Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Step 11.16.12
Pathology I
| Question | Answer |
|---|---|
| Is ATP required for apoptosis? Does apoptosis cause inflammation? | requires ATP, no inflammtion |
| What is the intersection of both the intrinsic and extrinsic apoptotic pathways? | both pathways end in the activation of cytosolic caspases |
| What histological features characterize apoptosis? | cell shrinkage, nuclear shrinkage, basophilia (pyknosis), membrane blebbing, karryohexis, kayolysis, formation of apototic bodies |
| What is the intrinsic apoptotic pathway? | incr Bax (proapototic) decr BCl-2 (anti apoptotic) leading to Cyt C release and activation of cytosolic caspases |
| When is the intrinsic apoptotic pathway active? | embryogenesis, hormone induction, atrophy, result of inurous stimuli like hypoxia or toxins |
| What are the 2 extrinsic pathways of apoptosis? | 1. ligand receptor interactions (Fas binds to Fas[CD95] 2. Immune cell (Tc releases perforin and granzyme) |
| What is necrosis and what histological features are seen? | enzymatic degradation and protein denaturation of cell. inflmmatory process and intracellular components extravasate |
| What organs can undergo coagulative necrosis? | heart, liver, kidney |
| What organs can undergo liquefactive necrosis? | brain, bacterial absesses, pleural effusion |
| What are some examples of casseuous necrosis? | TB, systemic fungi |
| What are some examples of fatty necrosis? | pancreas (saponification) |
| What types of organs undergo fibrinoid necrosis? | blood vessels |
| What are the 2 types of gangrenous necrosis and where do they happen? | dry (iscemic coagulative) or wet (w bacteria) common in limbs and GI tract |
| What are some examples of cell injuries which are reversible with O2? | 1. decr ATP synth 2. cellular swelling (this is due to Na/K+ pump 3. nuclear chromatin clumping 4. decr glycogen 5. fatty change 6. ribosomal detatchment (decr protein synthesis) |
| What are some examples of cell injury that are irreversible? | 1. nuclear pyknosis, karyolysis, karyohexxis 2. Ca2+ influx and caspase activation 3. damage to the plasma membrane 4. lysosomal rupture 5. mitochondrial permeability |
| What watershed areas are most vulnerable to hypoxia? | splenic flexure, ACA/MCA |
| What part of the heart is most vulnerable to hypoxia? | subendocardial tissue |
| What part of the kidney is most vulnerable to hypoxia? | proximal tubule (cortex) and thick asending limb ( medulla) |
| What area of the liver is most vulnerable to hypoxia? | area around the central vein |
| When and where do red ( hemorrhagic) infarcts occur? | loose tissue with collaterals like liver, lungs, or intestine or following reperfusion. The injury is from free radical damage |
| What are pale infarcts and when and where do they occur? | in solid tissues with a single blood supply such as heart, kidneys, spleen |
| What is seen in hypovolemic/cardiogenic shock? | low output failure, incr TPR, low CO, cold, clammy patient |
| What is seen in spetic shock? | high output failure. see decr TPR, dilated arteriole, high venous return, hot patient |
| What are 6 major causes of atrophy? What is it? | reduction in size or number of cells. 1. decr hormones ( uterus/vagina) 2. decr innervation (motor neuron damage 3. decr blood flow 4. decr nutrients 5. incr pressure ( nephrolithiasis 6. occlusion of secretory ducts (CF) |
| What are the 4 hallmarks of inflammation? | 1.rubor 2. dolor 3. calor 4. tumor 5. function laesa (loss of function) |
| What causes fluid exudation in inflammation? | incr vascular permeability, vasodilation, endothelial injury |
| What causes fibrosis in inflammation? | fibroblast emigration and proliferation. deposition of ECM |
| What is granulation tissue? | highly vascularized, fibrotic tissue |
| What is an absess? | fibrosis surrounding pus |
| What is a fistula? | abnormal communication |
| What is scarring? | collagen deposition resulting in altered structure and function |
| What is the onset, duration, and what cells are invovled in acute inflammation? | rapid onset, lasts minutes to days. neutrophils, eosinophils, Ab mediated |
| What cells mediate chronic inflammation and what are some associted sx? | mononuclear cell mediated, characterized by persistent destruction and repair. associated with blood vessel proliferation and repair |
| What is a granuloma and what type of inflammation is it associated with? | chronic inflammation. nodular collections of epitheloid macrophages and giant cells |
| What receptors on the vasculature/stroma and the leukocyte mediate rolling? | Vasculature/stroma: E selectin, P selectin Leuk: sialyl LewisX |
| What receptors on the vasculature/stroma and the leukocyte mediate tight binding? | VAsculature/stroma: ICAM-1 Leukocyte: LFA-1 ("integrin") |
| What receptors on the vasculature/stroma and the leukocyte mediate diapedesis (exit of BV)? | Vasc/stroma: PECAM-1 Leuk: PECAM-1 |
| What receptors on the vasculature/stroma and the leukocyte mediate migration (travel of leukocyte to area of injury or infection)? | Vasc/stroma: bacterial products ,CILK: C5a, IL-8, LTB4, Kallikrein |
| What is the order of leukocyte extravasation from the BV? | rolling-->tight binding-->diapedesis-->migration--->phagocytosis |
| How do free radicals damage cells? | via membrane lipid peroxidation, protein modification, DNA breakage |
| What types of things can cause free radical injury? | radiation exposure, metabolism of drugs (phase I), redox reaction, nitric oxide, transition metals, leukocyte oxidative burst |
| what things can help eliminate free radicals? | catalase, superoxide dismutase, glutathione peroxidase, spontaneous decay, antioxidants ( vit A,C,E) |
| What are 6 pathologies associated with free radical injury? | 1. retinopathy of prematurity 2. bronchopulmonary dysplasia 3. CCI4 leading to liver necrosis (fatty change) 4. acetaminophen 5. iron overload 6. reperfusion after anoxia (superoxide), especially after thrombolytic therapy |
| What are the mediators of the inflammatory phase of wound healing? | platelets, neutrophils, macrophages |
| Wbhat are the major characteristics od the inflmmatory phase of wound healing? | clot formation, icr vessel permeability, neutrophilmigration, macrophages clear debris 2 days later |
| What are the mediators of the proliferative phase of wound healing and when does it occur? | 2-3 days after wound. fibroblasts, myofibroblasts, endothelial cells, keratinocytes |
| What are the major characteristics of the proliferative phase of wound healing? | deposition of granulation tissue and collagen, angiogenesis, epithelial cell proliferation, dissolution of clot and wound contraction by myofibroblasts |
| What are the mediators of the remodeling phase of wound healing and when does it happen? | 1 week after wound. mediated by fibroblasts |
| What are the major characteristics of the remodeling phase of wound healing? | type III collagen is replaced by Type I collagen, increased tensile strength of tissue |
| What are 8 causes of granullomatous disease? | 1. M tb 2. Fungi (histo) 3. treptonema pallidum (syphilis) 4. M. leprae (leprosy) 5. Bartonella hensale 6. sarcoidosis 7. Crohn's disease 8. Berylliosis |
| What is the process of granuloma formation? | TH1's secrete gamma INf which activatews macrophages to secrete TNF-alpha which maintains the granuloma. The granulloma make be broken with anti TNF drugs but this leads to disseminated disease |
| What are the characterisitcs of a transudate? | hypocellular, protein pooor, Specific G <1.012 |
| What causes a transudate? | incr hydrostatic P, decr oncotic P, Na+ retention |
| What are the characteristics of an exudate? | cellular, protein rich, specific gravity > 1.02 |
| What causes an exudate? | lymphatic obstruction or inflammation |
| What is the mech and use of the Eryhtrocyte sedimentation rate (ESR)? | fibrinogen, a product of inflammation, causes RBCs to aggregate. RBCs fall at a faster rate when they are aggregated |
| What types of things would cause and incr ESR? | things that cause inflammation: infections, temporal arteritis, cancer, pregnancy, SLE |
| What types of things could cause a decr ESR and what is the mechansim of each? | sickle cell (sltered shape), polycythemia (toomany), CHF (unknown) |
| What is the mechanism of iron poisoning in children? | cell death due to peroxidation of membrane lipids |
| What are the major Sx of iron poisoning? | acute: gastric bleeding chronic: metabolic acidosis, scarring leading to GI obstruction |
| What is seen in the microscope in amyloidosis and what does affected tissue look like? | See Beta pleated sheet demonstrable by apple gree birefringence of Congo-red stain under polarized light. affected tissue has a waxy appearance |
| What is the protein and what is it derived from in Bence Jones amyloidosis? What disease is it seen? | AL protein derived from Ig Light chains (multiple myeloma) |
| What is the protein and where is it derived from in Secondary amyloidosis? What is a common setting | AA protein derived from serum amyloid associted protein (chronic inflammatory disease) |
| What is the protein and from what is it derived in Senile cardiac amyloidosis? | Protein: transthyretin from AF |
| What is the protein and from what is it derived in DM type II amyloidosis? | amylin protein derived from AE |
| What is the protein and from what is it derived in medullary carcinoma of the thyroid? | A-CAL protein derived from calcitonin |
| What is the protein and from what is it derived in Alzheimer's disease amyloidosis? | Beta amyloid protein derived from amyloid precursor protein (APP) |
| What is the protein and from what is it derived in dialysis associted amyloidosis? | Beta 2 microglobulin derived from MHC class I proteins |
| What are some major hallmarks of cancer? | evasion of apoptosis, self sufficiency in growth signals, insensitivty to anti growth signals, sustained angiogenesis, limitless replicative potential, tissue invasion and metastasis |
| What is hyperplasia and dysplasia? | hyperplasia: cells have increased in number Dysplasia: abnormal proliferation of cells with loss of size, shape and orientation |
| What is seen in carcinoma in situ? | neoplastic cells have not invaded basement membrane, high N/C ratio and clumped chromatin, neoplastic cells encompass the entire thickness |
| What is seen in an invasive carcinoma? | cells have invaded the basement membrane using collagenases and hydrolases ( metalloproteases), can metastasize if they reach a BV or LV |
| What metastasis and what is the seed and soil theory of metastasis? | Met: spread to distant organ, seed= tumor embolus, soil=target organ= liver, lungs, bone, brain |
| What is the order of neoplasm growth? | normal-->hyperplasia-->carcinoma in situ-->invasive carcinoma-->metastatic carcinoma |
| What is metaplasia? | one adult cell is replaced by another. often secondary to irritation or environmental exposure (squamous metaplasia in trachea and bronchi in smokers) |
| Are hyperplasia, dysplasia, and metaplasia reversible? | yes |
| What is anaplasia? | abnormal cells that lack differentiation, resemble primitive cells of the same tissue. often equated with undifferentiated malignant neoplasms |
| What is a neoplasia? | clonal proliferation of cells that is uncontrolled and excessive. neoplasia can be benign or malignant |
| What is desmoplasia? | fibrous tissue fromation in response to a neoplasm |
| Are neoplasia, anaplasia, and desmoplasia reversible? | NO |
| What is a tumor grade? | degree of cellular differentiation based on histiological appearance of tumor. I-IV based on number of mitoses per field. character of tumor |
| What is a tumor stage? | degree of localization/spread based on site and size of primary lesion, spread to LN, metastases, spread of tumor in a specific pt |
| Which has more prognostic value stage or grade? | stage |
| What is the TNM staging system? | T= tumor size N= none involvement M= metastases (most important prognostic factor) |
| What are 2 benign tumors of epithelium? | adenoma, papilloma |
| What are 2 malignant tumors of epithelium? | adenocarcinoma, papillary carcinoma |
| What are 2 malignant tumors of blood cells? | leukemia, lymphoma |
| What are the benign and malignant tumors of blood vessels? | B:hemangioma M:angiosarcoma |
| What are the benign and malignant tumors of SMM? | B:leiomyoma M: leiomyosarcoma |
| What are the benign and malignant tumors of SM? | B: rhabdomyoma M: Rhabdomyosarcoma |
| What are the benign and malignant tumors of connective tissue? | B: fibroma M: fibrosarcoma |
| What are the benign and malignant tumors of bone? | B: osteoma M: osteosarcoma |
| What are the benign and malignant tumors of fat? | B: lipoma M: liposarcoma |
| What are the benign and malignant tumors of greater that one type? | B: women. mature tetroma M: men. immature tetroma and mature tetroma |
| What is the difference between carcinoma and sarcoma? | carcinoma= epithelial sarcoma= mesenchymal origin |
| What are the characteristics of a benign tumor? | usually well differentiated, slow growing, well demarcated, no metastases |
| What are the characterisitcs of a malignant tumor? | may be poorly differentiated, erratic growth, locally invasive/diffuse, may metastasize |
Created by:
tjs2123
Popular USMLE sets