SLIDE 19,ACUTE SUPPURATIVE MENINGITIS Acute bacterial meningitis is rapidly progressive bacterial infection of the meninges and subarachnoid space. Findings typically include headache, fever, and nuchal rigidity. Diagnosis is by cerebrospinal fluid (CSF) analysis. Suppurative meningitis (SM) or bacterial meningitis is a life-threatening condition, which is exceptionally due to pituitary tumors (PT). Its frequency among male macroprolactinomas (MPRL) deemed to be aggressive. THE SPECIMEN WAS TAKEN FROM A CHILD WHO DIED OF BACTERIAL MENING ITIS. NOTE THAT THE SUBARACHNOID SPACE IS DENSELY INFILTRATED WITH PMN 'S. THERE IS VASODILATION AND CONGESTION WITH FLUID EXUDATION. NECRO SIS OF NEURONAL AND GLIAL ELEMENTS IS NOT SEEN IN THIS SECTION. ETIOLOGY ▪Bacteria that enter the bloodstream and travel to the brain and spinal cord cause acute bacterial meningitis. But it can also occur when bacteria directly invade the meninges. This may be caused by an ear or sinus infection, a skull fracture, or rarely, some surgeries. ▪Likely causes of bacterial meningitis depend on ▪Patient age ▪Route of entry ▪Immune status of the patient PATHOGENESIS ▪Most commonly, bacteria reach the subarachnoid space and meninges via hematogenous spread. Bacteria may also reach the meninges from nearby infected structures or through a congenital or acquired defect in the skull or spine. ▪Because white blood cells (WBCs), immunoglobulins, and complement are normally sparse or absent from cerebrospinal fluid (CSF), bacteria initially multiply without causing inflammation. ▪Later, bacteria release endotoxins, teichoic acid, and other substances that trigger an inflammatory response with mediators such as WBCs and tumor necrosis factor (TNF). Typically in CSF, levels of protein increase, and because bacteria consume glucose and because less glucose is transported into the CSF, glucose levels decrease. Brain parenchyma is typically affected in acute bacterial meningitis. TYPICAL SYMPTOMS AND SIGNS OF MENINGITIS Fever Tachycardia Headache Photophobia Changes in mental status (eg, lethargy, obtundation) Nuchal rigidity (although not all patients report it) Back pain (less intense than and overshadowed by headache) ATYPICAL PRESENTATIONS IN ADULTS Fever and nuchal rigidity may be absent or mild in immunocompromised or older patients and in alcoholics. Often, in older patients, the only sign is confusion in those who were previously alert or altered responsiveness in those who have dementia. In such patients, as in neonates, the threshold for doing lumbar puncture should be low. Brain imaging (MRI or, less optimally, CT) should be done if focal neurologic deficits are present or increased ICP is suspected. If bacterial meningitis develops after a neurosurgical procedure, symptoms often take days to develop. Treatment is antibiotics and corticosteroids. SLIDE 3541/201. EXTERNAL HEMORRHOIDS ACTIVE CONGESTION This section of hemorrhoidal tissue shows congested blood-filled vessels. There is also a thrombus within a dilated vein. Look for the area where the thrombus has contracted, and a space is formed. Hemorrhoids develop when the veins of the rectum or anus become dilated or enlarged and can be either “internal” or “external.” External hemorrhoids are usually found beneath the skin that surrounds the anus CAUSES The most common cause of hemorrhoids is repeated straining while having a bowel movement. This is often caused by severe cases of constipation or diarrhoea. Straining gets in the way of blood flow into and out of the area. This results in the pooling of blood and enlargement of the vessels in that area. Pregnant women may also be at an increased risk of hemorrhoids because of the pressure that the uterus places on these veins. If your parents have had hemorrhoids, you may be more likely to have them as well. Hemorrhoids may also be caused by pregnancy. As we age, hemorrhoids can occur due to increased pressure caused by sitting a lot. And anything that causes you to strain during bowel movements can lead to external hemorrhoids. SIGNS AND SYMPTOMS Itching around the anus or rectal area, Pain around the anus, Lumps near or around the anus, Blood in the stool. TREATMENT Hemorrhoids can be treated a few ways depending on severity. Some general treatments include ice packs to reduce swelling, suppositories, or hemorrhoid creams. These options can offer relief to individuals who have a milder case of hemorrhoids. If you have a more severe case, it is suggested to do treatment with a surgical procedure. Surgical treatments include: Removal of hemorrhoids, known as hemorrhoidectomy, Burning of hemorrhoid tissue with infrared photo, laser, or electrical coagulation, Sclerotherapy or rubber band ligation to reduce the hemorrhoids. SLIDE 2873B/210 HEMORRHOIDS Hemorrhoids are swollen, enlarged veins that form inside and outside the anus and rectum. They can be painful, uncomfortable and cause rectal bleeding. Hemorrhoids are also called piles. We’re all born with hemorrhoids, but at baseline, they don’t bother us. It’s only when they become swollen and enlarged that they produce irritating symptoms. SLIDE 2873B/210 HEMORRHOIDS This section shows hemorrhoidal tissue with congested and thrombosed blood vessels. Look for the thrombus which has contracted and has undergone partial recanalization. TYPES OF HEMORRHOIDS Hemorrhoids can happen inside or outside the rectum. The type depends on where the swollen vein develops. Types include: External: Swollen veins form underneath the skin around the anus. External hemorrhoids can be itchy and painful. Occasionally, they bleed. Sometimes they fill with blood that can clot. This is not dangerous, but can result in pain and swelling. Internal: Swollen veins form inside the rectum. Your rectum is the part of the digestive system that connects the colon to the anus. Internal hemorrhoids may bleed, but they usually aren’t painful. Prolapsed: Both internal and external hemorrhoids can prolapse, meaning they stretch and bulge outside of the anus. These hemorrhoids may bleed or cause pain. CAUSES Straining puts pressure on veins in the anus or rectum, causing hemorrhoids. You might think of them as varicose veins that affect your bottom. Any sort of straining that increases pressure on your belly or lower extremities can cause anal and rectal veins to become swollen and inflamed. Hemorrhoids may develop due to: Pelvic pressure from weight gain, especially during pregnancy. Pushing hard to have a bowel movement (poop) because of constipation. Straining to lift heavy objects or weightlifting. SIGNS AND SYMPTOMS Internal hemorrhoids rarely cause pain unless they prolapse. Many people with internal hemorrhoids don’t know they have them because they don’t have symptoms. If you have symptoms of internal hemorrhoids, you might see blood on toilet paper, in stool or the toilet bowl. These are signs of rectal bleeding. Signs of external hemorrhoids include: Itchy anus. Hard lumps near the anus that feel sore or tender. Pain or ache in the anus, especially when you sit. Rectal bleeding. Prolapsed hemorrhoids can be painful and uncomfortable. You may be able to feel them bulging outside the anus and gently push them back inside. PREVENTION Apply over-the-counter medications hazel or hydrocortisone to the affected area. containing lidocaine, witch Drink more water. Increase fiber intake through diet and supplements. Try to obtain at least 20-35 grams of daily fiber intake Soak in a warm bath for 10 to 20 minutes a day. Soften stool by taking laxatives. Take nonsteroidal anti-inflammatory drugs (NSAIDs) for pain and inflammation. Use toilet paper with lotion or flushable wet wipes to gently pat and clean your bottom after pooping. You can also use a tissue or washcloth moistened with water. TREATMENT Rubber band ligation: A small rubber band placed around the base of a hemorrhoid cuts off blood supply to the vein. Electrocoagulation: An electric current stops blood flow to a hemorrhoid. Infrared coagulation: A small probe inserted into the rectum transmits heat to get rid of the hemorrhoid. Sclerotherapy, A chemical injected into the swollen vein destroys hemorrhoid tissue. There are surgical procedures already mentioned in external hemorrhoids for complicated cases. 1.GIVE THREE DIFFERENCES BETWEEN AND ANEMIC (PALE) INFARCT AND A HEMORRHAGIC (RED) INFARCT. ANEMIC INFARCT HEMORRHAGIC INFARCT This is otherwise known as white infarct This is otherwise known as Red infarct is due because of lack of haemorrhagic and extravasation of erythrocytes from necrotic limited red blood cells accumulation. small vessels. It occurs in solid organs where there is It occurs in organs with loose connective tissue single blood supply like heart, kidney and with collateral vessels to permit blood flow to spleen. tissues but not sufficient to prevent infarction like intestines, liver and lungs. So, basically it occurs due to arterial It is due to venous insufficiency. insufficiency/ occlusion. 2. WHAT IS THE SOURCE OF EMBOLI WHICH GIVE RISE TO PULMONARY EMBOLISM AND INFARCTION? Most the time blood clots form in the leg veins first, a condition called 'Deep Vein Thrombosis' and gradually moves up into the right heart and pulmonary arteries. In many cases, multiple clots are involved in pulmonary embolism. The portions of lung served by each blocked artery are robbed of blood and may die. This is known as pulmonary infarction. This makes it more difficult for your lungs to provide oxygen to the rest of your body. Occasionally, blockages in the blood vessels are caused by substances other than blood clots, such as: Fat from the marrow of a broken long bone Part of a tumor Air bubbles SLIDE 25. A10-10C2, A0752B2. PULMONARY EDEMA An important feature in these slides is the presence of pale pink material within the alveolar spaces (fluid or transudate). Take note that the alveolar septae are intact with no evidence of necrosis. Extravasated red blood cells and congested capillaries can be appreciated. PULMONARY EDEMA: Pulmonary edema refers to the accumulation of excessive fluid in the alveolar walls and alveolar spaces of the lungs. The morphology of pulmonary edema typically progresses over two basic stages. Initially, edematous fluid ( Edema is swelling that is caused by fluid trapped in your body's tissues) remains within the pulmonary interstitium and any excess is emptied by the pulmonary lymphatics. However, once lymphatics are overloaded, edema fluid leaks into alveoli which can become filled. Causes : Pulmonary edema is often caused by congestive heart failure. When the heart is not able to pump efficiently, blood can back up into the veins that take blood through the lungs. As the pressure in these blood vessels increases, fluid is pushed into the air spaces (alveoli) in the lungs. Clinically, patient may feel very difficult in breathing due excessive fluid in alveolar sacs SLIDE 3552-C ENDOMETRIOSIS Endometriosis is the growth of implanted endometrial tissue outside the uterus. This tissue responds to cycle hormonal changes and periodically bleeds Old or previous hemorrhage is evident with the presence of hemosiderin-laden macrophages [brown pigment] MORPHOLOGY AND CAUSES Morphology: Endometriosis has been described in a few cases at the umbilicus, even without prior history of abdominal surgery. It has been described in various atypical sites such as the fallopian tubes, bowel, liver, thorax, and even in the extremities. Causes of Endometriosis Retrograde menstrual flow (woman’s menstrual flow moves in the wrong direction) is the most likely cause of endometriosis. Some of the tissue shed during the period flows through the fallopian tube into other areas of the body, such as the pelvis. Genetic factors because endometriosis runs in families, it may be inherited in the genes. Lesions: superficial “powder-burn” or “gunshot” lesion that is black, dark-brown, or blue, but subtle lesions which are red or clear, small, cysts with hemorrhage or white areas of fibrosis. SLIDE 2010-DM/215. DIAPHRAGMATIC MUSCLE, HEMORRHAGE A longitudinal section through the right diaphragm crura. Muscle tissue with edema, congestion, and interstitial hemorrhage Hemorrhage is the escape of blood from a blood vessel and extravasation of red blood cells into tissue. When a vessel is injured, hemorrhage continues as long as the vessel remains open and the pressure in it exceeds the pressure outside of it. Normally, coagulation closes the vessel and stops the bleeding. Uncontrolled hemorrhage can result from anticoagulant therapy, hemophilia, or severe blood-vessel damage, leading to excessive blood loss and shock. Causes: This may be due to a wide number of causes one of which is trauma. Note the presence of red blood cells extravasated into skeletal muscle. Diaphragmatic muscle hemorrhage: Rupture of the diaphragm occurs when intra-abdominal pressure suddenly rises above the tensile strength of the diaphragmatic tissue. Diaphragmatic rupture / hemorrhage is an uncommon injury seen in about 5% of patients undergoing laparotomy or thoracotomy for trauma. Lesions: Internal bleeding, traumatic brain injury, trauma produces larger, radial tears, often measuring 5 cm to 15 cm. Mechanisms: The postulated mechanism for blunt diaphragmatic injuries is a lateral blow causing shearing of the diaphragm and disruption of the attachments to the chest wall with concomitant increase in intra-abdominal pressure resulting from a frontal impact. Hence, diaphragm rupture is more common with lateral impact motor vehicle collisions. QUESTIONS Study the mechanisms by which a thrombus forms within the lumen of a blood vessel. Thrombus formation begins when platelets bind to collagen exposed at the site of vascular injury. Such binding leads to platelet activation, as a result of which platelet membranes acquire the ability to provide catalytic support for the biochemical reactions that lead to thrombin formation. Why is fracture of long bones closely associated with fat embolism ? when large bones break, fat from the bone marrow, which is made up of fatty cells, seeps into the bloodstream and causes of fat embolism syndrome. SLIDE #30. ILEUM INFARCTION ▪Infarct Because of the looseness of GIT tissue, any Ischemia that occurs, whether due to mesenteric arterial occlusion or mechanical obstruction compromising arterial supply, may lead to the development of an infarct which is red and hemorrhagic rather than pale or anemic as what would occur in solid organs. ▪The entire wall of the ileum is edematous due to the escape of plastic in tissues with many extravasated red blood cells seen from the mucosal layer to the serosal wall. Most of the mucosa no longer shows glandular structures but only ghost outlines of villi. Blood vessels in the submucosa and muscularis are dilated and congested. SLIDE #31. LUNG, PULMONARY THROMBOEMBOLISM Pulmonary embolism is the most common and fatal form of venous thromboembolism in which there is occlusion of pulmonary arterial tree by thromboemboli. In contrast, pulmonary thrombosis is uncommon and may occur in pulmonary atherosclerosis and pulmonary hypertension Morphology: No distinction in head and tail; smooth-surfaced dry dull surface, Mixed with blood clot Lines of Zahn rare. ETIOLOGY: Pulmonary emboli are more common in hospitalized or bedridden patients, though they can occur in ambulatory patients as well ▪ Thrombi originating from large veins of lower legs (such as popliteal, femoral and iliac) are the cause in 95% of pulmonary emboli. ▪ Less common sources include thrombi in varicosities of superficial veins of the legs, and pelvic veins such as periprostatic, periovarian, uterine and broad ligament veins. PATHOGENESIS: The risk factors for pulmonary thromboembolism are stasis of venous blood and hypercoagulable states. Detachment of thrombi from any of the abovementioned sites produces a thromboembolus that flows through venous drainage into the larger veins draining into right side of the heart. SLIDE 162-A. LUNG. THROMBOSIS AND INFARCTION The area supplied by the artery has undergone coagulative necrosis and this is seen as a paler staining area. The outlines of the alveoli are still appreciable. This condition is commonly manifested as sudden onset of dyspnea, cyanosis and chest pain. A pulmonary thrombosis happens when a blood vessel in your lungs becomes blocked. Most of the time, this blockage is caused by a blood clot and happens suddenly. Usually, a pulmonary thrombosis caused by a blood clot that formed locally in small arteries and branches and Firmly adherent to vessel wall. Morphology: Thrombi can have grossly (and microscopically) apparent laminations called lines of Zahn; these represent pale platelet and fibrin layers alternating with darker red cell–rich layers. Predisposing factors to the development of thrombosis and thromboembolism: • A family history of a blood clot in a vein deep in the body, called a deep vein thrombosis (DVT) • A history of DVT • Hormone therapy or birth control pills • Pregnancy • Injury to a vein, such as from surgery, a broken bone, or other trauma • Lack of movement, such as after surgery or on a long trip QUESTIONS What is amniotic fluid embolism? This is the most serious, unpredictable and unproven table cause of maternal mortality. During labour and in the immediate postpartum period, the contents of amniotic fluid may enter the uterine veins and reach right side of the heart resulting in fatal complications. Once a thrombus has formed within the lumen of a blood vessel, what are the possible changes in this thrombus (outcomes or fate of the thrombus)? 1. Lysis – the body naturally dissolves via fibrinolytic mechanisms 2. Propagation – occurs if a vein is completely occluded. The column of blood above the thrombus will clot and enlarge the thrombus. If this encounters the tributary of another vein, then the blood in that can also thrombose. The process of thrombosis extends into bigger and bigger veins. 3. Embolism – part of the thrombus can detach and travel to a distant site 4. The thrombus enlarges and occludes the blood flow through the artery or vein. Depending on the organ that is involved it can have varying consequences 5. Organization – an occluding thrombus is reorganized SLIDE #28. CHRONIC PASSIVE CONGESTION. SPLEEN Take note of the presence of Gamma-Gandy bodies) or siderofibrotic nodules(hemosiderin plus fibrosis). These appear as yellow-brown splinters. This condition occurs in the setting of portal hypertension SLIDE #28. CHRONIC PASSIVE CONGESTION. SPLEEN This condition usually occurs when there is portal hypertension such as that which Is associated with liver cirrhosis or in portal vein thrombosis (Budd Chiari Syndrome). Important features include increased cellularity of splenic pulp, sinusoidal Congestion, thickening of trabeculae and the presence of sidero fibrotic nodules known as Gamma Gandy bodies (pathognomonic for this disease). The brown pigment within these nodules is hemosiderin and the basophilic amorphous material is calcium. SLIDE #26, 193. CHRONIC PASSIVE CONGESTION, LUNG Sections show hemosiderin-laden macrophages (brown pigment) inside alveolar spaces. The Darker brownblack pigment is carbon (anthracotic pigment). Passive hyperemia (congestion), also termed stasis, is a consequence of an impaired venous drainage (heart failure, compression or obstruction of veins), followed by dilatation of venules and capillaries Etiology of passive congestion of the lung : chronic left heart (ventricular) failure. Alveolar walls are thickened due to dilated capillaries. Alveolar lumens are filled with transudate (amorphous, eosinophilic and homogenous) which replaced the air, red blood cells (microhemorrhages) and hemosiderin-laden macrophages (also called "heart failure cells"). With progression, interstitial fibrosis may appear and, together with hemosiderin pigmentation, generates the aspect of "brown induration". Extensive fibrosis leads to intrapulmonary hypertension. SLIDE 30. INTERSTITIAL PNEUMONITIS In this disease, the fluid collects first in the alveolar walls and not inside the alveolar spaces. The peribronchial walls are also infiltrated with lymphocytes and plasma cells. Microscopically: I. Hallmark finding is collections of large number of intra-alveolar macrophages having abundant cytoplasm and containing brown-black pigment and are termed as smokers’ macrophages. II. The intervening septa contain a few lymphocytes, plasma cells and an occasional eosinophil. III. Late cases show mild interstitial fibrosis. Essential features: • Rare and aggressive type of idiopathic interstitial pneumonia with diffuse alveolar damage (DAD), characterized by diffuse inflammation with hyaline membrane and fibroblastic proliferation • Acute interstitial pneumonia shares common features with acute respiratory distress syndrome (ARDS) clinically and morphologically Pathophysiology: • Both endothelial and epithelial injury result in decreased integrity of the alveolar capillary membrane • Imbalance of proinflammatory and anti-inflammatory mediators • Neutrophils increase in alveoli and interstitium and release metabolites leading to lung injury • Alveolar epithelial cells may go through epithelial - mesenchymal transition to become myofibroblasts, resulting in interstitial organization and fibrosis QUESTIONS Where is the fluid located in pulmonary edema? Is this fluid an exudate or transudate? Pulmonary edema is a condition caused by excess fluid in the lungs. This fluid collects in the numerous air sacs in the lungs. Cardiogenic pulmonary edema is caused by elevated pulmonary capillary hydrostatic pressure, which leads to a transudate of fluid into the interstitium and alveoli. Study the etiology, pathogenesis and clinical course of pulmonary edema. What makes it a serious condition? The most common cause of pulmonary edema is congestive heart failure (CHF). Heart failure happens when the heart can no longer pump blood properly throughout the body. This creates a backup of pressure in the small blood vessels of the lungs, which causes the vessels to leak fluid. In a healthy body, the lungs will take oxygen from the air you breathe and put it into the bloodstream. But when fluid fills your lungs, they cannot put oxygen into the bloodstream. This deprives the rest of the body of oxygen SLIDE NO 27. LIVER, CHRONIC PASSIVE CONGESTION The section was taken from a patient who died of congestive (chronic) cardiac failure. Chronic passive congestion of the liver occurs when these is right-sided heart failure other from chronic lung disease with pulmonary hypertension or chronic passive congestion of the lungs progressing into right-sided heart failure, or the presence of congenital heart disease with left to right shunts. The centrilobular zone shows marked degeneration and necrosis of hepatocytes accompanied by hemorrhage while the peripheral zone shows mild fatty change of liver cells. MORPHOLOGY Liver with chronic passive congestion and hemorrhagic necrosis. Central areas are red and slightly depressed compared with the surrounding tan viable parenchyma, creating “nutmeg liver” (so called because it resembles the cut surface of a nutmeg). Microscopic preparation shows centrilobular hepatic necrosis with hemorrhage and scattered inflammatory cells. PATHOGENESIS AND CAUSES Necrosis, hemorrhage, and hemosiderin-laden macrophages). In long-standing, severe hepatic congestion (most commonly associated with heart failure), hepatic fibrosis (“cardiac cirrhosis”) can develop. Because the central portion of the hepatic lobule is the last to receive blood, centrilobular necrosis also can occur in any setting of reduced hepatic blood flow (including shock from any cause); there need not be previous hepatic congestion Most common causes of passive hepatic congestion is congestive heart failure. restrictive cardiomyopathy or constrictive pericarditis. right-sided valvular disease involving the tricuspid or pulmonary valve THROMBOSIS Organizing thrombi: Many dilated and congested blood vessels are present. Few of the vessels show organizing thrombi with ingrowing proliferating vascular channels Thrombosis is the process of formation of solid mass in circulation from the constituents of flowing blood; the mass itself is called a thrombus. Thrombi can develop anywhere in the cardiovascular system. Arterial or cardiac thrombi typically arise at sites of endothelial injury or turbulence; venous thrombi characteristically occur at sites of stasis. Morphology: ❑Thrombi can have grossly (and microscopically) apparent laminations called lines of Zahn; these represent pale platelet and fibrin layers alternating with darker red cell–rich layers. ❑Such lines are significant in that they are only found in thrombi that form in flowing blood; their presence can therefore usually distinguish antemortem thrombosis from the bland nonlaminated clots that form in the postmortem state. PATHOPHYSIOLOGY ❑Since the protective haemostatic plug formed as a result of normal homeostasis is an example of thrombosis. ❑Human beings' posses' inbuilt system by which the blood remains in fluid state normally and guards against the hazards of thrombosis and hemorrhage. ❑Injury to the blood vessel initiates haemostatic repair mechanism or thrombogenesis. PATHOPHYSIOLOGY Virchow described three primary events which predispose to thrombus formation (Virchow’s triad): endothelial injury, altered blood flow, and hypercoagulability of blood. 1.Endothelial Injury: Endothelial injury is an important cause of thrombosis, particularly in the heart and the arteries, where high flow rates might otherwise impede clotting by preventing platelet adhesion or diluting coagulation factors. (by toxins, hypertension, inflammation, or metabolic products) 2. Abnormal Blood Flow: Turbulence contributes to arterial and cardiac thrombosis by causing endothelial injury or dysfunction, as well as by forming countercurrents and local pockets of stasis. Stasis is a major factor in the development of venous thrombi. 3. Hypercoagulability: Hypercoagulability contributes infrequently to arterial or intracardiac thrombosis but is an important underlying risk factor for venous thrombosis. It is loosely defined as any alteration of the coagulation pathways that predisposes affected persons to thrombosis and can be divided into primary (genetic) and secondary (acquired) disorders. (by factor V Leiden, increased prothrombin synthesis, antithrombin III deficiency). OUTCOMES OF THROMBOSIS AND EFFECTS ❑PROPAGATION : The thrombus may propagate and eventually cause obstruction of some critical vessels. ❑EMBOLIZATION : Thrombi may dislodge to distal sites in the vascular tree. ❑DISSOLUTION : They may be removed by fibrinolytic activity. ❑ORGANIZATION AND RECANALIZATION : Thrombi may induce inflammation and fibrosis – termed organization and may eventually become recanalization. CLINICAL EEFECTS OF THROMBOSIS ❑Cardiac thrombi : Large thrombi in heart that may cause sudden death. ❑Arterial thrombi : These cause ischemia necrosis of the deprived part which may lead to gangrene. ❑Capillary thrombi : Microthrombi in microcirculation may give rise to DIC ( disseminated intravascular coagulation ) ❑Venous thrombi (Phlebothrombosis) : These may cause following effects : Thromboembolism, Edema of area drained, Skin ulcers, Painful white legs and Poor wound healing, etc. SLIDE 12, RENAL INFARCT Renal tubules and glomeruli show typical coagulative necrosis i.e. intact outlines of necrosed cells. There is acute inflammatory infiltrate at the periphery of the infarct MORPHOLOGY Grossly, renal infarcts are often multiple and may be bilateral. Characteristically, they are pale or anemic and wedge-shaped with base resting under the capsule and apex pointing towards the medulla. Generally, a narrow rim of preserved renal tissue under the capsule is spared because it draws its blood supply from the capsular vessels. Microscopically, the affected area shows characteristic coagulative necrosis of renal parenchyma i.e., there are ghosts of renal tubules and glomeruli without intact nuclei and cytoplasmic content. The margin of the infarct shows inflammatory reaction— initially acute but later macrophages and fibrous tissue predominate ETIOLOGY AND PATHOPHYSIOLOGY Renal infarction is common. Majority of them are caused by thromboemboli, most commonly originating from the heart such as in mural thrombi in the left atrium, myocardial infarction, vegetative endocarditis and from aortic aneurysm. Less commonly, renal infarcts may occur due to advanced renal artery atherosclerosis, arteritis and sickle cell anaemia. The two major causes of renal infarction are thromboemboli and in situ thrombosis. Thromboemboli usually originate from a thrombus in the heart or aorta, and in situ thrombosis is usually due to an underlying hypercoagulable condition or injury to or dissection of a renal artery. QUESTIONS What are "heart failure cells"? Heart failure (HF) cell or siderophages are pulmonary macrophages that phagonicytize erythrocytes leaked from the congested capillaries due to HF. Degradation of erythrocytes and hemoglobin increases concentrations of heme in the lung. What are the causes of chronic passive congestion of the lungs? Of the liver? Mitral stenosis, narrowing of the valve between the upper and lower chambers in the left side of the heart, causes chronic passive congestion. Iron pigment from the blood that congests the alveoli spreads throughout the lung tissue and causes deterioration of tissue and formation of scar tissue. Most common causes of passive hepatic congestion are congestive heart failure. restrictive cardiomyopathy or constrictive pericarditis. right-sided valvular disease involving the tricuspid or pulmonary valve. SLIDE 13. SPLENIC INFARCT • Splenic infract is an area of ischemic necrosis within a tissue or organ, produced by occlusion of either its arterial supply or its venous drainage. • TYPES: 1. Red infarcts (hemorrhagic) 2. Pale infarcts 3. Liquefactive infarcts SPLENIC INFARCT: 2 types 1. segmental (global) 2. arterial (venous NORMAL VS PATHOLOGY OF SPLEEN ETIOLOGY • ATERIAL OBSTRCTION this is the most important factor (97% of cases) CAUSE: Most common cause of splenic infarction are Haematological Disease and Embolic Disorders PATHOPHYSIOLOGY A. Brief descriptions: Nearly 99% of infarcts are caused by thromboembolic events, and almost all are the result of arterial occlusions. White infarcts are encountered with arterial occlusion and in solid tissues. B. Gross Findings： Recent infarcts are Hemorrhagic, where as older, more fibrotic infarcts are pale yellow-gray. C. Micro Findings： Necrotic area with homogenous pinkish appearance. Hematoidin crystals can be found in this section. Inflammatory cells seated on the margin of infarct area. DIAGNOSIS AND PROGNOSIS • It can occur asymptomatically, the typical symptom is severe Pain in the left upper quadrant of the abdomen, sometimes radiating to the left shoulder. Fever and chills develop in some cases. It has to be differentiated from other causes of acute abdomen. • An abdominal CT scan is the most commonly used modality to confirm the diagnosis, although abdominal ultrasound can also contribute. • PROGNOSIS: Patients with benign underlying disease and asymptomatic infracts will have an extremely good prognosis SYMPTOMS Approximately one third of splenic infarcts are clinically occult. The most common presenting symptom is left-upper-quadrant abdominal pain (up to 70%). Additional symptoms include fever and chills, nausea and vomiting, pleuritic chest pain, and left shoulder pain. COMPLICATION AND TREATMENT • COMPLICATION : Hemorrhage, Rupture, Abscess, Pseudocyst formation. • Depends on etiology conservative treatment or splenectomy. • Initial treatment of splenic infarction is generally conservative and directed at the precipitating factors. Many patients will make a full recovery with supportive care and anticoagulation. • Therapies directed at Vaso-occlusion without anticoagulation are indicated in those with sickle-cell disease. • Surgical treatment will only be necessary in the presence of complications (hemorrhage, abscess, or pseudocyst) and in massive infarction when symptoms persist MYOCARDIAL INFARCTION MI is a diseased condition which is caused by reduced blood flow in a coronary artery due to atherosclerosis & occlusion of an artery by an embolus or thrombus. MI or heart attack is the irreversible damage of myocardial tissue caused by prolonged ischemia & hypoxia. Etiology: Myocardial infarction (MI) usually results from an imbalance in oxygen supply and demand, which is most often caused by plaque rupture with thrombus formation in an epicardial coronary artery, resulting in an acute reduction of blood supply to a portion of the myocardium. PATHOPHYSIOLOGY HISTOPATHOLOGY A B DIAGNOSIS Acute myocardial infarction is myocardial necrosis resulting from acute obstruction of a coronary artery. Symptoms include chest discomfort with or without Dyspnea, Nausea, and Diaphoresis. Diagnosis is by ECG and the presence or absence of serologic markers. DIAGNOSIS TEST : • Stress test to see how your heart responds to certain situations, such as exercise • Angiogram with coronary catheterization to look for areas of blockage in arteries • Echocardiogram to help identify areas of heart that aren’t working properly SYMPTOMS • Pressure or tightness in the chest. • Pain in the chest, back, jaw, and other areas of the upper body that lasts more than a few minutes or that goes away and comes back. • Shortness of breath. • Sweating. • Nausea. • Vomiting. • Anxiety. • Cough. TREATMENT • Blood thinners, such as aspirin, are often used to break up blood clots and improve blood flow through narrowed arteries. • Thrombolytics are often used to dissolve clots. • Antiplatelet drugs, such as Clopidogrel, can be used to prevent new clots from forming and existing clots from growing. • Nitroglycerin can be used to widen your blood vessels. • Beta blockers lower your blood pressure and relax your heart muscle. This can help limit the severity of damage to your heart. • ACE inhibitors can also be used to lower blood pressure and decrease stress on the heart. • Pain relievers may be used to reduce any discomfort you may feel.
