0:02 hello everyone welcome back to this
0:03 short tutorial from pathology Made
0:06 Simple at IOP pathology.com and
0:09 supported by vdia which is an amazing AI
0:12 study tool at the end of this session
0:14 you'll be having practice sessions via
0:17 violia so in continuation with the
0:19 autoimmune diseases series we were
0:22 talking about SLE right so we had
0:24 discussed about the autoantibodies
0:26 involved inle we have discussed about
0:28 the pathogenesis and mechanisms of
0:31 tissue injury in and now let's learn
0:34 about the various morphological features
0:38 of so remember the morphology ofle is
0:41 extremely variable the characteristic
0:44 lesions as we have learned results from
0:47 immune complex deposition in various
0:49 tissues and organs like the blood
0:52 vessels kidneys connective tissue and
0:54 skin now let's talk about the
0:56 morphological features in these tissues
0:58 and organs where there is immune complex
1:02 deposition firstly blood vessels the
1:04 characteristic feature ofle involving
1:07 the blood vessels is acute necrotizing
1:09 vasculitis you know it involves small
1:11 blood vessels particularly the
1:13 capillaries small arteries and
1:16 arterioles it can be present in any
1:18 tissue of the body but remember the
1:21 large vessel necrotizing vasculitis is
1:24 less common as compared to that of small
1:27 vessel necrotizing vasculitis you can at
1:30 times see thrombotic micro
1:33 angiopathy so morphological features in
1:35 acute stage include as we know it is
1:37 acute vasculitis meaning there will be
1:40 neutrophilic infiltration in the vessel
1:43 wall along with necrosis of the vessel
1:46 wall right so this vessel wall necrosis
1:48 when it combines with the deposits of
1:51 immune complexes the complement and
1:54 plasma protein it results in somewhat
1:56 smudgy eosinophilic area of tissue
1:58 destruction which is referred to as
2:02 fibrinoid necrosis so we look for
2:05 neutrophilic infiltration as well as
2:07 fibrinoid necrosis in the vessel walls
2:10 particularly the small blood vessels in
2:12 The Chronic stage what really happens is
2:14 that the vessels the blood vessels
2:17 undergo fibrous thickening causing
2:19 significant narrowing of the Lumen and
2:23 the consequences thereof so moving on to
2:24 understanding the morphological features
2:28 of kidney clinically significant renal
2:31 involvement happens in 50% of patients
2:34 with systemic Luper theosis and the
2:35 lesions in kidney can be categorized
2:38 into glomular lesions and tubulo
2:41 intertial regions glom regions are
2:43 referred to as glom nephritis and tub
2:46 interstitial are referred to as tubulo
2:49 interal nephritis so let's learn about
2:52 glomular lesions that's because of again
2:55 deposition of immune complexes and these
2:58 deposits can be in the glomular basement
3:01 membrane it can be in the m tangum and
3:04 sometimes throughout the glomas and
3:06 rightly the glomerular Legions are
3:10 referred to as lupus nephritis right so
3:13 this lupus nephritis has six different
3:15 morphological patterns starting from
3:19 class one to class six see the class one
3:20 is the least common pattern and the
3:24 class four is the most common pattern so
3:26 let's learn about different patterns in
3:29 lupus nephritis so I told you class one
3:31 to class six see the class one is
3:35 referred to as minimal mangial lupus
3:37 nefritis so as I told you earlier this
3:40 is the least common pattern where the
3:43 immune complex deposition is seen in the
3:46 mangium right there will be no
3:48 structural changes in the light
3:50 microscopic examination that means h&
3:52 stained sections do not show any
3:55 morphological features but then you do
3:57 find immune complex deposition when you
4:00 do a immunofluoresence and electron
4:03 microscopic examination the class two is
4:06 referred to as mangel proliferative
4:09 lupus nephritis okay as the name says
4:12 there will be proliferation of mangial
4:15 cells as well as accumulation of Matrix
4:18 in the Mangum that's a mangel matrix
4:21 okay so this is this know Pas stain
4:24 which shows the proliferation of the
4:26 meangel cells as well as some amount of
4:29 mangel Matrix accumulation remember
4:32 there will be no involvement of the
4:35 glomular capillaries that means the
4:37 endothelium of the glomular capillar is
4:40 not involved it's purely mangial imof
4:43 fluoresence and electron microscopy do
4:46 demonstrate granular mangial deposite of
4:48 imunoglobulin and complement so the
4:51 class three is referred to as focal
4:54 lupus nephritis so when we say focal it
4:57 means involvement of less than 50% of
5:01 the glomi okay among the GL glom
5:05 involved it can be segmental or Global
5:07 segmental meaning only the portion of
5:10 the glomas is involved Global means the
5:14 entire glomas is involved right see the
5:17 entire glom involvement in less than 50%
5:21 of all glom is focus lupus nefritis
5:23 which is a global pattern so what do you
5:27 see you find there will be swelling and
5:30 proliferation of the endothelial cell of
5:33 the capillaries as well as the mangial
5:36 cells right so there is proliferation of
5:38 endothelial and the mangel along with
5:41 infiltration by the lucos sites there
5:44 can be capillary wall necrosis you can
5:47 see some amount ofil in thrombi in few
5:49 of these blood vessels rarely very
5:51 rarely if the proliferation is too much
5:54 you can see cresant formation as well
5:56 right so that's type three now moving on
5:58 to class four which we told it is the
6:00 most common type and it is referred to
6:04 as diffuse lupus nephritis it's the most
6:07 common most severe which means diffuse
6:09 focal meaning less than 50% diffuse is
6:12 more than that right so this is the most
6:14 common and the most severe form of lupus
6:16 nephritis where you find proliferation
6:19 of the endothelial that's of capillary
6:22 lining proliferation of the meangel as
6:25 well as proliferation of the epithelial
6:28 cells lining The Bowman capsule right
6:30 Bowman space so you find proliferation
6:33 of everything endothelial mesangial and
6:36 epithelial cells that resulting in
6:38 formation of cresant sometimes these
6:41 crants which they can fill the entire
6:45 Bowman's space the glom involvement can
6:48 be segmental or Global segmental as I
6:50 told you only focal part of the glal is
6:52 involved whereas Global is the entire
6:54 glomas is involved so when it is
6:57 segmental it is called class 4S if it is
6:59 global it is called class 4 G this
7:02 subendothelial immune complex deposits
7:04 leads to you know circumferential
7:07 thickening of the capillary wall okay
7:09 you can find circumferential thurning of
7:11 the capillary walls that's because of
7:13 subendothelial tissue immune complex
7:16 deposits which you know is seen as wire
7:19 Loop that's these are referred to as
7:21 wire Loop lesions inle which is
7:25 characteristic of pattern four of lupus
7:27 nephritis which is diffuse lupus
7:30 nephritis and this is the the pattern
7:33 ofal environment which is often
7:35 symptomatic and the symptoms could be
7:39 hematuria proteinurea and hypertension
7:41 see the next pattern is class five which
7:43 is referred to as membranous lupus
7:46 nephritis where there is diffuse
7:48 thickening of the capillary WS due to
7:51 deposition of subepithelial immune
7:53 complexes so this is a classify showing
7:55 diffuse thickening of the capillary
7:59 walls This Is A Pas strain okay and that
8:01 the reason for that is increased
8:03 production of basement membrane like
8:05 material right this is a higher power
8:07 view showing diffus thickening of the
8:11 capillary walls and the last one is the
8:12 class six which is referred to as
8:15 advanced sclerosing lupus nephritis as
8:19 the name says there is sclerosis of more
8:23 than 90% of the glomi and this is end
8:27 stage renal disease moving on to tubular
8:29 lesions that's again because of deposit
8:32 of immune complexes on the tubular or
8:35 peritubular capillary basement membranes
8:37 okay remember it is tubular or
8:40 peritubular capillary basement membranes
8:43 very rarely tubular know uh involvement
8:46 can be the dominant abnormality okay you
8:48 can sometimes see lymphoid follicles
8:51 along with numerous plasma cells and
8:54 these may be the source of
8:56 autoantibodies so that's about the renal
8:58 lesions moving on to understanding the
9:01 skin leion reasons the classical feature
9:04 the characteristic feature is the idema
9:06 which affects the face along the bridge
9:09 of the nose and Che okay this is
9:12 characteristic it resembles that of a
9:13 butterfly and that's why it's referred
9:15 to as butterfly rash which is seen in
9:18 around 50% of patients and of course
9:20 similar kind of rash may be seen on the
9:24 extremities as well and also the trunk
9:27 very rarely uh lesions can be manifested
9:30 as artic areia bulle or maculopapular
9:33 lesions and rarely ulcerations can also
9:36 be noted so histological examination of
9:39 these skin lesions will show
9:41 lymphohistiocytic infiltrate that means
9:42 there will be infiltration of
9:46 lymphocytes and histiocytes where in the
9:48 junction between the dermis and the
9:51 epidermis okay at times you know this
9:52 kind of infiltrate can lead to
9:56 separation of dermoepidermal Junction
9:58 you can also see vasculitis of the superficial
10:00 superficial
10:02 vessels in the dermis so that's about
10:04 the skin lesions now moving on to the
10:08 cardiac lesions so remember the damage
10:11 can occur to any layer of the heart okay
10:13 it can be pericardium endocardium or The
10:15 myocardium pericardial involvement is
10:18 seen up to 50% of patients myocard is
10:21 very less common as compared to that of
10:23 the pericardial involvement the
10:25 myocardial involvement results in
10:27 resting teic cardia and some you know
10:30 subtle electrocardiography
10:32 abnormalities there can be valvular
10:35 involvement also most often mital and
10:38 iotic valve involvement where there will
10:41 be diffuse leaflet thickening leading on
10:43 to the dysfunction no in form of
10:46 stenosis or regurgitation of these two
10:48 valves it I mean there can be
10:51 endocarditis involving the valve that's valvular
10:52 valvular
10:55 endocarditis so that is referred to as
10:58 Libman Sac endocarditis okay this is
11:00 also referred to as very because
11:02 marantic or non-bacterial thrombotic
11:04 endocarditis so in this kind of
11:06 endocarditis you find the vegetations on
11:09 the ventricular surface as well as on
11:12 the atrial surface and these vegetations
11:15 and these vegetations are wary deposits
11:19 which can be you know around 1 to 3 mm
11:22 very rarely up to 1 cm in size another
11:25 important cardiac manifestation is the
11:28 coronary artery disease right in the
11:31 form of the sclerosis of coronary blood
11:34 vessels okay the mechanism is
11:36 multifactorial see the risk factors for
11:37 atherosclerosis which includes
11:40 hypertension obesity hyper lipidemia
11:42 they are much more common in SLE
11:44 patients than compared to the normal
11:47 population there can be immune complexes
11:50 and antiphospholipid antibodies you know
11:52 that can result in the damage to the
11:54 endothelium of these coronary blood
11:57 vessels and because of the damage it can
11:59 promote atherosclerosis okay okay so
12:01 these are the possible mechanisms for
12:03 coronary atherosclerosis in systemic lupus
12:04 lupus
12:07 osis the morphological features in some
12:09 of the other organs include spleen there
12:11 can be spleen omegal that's because of
12:14 follicular hypoplasia you do find onion
12:17 skin-like lesions because of concentric
12:19 thickening around the blood vessels in
12:22 the spleen okay the pleuritis and plural
12:25 Fusion is seen in 50% of patients with
12:29 lung involvement in El there can be
12:31 chronic interstitial fibrosis in long-standing
12:32 long-standing
12:35 disease you can find I body or
12:38 hematoxilin bodies in the bone marrow of
12:41 these patients hypoplastic germinal
12:44 Center and very rarely the lymph nodes
12:47 show necrotizing lympha denitis so this
12:50 is all about the morphological features
12:54 of systemic lupus rosis now it's time to
12:56 solve the practice sessions this is why
12:59 our visia I suggest you to click on the
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13:03 the description just to solve these
13:05 multiple choice questions there are you
13:08 know short answer type of questions and
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13:20 wrong and I feel it's fun to learn this
13:22 way in the next session let's learn
13:25 about the clinical features and lab
13:29 diagnosis of systemic lupus OSIS thank
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