Hypertrophy and Hyperplasia PDF

Hypertrophy: Hyperplasia: Increase in cell size & functional capacity, in post-mitotic cells, Increase in cell number, in pre-mitotic cells capable of division in organ. Not capable of division, like cardiac muscles, skel...

Hypertrophy: Hyperplasia: Increase in cell size & functional capacity, in post-mitotic cells, Increase in cell number, in pre-mitotic cells capable of division in organ. Not capable of division, like cardiac muscles, skeletal muscles & neurons. Mechanism: Mechanism: Synthesis & assembly of additional intracellular structural Growth factor-driven proliferation of mature cells: components & organelles, resulting in an increased organ size. Liver regeneration from surviving cells, after loss or resection surgery. Causes: Increased output of new cells from tissue stem cells:  Increased functional demand. Intrahepatic stem cells in liver regeneration, when surviving cells fail.  Hormonal & growth factors stimulation. Physiological Examples: Physiological examples: Occurs due to controlled levels of hormones or growth factors signals.  Striated muscles during increased workload (Functional). Compensatory (GF): Regeneration of organs – liver, kidney & skin. I 2  Thyroid gland in pregnancy- higher metabolism for fetus development. Hormonal: Regulated organs in pregnancy/puberty – uterus & breast. 3  Uterus (estrogen) & lactating breast (prolactin) during pregnancy. Lymphoid hyperplasia in respond to infection Pathological examples: Pathological Examples: S14d Goiter: Left Enlargement heart hypertrophy: of by caused the thyroid systemic gland at the base of the neck. hypertension Occurs due to excessive trophic action & can lead to dysplasia/cancer. It can lead to pulmonary hypertension Due Rightto hypothyroidism heart or hyperthyroidism. hypertrophic: caused mainly by pulmonary hypertension Endometrial hyperplasia.  Colon Obstruction: due to proximal hypertrophy of smooth muscles. Benign Prostate Hyperplasia (BPH) – doesn't lead to cancer. Lipogenesis: Adipocytes Hypertrophy, due to triglycerides accumulation. Adipogenesis: Adipocytes Hyperplasia, due to precursor's differentiation. Myocardial Hypertrophy: Benign Prostatic Hyperplasia (BPH): Thickening of the ventricle walls & reduction of ventricle lumen size. Noncancerous increase in size of prostate, due to increase in the number Involves mechanical & trophic signals, causing hypercontractivity. - of prostatic glands & Stroma, in Nodular & not uniform way. Result in reduced diastolic function & usually normal systolic function. Typically seen in men after the age of 40. Causes: ↳ Cause:  Missense mutation in the genes encoding for contractile apparatus: Excessive hormonal stimulation of androgens, which leads to increased Will cause sarcomeric proteins, resulting in reduced cardiac pumping. conversion of testosterone, responsible for cells proliferation. main reason d  Systemic Hypertension: Due to atherosclerosis or aortic valve disease, Symptoms: The left ventricle must work harder & responds by thickening. Increased urination, weak stream, loss of bladder control, Complications: Dysuria (painful urination) & nocturia (night urination).  Congestion & heart failure: Due to prolonged S left hypertrophy.  Cor Bovinum: The heart become huge, due to massive hypertrophy.  ↑ we zin und G31 94-16Sht Endometrial Hyperplasia Metaplasia: d PaS Jak Exts pland Cancer Increased gland to stroma ratio, caused by increased proliferation of the Replacement of one differentiated cell type (epithelial / mesenchymal) endometrial glands, due to high estrogen, unopposed by progesterone. by another, to a more resilient cell type - Usually non reversible. Typically seen in women between the age of 40 & 50. It is not a normal physiological process, which occurs due to chronic Diagnosis: irritants & results in altered stem cells differentiation. Ultrasound showing thickened endometrial stripe, or hysteroscopy. It may progress to dysplasia, which is more dangerous. Clinical Features: Or neoplasia (squamous cell carcinoma). Abnormal and dysfunctional menstrual bleeding. Epithelial Metaplasia: Can progress to Adenocarcinoma / endometrial carcinoma. Columnar epithelia is replaced by Squamous epithelia (most common) Asymptomatic in rare cases.  In respiratory & corneal epithelium, due to Vitamin A deficiency. Causes:  In respiratory epithelium, due to cigarette smoking. Obesity:  In urinary bladder transitional epithelium, due to bladder stones. Causes increased conversion of androgens to estrogen.  In cervix glandular epithelium, due to low pH of the vagina. Polycystic Ovarian Syndrome (PCOS): Mesenchymal Metaplasia: & Multiple small cystic follicles accumulate in the ovary & secrete estrogen. Pathological & not adaptive process. Liver Dysfunction: Myositis ossification: Causes compromised estrogen metabolism. Calcification of skeletal muscles due to trauma, causing bone to form. Ovarian granulosa tumour, secreting estrogen Myeloid metaplasia: Menopause perimenopause Estrogen replacement therapy Endometrioid hyperplasia without atypia: normal 2 Proliferation of hematopoietic tissue in liver & spleen. Another example: Have enlarged, dilated mucous glands & rarely progress to carcinomas. Barret’s Atypical hyperplasia (AH) / Endometrioid intraepithelial neoplasia EIN): esophagus - Have irregular cells, showing extensive mitosis, stratification & tufting. squamous to colmunar It is a premalignant condition, with increased risk of adenocarcinoma. epithel due to Treated by progestin / hysterectomy (surgical removal of the uterus). chronic reflux Acute gastritis: Gastritis: Sudden inflammation of the gastric mucosa & neutrophils present. Inflammatory changes in the stomach mucosa & submucosa lining. Caused by disruption of protective mechanism by chemicals & drugs, Diagnosed by endoscopy of the mucosa & confirmed by biopsy. such as NSAIDS, alcohol, bile reflux, stress, injury & H. pylori. May be asymptomatic or painful, accompanied by nausea & vomiting. Left untreated, can lead to severe blood loss & increased risk of cancer. Chronic Gastritis (metaplasia) Acute Erosive Gastritis: Chronic & gradual inflammation of the gastric mucosa, without The loss of the superficial gastric epithelium & have hyperemic mucosa. neutrophils present, which leads to atrophy & epithelial metaplasia. Characterized by dyspepsia (impaired digestion) with vomiting & when Characterized by dyspepsia, upper abdominal discomfort & vomiting. erosions are numerous, hematemesis may occur (vomiting of blood). Morphology: Variation in size, shape & orientation of epithelial cells. Intestinal Metaplasia Nuclear enlargement & atypia of epithelial cells. It is a "wrong" process, where more resilient Squamous gastric epithelia In superficial chronic gastric, inflammation is confined to gastric pits. is replaced by a more fragile Columnar mucosal epithelia Causes: Can be seen in Barret's esophagus, usually caused by chronic reflux, Helicobacter associated gastritis (Most common): But may also be overlapping chronic gastritis. H. pylori is present beneath the thin mucus, causing epithelial damage. It is a pre-disposing condition, increasing the risk for adenocarcinoma. Antrum area most affected, causing increased acid production & ulcer. Small bowel metaplasia: Autoimmune Chronic Gastritis (Like Crohn's): Only Sialomucin is produced & stained aqua blue. Present of antibodies against gastric parietal cells & intrinsic factor. Large bowel metaplasia: Causing vitamin B12 deficiency & reduced production of gastric acid. Both Sialomucin & Sulfomucin are produced & stained brown-black. In severe cases, in elderly, atrophy of the mucosa may develop. Both may be: Reactive Gastritis: Incomplete metaplasia: Caused by toxic damage to the mucosa, due to reflux, alcohol, tobacco, The mucin content of the columnar cells is reduced & previous gastric surgery & non- steroidal anti-inflammatory drugs. Changes from the normal gastric neutral mucin to acidic mucin. Complications: SDS Complete metaplasia: Risk of malignancy development (2-4%) The loss of columnar mucus-secreting cells & their replacement by an Severe dysplastic epithelial changes that constitute in situ carcinoma. epithelium that contains goblet cells and absorptive cells.  41238 # Edema: Pulmonary Edema: Escape of fluid from vessels & its accumulation in surrounding tissues. The accumulation of low-protein fluids in the lungs. Most commonly found in subcutaneous tissues, lungs & brain. Cardiogenic Causes: Classification: Increased Hydrostatic pressure in pulmonary capillaries, caused by: Permeability Local: During inflammation, due to increased vascular perfectibility. & Left heart failure due to hypertrophy or MI of the left ventricle. everRight) Generalized: Caused by hearth failure. systemic - Mitral stenosis, Volume overload & pulmonary vein obstruction. Anasarca: Extreme generalized edema, in subcutaneous tissues, Non-cardiogenic Causes: Visceral organs & body cavities, often due to decrease oncotic pressure. Decreased oncotic pressure, caused by: Causes / Mechanisms: Liver disease & nephrotic syndrome & protein loosing enteropathies. Increased Hydrostatic pressure, due to impaired venous return: Microvascular injury, caused by: Caused by Right heart failure, Constrictive pericarditis, liver cirrhosis & Viral infection, Inhaled gases, Liquid aspiration & sepsis. Venus obstruction or compression (pregnancy/hypertension/long flight). Morphology: Concoti/hydrostati) Decreased Oncotic pressure, due to hypoproteinemia (low albumin) in; In case of hemodynamic disturbance: - Kidney insufficiency or nephrotic syndrome (albuminuria). altmininis  Lungs are wet, heavy & hyperaemic. - Reduced albumin synthesis in chronic liver disease / malnutrition.  Fluid accumulates in lower lobes (hydrostatic pressure is greater). small intestine - Protein loosing enteropathy (inflammation of intestine, like Crohn's).  Microhemorrhages & hemosiderin macrophages (heart failure cells). - starvation Microvascular / Capillary injury: viruses Joy Grawning G2 houis)  Fibrosis & thickening of alveolar walls. Caused by infections (physiological response), inhaled gas (anesthetics), In case of local microvascular injury: chemical weapons, drugs, alcohol, narcotics & high altitudes.  Fluid accumulates in the alveolar septa in interstitial tissue. Increased vascular permeability, due to allergic response (histamine).  Lymphatic vessels are widen & filled with edematous fluid. Isurfictant Lymphatic obstruction, due to malignant neoplasms & inflammation.  Can lead to ARDS- if the fluid leaks into the lungs. Acute respiratory distress syndrome Hemostasis: DIC (Disseminated Intravascular Coagulation): Highly regulated process A precisely orchestrated process, preventing excess bleeding. Widespread activation of the coagulation system & thrombi formation. Primary Hemostasis (2 steps): Caused by endothelial injury or release of thromboplastic substances. 1. Vascular constriction - narrows the vessel & slows the flow of blood. Seen in severe infections, trauma, neoplasia & obstetric complications. Jessiren 2. Formation of a platelet plug – by platelet adherence & activation. Outcomes: cause 62 Secondary Hemostasis: Ischemic tissue damage - when thrombi forms in small arteries in & Involves a coagulation cascade, of amplifying enzymatic reactions, by brain, heart, lungs, kidneys, and other organs. which clotting factors promote the formation of a fibrin clot. Bleeding diathesis - increased susceptibility to bleeding or bruising.  ↑ Thrombosis: Embolism: Aggregation mass of platelets, held together by fibrin meshwork. The occlusion of small vessel by a solid/liquid/gaseous mass, which was It is designed to protect us from haemorrhage, but unde is really dangerous. transported away from its origin site by the bloodstream. Heparin-like treatment may be used to reduce the risk of thrombosis. Systemic embolism: Mechanism: Arterial emboli travel downstream, cause ischemic necrosis (infraction). ⑳ Endothelial damage cause collagen & Von Willebrand factor exposure, From Abdominal Aorta  Kidneys & lower limb arteries. triggering platelets adherence & aggregation & fibrin clot formation. From Heart  Systemic circulation (Brain, Kidneys, Gut, Lower Limbs) After the vessel is repaired, the clot should be removed by fibrinolysis. ⑤From Common Carotid  Cerebral arterial circulation But when the fibrinolysis is insufficient, the thrombus enlarges. Fat embolism: solig Thrombus mass: structured, solid mass, in the cardiovascular system. Fat enters the bloodstream, due to orthopedic injuries (femur fracture). Coagulum mass: unstructured mass, outside the circulatory system. Causing pulmonary insufficiency (dyspnea) & petechial hemorrhage. Virchow's Triad- abnormalities that lead to thrombosis: Endothelial damage: caused by atherosclerosis& disturb anticoagulant. Amniotic fluid embolism – very uncommon: Liqui) Amniotic fluid enters maternal pulmonary circulation after childbirth. Abnormal blood flow: caused by stasis or turbulence in an aneurysm. Causing heart & lung collapse & massive bleeding. Hyper-coagulability: caused by alterations in coagulation factors. Gas embolism: Like in polycythemia Vera, hematologic changes & cancer. Ens Gas bubbles entering the blood stream, causing distal ischemic injury. Types of Thrombosis: Divers decompression sickness: sudden atmospheric pressure change, /to Previously Fast moving blood: Pale & firm, due to high content of platelet/fibrin. Causes nitrogen to dissolve & form bubbles in the blood. Slow moving blood: Red & soft gelatinous, due to many trapped RBC. In health care: Air wasn't removed from syringes before injection. we Mural yes thrombus: In walls of a blood vessel & cardiac cambers. on Pulmonary embolism: Occlusive thrombus: In arteries & veins, leads to ischemia & necrosis. Occlusion of pulmonary circulation due to embolism. Vegetation's: In heart valves, due to endocarditis infection. Usually occurs when DVT in legs travel through the inferior vena cava, Main Outcomes of thrombosis: right atrium & right ventricle & gets stuck in the pulmonary artery. spread Propagation, Occlusion & Infraction: when the thrombus enlarges. This will cause the right heart difficulty to push blood into the lung & Shrinkage & Dissolution: when a recent thrombus goes Fibrinolysis. may develop into right sided heart failure. Organization & Re-canalization: ingrowth to re-establish flow. The outcome depends on the emboli size: Thromboembolism: thrombus fragment travel & impact other vessels. Large emboli will cause death. m Deep vein thrombus (DVT) from legs -> inferior vena cava -> right atrium -> right ventricle -> stuck in pulmonary artery (embolism). Medium emboli will cause hemorrhagic pulmonary infraction. Small emboli will be clinically silent & will be removed fast. Infarction: Hyperemia: Critical/complete obstruction of the supplying artery, Increased inflow of arterial blood into an organ/tissue, Resulting in irreversible necrosis of the supplied tissue, due to ischemia. It is an active process, resulting from arteriolar dilation. The body need to remove it or it will require surgical resection. It is mediated by hormones & neurological reflexes. Pale Infraction (Anaemic): Physiological Examples: Erection, Exercise & Blushing. Occurs in organs with single blood supply (brain, kidney, heart, spleen). - Pathological Examples: Classic Inflammation – causing edema. Mainly caused by thromboembolitic events & acute ischemia. Congestion: Red Infraction (Haemorrhagic): Stasis of venal blood inside an organ/tissue, Occurs in loose tissue with dual blood supply (lung, GI, ovaries & testis). It is a passive process resulting from disturbed outflow of venal blood. May be caused by venous infraction (e.g testicular torsion), obstruction of It is always pathological & commonly leads to edema. loose spongy tissues (lung) & after reperfusion of white infracts. Congested tissues show cyanosis (abnormal red-blue colour), Septic Infraction: Due to accumulation of deoxygenated haemoglobin. Occurs when infected material travels to another site (after endocarditis). Causes of congestion: Bland Infraction: Cardiac failure – will cause systemic congestion (like liver congestion) Occurs when there is no infection in the infracted area. Isolated Venous obstruction (DVT) – will cause localized congestion. No infarction tissues: Penis, Uterus, Urinary bladder, Thyroid, Tongue Long flights immobility: increased hydrostatic pressure in lower limb. Hemorrhagic Lung Infarction / Pulmonary Infraction: * Pregnancy 3rd trimester due to the uterus compressing the veins. Ischemic coagulative necrosis in the lung within an area of hemorrhage. Dehydration due to alcohol, caffeine, sweating or low humidity. Mainly caused by occlusion of pulmonary circulation due to embolism. Complication: Usually wedge-shaped in sub pleural region of the lung's lower lobes. Chronic congestion may lead to parenchymal necrosis & fibrosis. High risk in patients with problematic circulation (heart/lung disease). Liver Congestion / Hepatic venous congestion: Stages / Steps: Caused by increased pressure & impaired drainage of hepatic vein, Minuets-Hours: Vascular Occlusion of the pulmonary arteries, which results in liver dysfunction, due to right sided heart failure. Will result in their ischemic necrosis of lung parenchyma. Acute Liver Congestion: 4-12 hours: The dual blood supply by the bronchial arteries will keep Reversible ischemia & fatty changes of liver, due to stasis of venal blood. pumping blood to the dead are - not enough to prevent the infarction, Chronic Liver Congestion: but they will cause the infraction to be hemorrhagic red & wet. Nutmeg liver appearance, due to Irreversible ischemic necrosis & fatty 12-48 hours: brown area due to phagocytosis of RBC & hemosiderin. degeneration, which may lead to fibrosis liver, called cardiac cirrhosis. Weeks: Fibrosis - the necrotic area is replaced by scar tissue Hemorrhage: can be all over the body Cerebral Hemorrhage: * Extravasation of blood in its full content from the vessel, due to rapture. Bleeding in the brain, which may lead to liquefactive necrosis of brain. Caused by hypertension, trauma, atherosclerosis or inflammation. Causes: Hemoglobin is a good indicator of bleeding- lower than normal 12g/dL. 1. Trauma Classification by location Abdominal cavity, e.g hemorrhagic cyst of the ovary 2. Arterial systemic hypertension due to atherosclerosis. T rapture and bleeding into the abdominal cavity Internal hemorrhage: Bleeding which we can't see. 3. Tumors. External hemorrhage: Bleeding which we can see. 4. Aneurysm. Semi-external hemorrhage: Bleeding into tracts that come in contact 5. Amyloid angiopathy (Alzheimer). With the external environment, so it will show up sooner/later. 6. Bledding disorder (Leukemia, Hemophilia, etc). of weath E.g. bleeding into the lungs will eventually show blood during coughing. 7. Vascular abnormality cause the main Eg bleeding into lower GI - bloody stool / upper GI - bloody vomit Classification by type of vessel: Types: Epidural Hematoma: in all typesis [ Arterial hemorrhage: Fast & bright red in color. cere ! Resemble Due to traumatic injury, causing arterial tear. Venal hemorrhage: Slow & dark red in color. hematoma if they are not Subdural Hematoma: hernia huge Parenchymal hemorrhage: Small red dots from capillaries. · Due to trauma (may be mild), causing venal tear. Outcome: Subarachnoid hemorrhagic focus: fande it  Hematoma: Primarily pathological due to other pathology, or due to trauma. S like hypertension atherosclerosis Blood exit the vessel & compresses the tissue without destroying it. We Intraparenchymal hemorrhagic focus: , can see a bruise & hemosiderosis accumulation, but NO necrosis. Usually non-traumatic, due to hypertension / tumors / amyloid.  Hemorrhagic Focus: Blood exit the vessel & destroys the tissue, causing its necrosis. * We can see a mixture of blood & dead tissue cells. Epidural Hematoma: Types of hemorrhage (according to size): Bledding into the space between the dura & skull, caused by a tear in Petechial hemorrhage: Small 1-2mm pinpoint hemorrhage. middle meningeal artery, but no brain damage, due to blood drainage. Due to low platelet (thrombocytopenia) / sudden hypoxia / fat emboli. Usually caused by traumatic injury, like skull fracture. Purpura hemorrhage: Diffused, 3-5mm superficial skin hemorrhage. Characterized by lucid interval. & Due to low platelet / trauma / increased vascular fragility (e.g diabetes). Leads to cerebral herniation due to increased intracranial pressure. Ecchymosis hemorrhage: Large, 1-2cm superficial skin hemorrhage. Treatment is by drilling holes in the skull in order to release pressure. Change color (blue, green, yellow) & may appear with coagulation disorder. Subdural Hematoma: Shock: Capacity of the vascular system & circulating blood volume # Bleeding into the space between the meninges, caused by veins tearing, Disproportion between vasculature volume & circulating blood volume, which is self-limiting, so no damage occurs to the brain tissue. Caused by hypoperfusion & hypoxia. Usually caused by trauma. Stages: 2 types depending on the speed of their onset: Compensated: Vital organs perfusion maintained by reflex (heart,brain). Acute: Fast spread of bleeding, which is life threatening. Decompensated/progressive: Decreased perfusion to vital organs. Chronic: In elderly with brain atrophy, after minor head trauma. Irreversible: Organ failure & death. Subarachnoid hemorrhagic focus: Types of Shocks: Bleeding into the subarachnoid space, between arachnoid & pia mater. Hypovolemic Shock: Usually non-traumatic & spontaneous, due to other pathology. Caused by decreased intravascular blood volume. May be secondary to trauma. Due to hemorrhage or fluid loss (burns / vomiting / dehydration). Causes: Cardiogenic Shock: Rapture of Berry aneurysm (80%) / Tumor / Hematologic disturbance. Caused by pump failure, bradycardia !I Intraparenchymal hemorrhagic focus: Due to MI / tamponade / arrhythmia / pulmonary embolism. Focused bleeding into the cerebral parenchyma, Caused by a rapture of Distributive shocks = loss of vessels tonus due to vasodilation: small Intraparenchymal vessel, secondary to chronic hypertension. Circulatory volume is normal & we do not loose blood, Usually pathological (non-traumatic). But the vessels are dilated & need more blood to be filled. Causes: Septic Shock: Hypertension / Vascular malformation / Cerebral amyloid / Tumors / Caused by bacterial/fungal infection. 3 Infections / Hemorrhage in a previous brain ischemic infraction. of oxygen - Trigger vasodilation, capillary leakage & coagulation disturbances. an absence Stages: - Results in decreased perfusion & systemic inflammation & failure. - 1. Extraversion of blood, with compression of adjacent parenchyma. Neurogenic Shock: Caused by disruption of the autonomic nervous system, 2. Early lesions of clotted blood, surrounded by anoxic changes & edema. 3. When edema resolves, hemosiderin pigmented macrophages appear. Due to injury of the central nervous system (spinal cord). 4. After a month, cavern filled with clear fluid is seen (brain necrosis). - Trigger vasodilation & bradycardia & cause systemic damage. Outcome – depends on the size & location: Anaphylactic Shock: adrenaline level ? Increased intracranial pressure, causing brain herniation. Caused by IgE mediated hypersensitivity reaction to allergen. First 48h are critical, but if patient survives, hematoma slowly resorbed. - Trigger vasodilation by histamine & bradykinin release from mast cells. Complications: Liquefactive necrosis / hemosiderosis / coma / death. - Result in decreased blood pressure & bronchoconstriction. Left Cardiac Failure: Right Cardiac Failure: * The heart fails to pump efficiently, causing incomplete emptying of the The chambers dilated & pressure is increased, preventing adequate chambers & they become dilated, leading to a progressive rise in emptying of systemic venous blood from vena cava into right atrium. pressure in one chamber, which is reflected back into the vessels. The primary cause of right heart failure is left heart failure. Leads to poor systemic arterial perfusion: May also result from right ventricle infarction or pulmonary embolism. The insufficient blood pumped into the aorta & arterial system, leads to Leads to poor pulmonary perfusion of the lungs: hypotension, poor perfusion & poor oxygenation of tissues. The insufficient blood pumped into the lungs, leads to breathlessness. Leads - to increased pulmonary pressure: Leads to increased pressure in the systemic system: The high pressure in the pulmonary system, leads to accumulation of - High pressure in superior vena cava, leads to jugular v. engorgement. low protein fluid in the air sacs, causing pulmonary edema. - High pressure in inferior vena cava, leads to congested liver (nutmeg). - High pressure in small venules & capillaries of lower limb, leads to transudation of fluid into interstitial tissues & subcutaneous edema. Steatosis cardiaca: Adipositas Cordis (rare): * * Accumulation of lipid droplets in cardiac muscle, Diffuse fatty tissue infiltration into myocytes. Due to cells being unable of metabolizing fat. Occurs in the ventricular myocardium or the interventricular septum. Patterns of accumulation: In extreme causes, especially when the septal region is involved, In prolonged moderate hypoxia: 3 It can lead to secondary arrhythmogenic cardiomyopathies, Tiger effect of the myocardium – yellow (fat) & red-brown (normal). Where Non-ischemic scar fibrosis is formed & can lead to hypertrophy. In profound hypoxia / myocarditis: More uniformly affected myocytes – yellowing of the myocardium. Adiposis cardiaca: Red Infraction of the small intestine: Accumulation of adipose tissue within the heart. * When the Loop of small intestine slides into the hernia, causing the Mostly due to post myocardial infarction ischemia. gate of hernia to narrow so it is compressing the veins. In the early stage: Because we still have arteries working & only veins are obstructed, Fat is located beneath the epicardium. We will see congestion, edema & inflammatory process. In the later stage: Eventually the pressure on the gate of the hernia will be getting bigger, Fat accumulates between myocytes, leads to cardiac insufficiency. causing the arteries to be closed as well – this will cause red infraction, In the formally congested area & will be reddish, heavy & wet.