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Pathology 1 Block 1
Pathology NWHSU
| Question | Answer |
|---|---|
| What cells are normally replaced at different intervals? (Enterocytes, gastric and squamous epithelium) | Labile Cells |
| What cells do not normally regenerate but may in certain situations? (liver cells after hepatitis or partial liver donation) | Stable Cells |
| What cells do not regenerate during a lifetime? (Caridac cells) | Permanent Cells |
| Irreversible cell damage leads to _____________ or ____________. | Necrosis or Apoptosis |
| What is programmed cell death that leads to DNA fragmentation? | Apoptosis |
| What is a polymorphonuclear luekocyte? | Neutrophil |
| Name a pro-apoptotic protein. | Bax |
| Name an anti-apoptotic protein | BCL-2 |
| What leaks out of the cell before apoptosis? | Mitochondrial proteins |
| Decrease in O2 supply, toxins, and radiation all cause mitochondrial damage which leads to a decrease of_____ generation and increase production of ____ which eventually leads to multiple cellular abnormalities and eventually cell necrosis. | Decrease in ATP, increase in ROS (Decrease in energy, increase in Reactive Oxygen Species) |
| What two cellular reactions can happen from a reversible cell injury? | Hydropic Swelling Fatty Metamorphisis |
| Atrophy, Involution, Hypertrophy, hyperplasia, metaplasia, dysplasia, and lipfuscin pigment are all caused by ____________________ and are ___________ (irreversible or reversible). | Persistent stress All reversible |
| Lipofuscin Pigment is commonly seen in the __________ tissue. Also common in the ____ and the _______. It is ___________ in color under the microscope and shows up dark on HE staining. It is causes by ______________. | heart/cardiac tissue also common in the liver and brain Yellow-Brown and granular Repeated stress |
| Necrosis dealing with ischemia or infarcation. Most common type of necrosis. | Coagulative Necrosis |
| Necrosis dealing with excess liquid build up most commonly in the brain. | Liquefactive Necrosis |
| Necrosis dealing with lipase on adipocytes breaking down the triglyceride in the fat cell leaking into the surrounding fat. | Fat necrosis |
| Cheesy/curdlike foul smelling necrosis with gramulomas. | Caseous necrosis |
| Necrosis in small arteries, arterioles, and capillaries. Typically they lose elasticity. | Fibrinoid necrosis |
| Common in wrists, ankles, and femurs. Ischemia leading to hypoxia leading to ___________ necrosis. A sign of this necrosis is absence of ___________ in bone. | Avascular (Aseptic/osteonecrosis) necrosis osteocytes |
| Decrease in cell size. | Atrophy |
| Decrease in cell number. | Involution |
| Increase in cell size | Hypertrophy |
| Increase in cell number | Hyperplasia |
| Change of one normal cell to another normal cell. | Metaplasia |
| Microscopic cell abnormality indicating premalignant change | Dysplasia |
| Poorly differentiated tissue can be __________. | Cancer |
| __________ _____ _______ epithelium to squamous eptithelium. (1 type of metaplasia) | Bronchial ciliated columnar epithelium |
| _________ __________ epithelium to squamous epithelium. (1 type of metaplasia) | Transitional Bladder epithelium |
| _________ __________ epithelium to columnar epithelium. (1 type of metaplasia) | Esophageal squamous epithelium |
| ______ _________ to bone. (1 type of metaplasia) | fibrous tissue to bone |
| ____________ may occur in uterine cervical squamous epithelium, columnar epithelium in adenomatous colon polyps, and squamous epithelium in the bronchial tree. | Dysplasia |
| Lipofuscin is a pigment composed of degraded lipid and protein from broken down __________ ________. | Cytoplasmic organelles such as mitochondria and endoplasmic reticulum |
| A coagulative necrosis (occuring in gummas, tertiary syphilis, and respiratory tracts). Common to have granulomas. What type of necrosis is this. | Gummatous necrosis |
| Ischemia leading to necrosis is ________. Also known as a coagulative necrosis involving multiple tissue layers. | Gangrene |
| Decreased blood supply to a tissue or organ. | Ischemia |
| Tissue necrosis from severe ischemia, the blood supply may be cut off completely. | Infarcation |
| Three nuclear changes occuring in necrosis in order. | Pyknosis->Karyorrhexis->Karyolysis |
| Nuclear change in necrosis that involves shrinkage and pigment change/hyperchromatism | Pyknosis |
| Nuclear change in necrosis that involves fragmentation. | Karyorrhexis |
| nuclear change in necrosis that involves dissolution of the nucleus. The nucleus is no longer visible. | Karyolysis |
| Liquefactive necrosis occurs where there are many cells rich in _________, ________ and neutrophils. _________ contain many digestive enzymes which are released from these cells into the surrounding tissue causing liquefaction of the tissue. | Lysosomes, macrophages, and neutrophils Lysosomes |
| _________ necrosis occurs in granulomas. | Caseous necrosis |
| Center of granuloma is _______ tissue. | Necrotic/caseous tissue |
| Bordering the center of the granuloma is ___________. | Macrophages |
| The bigger cells inside of the macrophages in a granuloma are _________ _______ cells. | Langhans giant cells |
| _________ surround the macrophages in a granuloma. | Lymphocytes |
| The outtermost border of a granuloma is _____________ | Fibroblasts |
| Important cause of caseous necrosis in a granuloma in the lung. | Tuberculosis |
| ___________ are derived from circulating blood monocytes which are produced in the bone marrow. | Macrophages |
| Macrophages in a granuloma with an increased amount of cytoplasm are ___________ cells. | Epithelioid cells |
| Cell resulting from fusion of machrophages found in a granuloma. | Langhans giant cells |
| With ________ necrosis arteries can stay constricted and cause malignent hyertension. BP can be as high as 220/140 causing the patient to take medication. | Fibrinoid necrosis |
| Cell injury starts with damage to the __________ membrane with a loss of selective permiability.. | Cell membrane |
| Second in cell injury is damage to the _________ membrane with loss of aerobic respiration and ATP generation. | Mitochondrial membrane |
| Third in cell injury is a Ca++ influx causing damage to the _________ membrane with leakage of ________ _______ into the cytosol. | lysosomal membrane with digestive enzyme leakage |
| Three molecules injure lipid bilayer membranes by peroxidation. These toxic oxygen species are __________ _______ _____ ______, ________ __________, and ______ _________ | Super oxide anion radical (SAR, O2), Hydrogen Peroxide (H2O2), Hydroxyl radical (OH') |
| What scavenge free radicals or toxic oxygen species? | Antioxidants |
| Two systems our body has that work as natural antioxidants. | Glutathione and catalase |
| The fourth and final event of lethal cell injury is massive entry of ______ into the __________. The ________ activates multiple types of digestive enzymes in the cell that destroy all the critical parts of the cell resulting in death. | Calcium into the cytosol. calcium |
| A process by which phaocytic cells internalize and digest particulate material. (like bacteria) | Phagocytosis |
| What 3 cells are capable of phagocytosis? | Macrophages (Most common) Neutrophils Eosinophils |
| The cell membrane of the phagocyte wraps around the bacterium forming a ___________. Lysosomes within the cytoplasm of the pahgocyte fuse with the phagosome forming a __________. Digestive enzymes from the lysosome help digest and kill the bacterium. | Phagosome Phagolysosome |
| ____________ is often a physiologic process where cells that are normally short-lived die and are replaced by new young cells. | Apoptosis |
| Calcification that occurs in a previously abnormal tissue. (ex granuloma, atherosclerotic plaque) | Dystrophic calicification |
| Calcification that occurs because of increased calcium concentration in the extracellular fluid. (hyperparathyroidism with excess parathyroid thyroid hormone production) | Metastatic calcification |
| Inflammation that develops in house and may persist or may heal on its own. | Acute inflamtion |
| Inflammation that follow acute inflammation or may be the initial inflammatory response. | Chronic inflamtion |
| A specific type of chronic inflammation. | Granulomatous Inflamtion |
| Rubor or erythema is ______ | Redness |
| Calor is _______ | heat |
| Tumor is _________ | swelling |
| Dolor is _______ | pain |
| Functio laesa is ________ __ ________ | loss of function |
| Fluid accumulation in tissue outside the vascular system (Between ECF and ICF) | Edema |
| Fluid accumulation in a confined anatomic space (Joint, pleural or peritoneal cavity) | Effusion |
| Fluid with a low protein content, sp. gr. <1.015 | Transudate |
| Fluid with a high protein content, sp. gr. >1.015 | Exudate |
| 2 skin infections caused by staphylococcus aureus. | Impetigo Folliculitis |
| 2 skin infections caused by Group A beta hemolytic streptococcus. | Erysipelas Cellulitis of the arm |
| 3 types of blood vessels comprise the microvasculature. What are they? | Arterioles Capillaries Post capillary venules |
| 1st line of defense in the first 24 hours is _________. | Neutrophils/PMN's (polymorphonuclear leukocytes) |
| 1st line of defense 24-48 hours what two cells arrive. They are followed by _________ and _______ cells. | Monocytes and macrophages Followed by platelets and mast cells |
| Communication within the cell | Intracrine |
| Communication between two adjacent cells | gap junctions |
| communication between two attached celsl | juxtacrine |
| communication the cell talks to itself | autocrine |
| communication between nearby cells | paracrine |
| communication between distant cells | endocrine |
| communication at nerve synapses | neural |
| communication between distant cells | neuroendocrine |
| Five stages of cellular migration into an inflamed tissue | 1 margination 2 rolling along endothelium 3 activation of inflamatory cell 4 adhesion of the inflammatory cell to the endothelial cell 5 transmigration(emigration) inflamatory cell out of the postcapillary venule into the inflamed tissue |
| During cell rolling _______ interact with _________ and the cell surface to become activated. | Protein interact with neutrophils |
| Cell derived mediators can be derived from the cell membrane of many types. A common vasoactive mediator of inflammation is __________ acid. | Arachidonic acid |
| Specific cells involved in inflammation produce specific proinflammatory mediators in addition to arachidonic acid. What are four of these. | Platelets, mast cells, endothelial cells, monocytemacrophage cells |
| Arachidonic acid is a ___ carbon fatty acid that is joined to carbon 2 of phospholipids in the cell membrane of all cells. It is split off of the plasma membrane by an enzyme called ____________ ___. | 20 carbon fatty acid Phospholipase A2 (PLA2) |
| After arachidonic acid is acted on by other enzymes it forms various ____________ such as thromboxanes, prostaglandins, and luekotrines. | Eicosanoids |
| Cyclooxygenase causes formation of a ring at the middle of the 20C AA chain forming prostaglandins and thromboxanes now termed as __________. | Prostanoids |
| __________ adds an oxygen molecule to AA forming leukotrines and lipoxins. | Lipoxygenase |
| 4 classes of eicosanoids are ? | Prostaglandins (PGA-PGI), Thromboxanes (TX), Leukotrienes (LT), Lipoxins(LX) |
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