hello everyone welcome back to this
short tutorial from pathology Made
Simple at IOP pathology.com and
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you'll be having practice sessions via
violia so in continuation with the
autoimmune diseases series we were
talking about SLE right so we had
discussed about the autoantibodies
involved inle we have discussed about
the pathogenesis and mechanisms of
tissue injury in and now let's learn
about the various morphological features
of so remember the morphology ofle is
extremely variable the characteristic
lesions as we have learned results from
immune complex deposition in various
tissues and organs like the blood
vessels kidneys connective tissue and
skin now let's talk about the
morphological features in these tissues
and organs where there is immune complex
deposition firstly blood vessels the
characteristic feature ofle involving
the blood vessels is acute necrotizing
vasculitis you know it involves small
blood vessels particularly the
capillaries small arteries and
arterioles it can be present in any
tissue of the body but remember the
large vessel necrotizing vasculitis is
less common as compared to that of small
vessel necrotizing vasculitis you can at
times see thrombotic micro
angiopathy so morphological features in
acute stage include as we know it is
acute vasculitis meaning there will be
neutrophilic infiltration in the vessel
wall along with necrosis of the vessel
wall right so this vessel wall necrosis
when it combines with the deposits of
immune complexes the complement and
plasma protein it results in somewhat
smudgy eosinophilic area of tissue
destruction which is referred to as
fibrinoid necrosis so we look for
neutrophilic infiltration as well as
fibrinoid necrosis in the vessel walls
particularly the small blood vessels in
The Chronic stage what really happens is
that the vessels the blood vessels
undergo fibrous thickening causing
significant narrowing of the Lumen and
the consequences thereof so moving on to
understanding the morphological features
of kidney clinically significant renal
involvement happens in 50% of patients
with systemic Luper theosis and the
lesions in kidney can be categorized
into glomular lesions and tubulo
intertial regions glom regions are
referred to as glom nephritis and tub
interstitial are referred to as tubulo
interal nephritis so let's learn about
glomular lesions that's because of again
deposition of immune complexes and these
deposits can be in the glomular basement
membrane it can be in the m tangum and
sometimes throughout the glomas and
rightly the glomerular Legions are
referred to as lupus nephritis right so
this lupus nephritis has six different
morphological patterns starting from
class one to class six see the class one
is the least common pattern and the
class four is the most common pattern so
let's learn about different patterns in
lupus nephritis so I told you class one
to class six see the class one is
referred to as minimal mangial lupus
nefritis so as I told you earlier this
is the least common pattern where the
immune complex deposition is seen in the
mangium right there will be no
structural changes in the light
microscopic examination that means h&
stained sections do not show any
morphological features but then you do
find immune complex deposition when you
do a immunofluoresence and electron
microscopic examination the class two is
referred to as mangel proliferative
lupus nephritis okay as the name says
there will be proliferation of mangial
cells as well as accumulation of Matrix
in the Mangum that's a mangel matrix
okay so this is this know Pas stain
which shows the proliferation of the
meangel cells as well as some amount of
mangel Matrix accumulation remember
there will be no involvement of the
glomular capillaries that means the
endothelium of the glomular capillar is
not involved it's purely mangial imof
fluoresence and electron microscopy do
demonstrate granular mangial deposite of
imunoglobulin and complement so the
class three is referred to as focal
lupus nephritis so when we say focal it
means involvement of less than 50% of
the glomi okay among the GL glom
involved it can be segmental or Global
segmental meaning only the portion of
the glomas is involved Global means the
entire glomas is involved right see the
entire glom involvement in less than 50%
of all glom is focus lupus nefritis
which is a global pattern so what do you
see you find there will be swelling and
proliferation of the endothelial cell of
the capillaries as well as the mangial
cells right so there is proliferation of
endothelial and the mangel along with
infiltration by the lucos sites there
can be capillary wall necrosis you can
see some amount ofil in thrombi in few
of these blood vessels rarely very
rarely if the proliferation is too much
you can see cresant formation as well
right so that's type three now moving on
to class four which we told it is the
most common type and it is referred to
as diffuse lupus nephritis it's the most
common most severe which means diffuse
focal meaning less than 50% diffuse is
more than that right so this is the most
common and the most severe form of lupus
nephritis where you find proliferation
of the endothelial that's of capillary
lining proliferation of the meangel as
well as proliferation of the epithelial
cells lining The Bowman capsule right
Bowman space so you find proliferation
of everything endothelial mesangial and
epithelial cells that resulting in
formation of cresant sometimes these
crants which they can fill the entire
Bowman's space the glom involvement can
be segmental or Global segmental as I
told you only focal part of the glal is
involved whereas Global is the entire
glomas is involved so when it is
segmental it is called class 4S if it is
global it is called class 4 G this
subendothelial immune complex deposits
leads to you know circumferential
thickening of the capillary wall okay
you can find circumferential thurning of
the capillary walls that's because of
subendothelial tissue immune complex
deposits which you know is seen as wire
Loop that's these are referred to as
wire Loop lesions inle which is
characteristic of pattern four of lupus
nephritis which is diffuse lupus
nephritis and this is the the pattern
ofal environment which is often
symptomatic and the symptoms could be
hematuria proteinurea and hypertension
see the next pattern is class five which
is referred to as membranous lupus
nephritis where there is diffuse
thickening of the capillary WS due to
deposition of subepithelial immune
complexes so this is a classify showing
diffuse thickening of the capillary
walls This Is A Pas strain okay and that
the reason for that is increased
production of basement membrane like
material right this is a higher power
view showing diffus thickening of the
capillary walls and the last one is the
class six which is referred to as
advanced sclerosing lupus nephritis as
the name says there is sclerosis of more
than 90% of the glomi and this is end
stage renal disease moving on to tubular
lesions that's again because of deposit
of immune complexes on the tubular or
peritubular capillary basement membranes
okay remember it is tubular or
peritubular capillary basement membranes
very rarely tubular know uh involvement
can be the dominant abnormality okay you
can sometimes see lymphoid follicles
along with numerous plasma cells and
these may be the source of
autoantibodies so that's about the renal
lesions moving on to understanding the
skin leion reasons the classical feature
the characteristic feature is the idema
which affects the face along the bridge
of the nose and Che okay this is
characteristic it resembles that of a
butterfly and that's why it's referred
to as butterfly rash which is seen in
around 50% of patients and of course
similar kind of rash may be seen on the
extremities as well and also the trunk
very rarely uh lesions can be manifested
as artic areia bulle or maculopapular
lesions and rarely ulcerations can also
be noted so histological examination of
these skin lesions will show
lymphohistiocytic infiltrate that means
there will be infiltration of
lymphocytes and histiocytes where in the
junction between the dermis and the
epidermis okay at times you know this
kind of infiltrate can lead to
separation of dermoepidermal Junction
you can also see vasculitis of the superficial
superficial
vessels in the dermis so that's about
the skin lesions now moving on to the
cardiac lesions so remember the damage
can occur to any layer of the heart okay
it can be pericardium endocardium or The
myocardium pericardial involvement is
seen up to 50% of patients myocard is
very less common as compared to that of
the pericardial involvement the
myocardial involvement results in
resting teic cardia and some you know
subtle electrocardiography
abnormalities there can be valvular
involvement also most often mital and
iotic valve involvement where there will
be diffuse leaflet thickening leading on
to the dysfunction no in form of
stenosis or regurgitation of these two
valves it I mean there can be
endocarditis involving the valve that's valvular
valvular
endocarditis so that is referred to as
Libman Sac endocarditis okay this is
also referred to as very because
marantic or non-bacterial thrombotic
endocarditis so in this kind of
endocarditis you find the vegetations on
the ventricular surface as well as on
the atrial surface and these vegetations
and these vegetations are wary deposits
which can be you know around 1 to 3 mm
very rarely up to 1 cm in size another
important cardiac manifestation is the
coronary artery disease right in the
form of the sclerosis of coronary blood
vessels okay the mechanism is
multifactorial see the risk factors for
atherosclerosis which includes
hypertension obesity hyper lipidemia
they are much more common in SLE
patients than compared to the normal
population there can be immune complexes
and antiphospholipid antibodies you know
that can result in the damage to the
endothelium of these coronary blood
vessels and because of the damage it can
promote atherosclerosis okay okay so
these are the possible mechanisms for
coronary atherosclerosis in systemic lupus
lupus
osis the morphological features in some
of the other organs include spleen there
can be spleen omegal that's because of
follicular hypoplasia you do find onion
skin-like lesions because of concentric
thickening around the blood vessels in
the spleen okay the pleuritis and plural
Fusion is seen in 50% of patients with
lung involvement in El there can be
chronic interstitial fibrosis in long-standing
long-standing
disease you can find I body or
hematoxilin bodies in the bone marrow of
these patients hypoplastic germinal
Center and very rarely the lymph nodes
show necrotizing lympha denitis so this
is all about the morphological features
of systemic lupus rosis now it's time to
solve the practice sessions this is why
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way in the next session let's learn
about the clinical features and lab
diagnosis of systemic lupus OSIS thank
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