Exam Two Flashcards
1
Q
Two major lymphoid organs
A
Bone marrow
Thymus
2
Q
B cells
Surface markers?
Location?
Function?
A
CD19 or CD20, have specific antigen receptor called BCR
Develop in the bone marrow - sent to spleen and lymph nodes
Production of antibodies
Fully differentiated B cells are plasma cells
3
Q
T cells
Surface markers?
Location?
Function?
A
CD3+ markers and TCR to identify antigens
Cytotoxic T cells have CD8+
Helper T cells have CD4+
Develop in the thymus
Cytotoxic T cells kill tumor cells and virus infected cells
Helper T cells produce protein cytokines which influence immune cells
4
Q
Natural killer cells
Surface markers?
Location?
Function?
A
CD56+, killer inhibitory receptor
Differentiate and mature in bone marrow, thymus, tonsils, lymph nodes, and spleen
Enter circulation
Release lytic granules that kill virus infected cells and tumor cells
Does not need previous exposure to virus like CTLs, kill on first site
5
Q
Dentritic cells
Surface markers?
Location?
Function?
A
CD11c+
Present in tissues that are exposed to external environment - primarily the epidermis and mucous membrane
Antigen presenting cell that presents antigen to T and or B cells for activation
6
Q
Granulocytes
Surface marker?
Types?
A
Polymorphonuclear leukocytes (PMN)
CD66b+, but can be differentiated from one another by staining
Neutrophils
Eosinophils
Basophils
7
Q
Neutrophils
Surface markers?
Location?
Function?
A
CD66b+, but can be further differentiated
Produced in the bone marrow, enter circulation - often part of the pus observed at an infected site
Phagocytosis and activation of bactericidal mechanisms - kill pathogens
8
Q
Phagocytosis steps
A
Phagocyte ids the pathogen and engulfs the target
Phagosome is formed to contain pathogen
Phagosome fuses with lysosomal enzymes to form phagolysosome
Pathogen is degraded and destroyed
9
Q
Eosinophils
Surface marker?
Location?
Function?
A
CD66b+, but can be further differentiated
Most are found in the gut, mammary gland, uterus, thymus, bone marrow, adipose tissue, and in circulation
Kills antibody-coated parasites, role in allergies
10
Q
Basophils
Surface marker?
Location?
Function?
A
Least abundant granulocyte
CD66b+
Circulation
Promotes allergic responses and augmentation of anti parasitic immunity
Allergies and asthma association
11
Q
Monocytes and macrophages Surface markers? Location? Function? Specific names?
A
Largest WBC
CD14+
Develop in bone marrow, enter circulation as monocytes, become macrophages when they enter tissues
Phagocytosis and activation of bactericidal mechanisms; antigen presentation
CNS: microglia
Liver: kupffer cells
Lungs: alveolar macrophages
12
Q
Mast cells
Location?
Function?
A
Tissues
Release of granules containing histamine and active agents
Role in allergy, wound healing, and defense against pathogens
Histamines decrease permeability of capillaries to wbc to increase their presence and functionality
13
Q
WBC breakdown
A
Men and non pregnant women:
4500-11000/mcL^3 or
4.5-11 x 10^9/liter
Neutrophils: 50-62% Band neutrophils: 3-6% Lymphocytes: 25-40% Monocytes: 3-7% Eosinophils: 0-3% Basophils: 0-1%
14
Q
Innate immunity
A
Rapid - defense mechanisms exist before antigen exposure
Not antigen specific
Response time 0-4 hours
Cells include: granulocytes, mast cells, NK cells, complement proteins, and macrophages
Does not have memory
Promotes initiation of adaptive response: APCs
15
Q
Adaptive immunity
A
Slow: 96 or more hours
Antigen specific
Cells include: B cells (plasma), T cells (CTLs and Th), antibodies, and memory B cells
Has an enhanced response on second antigen exposure
Initiated by certain cells of the innate immune system
16
Q
Antigen
A
Any substance capable of cause an immune response
17
Q
Self/non-self
Central tolerance
A
Self cells have specific cellular surface markers for id
Process by which cells understand how to recognize self cells and non-self cells
18
Q
The 7 aspects of innate immunity
A
Physical/mechanical/chemical barriers Phagocytosis Inflammation Acute phase response Fever (pyrexia) NK cells and anti-viral immunity Plasma protein systems
19
Q
Physical/mechanical/chemical barriers
A
Many barriers in the body systems that act as first line of defense
Normal microbiota act as microbiological barriers for all systems
Skin: tight junctions and longitudinal flow of air/fluid (mechanical), fatty acids and beta-defensins (chemical)
Gut: tight junctions and longitudinal flow of air/fluid (mech), low ph of stomach and alpha-defensins (chemical)
Lungs: tight junctions and movement of mucus by cilia (mech); pulmonary surfactant, alpha-defensins, and cathelicidin (chemical)
Eyes/nose/oral cavity: tight junctions, tears, nasal cilia (mech); enzymes in tears/saliva, histatins, and beta-defensins (chemical)
20
Q
Opsonization
A
Enhances phagocytosis as antibodies bind to bacteria and the Fc receptors in the cell surface provide a glue like layer for the macrophage to easily stick to during engulfment
21
Q
Inflammation
A
Protective response intended to isolate infected tissues and prevent the spread of disease
Pain, redness, swelling, heat, and loss of function
Leads to increased vascular permeability and blood flow, exudation of plasma fluid (pus), and leukocyte recruitment and extravasation
22
Q
Acute phase response
Main goals?
A
Acute phase proteins play part in blocking spread of infection and activating complement
Cytokine IL-6 induces synthesis of proteins by stimulating liver to produce them
Promote phagocytosis
Promote blood clots in small vessels - traps infection
Activate the complement
23
Q
Fever
A
Elevating body’s temp impedes viral and bacterial replication
Cytokine IL-1 stimulates the production of prostaglandins to influence the hypothalamus to trigger ANS to raise temp
Fevers decrease path replication, increase antigen processing and specific immune responses
24
Q
NK cells and anti-viral immunity
Components?
A
Ways innate system responds to viral infections to prevent and kill infected cells
Type 1 interferons and NK cells
Interferons produce antiviral proteins to help prevent infection
NK cells directly recognize ligand on virally infected cells and kill them
25
Ligands are what kind of protein?
MHC class one
26
Plasma protein systems composed of?
3 systems that help with innate immunity process
Complement
Clotting
Kinin
27
Complement system
C3: enhances protein synthesis that helps with phagocytosis, opsonin production (flags cells)
A cascade pathway of 30 protein synthesized in the liver
Aides in direct damage to bacterium, enhanced phagocytosis, neutrophil migration, chemotaxis, and release of histamine
28
Clotting system
Results in formation of clots/mesh that help trap pathogen
Aides in neutrophil migration and increased permeability of blood vessels for wbcs
29
Kinin system
Bradykinin important
Breaks down clots (balances clotting system)
Works with prostaglandins to induce pain, fever, and vascular permeability
30
Types of adaptive immunity?
Humoral and cellular
31
Humoral
Think B cells, antibodies, immunoglobulins, opsonization
32
Cell mediated immunity
Think T cells and phagocytosis
33
Components of an antibody
Fc region: constant part of antibody (not antigen specific), includes hinge region where It branches off
Specific antigen binding sites: where antigen binds, contain both variable and constant regions
34
Five types of antibodies/immunoglobulins
```
IgM
IgA
IgD
IgE
IgG
```
35
Major histocompatibility complex
Cell types?
Function?
MHCs are glycoproteins found on surface of all cells except for rbcs
Aka HLAs
Class I: endogenous antigens
Class II: exogenous antigens
Bind peptide fragments derived from pathogens and display them on cell surface for recognition by appropriate T cells
Presents the antigen on the APC
36
MHC class II interacts with?
CD4 on Th cell to cause maturation of immunocompetent B cells into plasma cells
37
MHC class I interacts with?
CD8 on T cell when presenting an antigen to activate cytotoxic T cells
38
Humoral attachment
MHC II and CD4
39
Cellular attachment
MHC I and CD8
40
Antibody dependent cellular cytotoxicity involves?
Adaptive immunity
| NK cells kill target cells with help of antibodies
41
Types of T cells
| Functions?
T helper cells: recognize presented antigens on APCs, release cytokines to activate immunocompetent B and T cells
Cytotoxic T cells: kill cancer cells, infected cells, and damaged cells by releasing granzymes that produce apoptosis in target cell and punch holes in target cells for granzymes to enter and destroy
Memory T cells: remain in body after infection ends; converted to effector T cells when reexposed to same antigen for more effective response
42
How does inflammation aid in protecting against infection?
prevents spreading from localized spot - prevents systemic infection/sepsis
increases vascular permeability - allows WBCs to enter injury site to work more efficiently
recruits leukocytes to area
43
bacteria shapes?
| examples?
sphere: cocci (staph aureus and strep pyogenes)
can be diplo, tetrad, sarcina, staph, or strep
rods: bacilli
chain (bacillus anthracis)
flagellate rods (salmonella typhi)
spore-formers: (clostridium botulinum)
spirals:
vibrios (one flagellum, vibrio cholerae)
spirilla (multiple flagella)
spirochaets (long - treponema pallidum)
44
bacteria
| diagnosis?
done by culture and sensitivity to antibiotics (determines what med is most helpful)
45
gram-neg vs gram-pos
positive: thick peptidoglycan layer around bacteria in cell membrane; holds purple stain
negative: thinner peptidoglycan layer with outer membrane - does not hold purple dye, picks up pink counterstain
determines what antibiotics to use and virulence
46
septicemia
failure of body's defense mechanisms - leads to progressive growth of micro
bacterial toxins activate clotting cascades - leads to increased cap permeability and large passage of plasma to tissue (large blood vol drop - leads to hypotension and shock)
disseminated intravascular coagulation due to clotting cascade activation
47
viral disease
transmission?
drift?
shift?
most common affliction
viruses must use infection of host to replicate
transmission: aerosol, infected blood, sex, vectors
antigenic drift: gradual mutation on surface antigens (flu strains)
antigenic shift: major shifts in genetic recomb. such as species jumping (swine flu)
48
viral replication
attach to host cell
penetrate host cell
uncoat once inside
replicate inside nucleus using host cell enzymes
assembles and matures within
released by cell through budding of cell membrane
49
fungal infections
| examples?
thick, rigid cell walls made of polysaccharides without peptidoglycans found in bacteria - antibiotics that act on pep are not effective
can be single or multicelled
mycoses: superficial, deep, or opportunistic
dermatophytes: fungi that invade skin, hair, or nails (tineas - rignworm)
50
fungal infection pathogenicity
| example?
quickly adapt to host
suppress immune system
controlled by phagocytes and T lymphocytes
Candida albicans
most common - opportunistics
localized infection from overgrowth
disseminated infection if immunocompromised
51
parasitic infection
| examples?
organisms establish a relationship where the parasite benefits and the host is harmed
more common in developing countries
spread human to human through vectors (ingested)
leads to tissue damage in body
(malaria, hookworms, tapeworms, lice, ticks)
52
microbial mechanisms of drug resistance
reduction of drug concentration at its action site: microbes cease active uptake of drugs and can increase active export
alteration of drug target molecules: structure of target molecule (ribosome) to inhibit drug binding
antagonist protection: synthesize a compound that antagonizes drug actions
53
mechanisms of acquired resistance
spontaneous mutation: gradual increase in resistance to one drug
conjugation: extrachromosomal DNA is transferred from one bacterium to another; primarily gram neg; multiple drugs
54
principles of antibiotic use
pts must complete entire antibiotic course
don't use antibiotics to treat viral infections or for treatment of fever with unknown cause
start with broad-spectrum antibiotic
combos of antibiotics may be warranted for severe infections and infections caused by multiple organisms
55
desirable traits of antibiotic
selective toxicity: ability to injure the pathogen without harming healthy cells
56
bactericidal vs bacteriostatic
cidal kills bacteria
static suppresses aspects of bacterial life/replication
57
Adverse side effects: penicillin
allergic reaction
| electrolyte imbalances - hyperkalemia (cardiac)
58
Adverse side effects: cephalosporins
bleeding - interferes with prothrombin and vitamin K levels
| thrombophlebitis
59
Adverse side effects: tetracyclines
hepatotoxicity, nephrotoxicity, photosensitivity, yellowing of teeth, GI irritation, suprainfection
60
Adverse side effects: macrolides
GI effects
| QT prolongation - can result in sudden cardiac death
61
Adverse side effects: aminoglycosides
nephrotoxicity, ototoxicity, neuromuscular blockade - respiratory depression
62
Adverse side effects: sulfanomides and trimthoprim
hypersensitivity (stevens-johnson syndrome), photosensitivity, hematologic anemia, crystalluria
63
Adverse side effects: floroquinolones
tendon rupture, phototoxicity, reduced absorption from cationic solutions (milk)
64
antibiotic classification by susceptible organism
narrow-spectrum: active against a few microorganisms (gram pos cocci and gram pos bacilli: penicillin G and V)(gram neg aerobes: cephalosporins)
broad-spectrum: active against wide variety (gram pos cocci and gram neg bacilli: tetracyclines and sulfonamides)
narrow is preferred to broad
65
antibiotic classification by MoA
drugs that inhibit bacterial cell wall synthesis: weaken cell wall to allow lysis
drugs that increase cell membrane permeability: leakage of intracellular material
drugs that cause lethal inhibition of protein synthesis
nonlethal inhibition of protein synthesis
drugs that inhibit bacterial synthesis of DNA and RNA
antimetabolites: disrupt biochemical reactions
66
antibiotic classes of anti-fungals
polyene antibiotics: amphotericin B (broad spectrum but highly toxic) only IV
azoles: fluconazole (diflucan)(broad spectrum but less toxic)
echinocandins: caspofungin (narrow spectrum - aspergillus and candida)(newest class)
pyrimidine analogs: flucytosine (narrow spectrum for candidiasis and cryptococcosis)(combo with amphotericin)
67
stress response triggers?
| signs and symptoms?
```
psychological/emotional factor (fear)
physical factor (temp change, abuse)
physiologic stimuli (infection, inflamm.)
```
stress response due to bidirectional communication between brain and other physiologic systems
68
how does SNS respond to stress
aroused with HPA system during stress to release norepinephrine and stimulate adrenal gland to release catecholamines
fight or flight: HR and RR increase, blood vessels dilate, digestion slows, glucose increases
sudden acute activation to stress that subsides
69
catecholamines
hormones released by adrenal medulla during stress - epinephrine and norepinephrine
bind to adrenergic receptors to mimic direct sympathetic stimulation
70
Antibiotics
| Inhibition of cell wall synthesis
Penicillins
Cephalosporins
Bacitracin
Vancomycin
71
Antibiotics
| Inhibition of protein synthesis
Chloramphenicol
Erythromycin
Tetracyclines
Streptomycin
72
Antibiotics
| Inhibition of synthesis of essential metabolites
Sulfanilamide
| Trimethoprim
73
Antibiotics
| Inhibition of nucleus acid replication and transcription
Quinolones
| Rifampin
74
Major groups of antifungal agents
Drugs for systemic mycoses/infections
Drugs for superficial mycoses/infections
A few drugs are used for both
75
Types of vaccines
Weakened (attenuated) or dead pathogen
Toxoid
Recombinant viral proteins
76
effects of epinephrine
cardiac?
metabolic?
pulmonary?
beta 1: increases HR
beta 1: increases cardiac contraction force
beta 2: increases hepatic gluconeogenesis
beta 2: increased hepatic and muscle glycogenolysis
beta 1: increases glucagon and renin
beta 2: smooth muscle relaxation (bronchodilation)
77
what are adrenergic receptors?
| types?
membrane bound proteins that mediate the peripheral and central actions of epi and norepi
alpha receptors (1 and 2) focused on constriction of blood vessels and activation of effector cells (norepi and epi bind)
beta receptors are focused on relaxing effector cells and vasodilation (epi binds)
78
```
Primary responses of:
beta 1
beta 2
alpha 1
alpha 2
```
b1: heart - increased HR, conduction, and contractility
b2: lungs and GI - bronchodilation and decreased GI motility
a1: blood vessels and heart - increased vasoconstriction and increased heart contractility
a2: neurons - inhibition of neurons
79
dangers for pts with immune deficiencies
high susceptibility to acquire infection
| poorer response to infections
80
primary immunodeficiencies
caused by genetic anomaly
| congenital (inherited not acquired)
81
secondary immunodeficiencies
caused by another illness
| can't be genetically passed on to offspring; some are minor and some are lifelong
82
HIV
| cells involved?
Th cells are infected by HIV leading to their progressive destruction within the body
without Th cells, plasma and T cells can't be activated to supply adaptive immune response
83
HIV
| enzymes required?
reverse transcriptase: converts viral RNA into dsDNA
integrase: inserts new DNA into infected cell's genetic material to create more viruses
protease: necessary for processing proteins needed from the viral internal structure
84
HIV
| acute phase?
immediately follow infection with HIV
typical symptoms: fatigue, fever, headache
lasts 1-6 weeks
virus is actively proliferating in lymph nodes and Th cells are experiencing a sharp drop in #s
85
HIV
| clinical latency?
period where infected individual doesn't show any signs of infection following acute phase
can last many years
virus still replicating and T cells still being destroyed
86
HIV
| clinical manifestations
diminished response to wide array of infectious pathogens and cancers
at dx: serologically neg (no detectable antibodies), serologically pos but asymptomatic, early stage of HIV or AIDS
87
symptomatic HIV infection
variety of symptoms that don't involve opportunistic infections or malignancies
occurs once Th cells have reached low levels during latenc y
88
Viral loads and CD4 counts in each phase
early: sharp drop from 1000 to around 500
latency: gradual drop from 500 to 300
symptomatic: drop 300 to below 200 where diagnosis is established
89
CD4 count of progression from HIV to AIDS
less than 200 cells/mL
90
HIV treatment
ART
HAART
NRTIs: Zidovudine - competes with reverse transcriptase for interaction side for HIV genetic material
NNRTIs: Efavirenz - blocks reverse transcriptase from replicating by binding to virus structure
91
HAART MoA
combo drugs: 30-45 pills a day
death has reduced significantly since this treatment
```
reverse transcriptase inhibitors
HIV protease inhibitors
HIV integrase inhibitors
HIV fusion inhibitors
CCR5 agonist
antibiotics and anti-fungals for prophylaxis
```
92
Protease enzyme
essential in processing proteins needed from the viral internal structure (capsid)
93
Lab monitoring for HIV
presence of circulating antibodies against HIV proteins and HIV DNA indicates infection
levels of CD4+ t cell counts to monitor progression
drug therapy - efficient but not curative
94
overall treatment goal HIV CD4+ counts
maintain max suppression of viral load
| restore/preserve immune function improve quality of life
95
3 goals of immune response
Clears infection
Temporarily strengthens defenses to prevent reinfection
Establishes a state of long term immunological memory
96
Two involved in immunological memory
Antibodies and memory T cells
97
Memory T cells
Don’t undergo isotope switching and somatic hyper mutation like memory B cells
Have specific markers used to ID memory T cells
98
Overlapping phases of wound healing
Inflammation: coagulation, infiltration of wound healing cell, and angiogenesis
Proliferation and new tissue formation: (starts early) granulation, epithelialization (keratinocyte migration), fibroblast proliferation, collagen formation, and wound contraction
Remodeling and maturation: continuation of cellular differentiation, scar tissue formation, and scar remodeling
99
Types of healing: primary intention
wounds that heal under conditions of minimal tissue loss
100
Types of healing:
| secondary intention
wounds that require a great deal more tissue replacement (open wound), not restored to original form
101
Types of healing:
| resolution
returns injured tissue to original structure and function - can occur if there is minimal damage
takes up to 2 years
102
Types of healing:
| regeneration
replacement of the damaged tissue with healthy tissue
103
Types of healing:
| repair
replacement of destroyed tissue with scar tissue
| composed primarily of collagen to restore strength but not function
104
Types of dysfunctional healing: ischemia
collagen synthesis is impaired when tissue is oxygen deprived
105
Types of dysfunctional healing: excessive bleeding
barrier for oxygen perfusion, pooled blood doesn't allow oxygen to move around
promotes infection and bacterial growth
106
Types of dysfunctional healing: excessive fibrin deposition
fibrous adhesions formed in pleural, pericardial, and abdominal cavities can bind organs together and distort/strangle affected organ
107
Types of dysfunctional healing: predisposing disorders
diabetes: hyperglycemia can suppress macrophages and increase risk for infection
obesity: impaired leukocyte function, predisposition for infection, decreased growth factors, and increased levels of proinflammatory cytokines
wound infection: pathogens damage cells to stimulate continued release of inflammatory mediators to delay wound healing
inadequate nutrition
numerous drugs: NSAIDs and steroids
tobacco
108
dehiscence
complication of wounds that are sutured closed
| wound pulls apart at suture line generally 5-12 days after suturing when collagen synthesis is at its peak
109
keloid scar
raised scar that extends beyond the original boundaries of the wound and invades surrounding tissue
110
hypertrophic scar
raised scar that remains within the boundaries of the injured tissue
111
contracture of scar tissue
particularly common in the joints (especially burns), deformity caused by wound contraction resulting in loss of movement
112
Type I hypersensitivity
IgE and products of tissue mast cells mediated
most common allergic reactions are type one: asthma and seasonal rhinoconjuntivitis
most aggressive response: anaphylaxis
most important mediator: histamine: contracts bronchial smooth muscles, increases edema, and causes vasodilation
clinical manifestations: vomiting, diarrhea, hives, conjunctivitis, rhinitis, asthma
second exposure response much quicker
113
Type III hypersensitivity
IgG immune complex mediated
most caused by antigen-antibody complexes that are formed in the circulation and deposited later in vessel walls (formed from IgG and soluble antigens
not organ specific
harmful effects caused by complement activation
serum sickness
arthus reaction
114
Type II hypersensitivity
mediated by IgG
specific cell/tissue is target of immune response
symptoms: dependent on associated tissue/organ
antigen already bound to cell or tissue
mechanisms:
cell destroyed by antibodies and complement
cell destruction through phagocytosis
soluble antigen enters circulation and deposits on tissues - destroyed by complement and neutrophil granules
antibody dependent cell mediated cytotoxicity; involves NK cells
target cell malfunction - results in malfunction but not destruction of cells
115
serum sickness
the complex is in circulation and deposits around the body - affected tissues are blood vessels, joints, and kidneys
symptoms: fever, enlarged lymph nodes, rash, pain at site
type: raynaud phenomenon - fingers/toes pale or cyanotic with decreased temp
116
arthus reaction
repeated local exposure to antigen that reacts with preformed antibody and forms complexes in walls of local blood vessels - inflammatory response
symptoms: begin in an hour, peak 6-12 hours after
observed after injection, ingestion, or inhalation of allergens
117
Type IV hypersensitivity
cell mediated reactions
does not involve antibody
mediated by T lymphocytes (Tc cells or Th1 and Th17 cells) T cells attack and kill cellular targets , Th produce cytokines that recruit macrophages
ex: organ/graft rejection, skin test for TB, allergic reactions from poison ivy or metals
type IV components in autoimmune disease: rheumatoid arthritis
celiac disease is an ex.
118
goodpasture's
antibodies toward basement membranes and proteins associated with it in the lungs
affected to extent of bleeding
119
A blood type
can have A or O blood
120
B blood type
can have B or O blood
121
AB blood type
can have A, B, or O blood
122
O blood type
can only have O blood
123
universal donor
O (O-)
124
universal recipient
AB (AB+)
125
what occurs in blood transfusions
must ensure that transfused blood doesn't have an antigen present that the recipient blood has antibodies for
126
drugs for Herpes
Acyclovir: active against members of the herpesvirus family - first choice for HSV or varicella zoster
herpesvirus can develop resistance
Ganciclovir: used for HSV and cytomegalovirus infections, prevention and treatment of CMV in immunocompromised pts
SE: granulocytopenia - reduced granulocytes
thrombocytopenia - decreased platelets
used when there is displayed resistance to acyclovir
127
drugs for HepC
pegylated interferon alpha
(pegylated: drug is formulated with another protein which helps med stay in system longer)
no oral admin
adverse: flu-like sx, neuropsychiatric effects, fatigue, thyroid dysfunction, heart damage, neutropenia and thrombocytopenia
typically given with ribavirin (oral) used for RSV in children
128
HepB overview
| drugs
chronic infection that can lead to cirrhosis, hepatic failure, hepatocellular carcinoma, and death
hospitalization for fatigue, muscle pain, and jaundice
interferon alpha 2 beta and lamivudine (HIV prescription)
129
Influenza overview
| drugs
type A causes more infections than type B
lots of antigenic drift
primarily managed through vaccination: once a year
adamantanes and neuraminidase inhibitors (tamiflu) - more frequently used to help decrease spread in the body by preventing viral release from infected cells
130
H1 antagonists
stimulating H1 receptors leads to: vasodilation, increased cap perm, bronchoconstriction, CNS effects
mild allergy symptoms caused by histamine acting at H1 receptors
H1 antagonists produce selective blockade of receptors to treat mild allergic disorder
also for motion sick, insomnia, and common cold
131
major groups of H1 antagonists
| effects
1st gen: highly sedating (benadryl)
2nd gen: much less sedation, doesn't cross BBB well - less anticholinergic effects (claritin, allegra, zyrtec)
reduce localized flushing, itching, pain
CNS depression
132
H2 antagonist
H2 receptor stimulation leads to secretion of gastric acid
| produce blockade of receptors to treat gastric and duodenal ulcers
133
anaphylactic reaction treatments
epinephrine
antihistamines are little help, may be used in adjunct
shock includes bronchoconstriction, hypotension, and edema or glottis
maintaining open airway is treatment goal
134
drugs based on severity of allergic reaction
mild: antihistamines (H1 antagonists)
severe: epinephrine
135
clinical presentation of antihistamine overdose, anticholinergic syndrome
CNS stimulation
| insomnia, tremors, convulsions, confusion
136
Prednisone MoA
| safe use
suppresses WBC proliferations and lysis antigen active WBC to suppress immune response
use: suppress allograft rejection; treatment of asthma, RA, lupus, and MS
Safe use: dose of drug follows goal; increased risk of infection (maintain hygiene); kidneys promoted to retain Na and H2O - may lead to hypokalemia (may need supplement; refrain from use if on diuretic)
137
NSAID and ASA MoA
inhibits COX (enzyme that converts prostaglandins into prostanoids)
1st gen NSAIDs inhibit COX1 (good) and COX2 (bad) - nonselective
ASA inhibition is irreversible
NSAID 1st gen is reversible
2nd gen NSAID - only inhibit COX2 - lower risk for GI complications
Acetaminophen: inhibits prostaglandin syn. in CNS (analgesic and antipyretic)
138
clinical effects of COX1 inhibition
good: protection against MI and stroke
bad: gastric ulcers, bleeding, renal impairment
139
clinical effects of COX2 inhibition
good: suppress inflammation, alleviate pain and fever, protect against colorectal cancer
140
Clinical uses of NSAIDs
anti inflammatory, analgesic (mild to mod pain), and antipyretic
acetaminophen: no anti inflammatory properties
dysmenorrhea
prevention of Alzheimer's and cancer prevention - aspirin
suppression of platelet aggregation: COX1 - for thrombotic disorders
inflammatory disorders: RA, osteoarthritis, bursitis
141
precautions for NSAIDs
avoid alcohol use (especially with aspirin and acetaminophen)
no overuse/overdose: GI bleeding can lead to hospitalization or death
avoid using aspirin with children: increases risk of Reye's syndrome
142
averse side effects of NSAIDs
gastric ulcerations
bleeding
renal impairment
aspirin: salicylism (tinnitus, sweating, headache, dizziness), Reye's (avoid child use), pregnancy: (anemia, PPH, prolonged labor), hypersensitivity
acetaminophen: very few with normal dose: Stevens-Johnson syndrome, acute generalized exacnthematous pustulosis, toxic epidermal necrolysis, hepatotoxicity
143
NSAID effects on platelet aggregation
for nonselective anti-inflammatories, such as aspirin, there is inhibition of platelet aggregation that COX1 stimulates
leads to bleeding
144
drug-food interactions for NSAIDs
do not drink alcohol while using
145
autoimmunity
| causes?
immunity to self; occurs when immune system mistakenly attacks and destroys healthy body tissues
genes, immune reg, environment
not usually a single reason - complex diseases
146
autoimmune diagnosis
initial diagnosis may be missed due to general symptoms
general tests: low RBCs, C reactive protein, autoantibody titers, presence of rheumatoid factor
disease specific: neuro exam (MS), fasting glucose (diabetes), TSH levels (Graves')
147
key treatment for autoimmune disorders
immunomodulation
148
bullous pemphigoid
large fluid filled blisters on skin, typically in areas that flex
149
vitiligo
loss of melanin in skin
150
polymyositis
effects any muscle tissues, causes irritation and inflamm. making movement difficult
151
Myasthenia Gravis
progressive weakness and loss of muscle control
B cell disease
autoantibodies are formed against nicotinic acetylcholine receptors - acetylcholine NT that signals muscles to contract are blocked
152
Multiple Sclerosis
autoantibodies and self reactive T cells cause demyelination of nerve cells causing nerve signals to not be transported normally
153
organ specific autoimmune disorders
```
DM type 1
Goodpasture's
MS
Graves'
Hashimoto's thyroiditis
Hemolytic anemia
Addison's disease
Vitiligo
Myasthenia Gravis
```
154
systemic autoimmune disorders
```
RA
Scleroderma
SLE
Primary Sjogren's
Polymyositis
```
155
Alloimmunity
reactions due to non-self, but same species antigens
blood transfusions
