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Pathology
FA complete review Cellular Injury Part 1
| Question | Answer |
|---|---|
| What are cellular adaptations? | Reversible changes that can be physiologic or pathologic |
| What is Hypertrophy? | Increase structural proteins and organelles --> increase in size of cells |
| The cellular adaptation the causes increase in size of cells | Hypertrophy |
| What type of cellular adaptation results in increase number of cells? | Hyperplasia |
| What is hyperplasia? | Controlled proliferation of stem cells and differentiated cells --> increase in number of cells |
| What can be complications of excessive cell stimulation? | Pathological hyperplasia, which may progress to dysplasia and cancer |
| Definition of atrophy | Controlled tissue mass due to decrease in size and/or number of cells |
| How is a decrease in tissue mass due to decrease size done? | Increase cytoskeleton degradation via ubiquitin-proteasome pathway and autophagy. |
| What are some actions that lead to atrophy? | Disuse, denervation, loss of blood supply, loss of hormonal stimulation, and poor nutrition |
| Reprogramming of stem cells --> replacement of one cell type by another that can adapt to a new stress. | Metaplasia |
| What cellular adaptation occurs when one cell type is replaced by another? | Metaplasia |
| What are some common causes of metaplasia? | Cigarette smoking and irritation by gastric acid |
| What is dysplasia? | Cellular adaptation consisting of disordered , precancerous epithelial cell growth. |
| Loss of uniformity of cell size and shape; loss of orientation; nuclear changes. | Dysplasia |
| Precancerous epithelial uncontrolled growth. | Dysplasia |
| Severe dysplasia: | Usually becomes irreversible and progresses to carcinoma in situ. |
| Carcinoma in situ are commonly due to severe _______________. | Dysplasia |
| What nuclear irreversible cell injury changes? | 1. Pyknosis (condensation) 2. Karyorrhexis (fragmentation) 3. Karyolysis (fading) |
| What are clinical terms for Nuclear condensation, fragmentation, and fading? | Pyknosis, Karyorrhexis, and Karyolysis |
| Cellular membrane blebbing and nuclear chromatin clumping are examples of: | Reversible cell injury manifestations |
| Definition of Apoptosis: | ATP-dependent programmed cell death |
| Does Apoptosis require ATP? | Yes, it is a ATP-dependent activity |
| Apoptosis as ______________ and ______________ pathways. | Intrinsic and Extrinsic |
| What are the shared features between the intrinsic and extrinsic pathways of apoptosis? | Activate caspases --> cellular breakdown including cell shrinkage, chromatin condensation, membrane blebbing, and formation of apoptotic bodies, which are then phagocytosed. |
| What cellular action is characterized by deeply eosinophilic cytoplasm and basophilic nucleus, pyknosis, and karyorrhexis? | Apoptosis |
| How does Karyorrhexis occurs in apoptosis? | Fragmentation caused by endonuclease-mediated cleavage. |
| What is different in respect cell membrane between apoptosis and necrosis? | In apoptosis the cell membrane remains intact without significant inflammation. |
| What is an important and sensitive indicator of apoptosis? | DNA laddering |
| What is DNA laddering? | Fragments in multiples of 180 bp |
| The mitochondrial pathway refers to the ______________ pathway of apoptosis. | Intrinsic |
| When does the intrinsic pathway of apoptosis occurs? | As a regulating factor is withdrawn from a proliferating cell population. |
| What regulates the Intrinsic pathway of apoptosis? | Regulated by Bcl-2 family of proteins |
| Two PRO-apoptotic proteins: | BAX and BAK |
| Which Bcl-2 family proteins are anti-apoptotic? | Bcl-2 and Bcl-xL |
| What is the function of BAX and BAK? | Form pores in the mitochondrial membrane --> release of cytochrome C from inner mitochondrial membrane ito cytoplasm --> activation of caspases |
| Due to mitochondrial pore formation due to proapoptotic proteins what gets activated? | Caspases |
| What are caspases? | Cytosolic proteases |
| Caspase activation is associated with _______________. | Apoptosis |
| How does Bcl-2 prevent apoptosis? | Keeps mitochondrial membrane impermeable, thereby preventing cytochrome C release. |
| Bcl-2 overexpression ------->? | Decrease caspase activation ---> tumorigenesis |
| What are the two pathways of the Extrinsic Pathway of apoptosis? | 1. Ligand receptor interactions 2. Immune cell |
| What are the Ligand receptor interactions of the Extrinsic paths of apoptosis? | 1. FasL binding to Fas, or, 2. TNF-alpha binding to its receptor |
| What is the Immune cell pathway of the extrinsic apoptotic pathway? | Cytotoxic T-cell release of perforin and granzyme B |
| Fas-FasL interaction is necessary for: | Thymic medullary negative selection |
| What is the result of mutations in Fas? | Increased numbers of circulating self-reactive lymphocytes due to failure of clonal deletion |
| What is the result of defective Fas-FasL interactions? | Autoimmune lymphoproliferative syndrome |
| Necrosis is an ________________ process unlike apoptosis. | Inflammatory |
| What is the definition of Necrosis? | Enzymatic degradation and protein denaturation of cell due to exogenous injury --> intracellular components leakage. |
| When is Coagulative necrosis seen? | Ischemia/infarcts in most tissues (except brain) |
| Which is a tissue that does not show coagulative necrosis? | Brain |
| Coagulative necrosis is due to: | Ischemia or infarction; injury denatures enzymes ---> proteolysis blocked |
| Which type of necrosis is seen with Proteolysis blocked? | Coagulative necrosis |
| Histology of Coagulative necrosis: | Preceserved cellular architecture but nuclei disappear; Increased cytoplasmic binding of eosin stain |
| Histological view presents preserved cellular architecture, no nuclei, and increase cytoplasmic binding of eosin stain. | Coagulative necrosis |
| Liquefactive necrosis is seen with: | Bacterial abscesses and brain infarcts |
| What kind of necrosis is seen in brain infarcts? | Liquefactive necrosis |
| Why does liquefactive necrosis occur? | Neutrophils release lysosomal enzymes that digest the tissue |
| What are the main WBC type that carry out Liquefactive necrosis? | Neutrophils |
| What is the late histological view of Liquefactive necrosis? | Cystic spaces and cavitation (brain) |
| Which infections/conditions are seen with Caseous necrosis? | TB, systemic fungi (histoplasma capsulatum), and Nocardia |
| Macrophages wall off infecting microorganism --> granular debris. | Caseous necrosis pathogenesis |
| What is the histological features of Caseous necrosis? | Fragmented cells and debris surrounded by lymphocytes and macrophages. |
| Which type of necrosis is seen with the formation of granulomas? | Caseous necrosis |
| What are the main type of cells involved in Caseous necrosis? | Macrophages |
| Fat Necrosis is seen with: | 1. Enzymatic: acute pancreatitis 2. Nonenzymatic: Traumatic |
| Why does acute pancreatitis cause Fat necrosis? | Saponification of peripancreatic fat |
| Fat necrosis is due to; | Damaged cells release lipase, wich brask down triglycerides; liberated fatty acids bind calcium ---> SAPONIFICATION |
| Saponification is associated with _____________ necrosis. | Fat |
| Fat necrosis histological features | - Outlines of dead fat cells without peripheral nuclei - Saponification of fat appears dark blue on H&E stain |
| Vessel walls are thick and pink. Description of histological feature of ______________ necrosis. | Fibrinoid |
| What conditions produce Fibrinoid necrosis? | Immune reactions in vessels, preeclampsia, hypertensive emergency |
| How is fibrinoid necrosis produced? | Immune complexes combine with fibrin leading to vessel wall damage |
| Fibrinoid necrosis is considered what kind of hypersensitivity reaction? | Type 3 |
| What type of necrosis is seen in distal extremity and GI tract, after chronic ischemia? | Grangenous necrosis |
| Dry gangrenous necrosis is due to _________________. | Ischemia |
| Wet gangrenous necrosis is due to ________________. | Superinfection |
| Inadequate blood supply to meet demand. | Ischemia |
| What are the mechanisms that involve ischemia? | 1. Decreased arterial perfusion 2. Decreased venous drainage 3. Shock |
| What organ is the most vulnerable to hypoxia/ischemia? | Brain |
| What areas are of the brain most susceptible to hypoxia/ischemia? | ACA/MCA/PCA boundary areas |
| What are the most vulnerables regions to hypoxia? | Brain> Heart> Kidney> Liver> Colon |
| What type of cells are most affected by hypoxia? | Neurons, especially those include Purkinje cells of the cerebellum and pyramidal cells of the hippocampus and neocortex |
| What are two main types of infarcts? | Red infarcts and Pale infacts |
| What is another name for red infarcts? | Hemorrhagic infarcts |
| Red infarcts are due to: | Venous occlusion and tissues with multiple blood supplies, such as liver, lung, intestine, testes |
| What is the main concept behind the development of a red infarct? | Reperfusion |
| Damage or injury due to reperfusion is due to _________________. | Free radicals |
| What is another name for Pale infarcts? | Anemic |
| Which type of organs produce pale infarcts? | Solid organs with a single blood supply, such as heart, kidney, and spleen. |
| Which are the most common organs that have red infarcts? | Liver, lung, intestines, and testes |
| Heart, kidney, and spleen are often seen with __________ infarcts. | Pale |
| An organ with an end-arterial blood supply will most likely suffer on what kind of infarct? | Pale infarct |
| What is inflammation? | Response to eliminate initial cause of cell injury, to remove necrotic cells resulting from the original insult, and to initiate tissue repair. |
| What are the two main divisions of the inflammatory process? | Acute and chronic |
| What conditions lead to a harmful inflammatory response to itself (host)? | If it is: 1. Excessive (septic shock) 2. Prolonged (TB) 3. Inappropriate (autoimmune disease such as SLE) |
| What are the cardinal signs of inflammation? | 1. Rubor (redness), calor (warthm) 2. Tumor (swelling) 3. Dolor (pain) 4. Functio laesa (loss of function) |
| How is the rubor and calor developed in the inflammatory response? | Vasodilation (relaxation of arteriolar smooth muscle) --> increased blood flow. |
| What are the mediators of redness and warmth in inflammation? | Histamine, prostaglandins, and bradykinin. |
| What is the mechanism of action of Swelling caused by the inflammatory process? | Endothelial contraction/disruption --> increased vascular permeability --> leakage of protein-rich fluid from postcapillary venules into interstitial space (exudate) --> incrase in oncotic pressure |
| What is the end result of the process of swelling caused by inflammation? | Increased oncotic pressure due to increased level of proteins in the interstitial space. |
| What mediators cause or regulate endothelial contraction? | Leukotrienes (C4, D4, E4), histamine, and serotonin. |
| Sensitization of sensory nerve endings | Dolor (pain) |
| What are the mediators for dolor? | Bradykinin and PGE2 |
| What are the 3 systemic manifestations of inflammation? | Fever, leukocytosis, and increased plasma acute-phase reactants |
| When is leukocytosis commonly seen? | As a systemic manifestation of inflammation |
| What is leukocytosis? | Elevation of WBC count |
| What is a leukemoid reaction? | Severe elevation in WBC (> 40,000 cells) caused by some stressors or infections |
| What is the initial step in the pathogenesis of fever? | Pyrogens (LPS) induced macrophages to release IL-1 and TNF |
| Fever causes an increase in ______ in perivascular cells of the _______________. | COX activity ; Hypothalamus |
| What areas of the CNS is associated with the development of fever? | Hypothalamus |
| Which interleukin is notably for inducing acute phase reactants? | IL-6 |
| Where are acute-phase reactants produced? | Liver |
| Which are the POSITIVE acute phase reactants? | Ferritin, Fibrinogen, Serum amyloid A, Hepcidin, and C-reactive protein |
| Positive acute phase reactants _____________________. | Upregulate |
| What are the two most significant negative (downregulated) acute phase reactants in the process of inflammation? | Albumin and Transferin |
| Albumin and Transferrin are important ___________________. | Negative acute-phase reactants |
| What is the role of ferritin? | Binds and sequesters iron to inhibit microbial iron scavenging |
| What protein is known to inhibit microbial iron scavenging? | Ferritin |
| Ferritin binds to __________. | Iron |
| What is a coagulation factor, that is also a positive acute phase reactant? | Fibrinogen |
| Promotes endothelial repair; correlates with ESR; Coagulation factor involved in inflammatory process? | Fibrinogen |
| The level of fibrinogen is correlated with the amount of _______. | ESR |
| What are the two main roles of Hepcidin? | 1. Decrease iron absorption 2. Decrease iron release from macrophages |
| How does hepcidin decrease the amount of iron absorption? | Degrating ferroportin |
| What acute phase reactant is known to degrade ferroportin? | Hepcidin |
| The actions (prolonged) of hepcidin will result in the development of ___________________________. | Anemia of chronic disease (ACD) |
| C-reactive protein is an _________________________. | Opsonin |
| What is the main action or role of C-reactive protein? | Fixes complement and facilitates phagocytosis |
| Nonspecific sign of ongoing inflammation | C-reactive protein |
| What is the role of Albumin as an negative acute phase reactant? | Reduction conserves amino acids for positive reactants |
| Which two acute phase reactants are seen in lower levels during inflammation? | Albumin and Transferrin |
| What is the main reason for the low levels of albumin during inflammation? | Conservation of amino acids needed for positive reactants |
| What is the role of Transferrin (downregulated) during inflammation? | Internalized by macrophages to sequester iron |
| What is the abbreviation for Erythrocyte Sedimentation Rate? | ESR |
| What is ESR? | Products of inflammation coat RBCs and cause aggregation |
| The denser RBC aggregates ----> | Fall at a faster rate within a pipette tube --> Increase ESR |
| What is often co-tested with CRP levels? | ESR |
| What are common conditions with elevated ESR? | 1. Most anemias 2. Infections 3. Inflammation 4. Cancer 5. Renal disease (ESD or nephrotic syndrome) 6. Pregnancy |
| Which is the only anemia with a decreased ESR? | Sickle cell anemia |
| What product of inflammation is downregulated or lower in Sickle cell anemia? | ESR |
| Why is Sickle cell anemia manifested with a decreased ESR? | Altered shape of the RBC |
| List of conditions with decreased levels of ESR | 1. Sickle cell anemia 2. Polycythemia 3. Heart failure 4. Microcytosis 5. Hypofibrinogenemia |
| What is decreased in Polycythemia, heart failure, and microcytosis? | ESR |
| What WBC characterize acute inflammation? | Neutrophils in tissue |
| Acute inflammation is a manifestation of the ___________ immune system. | Innate |
| What is the most common clinical manifestation of acute inflammation? | Edema |
| Which are the MC mediators of acute inflammation? | Toll-like receptors, arachidonic acid metabolites, neutrophils, eosinophils, antibodies, mast cells, basophils, complement, and Hageman factor |
| What is the name of Factor XII? | Hageman factor |
| What is an inflammasome? | Cytoplasmic protein complex that recognizes procedures of dead cells, microbial products, and crystals |
| What is the result of an inflammasome activity? | Activation of IL-1 and inflammatory response |
| What is the vascular component of acute inflammation? | Vasodilation and endothelial permeability |
| What is the cellular component of acute inflammation? | Extravasation of leukocytes from postcapillary venules and accumulation in the focus of injury followed by leukocyte activation |
| What is the purpose of vasodilation in acute inflammation? | Bring cells and proteins to site of injury or infection |
| What are the 4 steps in leukocyte extravasation? | 1. Margination and rolling 2. Adhesión 3. Transmigration 4. Migration (chemoattraction) |
| What cells predominate in the late states of acute inflammation? | Macrophages |
| Which Interleukin indicates persistent acute inflammation? | IL-8 |
| What is the result of acute inflammation progressing into chronic inflammation? | Antigen presentation by macrophages and other APCs --> activation of CD4+ Th cells |
| Where does most of leukocyte extravasation occur? | Postcapillary venules |
| What condition is associated with defective Margination and Rolling, step of extravasation? | Leukocyte adhesion deficiency type 2 |
| What leukocyte component is decreased /absent/nonfunctional in LAD type 2? | Sialyl-Lewis x |
| Which proteins, serum markers are involved in Margination and rolling step of Leukocyte extravasation? | E-selectin, P-selectin, and GlyCAM-1, CD34 |
| What is another way to refer to adhesion step in Extravasation of leukocytes? | Tight binding |
| Defective Adhesion step in Leukocyte extravasation process leads to development of ___________________. | Leukocyte adhesion deficiency type 1 |
| LAD 2 is due to defective step ___ in Leukocyte extravasation | 1 |
| LAD type 1 is due to defective step ___ in leukocyte extravasation. | 2 |
| Decreased CD18 integrin subunit is seen in : | Leukocyte adhesion deficiency type 1 |
| ICAM-1 and VCAM-1 are involved in: | Tight binding (adhesion) step of Leukocyte extravasation |
| CD54 indicates? | ICAM-1 |
| CD106 indicates? | VCAM-1 |
| PECAM is represented by CD_. | 31 |
| What is another term used for transmigration? | Diapedesis |
| Description of Diapedesis (step 3) in Leukocyte extravasation | WBC travels between endothelial cells and exits blood vessel |
| What happens during migration (step 4) of WBC extravasation? | WBC travels through interstitium to site of injury or infection guided by chemotactic signals |
| What are some chemotactic products released during Migration in response to bacteria? | C5a, IL-8, LTB4, kallikrein, platelet-activating factor |
| Which are the main cells involved in chronic inflammation? | Macrophages, lymphocytes, and plasma cells |
| What are the most common stimuli for chronic inflammation? | Persistent infections --> Type IV hypersensitivity, autoimmune diseases, prolonged exposure to toxic agents, and foreign material |
| All the cells involved in chronic inflammation which are the most dominant? | Macrophages |
| Chronic inflammation is the result of macrophage interaction with? | T-lymphocytes |
| Which T helper cell is involved in the classical activation of inflammatory (proinflammatory)? | TH1 cells |
| Th2 cells secrete IL 4 and IL-13 --> | Macrophage alternative activation |
| What is the result of the macrophage alternative activation in the process of chronic inflammation? | Repair and anti-inflammatory |
| What is the composition of granulomas? | Composed of epithelioid cells with surrounding multinucleated giant cells and lymphocytes. |
| Granulomas are a pattern of chronic ____________. | Inflammation |
| What are epithelioid cells in granulomas? | Macrophages with abundant pink cytoplasm |
| What subtype helper T cells aid in the formation of granulomas? | Th1 cells |
| What is secreted by Th1 cells that activates macrophages, in the process of making granulomas? | INF-gamma |
| What cytokine is known to induce and maintain granuloma formation? | TNF-alpha |
| What is a possible adverse consequence of using anti-TNF drugs in a patient with a granulomatous disease? | Sequestering granulomas can break down leading to a disseminated disease |
| Why is a TB test always performed prior to starting anti-TNF therapy? | To prevent the breakdown of from granulomas in latent TB, and thus, avoid development of disseminated disease. |
| What is electrolyte condition is strongly associated with granuloma formation? | Hypercalcemia due to calcitriol production |
| What is needed on biopsy to diagnose Sarcoidosis? | Non-caseating granulomas |
| What are the most common granulomatous disease of BACTERIAL origin? | - Mycobacteria (TB, leprosy) - Bartonella henselae (cat scratch disease) - Listeria monocytogenes (granulomatosis infantiséptica) - Treponema pallidum (3 Syphylis) |
| Endemic mycoses are _____________________ diseases. | Granulomatous |
| What is a granulomatous disease due to a parasitic infection? | Schistosomiasis |
| Crohn disease si an autoinflammatory ___________________ disease. | Granulomatous |
| What foreign material ingestion (inhaled) materials are granulomatous disease? | Berylliosis, talcosis, hypersensitivity pneumonitis |
| Primary biliary cholangitis and Subacute (de Quervain) thyroiditis, are both _____________________ diseases. | Granulomatous |
| What are the two types of calcification? | Dystrophic and Metastatic calcification |
| Which type of calcification is seen in abnormal tissues? | Dystrophic |
| Dystrophic calcification extend tends to be _________________. | Localized |
| Metastatic calcification has an extend commonly described as _______________________. | Widespread |
| What are some associated conditions that exhibit dystrophic calcification? | TB (lung and pericardium) Granulomatous infections Liquefactive necrosis of chronic abscesses Fat necrosis Infarcts, thrombi, Schistosomiasis Congenital CMV, Toxoplasmosis, Rubella, Psammoma bodies CREST syndrome Atherosclerotic plaques |
| What areas are most commonly affected by metastatic calcification? | Interstitial tissues of the kidney, lung, and gastric mucosa |
| Dystrophic calcification is most likely due to: | Secondary to injury or necrosis |
| What is the etiology (reason of development) of Metastatic calcification? | Secondary to hypercalcemia or high Calcium-Phosphate product levels |
| What are some examples of high calcium-phosphate product level conditions? | CKD with secondary hyperparathyroidism, long-term dialysis, calciphylaxis, multiple myeloma |
| What is the serum calcium level of a person with evidence of dystrophic calcification? | Normocalcemic |
| Which type of calcification is seen with abnormal serum Ca2+ levels? | Metastatic calcification |
| A yellow-brown "wear and tear" pigment associated with normal aging. | Lipofuscin |
| How is Lipofuscin formed? | By oxidation and polymerization of autophagocytosed organellar membranes |
| Which organs usually show most Lipofuscin deposition upon autopsy of the elderly? | Heart, colon, liver, kidney, and eye. |
| What is the pigment usually found in during the autopsy of an elderly patient around the heart and kidneys? | Lipofuscin |
| How do free radicals cause damage to cell? | By membrane lipid peroxidation, protein modification, and DNA breakage. |
| What are ways to eliminate free radicals? | 1. Scavenging enzymes (catalase, superoxide dismutase, glutathione peroxidase) 2. Spontaneous decay 3. Antioxidants 4. Metal carrier proteins (transferrin, ceruloplasmin) |
| When does scar formation occurs? | When repair cannot be accomplished by cell regeneration alone. |
| In scar formation, the nonregulated cells, are replaced by ________________. | Connective tissue |
| What are the two types of scar formation? | Hypertrophic and Keloid |
| What collagen synthesis is increased in hypertrophic scar formation? | Type III collagen |
| Which collagen types are increased in synthesis in Keloid formation? | Type I and III collagens |
| Which type of scar formation has a much higher or significant (increased) collagen formation? | Keloid formation synthesis much more collagen |
| Hypertrophic scar has its collagen arrangement in _______________, which Keloid shows a ______________ collagen organization. | Hypertrophic ----------- parallel Keloid -------- disorganized |
| Which type of scar is confined to borders of original wound? | Hypertrophic |
| Description Of extent of keloid scar | Beyond borders of original wound with "claw-like" projection typically on earlobes, face, and upper extremities |
| Keloid formation has an increased recurrence in ethnic groups with _____________________. | Darker skin |
| What two tissue mediators solely stimulate angiogenesis? | FGF and VEGF |
| What is the role of PDGF? | 1. Induce vascular remodeling and smooth muscle migration 2. Stimulates fibroblast growth for collagen synthesis |
| What cells secrete PDGF? | Activated platelets an macrophages |
| Which tissue mediator is in charge of tissue remodeling? | Metalloproteinases |
| What is the specific role of EGF? | Stimulates cell growth via tyrosine kinases |
| What are the characteristics of Inflammatory phase of wound healing? | Clot formation, increased vessel permeability and neutrophil migration into tissue |
| What is the second phase of wound healing? | Proliferative |
| What cells are involved in the proliferative phase of wound healing? | Fibroblasts, myofibroblasts, endothelial cells, keratinocytes, and macrophages |
| What are the effector cell of the Inflammatory phase of wound healing? | Platelets, neutrophils , and macrophages |
| What are the effector cells of the Remodeling phase of wound healing? | Fibroblasts |
| What are the features of Proliferative phase of wound healing? | Deposition of granulation tissue and type III collagen, angiogenesis, epithelial cell proliferation, dissolution o clot, and wound contraction |
| What cells mediated wound contraction? | Myofibroblasts |
| What two deficiencies can delay wound healing? | Vitamin C deficiency and Copper deficiency |
| Which stage of wound healing is Type III collagen replaced by type I collagen, and incrase tensile strength of tissue? | Remodeling |
| While Vit C and copper deficiency cause delay in wound healing during the Proliferative phase, the deficiency of Zinc causes same effect in the ______________ phase of wound healing. | Remodeling |
| What enzymes break down type III collagen? | Collagenases |
| What metal (mineral) is required by Collagenases to function? | Zinc |
| Timeframe of proliferative phase of wound healing | Day 3 - weeks after wound |
| What is the common time frame for remodeling phase of wound healing? | 1 week --- 6+ months after wound |
| What is amyloidosis? | Abnormal aggregation of proteins into B-pleated linear sheets |
| What is the end result of amyloidosis? | Cellular damage and apoptosis caused by formation of insoluble fibrils |
| What is the composition of the insoluble fibrils in amyloidosis? | Abnormal aggregation of protein into B-pleated linear sheets |
| What methods and/or procedures can be used to visualize Amyloidosis? | 1. Congo red stain 2. Polarized light (apple green birefringence) 3. H&E stain |
| What is shown in a H&E stain of amyloidosis sample? | Deposits in glomerular mesangial areas and tubular basement membranes |
| What are the systemic types of amyloidosis? | Primary, Secondary, and Dialysis-related amyloidosis |
| What is the fibril protein involved in Primary amyloidosis? | AL (form Ig Light chains) |
| Which disorders are seen with primary amyloidosis? | Multiple myeloma and plasma cell disorders |
| What are the manifestations of systemic amyloidosis? | 1. Cardiac (RCM, arrhythmia) 2. GI (macroglossia, hepatomegaly) 3. Renal (nephrotic syndrome) 4. Hematologic (easy bruising, splenomegaly) 5. Neurologic (neuropathy) 6. Musculoskeletal (carpal tunnel syndrome) |
| What is the most significant Musculoskeletal manifestation of systemic amyloidosis? | Carpal Tunnel syndrome |
| What type of cardiomyopathy is seen with systemic amyloidosis? | Restrictive |
| Is nephritic or nephrotic syndrome associated with amyloidosis? | Nephrotic |
| What is defective protein in secondary amyloidosis? | Serum Amyloid A (AA) |
| What type of conditions (examples) produce secondary amyloidosis? | Rheumatoid arthritis, IBD, familial Mediterranean fever, protracted infection |
| B2-microglobulin protein defect is seen with _________________ amyloidosis. | Dialysis-related |
| What type of patients develop Dialysis-related systemic amyloidosis? | ESRD and/or long-term dialysis |
| What are examples of localized Amyloidosis? | Alzheimer disease, Type 2 DM, Medullary thyroid cancer, Isolated atrial amyloidosis, and Systemic senile amyloidosis |
| B-amyloid protein is involved in _________________ disease. | Alzheimer |
| What is the protein involved in amyloidosis in Type 2 DM? | Islet amyloid polypeptide (IAPP) |
| What is the etiology of Type 2 DM amyloidosis? | Deposition of amylin in pancreatic islets |
| What arrhythmia is more likely to develop in a patient with isolated atrial amyloidosis? | Atrial fibrillation |
| Which part of the heart is most affected in systemic senile amyloidosis? | Cardiac ventricles |
| What are the two types of hereditary amyloidosis? | Familial amyloid cardiomyopathy and Familial amyloid polyneuropathies |
| Mutated transthyretin (ATTR) causes---> | Familial amyloid cardiomyopathy and Familial amyloid polyneuropathies |
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rakomi
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