Kaposi Sarcoma

Legend
Predisposing:
Precipitating

Male (higher chance)

Immunosuppressed  

Predisposing and HIV (+)

sexual activity

Precipitating Gay
HIV (+)
Factor Idiopathic
Increased ability for
malignant cells to
Persistent/Recurrent Decreased immune
evade immune
Night Sweats Infection Tissue Damage and function
defenses and thereby
inflammation persist
Pathophysiology
Viral DNA enters the
cell
Increased
inflammation and or
Increased infections
increase proliferation
Clinical of oncogenic virus
Manifestation Synthesis of proviral
DNA damage 
DNA

Night Sweats
Diagnosis Insertion of proviral
DNA into host cell's
DNA
Disruption of tumor Insertion of actively
suppressor gene transcribed viral promoter
function sequence next to proto-
Introduction of
oncogene
oncogene

Decrease DNA repair,

decrease
control/inhibition of Proto-oncogene is
cellular division and transformed into an
decrease apoptosis oncogene

Cell death/disruption Virus enters epidermis,

of connections penetrates endings of
Purplish spots Increased risk of
between epidermal sensory and autonomic Excessive expression
uncontrolled cellular
cells nerves of oncogene
proliferation

Viremia produces a virus not held back in

Fever generalized immune check by immune
response system abnormal lesion Increased cancer risk

Virus tracks along

Damage to cell abnormal  vessel 
nerves and establishes
Nonproductive cough
lining in the lungs ;.
latent infection in local
SOB
Lesions in the lungs
ganglia (e.g. upper
Tachypnea might block part of Kaposi Sarcoma
thoracic and cervical
an airway 
ganglia) will create
inflammatory that will
infiltrate the vessels

Reduction in immune
Cell death/disruption
function leads to
of connections will create vascular
Purplish spots reactivation of latent
between epidermal mass/lesion
infection, virus tracks
cells
back out along nerves

Purplish spots
severing of
inflammatory 

creating flat macules 

subtle proliferation of
irregular vascular
channels between
normal stromal
collagen 

the extravasation of
erythrocytes and
hemosiderin into the
stroma

detection of
lymphoplasmacytic
infiltrate

worsening of
inflammatory will
made the flat macules
into plaques 

proliferating spindled
cells that form interlacing
bundles closely
approximated with blood-
filled vascular spaces 

intracellular hyaline
globules within lesion
cells

increased inflammatory
infiltrate consisting of
lymphocytes, plasma cells,
macrophages, and dendritic
cells 

severe inflammatory will

turn it into subsequently
nodular lesions which is
the tumor stage 

formation of intersecting
fascicles and sheets of
proliferating spindled
cells

Reference:

Douglas, J., et al. (2010). Kaposi Sarcoma Pathogenesis: A Triad of Viral Infection, Oncogenesis and Chronic Inflammation. National Library of Medicine. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3472629/?fbclid=IwAR281Rak429AfuODZZfn9OvDw7NGy2rQtQSMap4T5VkT_zbtMOfvey9SvL8

Sigmund, E. (2015). Retroviral Infection: Mechanisms of Oncogenesis. Calgary Guide. http://calgaryguide.ucalgary.ca/wp-content/uploads/2015/05/Retroviral-Infections-Mechanisms-of-oncogenesis.jpg

Spence, S. (2012).  Herpes Simplex Infection: Pathogenesis and Clinical FIndings. Calgary Guide. http://calgaryguide.ucalgary.ca/wp-content/uploads/2015/05/Herpes-Simplex-Virus-HSV.jpg