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41 Cards in this Set
- Front
- Back
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What is the initial vascular change associated with the acute inflammatory response?
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Vasoconstriction is the first vascular event, followed by the first sustained vascular event vasodilation
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How does the initial vascular event result in slowed circulation?
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Causes increased viscosity from release of Selectins (selected sugar compounds), causing slowing and sticking of WBCs
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What is chemotaxis, and which mediators of inflammation are responsible for the process?
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Chemotaxis is the phenomenon in which bacteria direct WBC movement from inside the BV to the extravascular space by C3b (opsonin), C5a (chemoattractant), leukotriene B4, and IL-8.
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Which WBC are seen in greatest amounts in the early phase of the inflammatory cascade?
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Neutrophils/Poly
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What is an opsonin?
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Opsonin is like "relish:" it makes things more appetizing for WBCs.
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Which of the local mediators of acute inflammation are preformed?
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Histamine, serotonin, and lysosomal enzymes.
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What role does histamine have in the inflammatory cascade?
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Histamine is a pre-formed local mediator found all over the body and quickly responds. It is the principal mediator of the immediate phase of increased vascular permeability, vasodilation.
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Why should you be cautious prescribing NSAIDs to asthmatic patients?
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NSAIDS cause bronchospasms. It stops the cyclooxygenase pathway and forces the patient into the 5-lipoxygenase pathway, which causes bronchospasms, vasoconstriction, and increased permeability.
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What is COX-1? COX-2? COX-3?
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COX-1 is always on, COX-2 is in response to inflammation. COX-3???>????
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What are cytokines?
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Cytokines are produced by any cells to signal other cells to be activated or divide on a particular side of the body.
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What roles do IL-1, TNF-α, and INF-γ play in the inflammatory response?
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Interleukin-1 increases thrombogenicity and endothelial activation for adhesion of white cells. Tumor Necrosis Factor Alpha aggregates WBCs. INF Gamma inhibits T-Helper T-cells and activates macrophages.
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What are the different "synthesized" mediators of inflammation?
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Arachadonic acid metabolites (Prostaglandins and Leukotrienes), platelet-activating factor, cytokines, nitric oxide, and activated oxygen species.
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What does complement do? Which complement components are involved with opsonization?
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The Complement System augments other components of the immune system. C3b is a chemoattractant for opsonization. C5b and C6-9 form MAC for cell lysis. Anaphylatoxins C3a and C5a increase vascular permeability by degranulation of mast cells. C5a; C5,6,7 complex generate mediators that attract phagocytes.
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What does bradykinin do?
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Bradykinin increases vascular permeability, vasodilation, bronchoconstriction and pain.
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What are the differences between acute and chronic inflammation?
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The main player in acute is neutrophils; in chronic it's macrophages. Acute inflammation lasts a short duration, while chronic lasts for at least several months.
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What is a granuloma?
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A granuloma is a specific type of chronic inflammation: it's the accumulation of modified macrophages. It's also a characteristic of type IV hypersensitivity.
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Which of the hypersensitivity responses is NOT antibody mediated?
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Type IV is the only hypersensitivity response that is cell mediated (by T-cells) and not Ab mediated. They take time to take affect.
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Identify some common ocular manifestations of hypersensitivity responses.
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Allergic conjunctivitis, episcleritis, uveitism, Mysthania Gravis, Grave's, Sjogren's, and SLE retinopathy.
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What's the difference between hyperplasia and hypertrophy?
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Hyperplasia is an increased number of cells. (Think lots of people in Asia!) Hypertrophy has the same number of cells but they get bigger. (Think bigger muscles get the trophy!)
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What is atrophy? Are the cells still alive?
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Shrinking of cells, but the cells are not dead.
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What is metaplasia? Why is there any concern about this adaptation occurring in the human body?
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Metaplasia is when one cell type is replaced by another, which could cause a change in cell function.
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What are some of the characteristics of dysplasia?
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Disorderly, non-neoplastic proliferation of cells. There's a loss of uniformity of individual cells.
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When does necrosis occur?
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After premature cell death
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What is apoptosis? Why do optometrists know to pronounce this “a-POE-tosis” and not “a-POP-tosis”? (Hint: how do you pronounce the condition that describes a droopy lid?)
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Apoptosis is programmed cell death. It's the "physiological" way for a cell to die. The cell shrinks, but the membrane doesn't rupture. Eventually phagocytosed.
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What is the difference between labile and permanent tissues?
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Labile tissues are continuously mitotic and can send signals when there's damage. Permanent tissues are nonproliferative and post-mitotic.
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What does asymmetric replication of stem cells mean?
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Asymmetric replication generates “committed” cells that enter a differentiation pathway.
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What is granulation tissue?
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When there is severe or chronic tissue injury, nonregenerating cells are replaced with connective tissue, beginning with granulation tissue. Granulation tissue is proliferation of fibroblasts and delicate capillaries.
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What is the difference between healing by first intention and healing by second intention?
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Healing by first intention means the wound was a clean, uninfected incision with little focal disruption and is covered with normal epithelium within a month. By second intention means the wound was large and there was extensive tissue damage; there is wound contraction by myofibroblasts and a large scar likely forms.
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What are the major factors that cause a delay in tissue healing?
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Infection, poor nutrition, poor perfusion, mechanical pressure/torsion, glucocorticoids, and foreign bodies
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All of the following are systemic side effects of topical NSAIDs EXCEPT:
a. gastrointestinal symptoms b. exacerbation of asthma c. headaches d. facial edema e. hypertension |
e. Hypertension
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The pain response in acute inflammation is:
a. inactivated by the Hageman factor b. enhanced by prostaglandins c. initiated by particle C3b of the complement pathway d. mediated by vascular endothelial cell retraction e. activated by the myeloperoxidase rxn |
b. Prostaglandin E2 are hyperalgesic; makes tissue hypersensitive to painful stimuli. Important bc NSAIDs decrease pain by blocking COX pathway, which produces prostaglandins.
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Patient has a hordeolum on upper lid margin of R eye. Which is a clinical sign of acute inflammation observed?
a. karyolysis b. hypertrophy c. swelling d. necrosis e. E. cyanosis |
C. Swelling is easy to observe clinically and is one of 5 clinical signs of acute inflammation. calor, rubor, tumor, dolor, and functio laesa.
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The principal mechanism by which vascular permeability is altered in acute inflammation is:
a. disruption of vascular basement membrane b. acceleration of vesicular transport c. separation of vascular endothelial jx d. increased hydrostatic pressure e. increased osmotic pressure of tissue fluid |
C. increased permeability of BVs during acute inflam mediated my histamine, bradykinin, LTs, etc and involves contraction of vascular endothelial cells to open gaps b/w endothelial cells
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Aberrant healing can produce a keloid, which is composed predominantly of:
a. necrotic tissue b. dense collagen c. loose CT d. endothelial cells e. adipose tissue |
B. keloids, composed mainly of collagen. scar tissue that grows beyond boundaries of original wounded area.
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Purulent exudate:
a. consists of neutrophils and necrotic tissue b. is a thin fluid secreted by mesothelial cells c. occurs in severe injuries w/ large vascular leaks d. forms an amorphous coagulum of threads e. is characterized by large numbers of fibroblasts |
A. purulent inflammation contains pus and may form an abscess. it consists of neutrophils, necrotic debris, and edema fluid
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Leukocyte pavementing during acute inflammation is mediated by:
a. chemotaxis b. adhesion molecules (integrins) c. phagocytosis d. vascular leakage e. myeloperoxidase |
B. During acute inflammation, leukocytes move from center of BV to margins (margination), stick to vessel wall (pavementing), pass through the vascular endothelium (transmigration), and then migrate to the site of inflam (chemotaxis). Pavementing is mediated by adhesion molecules on inflammatory cells that cause first rolling (selectins) and then sticking (integrins) of the cells to the vascular endothelium.
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Inheritance of HLA-B27 allele confers a 90% relative risk of which of the following disorders?
a. rheumatoid arthritis b. Sjogren’s c. type I DM d. ankylosing spondylitis e. lupus erythematosus |
D. many autoimmune disorders are assoc w/ HLA alleles.
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Antinulcear antibodies against double-stranded DNA are highly assoc w/ diagnosis of:
a. rheumatoid arthritis b. Sjogren’s c. type I DM d. ankylosing spondylitis e. systemic lupus erythematosus |
E. ANAs are common among patients w/ many autoimmune conditions, such as Sjorgrens and scleroderma. Antibodies specific for double-stranded DNA are highly correlated w/ SLE. Diagnosis of SLE currently is based on 11 criteria, one of which is anti-dsDNA.
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All of the following clinical findings are consistent with a diagnosis of ankylosing spondylitis EXCEPT:
a. anterior nongranulomatous uveitis b. negative HLA-B27, c. lower back pain d. sacroilitis that can lead to kyphosis e. posterior synechiae |
b. Ankylosing spondylitis has the strongest association with HLA B-27 with up to 90% of patients being positive. Other diseases that have a high association with HLA B-27 and can have ocular findings include Reiter’s syndrome, inflammatory bowel disease, and psoriatic arthritis.
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All of the following are medical treatment that are used in the treatment of systemic lupus erythematous EXCEPT:
a. D-penicillamine b. hydroxychlorquine c. prednisone d. cyclophosphamide |
a. D-Penicillamine is a degradation product from penicillin that is typically used in the treatment of severe rheumatoid arthritis, Wilson’s disease, heavy metal poisoning, and chronic active hepatitis. D-Penicillamine is known to be the cause of drug-induced SLE in patients receiving it over a prolonged course of time.
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All of the following findings are consistent with a diagnosis of adult rheumatoid arthritis EXCEPT:
a. bilateral swollen tender joints b. nodules at pressure points c. development of osteophytes d. elevated gamma globulins (mostly IgM and IgG) |
c. Osteophytes are abnormal bone growth at joint margins due to loss of joint cartilage from the mechanical wearing down of the joints are seen in the x-rays of patients with osteoarthritis. They do not occur in RA, where joint damage is from inflammation and enzymes found in the joint fluid.
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