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NR 283 Unit 2 ROK Immunity and inflammation Hypersensitivity revised
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NR 283 Unit 2 ROK Immunity and inflammation Hypersensitivity revised
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Atlanta CampReview of Knowledge
Review of Knowledge (ROK) (25 Points)
Course NR 283
Exam Exam 1
Purpose
The Review of Knowledge (ROK) focuses on course outcomes, unit outcomes and key concepts
to enhance student success on exams. Use this document as a focused guide for study in
conjunction with assigned readings, PowerPoint presentations, and other course resources.
Supplement this document by outlining your own notes from the textbook chapters and place
your expanded more detailed notes in the Student Notes column. This document should NOT be
used as a substitute for completing the assigned readings.
Chapter 5-7
Inflammation and immunity (10 Points)
Key Concepts Chapters Student Notes
Innate Immunity Chapter 5, Innate Immunity = immunity that one is born with. Thymus
6, 7 plays a large part in formulating this immunity. Also the white
blood cells are involved in this type of immunity.
(specific Adaptive Immunity = immunity that develops slowly after
portions) exposure to a specific pathogen. The lymphocytes create a specifi
antibody for the pathogen. They adapt to that exposure.
Adaptive immunity Acquired Immunity=immunity that develops after exposure to a
suitable agent. (i.e) attacked by a disease or by injection of
antigens (immunizations)
Specific Immunity = is a subsystem of the overall immune syste
that is composed of highly specialized systemic cells & processes
that eliminate or prevent pathogen growth.
Wound healing- involves a series of steps.
Acquired immunity Homeostasis
Inflammation-mast cells-histamine released
Proliferation-neutrophils are called to fight the bacteria-
macrophages will come in phagocytize bacteria-t-helper
Specific immunity take protein to lymphocytes and lymphocytes will make
antibodies- antibodies create lock and key-humoral
immunity.
Remodeling phase
Platelets play a key role in forming clots and stop the bleeding.
Wound healing
Inflammatory Mediators of Inflammation
Chemotaxis -Movement of cells or organisms in response to
POET - ROK Form 1
Revised 5.3.16
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, process chemicals. Examples of the chemicals are histamine, bradykinins
leukotriene, cytokines (Many different types, ex. interleukins,
TNF), prostglandins.
Leukotrienes
from mast cell membranes
Similar effects to histamine in later stages
Prostaglandins
they also induce pain
(NSAIDs) block the synthesis of prostaglandins,
thereby inhibiting inflammation
Bradykinin
Causes dilation of blood vessels, pain, smooth
muscle contraction, vascular permeability, and
leukocyte chemotaxis
Cytokines - Attract leukocytes to site of
inflammation
Synthesized by many cells (macrophages,
fibroblasts, endothelial cells). chemicals with
Chemotactic factors increase inflammation
Interleukins (IL)
Produced primarily by macrophages and
lymphocytes in response to a pathogen or
stimulation by other products of inflammation
Induces fever by acting as an endogenous pyrogen
Granulocytes- very grainy
Neutrophils are evident in the first stages of an infection or
inflammation.
If the need for neutrophils increases beyond the
supply, immature neutrophils (banded neutrophils)
are released into the blood. Called to site of
invasion by the chemotactic factors
Arrive within 6-12 hours - First and initial
responders for protection
Short lived at the inflammatory sites
Becomes a component of purulent exudate or pus.
Eosinophils Increased in parasitic invasions.
Hypersensitivity reactions trigger the release of
eosinophilic chemotactic factor of anaphylaxis fro
mast cells
Increased in allergic disorders
Present in chronic inflammation, releasing
chemotactic factors.
POET - ROK Form 2
Revised 7.1.16
This study source was downloaded by 100000857546843 from CourseHero.com on 02-09-2023 01:11:51 GMT -06:00
https://www.coursehero.com/file/31056084/NR-283-Unit-2-ROK-Immunity-and-inflammation-Hypersensitivity-reviseddocx/
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