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Patho And Pharm > Exam Two > Flashcards

Exam Two Flashcards

1
Q

Two major lymphoid organs

A

Bone marrow

Thymus

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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

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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

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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

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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

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6
Q

Granulocytes
Surface marker?
Types?

A

Polymorphonuclear leukocytes (PMN)

CD66b+, but can be differentiated from one another by staining

Neutrophils
Eosinophils
Basophils

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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

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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

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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

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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

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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

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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

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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%
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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

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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

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16
Q

Antigen

A

Any substance capable of cause an immune response

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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

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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
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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)

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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

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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

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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

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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

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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

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25
Q

Ligands are what kind of protein?

A

MHC class one

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26
Q

Plasma protein systems composed of?

A

3 systems that help with innate immunity process
Complement
Clotting
Kinin

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27
Q

Complement system

A

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

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28
Q

Clotting system

A

Results in formation of clots/mesh that help trap pathogen

Aides in neutrophil migration and increased permeability of blood vessels for wbcs

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29
Q

Kinin system

A

Bradykinin important

Breaks down clots (balances clotting system)

Works with prostaglandins to induce pain, fever, and vascular permeability

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30
Q

Types of adaptive immunity?

A

Humoral and cellular

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31
Q

Humoral

A

Think B cells, antibodies, immunoglobulins, opsonization

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32
Q

Cell mediated immunity

A

Think T cells and phagocytosis

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33
Q

Components of an antibody

A

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

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34
Q

Five types of antibodies/immunoglobulins

A 
IgM
IgA
IgD
IgE
IgG
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35
Q

Major histocompatibility complex
Cell types?
Function?

A

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

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36
Q

MHC class II interacts with?

A

CD4 on Th cell to cause maturation of immunocompetent B cells into plasma cells

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37
Q

MHC class I interacts with?

A

CD8 on T cell when presenting an antigen to activate cytotoxic T cells

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38
Q

Humoral attachment

A

MHC II and CD4

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39
Q

Cellular attachment

A

MHC I and CD8

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40
Q

Antibody dependent cellular cytotoxicity involves?

A

Adaptive immunity

NK cells kill target cells with help of antibodies

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41
Q

Types of T cells

Functions?

A

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

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42
Q

How does inflammation aid in protecting against infection?

A

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

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43
Q

bacteria shapes?

examples?

A

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)

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44
Q

bacteria

diagnosis?

A

done by culture and sensitivity to antibiotics (determines what med is most helpful)

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45
Q

gram-neg vs gram-pos

A

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

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46
Q

septicemia

A

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

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47
Q

viral disease
transmission?
drift?
shift?

A

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)

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48
Q

viral replication

A

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

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49
Q

fungal infections

examples?

A

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)

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50
Q

fungal infection pathogenicity

example?

A

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

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51
Q

parasitic infection

examples?

A

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)

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52
Q

microbial mechanisms of drug resistance

A

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

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53
Q

mechanisms of acquired resistance

A

spontaneous mutation: gradual increase in resistance to one drug

conjugation: extrachromosomal DNA is transferred from one bacterium to another; primarily gram neg; multiple drugs

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54
Q

principles of antibiotic use

A

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

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55
Q

desirable traits of antibiotic

A

selective toxicity: ability to injure the pathogen without harming healthy cells

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56
Q

bactericidal vs bacteriostatic

A

cidal kills bacteria

static suppresses aspects of bacterial life/replication

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57
Q

Adverse side effects: penicillin

A

allergic reaction

electrolyte imbalances - hyperkalemia (cardiac)

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58
Q

Adverse side effects: cephalosporins

A

bleeding - interferes with prothrombin and vitamin K levels

thrombophlebitis

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59
Q

Adverse side effects: tetracyclines

A

hepatotoxicity, nephrotoxicity, photosensitivity, yellowing of teeth, GI irritation, suprainfection

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60
Q

Adverse side effects: macrolides

A

GI effects

QT prolongation - can result in sudden cardiac death

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61
Q

Adverse side effects: aminoglycosides

A

nephrotoxicity, ototoxicity, neuromuscular blockade - respiratory depression

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62
Q

Adverse side effects: sulfanomides and trimthoprim

A

hypersensitivity (stevens-johnson syndrome), photosensitivity, hematologic anemia, crystalluria

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63
Q

Adverse side effects: floroquinolones

A

tendon rupture, phototoxicity, reduced absorption from cationic solutions (milk)

64
Q

antibiotic classification by susceptible organism

A

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
Q

antibiotic classification by MoA

A

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
Q

antibiotic classes of anti-fungals

A

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
Q

stress response triggers?

signs and symptoms?

A 
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
Q

how does SNS respond to stress

A

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
Q

catecholamines

A

hormones released by adrenal medulla during stress - epinephrine and norepinephrine

bind to adrenergic receptors to mimic direct sympathetic stimulation

70
Q

Antibiotics

Inhibition of cell wall synthesis

A

Penicillins
Cephalosporins
Bacitracin
Vancomycin

71
Q

Antibiotics

Inhibition of protein synthesis

A

Chloramphenicol
Erythromycin
Tetracyclines
Streptomycin

72
Q

Antibiotics

Inhibition of synthesis of essential metabolites

A

Sulfanilamide

Trimethoprim

73
Q

Antibiotics

Inhibition of nucleus acid replication and transcription

A

Quinolones

Rifampin

74
Q

Major groups of antifungal agents

A

Drugs for systemic mycoses/infections
Drugs for superficial mycoses/infections

A few drugs are used for both

75
Q

Types of vaccines

A

Weakened (attenuated) or dead pathogen
Toxoid
Recombinant viral proteins

76
Q

effects of epinephrine
cardiac?
metabolic?
pulmonary?

A

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
Q

what are adrenergic receptors?

types?

A

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
Q 
Primary responses of: 
beta 1
beta 2
alpha 1
alpha 2
A

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
Q

dangers for pts with immune deficiencies

A

high susceptibility to acquire infection

poorer response to infections

80
Q

primary immunodeficiencies

A

caused by genetic anomaly

congenital (inherited not acquired)

81
Q

secondary immunodeficiencies

A

caused by another illness

can’t be genetically passed on to offspring; some are minor and some are lifelong

82
Q

HIV

cells involved?

A

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
Q

HIV

enzymes required?

A

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
Q

HIV

acute phase?

A

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
Q

HIV

clinical latency?

A

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
Q

HIV

clinical manifestations

A

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
Q

symptomatic HIV infection

A

variety of symptoms that don’t involve opportunistic infections or malignancies
occurs once Th cells have reached low levels during latenc y

88
Q

Viral loads and CD4 counts in each phase

A

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
Q

CD4 count of progression from HIV to AIDS

A

less than 200 cells/mL

90
Q

HIV treatment

A

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
Q

HAART MoA

A

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
Q

Protease enzyme

A

essential in processing proteins needed from the viral internal structure (capsid)

93
Q

Lab monitoring for HIV

A

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
Q

overall treatment goal HIV CD4+ counts

A

maintain max suppression of viral load

restore/preserve immune function improve quality of life

95
Q

3 goals of immune response

A

Clears infection
Temporarily strengthens defenses to prevent reinfection
Establishes a state of long term immunological memory

96
Q

Two involved in immunological memory

A

Antibodies and memory T cells

97
Q

Memory T cells

A

Don’t undergo isotope switching and somatic hyper mutation like memory B cells

Have specific markers used to ID memory T cells

98
Q

Overlapping phases of wound healing

A

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
Q

Types of healing: primary intention

A

wounds that heal under conditions of minimal tissue loss

100
Q

Types of healing:

secondary intention

A

wounds that require a great deal more tissue replacement (open wound), not restored to original form

101
Q

Types of healing:

resolution

A

returns injured tissue to original structure and function - can occur if there is minimal damage
takes up to 2 years

102
Q

Types of healing:

regeneration

A

replacement of the damaged tissue with healthy tissue

103
Q

Types of healing:

repair

A

replacement of destroyed tissue with scar tissue

composed primarily of collagen to restore strength but not function

104
Q

Types of dysfunctional healing: ischemia

A

collagen synthesis is impaired when tissue is oxygen deprived

105
Q

Types of dysfunctional healing: excessive bleeding

A

barrier for oxygen perfusion, pooled blood doesn’t allow oxygen to move around
promotes infection and bacterial growth

106
Q

Types of dysfunctional healing: excessive fibrin deposition

A

fibrous adhesions formed in pleural, pericardial, and abdominal cavities can bind organs together and distort/strangle affected organ

107
Q

Types of dysfunctional healing: predisposing disorders

A

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
Q

dehiscence

A

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
Q

keloid scar

A

raised scar that extends beyond the original boundaries of the wound and invades surrounding tissue

110
Q

hypertrophic scar

A

raised scar that remains within the boundaries of the injured tissue

111
Q

contracture of scar tissue

A

particularly common in the joints (especially burns), deformity caused by wound contraction resulting in loss of movement

112
Q

Type I hypersensitivity

A

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
Q

Type III hypersensitivity

A

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
Q

Type II hypersensitivity

A

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
Q

serum sickness

A

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
Q

arthus reaction

A

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
Q

Type IV hypersensitivity

A

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
Q

goodpasture’s

A

antibodies toward basement membranes and proteins associated with it in the lungs
affected to extent of bleeding

119
Q

A blood type

A

can have A or O blood

120
Q

B blood type

A

can have B or O blood

121
Q

AB blood type

A

can have A, B, or O blood

122
Q

O blood type

A

can only have O blood

123
Q

universal donor

A

O (O-)

124
Q

universal recipient

A

AB (AB+)

125
Q

what occurs in blood transfusions

A

must ensure that transfused blood doesn’t have an antigen present that the recipient blood has antibodies for

126
Q

drugs for Herpes

A

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
Q

drugs for HepC

A

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
Q

HepB overview

drugs

A

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
Q

Influenza overview

drugs

A

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
Q

H1 antagonists

A

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
Q

major groups of H1 antagonists

effects

A

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
Q

H2 antagonist

A

H2 receptor stimulation leads to secretion of gastric acid

produce blockade of receptors to treat gastric and duodenal ulcers

133
Q

anaphylactic reaction treatments

A

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
Q

drugs based on severity of allergic reaction

A

mild: antihistamines (H1 antagonists)
severe: epinephrine

135
Q

clinical presentation of antihistamine overdose, anticholinergic syndrome

A

CNS stimulation

insomnia, tremors, convulsions, confusion

136
Q

Prednisone MoA

safe use

A

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
Q

NSAID and ASA MoA

A

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
Q

clinical effects of COX1 inhibition

A

good: protection against MI and stroke
bad: gastric ulcers, bleeding, renal impairment

139
Q

clinical effects of COX2 inhibition

A

good: suppress inflammation, alleviate pain and fever, protect against colorectal cancer

140
Q

Clinical uses of NSAIDs

A

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
Q

precautions for NSAIDs

A

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
Q

averse side effects of NSAIDs

A

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
Q

NSAID effects on platelet aggregation

A

for nonselective anti-inflammatories, such as aspirin, there is inhibition of platelet aggregation that COX1 stimulates
leads to bleeding

144
Q

drug-food interactions for NSAIDs

A

do not drink alcohol while using

145
Q

autoimmunity

causes?

A

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
Q

autoimmune diagnosis

A

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
Q

key treatment for autoimmune disorders

A

immunomodulation

148
Q

bullous pemphigoid

A

large fluid filled blisters on skin, typically in areas that flex

149
Q

vitiligo

A

loss of melanin in skin

150
Q

polymyositis

A

effects any muscle tissues, causes irritation and inflamm. making movement difficult

151
Q

Myasthenia Gravis

A

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
Q

Multiple Sclerosis

A

autoantibodies and self reactive T cells cause demyelination of nerve cells causing nerve signals to not be transported normally

153
Q

organ specific autoimmune disorders

A 
DM type 1
Goodpasture's
MS
Graves'
Hashimoto's thyroiditis
Hemolytic anemia
Addison's disease 
Vitiligo
Myasthenia Gravis
154
Q

systemic autoimmune disorders

A 
RA
Scleroderma
SLE
Primary Sjogren's
Polymyositis
155
Q

Alloimmunity

A

reactions due to non-self, but same species antigens

blood transfusions

Patho And Pharm (6 decks)

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