Exam 1 Study Guide Flashcards
(206 cards)
1
Q
What is hyperpyrexia
A
fever
body temp exceeds normal in response to pyrogen
NORMAL: 97 to 99.5 F & 36 to 27.5 C
2
Q
Variation of hyperpyrexia
A
lowest in morning
highest in late afternoon
3
Q
What is the role of the hypothalamus
A
thermoregulatory center regulating body temperature
Helps balance heat production and loss
4
Q
Hypothalamus: Cooling of the body
A
sweat glands excrete sweat
blood vessels dilate
heat loss through radiation and conduction
5
Q
Hypothalamus: Heating of the body
A
erector muscle constriction, trapping air
shivering
blood vessels constrict
6
Q
What is thermostatic set point
A
keeps core temperature at normal level (raise/lower_
7
Q
Where is heat production derived from?
A
metabolic activity in the muscles and liver
8
Q
What gets activated to increase temperature
A
the sympathetic nervous system activated
fight or flight
neurotransmitters (epinephrine/norepinephrine
9
Q
What is the importance of epinephrine and norepinephrine
A
both neurotransmitters are released into bloodstream when body senses a need to increase heat
10
Q
Which body signs leads to increase heat production?
A
- Shivering
- Goosebumps
- excretion
11
Q
What are the causes of Heat production
A
- work/exercise
- heat stroke
- drug-induced
- malignant hyperthermia
- neuroleptic malignant syndrome
- central nervous system damage
12
Q
What are the 5 process of heat loss?
A
- Radiation
- Conduction
- convection
- evaporation
- respiration
13
Q
What is Radiation?
A
transfer of heat from one place to another
14
Q
What is Conduction?
A
Requires direct contact
15
Q
What is evaporation?
A
Sweat
16
Q
What is the Febrile Response?
A
- Thermostatic set point during the fever is reset to a higher temperature
- resting is caused by cytokines
- hypothalamus raises the set point (your body thinks normal temperature is low and will increase to a new higher set point)
- infection/inflammation starts resolving from taking antipyretic which reduces cytokines causing to loss heat
17
Q
What is cytokines and the role of it?
A
signaling molecules released by immune system, during infection/inflammation
18
Q
What is antipyretic?
A
fever reducing medication like acetaminophen or ibuprofen
19
Q
What are the stages of fever?
A
Prodrome
Chill
Defervescence
20
Q
Prodrome: fever stage
A
nonspecific complaints (aches, pain)
21
Q
Chill: fever stage
A
shivering
complaints of freezing to death
vasodilation caused red flushes skin once the set point has been reached
22
Q
Defervescence: fever stage
A
complains of burning up
diaphoresis
23
Q
The components of fever
A
24
Q
What are the associated symptoms of fever?
A
heart rate
myalgias
fatigue
joint pain
respiration increase
dehydration from sweating
chills
headaches (vasodilation of cerebral vessel)
delirium
confusion
25
Hyperthermia: Heat Stroke
overheated: heat regulation ability of the hypothalamus fails
treatment: cool the person
26
Hyperthermia: Malignant
rare hereditary disorder
related to exposure to anesthetic and muscle relaxants
rapid increase in intracellular calcium level
hyper metabolic state
temp increase 1-2 degree within 5 min
treatment: ice ice and dantrolene
27
Management of fever are:
determining cause
monitoring CBC differential
Assess vital signs
fixation of external environment
hydration
28
Medication Lowering Fevers
TYLENOL, IBUPROFEN and ASPIRIN lower fever by interfering with production of molecule called prostaglandin E2
29
What is the role of Prostaglandin E2 in fever
group of lipid compounds
inflection/inflammation, cytokine trigger the release of arachidonic acid from the cell to immune cells
acts of hypothalamus to raise point causing fever
30
What is the cyclooxygenase (COX) pathway?
COX is responsible for converting arachidonic acid into various types of prostaglandis
31
Two form of cyclooxygenase
COX-1 is generally involved in normal, everyday physiological processes (like protecting the stomach lining).
COX-2 is primarily induced during inflammation and plays a large role in the production of PGE2 during an immune response
32
What is Hypothermia
loss of body heat over prolonged period of time
>95 F
prolonged vasoconstriction/shivering become ineffective
loss of thermoregulatory ability
>87.8 F : neurologic sign (confusion) arrhythmias (a-fib, J wave)
33
Fever across the lifespan: children
very common
may be asymptomatic or symptomatic
34
Fever across lifespan: older adults
presentation with fever
>=99 may be concerning
35
What are the adaptive changes
changes due to disease process, altered cell function of renviromental influences
36
When do adaptive changes occur?
Changes occur when extracellular signals and cues “turn on” signaling mechanisms inside the cell identifying some thing needed by the cell
37
How do adaptive changes work?
These signals send chemical messengers that alter gene expression
Increase work demand or threats to survival by changing cell size, number, or form
Serve as a protective mechanism, to prevent cellular and tissue damage
When the reason for cell adaptation is removed, the need for changing gene expression stops and in some instances the cell will go back to normal
38
What is atrophy?
cells revert to smaller size in response to change in metabolic requirement or environment
39
What is atrophy: cells not in use
not in use there is a decreased demand
cells go back to smaller size and function at a level that is compatible for survival
40
What can the cells do in atrophy?
cells reduce oxygen consumption and cellular function by decreasing number of organelles
41
What happens when cells atrophy?
42
what are the causes of atrophy?
Disuse: decreased skeletal muscle use
Denervation: Occurs when limb is paralyzed
Loss of endocrine stimulation: Menopause
Inadequate nutrition
Ischemia: from decreased oxygen to tissues
Aging
43
What is hypertrophy
an increase in cell size and resulting in increase in the amount of functioning tissue
44
What can cause hypertrophy
increased workload placed usually on cardiac and skeletal muscle
can't make more cells
increase in size
45
How does hypertrophy work?
increasing functional components of the cell to find balance between what is needed and how far i can be pushed.
muscle cells make more actin and myosin and adp
46
Physiological/pathologic hypertrophy
47
What are compensatory hypertrophy
enlargement of a remaining organ or tissue after portion has been removed or inactive
nephrectomy: kidney
partial hepatectomy
48
What is hyperplasia?
increase in the number of cells in organ or tissue
49
Where does hyperplasia occur in?
occurs in tissues which have mitotic division such as the epidermis, intestinal epithelium, and glandular tissue
50
Hyperplasia relation to normal adaptive process?
occurs from a stimulus. Likely genes responding to messengers in the cell to increase replication
It is controlled
It usually stops when the stimulus is removed.
51
What is hyperplasia stimulated by
hormonal or compensatory mechanisms
part of would healing
52
What is chronic inflammation?
Occurs due to low grade/long lasting stage with obesity
Presence of macrophages and lymphocytes
asymptomatic
53
What is metaplasia
reversible change in cells where one type is replaced with another type
54
What does metaplasia respond to?
respond to chronic inflammation and irritation
replaces the original cells with ones what can better tolerate conditions
55
Metaplasia in relevance to tissue type
1. Epithelial cell becomes another epithelial cell.
Example: When the stratified squamous cells are replace the ciliated columnar cells in the in the trachea and large airways.
The squamous is better able to tolerate the smoke and damage there of but the cilia are loss
56
Metaplasia: conversion of cells
Conversion of normal cells to a different cell type often following an injury or insult from outside stimuli
Example of cell types: Columnar to squamous
Examples of external stimuli: Changes in ph., acid-base changes, hormones, smoking, alcohol
57
What is the physiological change in the cell type?
Considered to be non-cancerous
Some metaplasia can be pre-cancerous (i.e. Barrett’s esophagus)
58
What is dysplasia
Characterized by “deranged” cell growth of a specific tissue which results is cells of all shapes and sizes
59
what does dysplasia result from?
Often results from irritation or inflammation and can be a be precursor of cancer
60
what does adaptive in relevance to dysplasia
It is adaptive meaning once the irritation is gone, the dysplasia can resolve or progress to cancer in situ
61
What is necrosis?
occurs when cell die
stressors or insults exceed abiliy to survive
62
What is intracellular accumulation
buildup of substances that cells cannot immediately use or eliminate
May be abnormal or stored products from other parts of the body
63
Intracellular accumulation substances
Substances may accumulate transiently or permanently
Normal body substances (i.e. Lipids)
Abnormal exogenous Products, from errors in metabolism
Exogenous products that cannot be broken down by the cell
64
what is Proliferation
increase in number of cells
65
what is differentiation
Changes in physical and functional properties of cells, directs the cell to develop into specific cell type
66
what is apoptosis (programmed cell death)
Is programmed cell death prompted by a genetic signal and is designed to replace old cells with new.
67
what is ischemia
decreased blood flow to cells
68
what is necrosis
Death of cells related to cell injury. Damage occurs to cell structures ( mitochondria) depleting ATP. Need ATP for cell function. Damage to cell membrane, allows water into cell causes swelling
69
What is Inflammation?
reaction to injury to the cells or actual death of a cell
70
What is the innate, natural immune response of inflammation?
1. neutralizes harmful agents
2. removes damaged and dead tissue
3. generates new tissue
4. promotes healing
71
Good Inflammation
normal function to fight off infection and heal from an injury
72
Bad Inflammation
Involved in
coronary disease and MI
emphysema, asthma, chronic bronchitis
allergic rhinitis
can be chronic (long term)
73
What is the suffix for inflammation
itis
74
what are the classic signs/symptoms of inflammation
redness
swelling
heat
pain
loss of function
75
What cells are involved in inflammation?
Leukocytes
Granulocytes: Poly nucleated
Agranulocytes: Single nucleus
76
Leukocytes Charcteristics
Lymphocytes smallest form
work with macrophages in chronic inflammation
plasma cells develop from B Lymphocytes
77
Sub-cells of Granulocytes: Poly nucleated
Neutrophils
Eosinophils
Basophils
Mast cells
78
Sub-cells of Agranulocytes: Single nucleus
Monocytes
macrophages
lymphocytes
79
What are the cells involved in acute inflammation?
Neutrophils and Eosinophils
Basophils and Mast cells
80
Neutrophils in an acute inflammation
60 to 70% WBC
Non-Specific
Phagocytosis
Mobile
Able to reach injury in 90 minutes
short life span 24-48 hrs
81
Eosinophils in an acute inflammation
2 to 3% of WBC
mild phagocytic
react slower
able to reach injury in 2-3 hrs
live longer
82
What is acute inflammation
immediate reaction to injury to blood vessels and tissue
triggers: injury, infection, malignancies, immune reaction
83
Which acute inflammation cells is involved in allergic reactions
Eosinophils which work with basophils in allergic rhinitis and asthma
84
Basophils in an acute inflammation
>1% of WBC
release histamine/heparin in area of tissue damage
85
Mast Cells in an acute inflammation
activates inflammation
membrane permeability
leaukocyte chemotoxis
86
What are monocytes/macrophages
Agranulocyte
monocyte 3% of WBC
role in IR and immune response
MONOCYTE MATURE TO MACROPHAGES
live longer=chronic inflammation
87
What is the role of platelets
stop bleeding
RECOGNIZE FOREIGN INVADERS
Secrete cytokine and chemokines
Suppress pro-inflammatory mediators
Express MHC during infections
88
What are the two inflammatory response in relation to acute inflammation?
Vascular stage
Cellular stage
89
What occurs in the vascular stage?
1. increased blood flow
2. increased vascular permeability
2. fluid moves out, blood thickens and stagnates so clotting occur
90
Vascular Stage: Process of increased blood flow
Starts with transient vasoconstriction followed by rapid vasodilation
Injured tissue secretes nitric oxide and histamine
Causes Heat, Redness, and Pain
91
Vascular Stage: What does increased vascular permeability cause?
Causes leakage into the extravascular space and then into the tissues
Swelling and pain
92
Vascular stage: what changes are involved?
involves changes to the microcirculation in the capillaries, arterioles, and venules
93
What are the 4 phases of cellular stage?
1. Margination and adhesion
2. transmigration
3. chemotaxis
4. phagocytosis
94
Cellular Stage: Describe Margination and Adhesion phase
1. Contact of leukocytes with the endothelial tissue
2. Cytokines cause the endothelial cells to give off cell adhesion molecules (selectin).this slows flow and causes the leukocytes to roll along the endothelial surface. The neutrophils secrete integrins and they stick to the endothelium
3. The accumulation of leukocytes which occurs when there is decreased volume.
95
Cellular Stage: Describe Transmigration Phase
Leukocytes migrate through the vessel wall and into the tissue
96
Cellular Stage: Describe Chemotaxis
1. Guide leukocytes to the site of injury
2. Are mediated by proteins released from the local immune cells which cause neutrophils to squeeze through the endothelial cells
3. Endothelial cells help this process by releasing nitric oxide
97
Cellular Stage: Describe Phagocytosis
1. Attachment of leukocyte to offending agent
2. Engulfment:
Cytoplasm move around and enclose the particle in a phagosome
3. The phagosome fuses with lysosome which contains antibacterial molecules
4. Kills and degradation of the bacteria
98
What is the endothelial activation
1. Endothelial Cells – are a single cell layer that lines blood vessels and separate intravascular and extravascular spaces
2. Normally Non-thrombogenic, smooth
3. Changes in endothelial cells during inflammation result in activation
tight and held together by tight junctions
99
What are the two types of pro-inflammatory mediators?
Plasma Derived
Cell-derived
100
What are types of plasma-derived mediators
1. Kinin sytem
2. coagulation system
3. complement system
4. fibrinolysis system
NON reactive till activated
101
plasma-derived mediators: Role of Kinin System
1. Increase capillary permeability and stimulate pain receptors
2. factor XII int he coagulation cascade can activate this system
102
What happens when Kinin System is activated?
formation of BradyKinin
binding to beta1 & beta2 receptors
increases dilation and Vascular permeability
smooth muscles contract
work with prostaglandin
103
plasma-derived mediators: Role of Coagulation System
1. formation of fibrin clot
2. traps exudate, microorganisms, foreign bodies
3. send chemotactic signals to neutrophils
4. trigger kinins
104
plasma-derived mediators: Role of complement system
1. over 30 plasma protein
2. inflammatory response better and stronger
a. cell lysis
b. opsonization
c. chemotaxis
3. anaphylation
a. Degranulation of mast cells
b. release of histamine
c. vasodilation and increase vascular permeability
105
plasma-derived mediators: Role of Fibrinolysis System
1. Acts into opposition to the coagulation system
2. Main inflammatory mediator is Plasmin
3. Plasmin
a. Breaks down fibrin clot which increases permeability
b. Plays role in complement cascade
4. When clot breaks down results in FDP’s which increases vascular permeability
106
What are the cell derived Mediators
produced by cells and release when injury occurs
1. macrophages (monocytes)
2. mast cells (basophils)
3. endothelial cells
4. leukocytes
5. platelets
107
Cell Derived Mediator: What is Histamine
1. A Principle inflammatory mediator in acute response
2. Found In all the tissues, but the highest concentration in mast cells, basophils, and platelets
108
Cell Derived Mediator: What does Histamine cause
vasodilation and increased vascular permeability
109
Cell Derived Mediator: How does Histamine work
1. Binds to H1 receptors on the endothelial cells, especially on the bronchi and causes bronchoconstriction (Lungs)
2. Binds to H2 receptors it is anti-inflammatory. Found in large number in the stomach and produces acid (GI tract)
110
Cell Derived Mediator: what is Serotonin
1. Found in the platelets, mast cells, and certain cells in the Gi Tract, spleen, and nerve cells
2. Have a receptor for Immunoglobulin E (IG E)
3. Along with Histamine increases vascular permeability and vasodilation
111
Cell Derived Mediator: what is Prostaglandins
1. Inflammatory mediators
2. Made from Arachidonic acid by the action of COX
3. Strengthen histamine
112
Cell Derived Mediator: what does Prostaglandins do?
1. Increase vascular permeability
2. Neutrophil chemotaxis
3. Causes pain by a direct effect on nerves
113
Cell Derived Mediator: what is Prostaglandins manufacture?
1. COX-1:
Found in most tissues
Macrophage differentiation
Platelet aggregation
Renal function
2. COX-2:
Associated with inflammation
114
What is the arachidonic acid metabolites?
activation of mast cells lead to synthesis of other factors
115
where is the arachidonic acid metabolites located ?
Found in phospholipids, the release of the arachidonic acid leads to eicosanoid mediators
116
What does arachidonic acid metabolites make?
Make prostaglandins and leukotrienes
117
what is the arachidonic acid metabolites relation to thromboxane?
Thromboxane A – helps with platelet aggregation and constriction
118
what is the arachidonic acid metabolites relation to Leukotrienes?
1. Slower and last longer than histamine.
2. Permeability, adhesion of endothelial cells, chemotaxis of neutrophils, eosinophils and monocytes.
3. LTD4-causes slow and sustained constriction of bronchioles--asthma
119
What is the Non-Steroidal Anti-inflammatory Drugs (NSAIDS)?
1. working inhibiting prostaglandin synthesis
2. inhibit cox-1 and cox-2
3. suppress inflammation
4. pain relief
5. anti-pyretic
120
What is the black box warning of NSAIDS?
increase risk of cardiovascular events/stroke
121
Which pts should you avoid NSAIDS with
1. hypertension
2. heart and kidney disease
3. diabetes
122
What are NSAIDS nonselective COX inhibitors
Aspirin (Not an NSAID)
Ibuprofen
Naproxen
Diclofenac
Meloxicam
Indomethacin
Diclofenac
Ketorolac
123
What are NSAIDS nonselective COX-2 inhibitors
Celebrex
124
What is Ketorolac NSAIDS?
nonselective COX inhibitor
PO, IV, IM
alternative opioid therapy
not use more than 5 days
weaned to oral
NO PEDIATRIC use
125
What is Indomethacin NSAIDS?
used for pericarditis and gout
very irritating to Gi tract
126
What are the side effects of NSAIDS: Gastrointestinal?
Pain, heartburn, nausea
Gastric mucosa damage
GI bleeding
127
What are the side effects of NSAIDS: Kidney?
A major cause of renal disease and renal failure
Increased in those with HTN, Heart Failure, DM, and in older adults
128
What are the side effects of NSAIDS?
electrolyte imbalance
pregnancy category C
129
What are Nursing consideration for NSAIDS ?
1. Administer with food
2. Assess for gastritis, ulcers and GI bleed
3. Long term use may have PPI or H2 blocker use as well
4. Watch the creatinine
5. Assess for CV risk
6. Stop at least one week before surgery
7. Assess for fluid retention/weight gain
8. IV ibuprofen should be administered over 30 minutes
9. Be certain well hydrated
130
What is the action of acetylsalicylic acid (aspirin)?
anti-pyretic
analgesia
131
What does acetylsalicylic acid (aspirin) inhibit
prostaglandin production
1. reducing swelling/pain
2. lowers fever
132
What are nursing considerations for aspirin
Same as NSAIDS
DO NOT STOP ASA WITHOUT CONFIRMING WITH THE PRESCRIBING PROVIDER
133
what is the pt education for aspirin?
Similar to NSAIDS
Do not combine with NSAIDS
Be careful with bleeding
Soft toothbrush, good oral care
Careful with razors
134
What are the contraindications of aspirin?
1. Allergy (watch closely in asthmatics)
2. Bleeding abnormalities
3. Renal dysfunction
5. Never give to children under age 18, causes 5. Reye Syndrome
6. No pregnancy: May see however in those with coagulation issues
135
What are the toxicities of aspirin?
TINNITUS
Can progress to sweating, fever, dehydration, metabolic acidosis, and LOC changes
Medical emergency, if overdose
136
What are the indications of acetaminophen (Tylenol)?
Anti-pyretic
Analgesia
It is not an anti-inflammatory. IT IS NOT AN NSAID!
137
What is the purpose of acetaminophen (Tylenol)?
1. Fever reduction occurs from directly action on hypothalamus and thermostatic set point
2. The mechanism of pain relief in not clear. Possible interaction with the prostaglandins
138
What are the nursing considerations of Tylenol?
1. don't exceed 3-4 gm/day
2. Should be used cautiously in those who are undernourished
3. If drinking more than 3 Alcoholic drinks/day – Avoid or limit to 2gm per day
139
What is pt education for Tylenol?
Child doses vary
1. If giving for more than 5 days especially in children need to consults
2. Watch OTC combination meds with Acetaminophen
3. Call if skin rash occurs
140
What is the antidote for Tylenol?
Mucomyst (acetylcysteine)
141
What are adverse effects of Tylenol
1. People die from inadvertent poisoning
2. Parent give to much without realizing
3. No more than 3-4gm per day in adults
142
What is Cytokines
1. produced by macrophages and lymphocytes, endothelial cells
2. Help regulate immunity
3. Tumor Necrosis Factor (TNF) and Interleukin-1 and 6: Responsible for most of the symptoms experienced
143
What can Cytokine cause
1. Weight loss and cachexia
2. Cause fever, hypotension, and increased heart rate, increase cortisol levels, decreased appetite
144
What is Nitric Oxide?
1. potent vasodilator
2. keep endothelial cells healthy and smooth
145
How does nitric oxide work?
Blocking of Nitric oxide production in normal promotes the leukocyte rolling and adhesion
146
What occurs due to nitric oxide?
1. Decreases leukocyte recruitment– reduces inflammation
2. Inflammation in endothelial cells leads to NO blockage
147
What is exudate?
varying on fluid type, plasma protein content and +/- of certain cells
148
What is Serous exudate?
watery protein low in protein content result in plasma entering the affected site
149
What is Transudate?
low protein
150
What is Serosanguinous?
Red blood cells that leak from capillary injury
151
What is purulent exudate?
pus is filled with neutrophils protein and tissue debris
152
what is the Abscess formation
Walling off of the area of purulent (pus) exudate to form an abscess
core surrounded by neutrophils
153
What is Immunity?
1. Defense system against pathogens, foreign substance that cause disease
2. responsible for maintaining the bodies internal homeostasis
154
What are the two immunity processes?
Innate
adaptive
155
What are the primary organs of the immune system?
1. Spleen
2. Tonsils
3. Thymus
4. Peyers Patches
5. Appendix
156
Immune System: sleep function
1. Largest of the lymph organs
2. White pulp
3. Red pulp
157
What is the white pulp for spleen?
contains concentrated areas of the T and B lymphocytes, dendritic cells
158
What is the red pulp for spleen?
where old or damaged RBCs are destroyed
159
Immune System: thymus function
maturation of functional t-cells
160
Immune System: Tonsils function
Collection of lymph located at entrance to digestive and respiratory tracts
No afferent lymphatic vessels
161
Immune System: sleep function
Lymphoid tissues in the GI, Respiratory and Urogenital tracts
Only contain B cells
Not encapsulated
162
What are the two lines of defense?
first line
second line
163
What are the physical barriers of First Line of Defense
skin
mucous membrane
164
What are the chemical barriers of First Line of Defense
tears
sweat
stomach acid
165
What are the mechanical barriers of First Line of Defense
coughing
sneezing
166
What are the epitheial barriers of First Line of Defense
1. Closed packed cells, layers, constant shedding and protective layer of keratin. Salty acidic environment inhibit colonization
2. Lysozyme makes cells easier for phagocytosis
4. Mucous membranes- tight epithelial cells. Mucus traps and washes away along with saliva.
5. Cilia- moves microbes towards the throat so can be expelled by coughing.
6. Surfactants in respiratory tract “opsonize” or tag the cells which need to have phagocytosis
7. GI tract goblet cells secrete mucin ⇢ hydrated form ⇢ mucus. Traps pathogens for destruction.
167
What is the second line of defense
inflammatory response
antimicrobial protein
phagocytosis
168
What are the phagocytic cells?
neutrophils
dendritic cell
monocytes/macrophages
natural killer cells
169
Where are dendritic cells found
nose, lungs, mucosal lining of GI and skin
170
How do dendritic cells link innate and adaptive immunity
Takes the organism to the B and T lymphocytes (antigen presenting cell)
Some can produce interferon to suppress viral replications
171
What is a Natural Killer cell
involved in innate immune system
first line defense
recognize and kill bacteria, virus
172
How does natural killer cell result in apoptosis
by releasing cytotoxic granules
173
What is Innate Immunity
non-specific
no memory
inflammatory process which can lead to disease
174
What cells are involved in innate immunity?
neutrophils
monocytes/macrophages
natural killer cells
175
What are chemokines: innate immunity
subgroup of cytokines by thymus and lymphoid tissue
CONTROL MOVEMENT/POSITIONING OF IMMUNE CELLS
warn other host cells of danger
176
What is adaptive immunity
3rd line defense
antigen-specific response
177
What are the three types of adaptive immunity
humoral
cell-mediated
regulatory t-cell
178
What is humoral immunity: adaptive?
produce B cells
work to rid body of microbe and toxins
179
How does humoral immunity: adaptive work to rid body of microbe and toxins?
Antigen –antibody complexes
Clumping of cells
Neutralization of toxins, bacteria and viruses,
Destruction of pathogens
Adherence of the antigen to immune cells
Phagocytosis
Complement Activation
180
What are antigens
1, substances generating response from host
2. epitopes
181
what are epitopes?
part of an antigen that binds to a specific antigen receptor on the surface of a B or T cell that triggers a cellular immune response.
182
What are antigen presenting cells (humoral immunity: adaptive)
1. immune cells mediate cellular response by process and presenting antigens for recognition by lymphocytes
2. BEGIN TRANSITION FORM INNATE TO ADAPTIVE)
183
What are the functions of antigen presenting cells (humoral immunity: adaptive)
1. There express the MHC molecules on their membrane
2. Involved in T cell activation
3. “Present” the antigen to the immune system
184
What is the clusters of differentiation of humoral immunity: adaptive?
Are cell surface markers/receptors
Expressed by cells at different stages of maturation and activation
185
What are the two responses of humoral immunity: adaptive?
primary
secondary
186
What is the primary response of humoral immunity: adaptive
Cell waiting for antibody to be detected. Clonal selection occurs
B cells differentiate into plasma cells which create the antibodies
Activation takes 1-2 weeks and many get better during primary stage
IgM is produced in large amounts and then IgG
187
What is the secondary response of humoral immunity: adaptive
occurs with repeated exposure .
Recognition occurs faster
Minimal IgM but large amounts of IgG
Titers
Booster shot
188
What is cell mediated immunity: adaptive?
Functions against microbes, parasites, bacteria, viruses which replicate inside cells where they can not be destroyed by antibodies
189
What cells are involved in cell-mediated immunity: adaptive
T cells
Cytokines T cell
Helper T cells (CD4)
190
Helper T cells Description (cell-mediated immunity: adaptive)
1. Express the CD4 protein
2. Direct B lymphocytes and macrophages
3. Secrete cytokines, chemokines etc. which kill the infected dead cells and stimulate new macrophages
4. Play a role in the amplifying and activation and of the humoral response
191
Cytotoxic T (Killer Cells) Description (cell-mediated immunity: adaptive)
1. Express the CD 8 protein
2. Once activated, they search out and destroy antigens
3. Able to differentiate what are normal and what are bad
4. Cause apoptosis or programmed death.
192
what is the relevance of macrophages to adaptive immunity
1. Gets rid of pathogens and infected cells through the adaptive system
2. Antigen presenting cells (APC): bring the antigen to the lymphocytes
3. Acts like a recruiter—Produces signaling proteins that activate other immune cells
4. Release cytokines/chemokines
193
What is the complement system
1. group o circulating plasma protein that helps defend against mirco-organism
2. BRIDGE BETWEEN INNATE AND ADAPTIVE IMMUNTIY
194
what are the 3 stages of complement system
1. Initial activation phase
2. Amplification of inflammation
3. Late-stage membrane attack response
CELL LYSIS
195
What is the major histocompatibility complex?
1. Enables the t-lymphocytes to determine “healthy vs unhealthy” cells.
Recognition of self/non-self recognition
2. Large cluster of genes on chromosome 6
Divided into 3 classes (I,II,III) based upon function.
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What are antibodies (immunoglobulins)
y shaped glycoprotein
produced by mature B-lymphocytes
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what are Functions of antibodies (immunoglobulins)
1. Directly impede the function of the pathogen
2. Neutralize secreted toxins and enzymes
3. Facilitate the removal of antigens by phagocytic cells
4. Participate in cell-mediated immunity
5. Activation of opsonization
6. Activation of inflammation
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What type of lymphocytes are involved in immune system
B lymphocytes (Bcells)
T lymphocytes (T cells)
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What is the role of B- lymphocytes
maturity in bone marrow
humoral immune response
differentiate into
plasma cells and production of antibodies and memory cells
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What is the role of T-lymphocytes
matured in the thymus
cellular-mediated immunity
types:
helper
cytotoxic (killer)
regulatory)
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What are the immune related cells
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What is opsonization: immunity
immune system marks harmful invaders
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How does opsonization connect to memory cells
knows how to fight off the same infection when it comes back
remembers the invader and quicker to make antibodies dependent on the mark
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What is the hematopoietic cascade: immunity
process the body uses to create all different kinds of blood cells to stay healthy
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In hematopoietic cascade: immunity what is Hemocytoblasts
starting creation with stem cells in bone marrow which can turn into any type of blood cell
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What are the two categories developed for hemocytoblasts
Myeloid Lineage: RBS, WBC, platelets
Lymphoid Lineage: Different WBC (T/B cells)
