Anapath
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| What techniques are used for liquid cytology? | Centrifugation (cell block, fixation, tissue processing and embedding) |
| How to get tissue samples? what are the types? | Biopsy Needle biopsy (0.6-1.5 cm) Endoscopic biopsy (0.5-5 mm) Surgical biopsy (excision) Large surgical specimens (in OR) partial organ excision, or complete organ excision |
| What are the different technical routine steps? | Fixation, Examination, TIssue processing, Embedding, Cutting and Staining |
| What is fixation? | Essential to preserve cell morphology, should be immediately done after sampling. Fixation done by formol (LM) and Gluta (EM) Duration of fixation depends on size, 2-5 hours for biopsy and 24-48 hours for surgical specimens |
| What is tissue processing? | Dehydration by putting it in alcoholic mediums, then remove alcohol and transfer to xylol then heated paraffin at 50 degree infiltrate the tissue. Takes 12-16 hours, automated process by a machine For hurry specimens we can make a 3 hour processing but not so reliable |
| What is embedding? | Manual process, heated paraffin is put to freeze in -5 degrees |
| What is cutting? | Using a microtome for very thin sections, 3-5 microns. Then sections are put on a slide on water drop |
| What is staining? | First remove paraffin, then put stain (nuclear or acidic cytoplasmic stain) Safaran stains collagen. A coverslip protects stained tissue Takes 1 hour or less than 15 min |
| What are frozen sections? | Less than 15 mins, for need of fast decision for surgery, -25 degrees sections are 3-5 micons Limited since change cell morphology, limited nb of samples submitted, calcified tissues cant be cut. Used for determine nature of lesions (cancer or inflammatory) |
| What are special stains? | There are two kinds, natural and man-made, aqueous or alcoholic usually cytoplasmic stains (Eosine (pink), phloxine (manmade, stains acidophillic), Safran (from crocus flower, stains collagen) Nuclear stains (Carmen (from cochineal flower), Orceine (From lichens) and hematoxylin (from campeche wood, colorless should be oxidized to give a purple color) |
| What is EM? | ➢ Need for a special fixative solution : glutaraldéhyde, … ➢ Embedding in resin ➢ The indications for diagnostic purposes are very limited (abnormalities of the bronchial cilia, hereditary diseases of the basal membranes of the skin and of the renal glomerulus) |
| What happens when cells encounter physiological stress or pathological stimuli? | Cells undergo adaptation to achieve a new state and preserve viability and function These adaptations are Hypertrophy, hyperplasia, atrophy, metaplasia This may be reversible when stress is done, and may lead to cell injury if stress level exceeds adaptive capacity. Some injuries are reversible, others are not and lead to cell death by necrosis or apoptosis |
| What is hypertrophy? | Cell size increase thus organ size increase, occurs when cells have limited capacity to divide, in response to increased workload. Induced by growth factor, could occur with accompanying hyperplasia leading to enlarged organ |
| What is hyperplasia? | It occurs for tissues capable of replication, induced by growth factors, can be pathologic or physiologic. Two types: hormonal (like female breast hypertrophy) or compensatory (by removal or loss of an organ part) Most pathological ones are caused by hormonal excess |
| Give examples on pathological hyperplasia? | Endometrial hyperplasia by disturbed estrogen and progesterone levels, causing abnormal menstrual bleeding. Growth factors repair vessels and tissues by proliferating fibroblasts Viral infections also increase growth factor (like papilloma causing skin warts and mucosal lesions) |
| What is the relationship between hyperplasia and cancer? | Usually hyperplasia is responsive to normal regulatory control mechanisms, if they get out of control , we reach cancer. Also hyperplasia is a fertile soil to get cancer (pt with endometrial hyperplasia have an increased risk to get endometrial cancer) |
| What is atrophy? | It is the shrikage in size of cells, may lead to shrikage in organs if nb of cells is big. Due to decreased cell activity by decreased workload (immoblization of limb), loss of innervation, diminished blood supply, nutrition, endocrine stimulation , and aging |
| What is metaplasia? | It is replacement of a cell type to another in response to chronic stress and irritation in order to further adapt to this irritation Like squamous metaplasia, although protective to cells, but leads to loss of function (like mucus secretion) and may be malignant (lung cancer) Sometimes can get from squamous to columnar (like in case of gastric reflux Can occur to mesenchyma pathology (bone erosion to soft tissue) |
| What is reversible cell injury? | During early injury it is still reversible where no severe membrane damage or nuclear dissolution occurs |
| What are the causes of cell injury? | Hypoxia, chemical agents, infection, autoimmunity, genetic defects, nutritional imbalances, physical agents, and aging |
| How does hypoxia cause cell injury and death? | It interferes with oxidative respiration, it is different then ischemia which is loss of blood supply, as it may also be caused by pneumonia, anemia, or CO poisoning (which complexes with Hb and form a stable form) |
| How to distinguish a reversible cell injury? | Two manifestations (swelling and fatty change) swelling due to no ion pumps, fatty change is appearance of small or large lipid vacuoles in cytoplasm |
| What is cellular swelling? | First manifestation of cell injury, reversible, seen better when whole organ is affected by increasing its mass, turgor and pallor (capillary compression) AKA hydropic change or vacuolar degeneration |
| What is fatty change? | Appearance of lipid vacuoles in cytoplasm, cells participating in fat metabolism (liver cells) also shows eosinophilic staining with progression to necrosis becomes more pronounced |
| What are cellular changes in reversible injury? | Plasma membrane alteration (blebbing, distortion of microvilli) Mitochondrial changes (swelling, phopholipid rich density) ER dilation (detachment of ribosomes) Nuclear alterations (clumping of chromatin) |
| What is cell death? | As damage continues, cells get to a point of irreversible damage and thus death, two types (necrosis and apoptosis) that differ in mechanism, morphology and disease physiology |
| What is necrosis? | It is a pathway of cell death, where cytoplasmic membranes are damaged releasing toxins to the cell. Cytoplasm gets more eosinophilic, more glassy appearance due to glycogen loss, increased myelin figures, vacuolated month-eaten cytoplasm due to organelle digestion by enzymes Nuclear changes are karyolysis (no more basophilia due to DNA damage), pyknosis (nuclear shrink due to DNA decondesation), karyorrhexis (fragmented nucleus) 1-2 days nucleus disappears |
| What happens to necrotic cells after death? | May either be digested by enzymes, or replaced by myelin figures and either phagocytosed or degraded into fatty acids which may bind calcium and get tissue calcification. |
| What are the patterns of necrosis? | Coagulative, liquifactive, gangrenous, caseous, fat necrosis, fibrinoid necrosis |
| What is coagulative necrosis? | Characteristic of infarcts in all solid organs except brain. It is death of cells with preservation of underlying architecture, and dead tissue forms a firm texture. Dead cells are not directly removed, it need leucocytosis in order to start degradation (takes days or weeks) |
| What is liquefactive necrosis? | In bacterial/ fungal infections where inflammation and enzymes liquify the tissue, usually in CNS, completely digested dead cells. If by bacteria it forms pus |
| What is gangrenous necrosis? | Limb lost blood supply and had caogulative necrosis involving many tissue layers, could be accompanied by liquification if bacteria is present and attracts leukocytes (wet-gangrene) |
| What is caseous necrosis? | In TB, cheese like, Fragmented or lysed cells, amorphous pink appearance in H&E stain, completely obliterated cellular outline and tissue architecture. If enclosed in an inflammatory border then it is called a granuloma. |
| What is fat necrosis? | Focal areas of fat destruction, due to release of pancreatic lipases in acute pancreatitis, liquify membranes of fat cells in peritoneum that may combine with calcium (fat saponification) |
| What is fibrinoid necrosis? | Special form where Ab-Ag complexes accumulate in arterial walls, leaks out of the vessels producing an amorpous bright pink appearance called fibrinoid |
| What is apoptosis? | When no GF or DNA is damaged cell kills itself. Nuclear dissolution without loss of membrane integrity. Not necessarily pathological, no inflammatory response. |
| What are intracellular accumulations? | Cells may accumulate substances, may be harmless or cause cell injury, due to an abnormality in cell metabolism. May be endogenous or exogenous substances. |
| What are the three main pathways of intracellular accumulations? | Inadequate removal and degradation of an endogenous substance (hepatic steatosis, cholestasis) Excessive production of endogenous product (hemosiderosis, a1-antitrypsin deficiency, lysosomal disease glycogenosis...) Abnormal exogenous substance accumulate (carbon, silica) |
| What is steatosis (fatty changes)? | Accumulation of TGs in parenchymal cells, most often in liver but may occur in heart, muscle, kidney or other organs Causes: toxins, protein malnutrition, DM, Obesity (most common cause in industrial countries, hypoxia, infection. |
| How is the gross appearance of steatotic liver? | Size increase, soft consistency, yellow color, leaves a mark of fatty deposits on the blade |
| What are the microscopic appearances of liver steatosis? | Cytoplasm of hepatocytes have optically empty vacuoles (with paraffin embedding) Steatosis appears in two forms (macrovauolar - push nucleus to the periphery, microvacuolar - central nucleus) It is a reversible lesion resolved by cessation of agression |
| How do cells get cholesterol intracellular accumulations? | Usually cholesterol is controlled by membrane generation, but cells may get overloaded with lipids (cholesterol and TGs) by increased intake or decreased catabolism Atherosclerosis is most important one |
| How to proteins accumulate intracellular? | Less common than fat accumulation, in kidney nephrotic syndrome causes heavy protein leakage of glomerular filter thus increased reabsorption (of albumin) giving pink hyaline cytoplasmic droplets in cells of proximal tubule If it persists, proteinuria abates (decreases) Another example is Igs accumulate in RER of plasma cells forming eosinophilic Russel bodies |
| How do glycogen accumulate intracellular? | Associated with abnormal glucose/ glycogen metabolism. Most typical is poorly controlled DM with glycogen accumulation in renal tubule epithelium, cardiac myocytes, beta cells of langerhans Glycogen could also accumulate in cells with genetic disorders called glycogenoses |
| How is intracellular pigment accumulation? | Exogenous (carbon) or endogenous (lipofuscin, melanin, Hb derivatives) accumulate. Most commonly carbon going to tracheobronchial lymph nodes blackening the nodes and the pulmonary parenchyma (anthracosis) |
| Talk about lipofuscin pigment intracellular accumulation. | Brown-yellowish pigment accumulates with cell aging, complex of lipid and protein accumulate in a variety of tissues with aging or atrophy not injurious but a marker of past free radical injury Could cause brown atrophy |
| Talk about melanin pigment intracellular accumulation. | Could go to basal keratinocytes of skin or dermal macrophages causing black color to screen against UV) |
| How is cholestasis intracellular accumulation? | Visible accumulation of bile in liver tissue, turns liver green, accumulation in interhepatocyte canaliculi or interlobular bile ducts and sometimes seen in heptocytes Caused by bile duct obstacles, toxic liver injury, viral liver injury |
| How is hemosiderin intracellular accumulation? | Hb derived pigment, golden yellow - brown, in tissues with excess iron (ferritin micelles...) identified by Prussian blue histochemical rxn (Perls) usually pathological, but small amounts in bone, spleen, liver may be normal. Excessive accumulation - Hemosiderosis- is seen in hemochromatosis rarely could be exogenous |
| What is localized hemosiderosis? | Related to gross bleeding , lysed RBCs, lysosomes of macrophages transform Hb to hemosiderin explaining variation in color of traumatized areas. Like: cardiac lung siderosis, tatooed scars from hemorrhagic infarcts, evolution of thrombosis |
| What is generalized hemosiderosis? | Increase body iron in poly visceral overload, in macrophage and parenchymal cells. Macroscopically visible by brown discoloration of viscera, hardness of viscera, screeching noise in cutting |
| What are the causes of generalized hemosiderosis? | Primitive or secondary mechanisms involved : increased duodenal absorption of dietary iron, abnormal iron use, refractory anemia/ hemolysis, repeated blood transfusion |
| What is primitive generalized hemosiderosis/ hemochromatosis? | Inherited autosomal recessive transmission, iron accumulate in parenchyma causing destruction and fibrosis Mostly affects liver, pancreas, heart and endocrine glands From iron stock 30-50 g (10 times normal) |
| How is liver hemochromatosis? | Iron present in hepatocytes, kupffer cells, portal space macrophages. Hypertrophic rust-colored micronodular cirrhosis. Commonly causes hepatocellular carcinoma, with massive iron overload. |
| Talk about organs other than liver involved in hemochromatosis. | Myocardium (leads to subendocardial fibrosis can be cause of heart failure) Endocrine Glands (Involved in hormonal insufficiency- ant pituitary decreasing GnRH..) Skin and Mucosa (special hyperpigmentation, due to presence of hemosiderin in histiocytes of dermis and sweat glands/ epidermal melanosis following pituitary insufficiency) |
| What is secondary generalized hemosiderosis? | Pure hemosiderosis without sclerosis Iron accumulates in phagocytes in liver/lymph nodes/skin, parenchyma are affected. |
| What is pathological calcification? | Increase in Ca, iron, Mg and other minerals all together. Occur in 2 ways, dystrophic calcification, Metastatic calcification |
| What is dystrophic calcification? | Normal Ca deposition but deposit in injured tissues, usually in advanced atherosclerosis, but can be found incidentally with insignificant past cell injury, and may cause organ dysfunction (of damaged heart valves -->compromised valve motion, like aortic stenosis) Starts from extracellular accumulation due to injury, usually calcium and phosphate |
| What is metastatic calcification? | Associated with hypercalcemia, by increased PTH, destruction of turnover mechanisms, tumors, immobilization, vitamin D intoxication and sarcoidosis, and renal failure in which phosphate retention leads to secondary hyperPTH |
| How is the morphology of pathological intracellular calcification? | Fine white granules, felt as gritty deposits Dystrophic is common in caseous necrosis TB and could become radiopaque stone. Basophilic deposits. In lungs could cause respiratory deficits and massive deposits in kidney can lead to renal damage. |
| What are lysosomal overloaded diseases? | Genetic abnormality in a protein important for lysosomal function, causes accumulation of metabolite, may affect glycogenesis, sphingolipids (GM1 and GM2) and mucopolysaccharides Dx by biopsy and stains |
| What is amyoidosis? | Intercellular deposit, extracellular fibrillar proteins accumulate and causes tissue damage. Same morphology with all various protein types causing amyloidosis (30 different proteins) Formed of interwind beta pleated sheath, 95% fibrils and 5% glycoproteins. |
| What are the three most common forms of amyloid? | AL (light amyloid) : Ig light chain as a whole or amino terminal or both. AA (amyloid-associatated) : composed of protein derived from proteolysis of a larger precursor protein called serum amyloid-associated (SAA) synthesized in the liver. beta amyloid (Abeta) derived from proteolysis of much larger glycoprotein called amyloid precursor protein |
| What are the classifications of amyloidosis? | Amyloidosis results from abnormal folding of proteins causing beta pleated sheath and with the inability to get degraded causes their accumulation extracellularily. Primary amyloidosis, Reactive systemic amyloidosis and other forms of amyloidosis are present |
| What is primary amyloidosis of plasma cell proliferation? | AL type, systemic distribution, most common form of amyloidosis. clonal proliferation of plasma cells forming Igs Occurs with pt of multiple myeloma (15%) tumor, but most are not associated with the tumor. |
| What is reactive systemic amyloidosis? | AA type, systemic distribution, previously called secondary amyloidosis (secondary to inflammation) Causes: TB, bronchiectasis and chronic osteomyelitis and Abx treatment, RA, Ankylosing spondylitis, IBD (Crohn and ulcerative colitis) |
| What are other forms of amyloidosis? | Heredofamilial (familial med fever) Hemodialysis associated (deposits form beta2-microglobulin) Localized amyloidosis (nodular deposits in lung, larynx, bladder, tongue, eye...) Endocrine amyloid (medullary carcinoma thyroid, islet tumors of pancreas, pheochromocytoma...) Aging amyloid (systemic in elderly) |
| How does amyloidosis appear macroscopically? | Accumulates in large amounts, organ enlarged, gray tissue, waxy firm consistency |
| How is the histology of amyloidosis? | Always extracellular, between cells close to basement membrane. Plasma cell proliferation is associated with perivascular and vascular deposits H&E stain amorphous eosinophilic extracellular substance. Congo red stain pink but green perifringence of stained amyloid. subtyping by mass spectroscopy. |
| How does amyloidosis affect the heart? | Involved in senile systemic amyloidosis, enlarged and firm with no change on gross inspection. Histologically starts as focal subendocardial accumulations and within myocardium between myofibrils, causing pressure atrophy of heart muscle. In addition to EKG changes due to subendocardial deposits |
| How does amyloidosis affect the liver? | Inapparent grossly but may cause hepatomegaly. Starts at space of disse then goes to hepatic parenchyma and sinusoids. Could cause with time deformity, pressure atrophy, hepatocyte disappearance -->total replacement of a large part of the liver. Vascular involvement and deposits in kupffer cells, usually preseved liver function |
| How does amyloidosis affect the kidneys? | Most common and serious complication of amyloidosis, normal usually but if severe they may shrink because of ischemia by vascular narrowing due to the deposits within arterial walls. May deposit in glomeruli as subtle thickening of mesangium, causing distortion of glomerular vascular tuft and capillary narrrowing |
| How does amyloidosis affect the spleen? | May be inapparent or splenomegaly. 2 distinct patterns of accumulation: Splenic follicules (tapoica-like granules, sage spleen), and Splenic sinuses walls and connective tissue framework in red pulp Could create lardaceous spleen if connected amyloidosis |
| What are effects of amyloidosis on various organs? | Tongue: Nodules causing macroglossia tumor forming. Respiratory tract: Larynx down to smallest bronchioles Brain: Alzheimer plaques , or autonomic NS for familial amyloidotic neuropathies. |
| What are lesions related to aging? | Related genes of aging are acrogeria and progeria, cellular aging causes organ aging. Some organ systems get damaged due to aging by 2 mechanisms: determined genetic clock (Incomplete replication causing telomere shortening and clock gene involvement) And external factors (repari stopped) |
| How does cell function get affected by aging? | Reduced cell function, irreversible oxidative damage accumulation (lipofuscin for example), reduced chromosome repair, decreased ability to multiply, acceleration of apoptosis... |
| How is the morphological aspect of organ aging? (lung, vessesls and heart) | Not all organs age at the same rate. Production of elastase increasing with age, Organs rich in elastic fibers age the fastest. The aging of many organs is characterized by atrophy. Lung : destruction of alveolar elastic fibers. Vessels : calcification and stiffening of the wall of elastic arteries, intimal thickning of aortic wall Heart : decrease of myocardial cell, accumulation of lipofuchsine, and calcifications of aortic and mitral valves |
| How is morphological aspect of aging on osteoarticular, kidney and GI? | Osteoarticular system : almost inevitable beyond the age of 60; bone mass is reduced (osteoporosis); muscles atrophy and are partially replaced by fatty tissue; joint cartilages deteriorate and are no longer repaired by chondrocytes, tendons Ligaments stiffen under the effect of glycosylation. Kidney : Glomerular anf interstitial fibrosis. GI tract: Progressive atrophy of mucosa Decrease of the regeneration potential of epithelial cells Decreased activity of glandular cells. |
| How does skin appear with aging? | The distribution of lesions is heterogeneous according to the different parts of the body; thinning of the skin, especially by thinning of the dermis, the elastic fibers of which become scarce, and the collagen of which becomes rare and stiffens under the effect of glycosylation. The basal layer flattens out by reduction of the elastic fibers of the papillary dermis. Wrinkles appear with a decrease in the subcutaneous adipose tissue. The skin becomes dry, and the secretions of the sebaceous and sweat glands decrease. The hair follicles are less numerous and the melanocytes become scarce leading to the bleaching of hair and body hair. In addition, there are lesions related to exposure to solar radiation: elastosis, actinic keratosis, Dubreuilh's melanosis. |
| How is CNS aging? | During normal aging the weight of the brain decreases slightly The meninges thicken and are fibrous The cortex atrophies and the ventricles are dilated. The number of neurons in the cortex and the hippocampus decreases Senile plaques can be seen in the hippocampus as well as neurofibrillary degeneration. Changes in enzymes and neurotransmitters can have a physiological impact on functional networks Alzheimer's disease is not linked to aging, but its frequency increases with age |
| What is an inflammation? | Beneficial host response to foreign invaders and necrotic tissues, but can cause tissue damage. Main components are vascular reaction and cellular response. Steps are recognition of injured agent, recruitment of leukocytes, removal of agent, repair |
| What are the general causes of inflammation? | Infection, tissue necrosis, foreign bodies, trauma, immune response. Epithelia, macrophages, DC, leukocytes recognize the microbes and necrotic tissues by their PRRs, while microbes in blood are recognized by circulating proteins. Outcome of acute inflammation is elimination of the stimulus, repair of damaged tissue or persistent injury thus chronic inflammation. |
| What is acute inflammation? | It consists of 3 components: Dilation of small vessels, Increased permeability of microvessels, migrating leukocytes from microcirculation to the injury focus to eliminate the offending agent |
| What are the different features of chronic and acute inflammation? | Onset (fast vs slow) Cellular infiltrate (neutrophils vs macrophages and lymphocytes) Tissue injury (mild vs severe progressive) Local signs (prominent vs less) |
| What is the blood vessels reaction in acute inflammation? | Changes in blood flow and permeability, to maximize movement of plasma proteins and leukocytes to site of injury. Fluid and proteins leave the vascular system by exudation process (exudate: rich in proteins, Transudate : poor in proteins via osmotic imbalance) |
| What is edema? | Excess fluid in interstitial tissue, can be exudate or transudate. Pus is a purulent exudate rich in leukocytes, dead cell debris and microbes (maybe) |
| How do vessels react with inflammation? | Vasodilation induced by mediators (histamine), it is the first manifestation of inflammation (may be preceded by vasoconstriction. Starts with arterioles and moves to capillaries leading to increased blood flow to site of inflammation (causing erythema and chalour) It is followed by increased permeability of vessels outpouring exudate. Slower blood flow and increased viscosity occurs. Resulting in stasis of blood flow and seen as vascular congestion with localized redness causing neutrophils to accumulate. |
| How is increased vascular permeability occurring in endothelial cells? | Retraction of endothelial cells (opening interendothelial spaces, elicited by histamine, bradykinin, leukotrienes, other chemicals. Occurs after exposure to mediator short lived, immediate transient response. Occurs at post-capillary venules Endothelial injury also increases vascular permeability due to necrosis and detachment, so direct damage to endothelium is encountered in severe injuries, neutrophils adhere to injured endothelia and amplify this reaction. Starts just with the injury and stays hours until damaged vessels are thrombosed or repaired |
| How is the leukocyte recruitment to site of inflammation? | Mostly neutrophils (rapid) and macrophages, neutrophils use enzymes to mount response while macrophages use new transciption. Mediated by adhesion molecules and cytokines. |
| How is leukocyte adhesion to endothelia? | Laminar flow gets leukocytes to post-capillary venules wall, then when blood stasis occurs white cells position along endothelial surface (margination), then they detect endothelial change and adhesion molecules to roll through endothelia and adhere to injury point (all mediated by cytokines) |
| How is leukocyte migration through endothelia? | By squeezing in between process called transmigration (in post-capillary venules) Driven by chemokines Igs and Platelet Endothelial Cell Adhesion Molecule (PECAM-1) mediate binding event. They pierce the basal lamina secreting collagenase, vessel wall not injured. |
| What are adhesion molecules? | Selectins (weak interaction between leukocytes and endothelium) e.g: L, E and P selectins ( L neutrophils other endothelium) Integrins (firm reaction) e.g: LFA, MAC, VLA, a4b7 |
| What is chemotaxis of leukocytes? | Leukocyte movement to site of injury after leaving the circulation stimulated by chemical. Exogenous and endogenous chemotactic molecules (bacterial, cytokines, complements (C5a), Lipooxygenase pathway of AA) Nature of leukocyte infiltrate depends on the age of inflammation and type of stimulus (starts neutrophils becomes lymphocytes and macrophages) |
| How is phagocytosis and clearance of offending agent? | Leukocyte activation after recognition of microbes, then they destroy them by phagocytosis and intracellular killing (after becomes active) Sequential steps of phagocytosis are Recognition, Engulfment, and Killing |
| How is the recognition by phagocytic receptors for phagocytosis? | Its effieciency increases when microbes are opsonized (by Igs, C3b and lectins which are recognized by leukocytes) |
| How is engulfment process of phagocytosis? | Pseudopods (cytoplasm extensions) flow around microbe, then enters as a phagosome, which fuses lysosome and starts degrading it. Phagocyte may also release some granule contents to extracellular space damaging innocent cells |
| How is intracellular destruction of microbes and debris occurring? | By ROS, reactive nitrogen species (RNS), derived from NO and lysosomal enzymes. This is the final step of elimination of microbes and necrotic cells. Cells may also release toxins and proteases extracellularly |
| What are ROS? | Reactive oxygen species, produced by rapid assembly and activation of enzyme phagocyte oxidase (NAPH oxidase) forming superoxide (O2.) In neutrophils it is called respiratory burst, and ROS are produced in phagolysosomes where superoxide is then transformed into H2O2. Then myeloperoxidase enzyme converts H2O2 to OCl2- hypochlorite, which is the anti-microbial agent destroying bacteria by halogenation or oxidation. |
| Talk about NO? | NOS induces production of NO when macrophages are activated by cytokines or microbial products, NO reacts with O2. generating high reactive peroxynitirite which attack damage lipids, protein nucleic acids of microbes NOS presents in cytoplasm and exerts NO to lysosome |