute T-cell leukemia in HTLV-1?

A

AZT+lfn
Lenalidamide
Mogamulizumab

141
Q

What virus causes tropical spastic paraparesis?

A

HTLV-1

142
Q

Presentation of tropical spastic paraparesis?

A

Spastic paraparesis with lower > upper
Proximal > distal muscles
There is hyperreflexia, urinary incontinence
+ Babinski reflex

143
Q

Who gets tropical spastic paraparesis?

A

Jamacians [Caribbeans]

F > M

144
Q

Treatment of HTLV-1 TSP/HAM?

A

Corticosteroids may slow progression

–> ART is NOT effective.

145
Q

What is a “flower cell”

A

Lymphocytes with HTLV provirus present
Occurs in higher frequency with acute t-cell leukemia and HAM/TSP. Seen on peripheral blood smear.
NOT associated with disease

146
Q

NOTE:

A

Home HIV testing may have false negative results in the first 3 months of infection.

147
Q

How often should those on PrEP be followed

A

Every 3 months with HIV testing

ID Review (25 decks)

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