Histology of Connective Tissue II PDF

Histology of Connective Tissue II By: Dr. Moustafa Al Sawy Dr. Shaimaa Mohamed Amer MBBCH, M.SC. M.D HISTOLOGY MBBCH, M.SC. M.D HISTOLOGY Associate Professor of Histology & Cell Bi...

Histology of Connective Tissue II By: Dr. Moustafa Al Sawy Dr. Shaimaa Mohamed Amer MBBCH, M.SC. M.D HISTOLOGY MBBCH, M.SC. M.D HISTOLOGY Associate Professor of Histology & Cell Biology Associate Professor of Histology & Cell Biology Certified Medical Educator Learning objectives Knowledge: Learning Objectives At the end of the lecture , each student will be able to: 1.Describe the histological structure of connective tissue cells (plasma & mast cells) by LM & EM and mention their function. 2. List the types of the connective tissue fibers & describe the histological features of each one 6. Plasma cells *They are originated from B lymphocytes. L.M: *They are ovoid in shape with small eccentric nucleus. * Their nucleus has heterochromatin radiating out from the center, giving it a characteristic cartwheel appearance (clock face). *The cytoplasm is strong basophilic with pale area represent Golgi apparatus called negative Golgi image. E.M: extensive RER, Golgi and numerous mitochondria. Function: 1-They are responsible for humeral immunity (Antibodies). 2-They are apparently present in submucosa of GIT.  Medical Application Multiple myeloma: Abnormal plasma cells called myeloma cells accumulate in bone marrow resulting in activation of osteoclasts which leading to painful, lytic bone lesions and consequent hypercalcemia. Also, causes suppression of hematopoiesis, which often results in anemia, leukopenia, and thrombocytopenia. The overproduction of immunoglobulin leads to myeloma nephropathy, which manifests with increased serum creatinine and hematuria. 7.Mast cells LM: They are oval or rounded in shape , abundant in loose CT along the blood vessels. *The nucleus is central & rounded. *The cytoplasm is full of basophilic secretory granules. EM: It has well developed Golgi, Mitochondria, Ribosomes and electron dense granules. Functions: 1-Secret heparin which is anticoagulant and act as cofactor for lipoprotein lipase to clear plasma from lipids. 2-Secret histamine which participate in antigen –antibody reaction in allergy. 3-Secret Eosinophilic chemotactic factor which stimulate Eosinophils migration to site of action. LM Mast cell EM mast cell  Sequence of events in anaphylaxis (Activation & degranulation): 1- The first exposure to an allergen as bee venom or tetanus antitoxin results in production of IgE by plasma cells. 2- IgE will bound to mast cells. 3- A second exposure to same antigen results in binding of antigen to IgE on the mast cell activating receptor coupling factors. 4 -This triggers release of primary mediators from granules liberating histamine, heparin, & ECF- A. o Histamine: Contraction of smooth muscle (mainly bronchioles). Dilates blood capillaries & increases their permeability. So that plasma leaks out; the skin appears red (wheals) and edematous (urticaria).  Sequence of events in anaphylaxis (Activation & degranulation): o Leukotriens (SRS-A): produce slow contraction of smooth muscle & increase vascular permeability. o ECF-A: attracts blood eosinophils. Heparin: blood anticoagulant, but blood clotting remains normal. 5. This leading to sever hypotension, mucosal edema of respiratory tract that can suffocation. N.B: Some drugs as penicillin and cephalosporins can cause acute urticaria by triggering IgE- mediated mast cell activation (type 1 hypersensitivity reaction).  Fibroblast Macrophage Mast cell Plasma cell Origin UMC Blood Monocyte UMC B-lymphocyte L/M: Shape Irregular branched Irregular branched oval or rounded. Oval cytoplasm basophilic Pale basophilic basophilic granular basophilic with-ve Golgi image, vacuolated spherical nucleus central pale nucleus, central nucleus Eccentric nucleus with cart with prominent eccentric kidney shaped wheel appearance of nucleolus nucleus chromatin. E/M Rich RER, well many lysosomes. Prominent RER & rich in RER & well-developed developed Golgi. well-developed Golgi, Golgi. membrane rounded heterogeneous granules, few mitochondria.  Fibroblast Macrophage Mast cell Plasma cell Sites C.T take different names in each -Skin -Areas subjected to organs: e.g. -GIT bacterial invasion as -Osteclast in bone -Respiratory intestine. -Microglia in CNS -Areas of chronic -Kupffer cell in liver inflammation. Function Fibroblast -Phagocytosis (ingestion and -Secretion of Synthesis of antibodies. produce all digestion) heparin. types of fibers -Make allergic & ground reaction substances. (histamine).  2.Connective tissue fibers C.T. fibers Collagen fibers Elastic fibers Reticular fibers 1.White Collagenous Fibers Triple helix (3polypeptide α-chains)  1.White Collagenous Fibers Characters: Color: the bundles are white in color in the fresh state. Tuff and resist stretch. It forms wavy bundles. The bundles branch but the single fiber does not branch. L.M. Acidophilic by H & E. Blue with mallory trichrome stain. E.M. (fibrils- fibers) *Each collagenous fiber is composed of fibrils. *Each fibril is formed of type-I tropocollagen molecules that are synthesized by fibroblasts. White Collagenous Fibers 2. Yellow elastic fibers  2. Yellow Elastic Fibers Characters: Color: yellow in the fresh state. Elastic in nature (can be stretched but recoil after release of the stretch). The fibers branch and may form elastic membranes. L.M.: Acidophilic with H & E. Yellow by Van- Gieson stain. E.M : Each fiber is formed of; Amorphous protein in the center called elastin. Microfibrills in the periphery called oxytalan fibers. Sites : *In the walls of arteries. * In the trachea, bronchi and bronchioles. *Ligamentum flavum between vertebrae. Yellow elastic fibers  Medical Application *Fibrillin is a family of proteins related to the scaffolding necessary for the deposition of elastin. *Mutations in the fibrillin gene result in Marfan syndrome, a disease characterized by a lack of resistance in the tissues rich in elastic fibers. Because the large arteries are rich in components of the elastic system and because the blood pressure is high in the aorta, patients with this disease often experience aortic swellings called aneurysms, a life-threatening condition.  Medical Application Degradation of elastic fibers occurs enzymatically via pancreatic elastase enzyme. Elastase enzyme is inhibited by α1- antitrypsin. Autosomal dominant defect in α1- antitrypsin leads to increased elastase activity, which can cause lung emphysema (damage of lung alveoli due to loss of supporting elastic fibers)  3. Reticular fibers Characters: They are very thin fibers that branch and anastomose to form a network. L.M. Not stained with H & E. Stained brown to black with Silver. E.M. Composed of type- III collagen coated by glycoprotein. Sites: Stroma of parenchymatous organs e.g. Liver, spleen and lymph nodes. Reticular fibers  3.Ground substance *It is the intercellular in which the fibers and cells are embedded. *Ground substance is soluble in most of the solvents used to prepare histological sections and therefore not visible in ordinary sections. *It is made of a complex mixture of glycosaminoglycans & glycoproteins. 1-Proteoglycans (Glycosaminoglycans , GAGs) *Consist of proteins (5%) and repeating of disaccharide units (polysaccharide chains) (95%) *For example, Hyaluronic acid ( non sulfated). ,Chondroitin sulfate , Dermatan sulfate, Keratan sulfate and Heparan sulfate. 2-Glycoproteins: *Conjugation of protein & carbohydrates. * For example : chondronectin, fibronectin, integrins and laminin. 3-Water. 4-Salts.  Medical Application *The degradation of proteoglycans is carried out by several lysosomal enzymes in certain cells. Deficiency of these lysosomal enzymes that degrade specific GAGs, leading to accumulation of these macromolecules in tissues causing of several disorders, including the Hurler and Hunter syndromes. Hurler syndrome is caused by a deficiency of a lysosomal enzyme that breakdown the dermatan sulfate and heparin sulfate (GAG). This finally results in the accumulation of large amounts of GAG in the body, eventually causing severely dysfunctional of the cells leading to their death. Hunter syndrome is a rare, inherited disorder in which the body does not properly digest (break down) sugar molecules (mucopolysaccharides) in the body. When these molecules build up in organs and tissues over time, they can cause damage that affects physical and mental development and abilities. Medical Application  Case Scenario A 43-year-old woman is brought to the emergency department 10 minutes after the sudden onset of shortness of breath, dry cough, nausea, and an itchy rash. The symptoms started 15 minutes after she had dinner with her husband and her two sons at a local seafood restaurant. She appears uncomfortable and anxious. Her pulse is 124/min, respirations are 22/min and slightly labored, and blood pressure is 82/68 mm Hg. Examination of the skin shows erythematous patches and wheals over her trunk, back, upper arms, and thighs. Which of the following cells are responsible for this condition? A) Fibroblast B) Plasma cells C) Mast cells D) Monocytes Any Questions? References: 1.Basic Histology: Text & Atlas. Editor: Luiz Carlos Junqueira, MD, PhD; Jose Carneiro, MD, PhD. 14th Ed. 2. Wheatear’s functional histology: A text & color atlas.15th Ed. 3. AMBOSS platform. Thank You