 Welcome to Matt's model lecture series. Before we start just take a minute and subscribe so you can get notified when we post a new video. Okay so let's see what do we have over here. It's an x-ray of a spine and the clue that they give you in the test is going to be bamboo spine on x-ray. So there is what do we see. It's going to be seen in ancholizing spondylitis. So ancholizing spondylitis is a chronic inflammatory arthritis. It's associated with HLAB 27. So what do we see over here that there is ossification along the margins of the disc spaces in this patient's lumbar spine. So what they are going to produce they are going to produce an appearance that is similar to a stick of bamboo. Okay so it is going to be fused spine we see it. So bamboo spine. Ancholizing spondylitis. Now what do we see over here. Needle shapes and crystals are there. So these crystals are monosodium urate crystals. These are needle shaped negatively bifuringian crystals. Okay so monosodium urate crystals. Where do we see them? We see them in gout. Next one rhomboid shaped crystals. So where are we going to see these? We do see them in suruga. So these are known as calcium pyrophosphate dihydrate crystals. Rhomboid crystals positive bifuringians. High yield topic. Nice. We have swanic and vitroendiformities. Okay so swanic is the one that is by the hyperextension of the proximal interferringial joint with selection of the distal interferringial joint. This is our swanic whereas the vitroin is the one that is by the inverse portion of posture of this one. So you can see that that's our hyperextension and that's inverse of that. Where are we going to see that in rheumatoid arthritis? Next we have an x-ray of a knee with wing sarcoma. So wing sarcoma, they are going to give you the buzzword as onion husking periostal reaction. So the tumor is towards the top of the fibula and has destroyed the portion of the bone. So wing sarcoma. Next, melignant small blue cell tumors. So small round blue cells of the wing sarcoma that we see under the microscope. So then again in wing sarcoma. Codmin triangle. So codmin triangle like a triangular elevation of the periosteum that is going to be from an aggressive melignant bone tumor that is osteo sarcoma. Codmin triangle. So they will give you the raised periosteum. Next, so bubble appearance. So this one over here is the front, okay, and that's the right of the thigh bone and we are going to see this one in giant cell tumor of the bone and that's usually benign. Giant cells. So we are still talking about the giant cell tumor, okay. These are multi-nuclear giant cells with up to 100 nuclei that have prominent nuclei. So nuclei are over here. Giant cells, 100 multiple nucleus. And we are going to see that in giant cell tumor of the bone. Pretty commonly asked, what is it? Tennis racket shape, cytoplasmic organelles and linger hand cells, morbid granules. Where do we see those? Linger hand cell, histocytosis. These are the vesicles and then tennis racket shape cytoplasmic organ. Where do we see that? So these are known as kesur fresher rings, golden brown rings around peripheral cornea. So these rings are caused by deposition of excess copper on the inner surface of the cornea in the desment membrane and we are going to do the silt exam, lamp examination, that's the diagnosis of the kesur fresher rings, particularly in the early stages, unless the rings are visible to the naked eye and the conditions will be when we have severe copper overload. Otherwise we need to do silt, lamp examination and we are going to see that in Wilson disease where we have excess copper deposition. Next, antimitrochondriol antibodies. This is highly, highly diagnostic of primary barycologitis, okay. So a positive antimitrochondriol antibodies means that they are detectable levels of antibodies in the bloodstream. So we are going to see that in prime debilary cirrhosis that what we used to name as now it is known as prime debilary colongitis. Next one, nutmeg appearance of liver. So this is due to the perfusion abnormality of the liver and that's going to be result as of a hepatic venous congestion. So when the hepatic veins are congested, contrast is prevented from diffusing through the liver in a normal manner. So we are going to see nutmeg appearance of the liver. So because of chronic passive congestion of liver due to right heart failure or butchery form syndrome. Antilever kidney microsomal 1 antibodies. So we are going to see those in the autoimmune hepatitis in the liver and kidney. We are going to see that. Enta smooth muscle antibodies. Antibodies that attack smooth muscles, okay. And smooth muscle antibodies are auto antibodies. These are the proteins they are produced by the body's immune system. They're recognized in attack. It's own actin, a protein that is found in smooth muscle and other tissues especially in the liver. So that's why where do we see that in autoimmune hepatitis. Triglycerides accumulation in the liver cell vacuoles. So this is our hepatic macrovesicular histitosis, fatty chain changes there. So the lipid accumulates in the herbarocytes as vacuoles. These vacuoles have a clear appearance. Okay, we can see that. This is a clear appearance. Okay. And the most common cause of the fatty chain in developed nations is termed as non-alcoholic fatty liver disease. It can be associated like diabetes, obesity, metabolic syndrome. And in our underdeveloped countries it's contributes to kosher cause syndrome in children. And it can be because of the severe GI malabsorption are the additional causes in underdeveloped countries. But over here we will see that that's fatty liver. It can be alcoholic or metabolic syndrome. So metabolic syndrome means diabetes, malitis, obesity is there. Next one. Bilory bodies. Is nophyloxidoplasmic inclusion in the liver cell. Okay. Twisted rope appearance with the balloon shape liver cell. Okay. And then we see twisted rope appearance over here. And this is going to be seen in alcoholic liver disease. Next one. Apple core lesion on barium x-ray. So this is our apple core. Where do we see that? Colorectal cancer. Geralar cast is the second most common type of cast and it can result from the breakdown of cellular cast or the inclusion of aggregates of plasma proteins like albumin or immunoglobin light chains. And the most common findings will be in acute tubular necrosis, schematic or toxic injury. Very high yield tested question. Thyroid like appearance of kidney. Thyroid like appearance of kidney. So this is known as like thyroidization of tubules means that a trophic tubules filled with casts that resemble thyroid follicle. Interstitial lymphoplasmocytic infiltrates in often perigluminal fibrosis and secondly segmental gluminal sclerosis. So these are the ones they are known as thyroidization. So this is means that they are going to resemblance to the normal thyroid follicles. The dilated tubules contain a bit in proteins. They will resemble the thyroid colloid which is surrounded by flattening epithelial cells. So thyroidization. So where do we see that? We see that in chronic pallonephritis and it's because of recurrent infections. Next spikes on basement membrane don't like sub epithelial deposits. So this one we are going to see in membrane is nephropathy. That's your nephrodic syndrome. On electron microscope. Dome shape. Normally look at that these putocytes fuse putocytes, a festment like Hershey kisses are there and now they are melted. So putocytes what they do they play an important role in gluminal function. So together with endothelial cells of the gluminal capillary loop and gluminal basement membrane they form a filtration barrier. So these putocytes cooperate with misingial cells to support the structure and function of the gluminal rest. So what they do they are specialized epithelial cells that cover the outer surface of gluminal capillaries and these are like our unique cell junctions. They have cell diaphragms which features the nephrodic and nephrodic syndrome proteins in addition to the components of the adherence, tight and gap junctions. They are going to connect the adjacent putocyte foot processes. So means that these foot processes play a very important role in gluminal function. So they are going to act as a filtration barrier. Where do we see that? We see that in minimal change disease in children with nephrodic syndrome. Clemleston nodules. So nodular glumloschlorosis of the diabetes mellitus. So the nodules of pink highly material form in the region of gluminal capillary groups in the glumal rest. And it is because of the increase in misingial metrics from damage as a result of non-enzymatic glycosylation of proteins. High yield. High yield, high yield, high yield. We cannot emphasize that how much this topic is important. So we are going to see that in diabetic nephropathy. So nodular hyaline deposits in glumular eye is diabetic nephropathy. Lumpy bumpy appearance. Lumpy bumpy appearance on glumular eye. We are going to see that in post streptococcal glumular nephritis. And it is due to deposition of IgG, IgM, and C3. Linear. Linear. Okay. Linear deposition on the glumular and ulular basement membranes. And this is our IgG deposition. We are going to see in good pasture syndrome. They can capillary loop. So wire loop. Wire loop appearance. So wire loop appearance, where do we see? Diffuse polyforative glumular nephritis. And as seen with lupus. Wire loop. Let pi appearance of colon on abdominal imaging. So it's a classical barium enema finding in chronic ulcerative colitis. Okay. And it can be seen on CT MRI or plane radiograph. Over here we have a complete loss of illustration markings in the disease segment of the colon. So smooth walled and cylindrical are going to be seen. So lead pipe. Where do we see in ulcerative colitis? String sign. Narrowing of bowel lumen on barium x-ray. So it is going to be severe narrowing of the loop of bowel. Which going to make the lumen resemble as a string. And string sign is a term often applied to the appearance of any mock narrowing of the lumen. But it is the description of our reversible narrowing in our Crohn's disease. Now next one we have over here. Musin filled cell with paraffin nuclei. It's known as signet cell. So what are those signet cells? Cell with a large vacuole. Okay. The malignant type is seen predominantly in carcinomas. Are frequently associated with stomach. But it can arise in prostate, bladder, gallbladder, breast, colon, ovarian, stroma and testes. But the main common is going to be in gastric carcinoma. Musin filled paraffin nucleus is signet rings. Next one. What do we see on this x-ray? They said that deposit hemocytrine from hemorrhage given brown color. So brown tumor of the bone. So it's a bone lesion that arises in the setting of excess of osteoclasts activity, like in hyperperatoridism. And they are a form of osteitis fibrosus tica. It's not a neoplasm, but rather simply a mass. And it affects the maxilla and mandible, though any bone can be affected. And these bone tumors are brown tumors are radial leucine. So where are we going to see them in hyperperatoridism or osteitis fibrosa cystica? Orphan NEI nuclei. So a large thyroid cell with ground glass nuclei and central clearing. Okay, ground glass nuclei. So large nuclei oval molded with singular membranes, nuclear clearing, okay, nuclear grooves, one or more marginally placed micro nuclear lie. So these are going to be seen in our papillary carcinoma of the thyroid. Next one. Where are we going to see these two bodies? Oshkov bodies are granuloma with giant cells after pharyngeal infection. So our cells associated with our rheumatic heart disease. So these are surrounding centers of fibrinoid necrosis and our iniscus are the year cytoplasm is more basophilic and contain up to four nuclei. So in this cause cells are a large macrophages found within granuloma. So this is like a granuloma. Okay, the whole thing that are containing the granuloma is Oshkov. Inside this granuloma is known as Etiskov. So this is going to be our associated with rheumatic fever. Blue sclera. Where do we see that? This is osteogenesis imperfecta and is caused by thin sclera collagen along the underlying darker colloid vasculature to be seen. And patients with osteitis imperfecta have shown a reduction in thickness of the corneal and sclera collagen fibers which can result in low ocular rigidity. Okay, so these are going to be your blue sclera. Where do we see that? We see in osteogenesis imperfecta type one collagen defect. Thank you everyone. I hope this video was a source of information for you. Thank you.