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253 Cards in this Set

  • Front
  • Back
what are the cellular components of the immune system derived from?
pluripotent hematopoietic stem cells
at six weeks, hematopoiesis shifts from _____ to ______.
fetal liver to bone marrow
Where do T cells develop?
Where do B cells develop?
T cells - thymus
B cells - Bone marrow
Cell mediated immunity involves which type of lymphocyte?
T cells
humoral immunity involves which type of lymphocyte?
B cells
regarding costimulation of T cells - what happens if...
1. there is no 2nd signal?
2. there is a 2nd signal?
1. T cells will not be stimulated
2. T cells will produce IL-2: this causes differentiation of T cells into effector cells and memory cells.
what is the first cosignal involved in T cell stimulation?
CD4 binding to MHC class II
CD8 binding to MHC class I
what are the 2 subsets of CD4 T cells?
Th1 (T helper 1)
Th2 (T helper 2)
1. What does Th1 secrete?
2. What is the Th1 response important in?
1. IL-2 and IFN-gamma
2. important in:
delayed hypersensitivity rxns.
macrophage activation
1. What does Th2 secrete?
2. What is the Th2 response important in?
1. IL-3, 4, 5,
2. aids in synthesis of IgE and eosinophils
What type of antibodies do B cells have on their cell surface?
(membrane bound) IgM
which cell type of the immune system is able to kill virally infected cells w/o previous sensitization?
NK cells
what are the two major types of APCs in the immune system?
dendritic cells
1. macrophages present their antigens to?
2. dendritic cells present their antigens to?
1. T cells
2. activated CD4+ cells (interdigitating)
B cells (follicular)
macrophages look for what coating (opsonization) molecules?
1. where are interdigitating dendritic cells found?
2. where are follicular dendritic cells found?
1. under epithelia and in interstitium
2. in germinal centers of lymphoid follicles
Histocompatibility class I is effective against what type of microbe?
(It binds to peptides synthesized within cells)
Histocampatibility class II is effective against which class of microbes?
exogenous microbes, bacteria
(binds peptides that are internalized and processed in lysozomes)
which histocompatibility class is expressed on all nucleated cells and platelets?
MHC Class I
which histocompatibility complex is expressed on APCs? (B cells, macrophages)
MHC Class II
which types of hypersensitivity are antibody mediated?
describe a type I hypersensitivity
First and Fast
antigen binds to IgE on mast cells and basophils: this triggers release of vasoactive amines.
What are some primary mediators in a Type I hypersensitivity?
1. Biogenic amines(Histamines)
2. enzymes (chymase, tryptase, acid hydrolase)
3. Proteoglycans (heparin and chondroitin sulfate)
what are the actions of histamine in a type I hypersensitivity?
smooth muscle contraction resulting in increased vascular permeability. This results in increased secretions
what are the actions of enzymes such as chymase, tryptase and acid hydrolase in a type I hypersensitivity?
cause tissue damage by generating kinins and complement fragments
Leukotrienes C4 and D4 are secondary mediators in a type I hypersensitivity. what is their role?
chemotactic for neutrophils, eosinophils, monocytes
which secondary mediator of a type I hypersensitivity causes increased bronchospasm and mucus secretion?
Prostaglandin D2
which secondary mediator of a type I hypersensitivity causes platelet aggregation, histamine release, bronchospasm, vasodilation and vascular permeability?
PAF (Platelet Activating Factor)
what is the role of eosinophils in the type I hypersensitivity response?
amplify and sustain inflammatory response
(they produce major basic protien and eosinophilic cationic protien)
What is atopy?
a genetically determined susceptibility to a type I hypersensitivity reaction
what changes are seen in the serum levels of an atopic individual?
higher IgE levels
more IL-4 producing Th2 cells
give some examples of type I hypersensitivity reactions
hives, allergies
local wheal and flare
describe the general mechanism of a type II hypersensitivity reaction
IgM and IgG bind to antigen of "enemy cell" leading to cytotoxicity
what are the three mechanisms of antibody mediated injury in a type II hypersensitivity?
1. Compliment mediated and Opsonization
2. Antibody Dependent Cell Mediated Cytotoxicity (ADCC)
3. Antibody Mediated Cellular Dysfunction
Give some examples of Complement mediated and opsonization pathologic conditions seen in type II hypersensitivity rxns.
transfusion reactions
drug reactions
autoimmune hemolytic anemias
erythroblastosis fetalis
Which hallmark thing is seen in complement mediated and opsonization cytotoxicity?
MAC (membrane attack complex)
describe the mechanism of antibody dependent cell mediated cytotoxicity
IgG coats target cells. then nonsensitized cells (monocytes, neutrophils, NK cells) kill the target cells.
describe the mechanism of antibody mediated cellular dysfunction
antibody impairs cell function without cell injury or death
Give two examples of a type II hypersensitivity caused by antibody mediated cellular dysfuntion.
1. Myasthenia Gravis (antibodies impair Ach receptor)
2. Graves Disease (hyperthyroidism)
cyroglobulinemias, Henoch-Schonlein purpura, SLE and Rheumatoid arthritis are examples of?
Type III hypersensitivity
describe the mechanism of a type III hypersensitivity rxn
TYPE III = III things stuck together (antigen-antibody-compliment)
antigen-antibody complexes activate compliment, which attracts neutrophils. Neutrophils release lysosomal enzymes.
what happens to the immune complex formed in the type III hypersensitivity rxn?
it is deposited on tissues
two types of inflammatory reactions can occur in a type III hypersensitivity.
1. Which one is systemic?
2. Which one is local?
1. Serum Sickness
2. Arthrus rxn
compare the timeframes of the arthrus reaction to serum sickness.
arthrus rxn: appears in 2-6 hrs.
serum sickness: appears in 6 days, lasts at least 10.
describe the three phases of serum sickness.
1. Phase I: Immune complex formation
2. Phase II: Immune complex deposition
3. Phase III: Immune complex mediated inflammation
describe the arthus rxn
antibody-antigen complexes cause local tissue necrosis. result is edema, hemorrhage, fibrinoid necrosis.
antibodies are not involved in a type IV hypersensitivity rxn. What, then, initiates this rxn?
initiated by soluble circulating antigens
these antigens activate T cells
what are the two types of Type IV hypersensitivity rxns and which cell types mediate them?
1. Delayed-type hypersensitivity (CD4+)
2. Direct T cell toxicity (CD8+)
what is the classic example of a delayed type hypersensitivity?
Describe the time frame of this example
tuberculin reaction
redness, induration -> 8-12 hrs
peaks 24-48 hrs
transplant rejection is an example of which type of hypersensitivity?
Type IV
myasthenia gravis is an example of which type of hypersensitivity?
Type II (cytotoxic)
SLE is an example of which type of hypersensitivity?
Type III (Immune complex)
Sjogren syndrome is an example of which type of hypersensitivity?
Type IV
rheumatic fever is an example of which type of hypersensitivity?
Type II (cytotoxic)
which type of hypersensitivity is a classic reponse to mycobacterium tuberculosis?
Type IV
when you see a granuloma you should think this kind of hypersensitivity
Type IV (delayed type)
what are some examples of delayed type (IV) hypersensitivity? (3)
contact dermatitis
type I diabetes
In the type IV hypersensitivity, CD8+ T cells kill cells by what two major mechanisms?
1. perforin/granzymes
2. Fas-Fas ligand
what are the glycoprotiens that stud the HIV viral envelope?
gp120 and gp41
gp 120 binds to the host CD4+ T cell
gp 41 penetrates membrane so HIV can enter host cytoplasm
what are the three subgroups of HIV-1?
1. M - most
2. O - outliers
3. N - neither
what type of host cells does HIV target? (3)
1. T cells
2. macrophages
3. dendritic cells
what must happen in order for a person to have "full blown AIDS"
CD4+ count must be below 500/mL
what is the significance of macrophages and HIV?
microphages are a virus factory (they don't lyse like the T cells do). So they carry the virus throughout the body (especially to the nervous system)
where in the body are the major sites of HIV infection and persistance?
lymphoid tissues
which organisms cause opportunistic pulmonary infection in AIDS? (3)

HHV8 causes what in AIDS patients?
1. P. carinii (jerovicii)(2/3)
2. CMV
3. Myobacterium avium

Kaposi's sarcoma
what type of antibodies are diagnostic of SLE?
antibodies to dsDNA and Smith(Sm) antigen
why would lupus pts have a false test for syphilis?
SLE antibodies against phospholipid B2-glycoprotien complex also bind cartiolipin antigen (used in syphilis test)
what is the antiphospholipid antibody syndrome seen in SLE?
procoagulant and anticoagulant features.
anticoagulant - antibodies interfere with PTT
procoagulant - associated with miscarriages, cerebral or occular ischemia
Besides SLE, what other type of lupus exists?
Drug-Induced Lupus
Which three drugs are associated with inducing Lupus?
What is the ANA targeted towards in drug-induced Lupus?
ANA is target towards histones
what is the most common autoimmune disease after SLE?
Sjogren's syndrome
what is the triad of symptoms commonly seen in Sjogrens syndrome?
Xeropthalmia (dry eyes)
Xerostomia (dry mouth)
in Sjogrens syndrome: what is observed in lacrimal and salivary glands?
lymphocytic infiltrate
serologic markers of Sjogren's disease?
SS-A (Ro)
SS-B (La)
significance of lymphocyte abnormality in Sjogren's syndrome?
*increased risk of B cell lymphoma
* increased occurance of another autoimmune disorder
what is the underlying pathology behind scleroderma?
- excessive collagen deposition in skin and internal organs
- caused by abnormal immune response resulting in growth factors that act on fibroblasts to stimulate collagen production.
what are the two types of scleroderma?
1. Diffuse
2. limited (CREST) form
1. what is the antibody type specific to diffuse scleroderma?
2. what is the antibody type specific to the CREST variant of scleroderma?
1. antibody to Scl-70
2. Anti-centromere antibodies
describe some skin/skeletal changes seen in Scleroderma (3)
1. Claw-like flexion deformity (Sclerodactyly)
2. Cutaneous ulceration
3. thick, tough skin (due to dense collagen in dermis)
describe two vascular changes that occur in scleroderma
1. thickening and fibrosis of vessel walls
2. occlusion by a thrombus
what are three renal changes seen in scleroderma?
1. cortical infarcts
2. fibrinoid necrosis of renal vessels
3. hypertension (30%)
how often are renal changes observed in scleroderma?
2/3 of scleroderma patients have renal symptoms
how often are GI tract symptoms seen in scleroderma

what are three GI symptoms seen in scleroderma?
90% of the time
esophageal dysfunction
Malabsorption syndrome
what are the two organ systems effected in Goodpasture's syndrome?
1. Renal (Glomerulus)
2. Pulmonary

"2 Good Pastures for this disease: Glomerulus and Pulmonary"
what type of hypersensitivity is Goodpasture's disease?
Type II

(2 good pastures = type 2)
1. In Goodpastures: describe the pattern of anti-glomerular basement membrane antibodies on immunoflourescence
2. In SLE: describe the pattern of antiglomerular basement membrane antibodies via immunoflourescence
1. linear staining
2. "wire loop" lesions
What are the three characteristics of a biofilm?
1. Attached to a surface
2. Secretion of EPS ("slime layer")
3. Altered phenotype
1. sessile
2. planktonic
1. attached to a surface
2. free
what is the connection between biofilms and bacterial resistance?
biofilms increase the resistance of the bacteria
why is biofilm more resistant than planktonic bacteria?
biofilm is a molecular filter
(therefore will not allow antimicrobial "through")
what is the tradeoff for bacteria in a biofilm that has antimicrobial resistance?
bacteria in a biofilm grow more slowly than planktonic bacteria
the property of a biofilm to sense when the minimal population has been achieved is called_________?
Quorum sensing
In quorum testing, what occurs once the minimal population has been achieved?
gene expression is regulated
which operon is associated with quorum sensing?
The Lux operon
where is the LuxR/LuxI regulatory (quorum) system seen?
it is seen in over 25 species of Gram negative bacteria
what are five examples of Biofilms causing human infections?
1. Native Valve Endocarditis
2. Otitis Media
3. Chronic Bacterial Prostatitis
4. Cystic Fibrosis
5. Peridontitis
which organism has an 80% colonization rate as a biofilm in Cystic Fibrosis?
P. auruginosa
P. auruginosa produces what molecule that forms the biofilm?
which two organisms most often form biofilms that cause native valve endocarditis?
what are some medical devices that commonly get biofilms?
Prosthetic Heart Valves
Central venous catheters
urinary catheters
(contact lenses, dental unit water lines)
why can't the host immune system get rid of these biofilm infections?
biofilm prevents access to the bacteria to be killed.
what toxic thing can bacteria in the biofilm release?
what is the "definition" of asthma?
chronic INFLAMMATORY disorder of the airways, usually associated with widespread but variable airflow OBSTRUCTION
at what time(s) of day would a coughing pattern make us suspicious of asthma?
* Night and early morning
(non-asthmatics usually don't experience that)
* always returns to baseline
What is the effect of inflammation on the bronchioles?
(bronchospasms & asthma easily triggered)
what occurs (cellular level)in the early asthmatic reaction?
allergen causes IgE to bind to mast cell. mast cell is activated and degranulates, releasing many inflammatory factors. this results in acute bronchoconstriction
what contents are released when a mast cell degranulates?
chemotactic factors (for neutrophils and eosinophils)
what physical symptoms are associated with acute airway obstruction? (3)
1. bronchoconstriction
2. microvascular leakage with edema
3. reduced mucous clearance
compare the timeframes of the acute and late asthmatic reaction
acute - onset: minutes
lasts 1.5-2 hrs.

chronic - onset: 2-8 hrs
lasts: days to weeks
what are the cellular "happenings" responsible for the late allergic reaction?
In the acute phase, cytokines are released from mast or T cells. they attract eosinophils and neutrophils -> they get there and induce inflammation: this results in late allergic rxn.
what physical symptoms are associated with the late asthmatic reaction?
submucosal edema
mucous hypersecretion
increased hyperresponsiveness
what class of drug do we use to target:
1. the early phase of an asthma reaction
2. the late phase of an asthma reaction
1. bronchodilators (most often B2 agonists)
2. antiinflammatories
regarding corticosteroid use in asthma: which route would you administer for:
1. an acute reaction
2. long term control
1. systemic (want to prevent a late phase reaction)
2. inhaled (local)
what are the three classes of bronchodilators used to treat acute asthma?
1. B2 agonists
2. Anticholinergics
3. Methylxanthines
what is the MOA of Theophylline?
*phosphodiesterase (PDE) inhibitor*
prevents the breakdown of cAMP resulting in cAMP accumulation. Excess cAMP stimulates bronchorelaxation.
MOA of anticholinergics?
anticholinergics inhibit the parasympathetic effects (vagal tone = bronchoconstriction)
Parasympathetic effects are mediated by Acetylcholine
do Beta agonists have antiinflammatory activity?
NO, they do not have any clinically significant antiinflammatory activities
what are the effects of B2 agonists combined with steroids?
1. B2 augments inhibitory activity of steroids on cell activation
2. steroids increase B2 receptors
3. inhibit inflammatory mediator release from airway smooth muscle cells.
B2 agonists have what effect on:
1. late allergic response
2. inflammation
3. airway hyperresponsiveness
(this is why they can't be prescribed as monotherapy)
which bronchodilator has equal B1-B2 activity?
which bronchodilators are B2 selective (3)
1. Albuterol (least selective of the 3)
2. Salmeterol
3. Formoterol
which bronchodilator is the anticholinergic?
1. which B2 agonist is used for acute asthma?
2. which B2 agonists are long acting and therefore are used for long term asthma treatment?
1. Albuterol
2. Salmeterol, Formoterol
what is the medication of choice for EIB (excercise induced bronchospasm)?
Short Acting B2 Agonists
To treat COPD exacerbation: what medication can we combine with a short acting B2 agonist?
in what form do Salmeterol and Formoterol come?
powder for inhalation
*used for chronic maintenance of asthma*
adverse effects of B2 agonists?
when prescribing salmeterol: what must you educate patient about?
* recognizing signs of deteriorating asthma control, then seek medical help*
*also emphasize that it is not an acute bronchodilator*
(a sign of deteriorating asthma control is more frequent need for the short acting bronchodilator)
what are the two sites/mechanisms of action of Theophylline?
1. nonselective PDE inhibition
2. competitive antagonist of adenosine receptors (results in bronchodilation)
why is theophylline not used so much in asthma anymore?
- what is it still used for?
it is TOXIC (small therapeutic index)
- still used for COPD
why is theophylline useful in COPD?
1. respiratory stimulant
2. bronchodilation
3. increase diaphragmatic contractility
what is one reason why theophylline is so toxic?
it is involved with the P450 system
what is the therapeutic range of theophylline?
5-15 mcg/mL
would we use theophylline in chronic or acute asthma?
regarding anticholinergics:
1. do they have antiinflammatory activity?
2. which is a stronger bronchodilator: this or B2 agonists?
1. no
2. B2 agonists
what is the difference between ipratropium and tiotropium?
ipratropium - 4x per day
tiotropium (Spiriva) - once daily
what type of asthma attack would anticholinergics be useful for?
acute asthma attacks
what can be combined with ipratropium to make it more useful in the treatment of acute asthma and COPD?
(Combivent, DuoNeb)
what are the 3 classes of antiinflammatory agents used in asthma treatment?
1. Corticosteroids
2. Mast cell stabilizers
3. Leukotriene modifiers
what are the two types of allergic rhinitis?
1. SAR - seasonal allergic rhinitis (outdoor allergens)
2. PAR - perennial allergic rhinitis (indoor allergens)
what is the chronic allergic respiratory syndrome hypothesis?
the thought that rhinitis and asthma may be manifestations of one syndrome
do antihistamines treat nasal congestion?
that is why we have decongestant/antihistamine combinations
which histamine receptor is relevent to s/s of allergic rhinitis?
(H2 = gastric acid)
what is the difference between first and second generation antihistamines?
first generation - drowsy
second generation - non-drowsy
what is the only OTC second generation antihistamine?
Loratadine (Claritin)
MOA of antihistamines?
competitive Histamine antagonist at the H1 receptor
(not currently true - inverse agonist of H1 receptor)
other effects of antihistamines besides inhibition at H1 receptor?
local anesthetic effect
which antihistamine is known for the serotonergic blockade?
which antihistamine is known for the local anesthetic effects?
diphenhydramine (benadryl)
(seen in Calamine)
which second generation antihistamine is the only one to have absolutely NO sedation effects?
fexofenadine (Allegra)
which effect of antihistamines is responsible for the most adverse effects?
anticholinergic activity causes the most adverse effects
(2nd generation has less anticholinergic activity)
what is the molecular explanation for the first generation antihistamines causing sedation (and the 2nd generation not)?
1st generation easily penetrate the BBB - they are not recognized by the efflux pump so they build up there.
(2nd gen. has little BBB crossing)
what is Azelastine?
H1 antagonist nasal spray
(not often used due to many adverse effects)
what is the MOA of decongestants?
VASOCONSTRICTION in mucosa of respiratory tract
a-adrinergic receptor agonist
what is the most common oral decongestant?
what about intranasal decongestants?
what is often seen in intranasal decongestant use?
rebound rhinitis
(headaches and worse congestion appear 3-5 days after use)
MOA of cromolyn?
prevents release of mediators from mast cells.
effective for prophylaxis of asthma/acute allergic response
what are two other uses (besides allergies) of first generation antihistamines?
motion sickness
sleep aid
what is considered the "gold standard" of treatment for Allergic Rhinitis?
Intranasal Steroids (Corticosteroids)
(prophylaxis of AR)
what is an adverse effect of intranasal steroids that is rare but serious when it happens?
septal perforation
(advise administration away from septum)
MOA of corticosteroids?
(inhibit formation of arachadonic acid from membrane phospholipids)
inhibits the synthesis of virtually all cytokines (thereby inhibiting inflammation)
what is the main leukotriene modifier used to treat seasonal AR?
Montelukast (Singulair)
what is an advantage of leukotriene inhibitors (vs. intranasal steroids)?
LIs can be used at a young age
MOA of leukotriene inhibitors? (2)
- block leukotriene receptors (Zafirlukast, Montelukast)
- inhibit conversion of arachadonic acid to leukotrienes (lipoxygenase inhibitor)(Zileuton)
what is the only rhinitis medication that does not improve rhinorrhea?
what is the only rhinitis medication that does not improve congestion?
(antihistamines also have little effect)
classes of rhinitis medications that improve eye symptoms? (3)
LT inhibitors
Nasal steroids
In relation to treatment of asthma: which corticosteroid has more adverse effects?
ORAL - more effects
(low adv. effects with inhaled steroids)
how can the local adverse effects of inhaled corticosteroids be reduced?
- use spacers, chambers
- rinse mouth out after each dose (reduces candidiasis)
what drug can you add for increased efficacy of inhaled corticosteroids?
- Salmeterol/inhaled steroid (fluticasone)
- Formeterol/inhaled steroid
when would we use oral systemic corticosteroids in the treatment of asthma?
use for acute attacks
(intranasal steroids are a chronic maintenance dose)
what are the 2 mast cell inhibitors and when would they be used?
1. cromolyn sodium, nedocromil
2. used to prevent EIB, also used in allergic rhinitis and conjunctivitis
does cromolyn sodium function as a bronchodilator?
it functions as an NSAID
what is the name of the pathway that yields leukotrienes?
Lipogenase pathway yields Leukotrienes
functions of leukotrienes? (3)
1. contraction of smooth muscle:
vasoconstriction -> increased vascular permeability
2. recruit and activate eosinophils and basophils in airway
3. increase mucous secretions
which is a more potent bronchoconstrictor: histamine or leukotrienes?
(1000 x more potent)
name the two LT receptor antagonists
name the leukotriene that is a 5-lipoxygenase inhibitor
which anti-asthmatic drugs are associated with Churg-Strauss Syndrome?
(unknown if causal)
what is omalizumab (Xolair)
new drug for moderate-severe allergy induced asthma (that is poorly controlled with inhaled steroids)
MOA of Omalizumab?
monoclonal Ab that binds to IgE - this prevents binding of IgE to mast cells and basophils
1. how is omalizumab administered?
2. adverse effects (2)
1. SubQ every 2-4 wks (long 1/2 life)
2. anaphylaxis, malignant neoplasms (0.4%)
what are the four classes of asthma?
1. Class I (Intermittent)
2. Class II (Mild Persistent)
3. Class III (Moderate Persistent)
4. Class IV (Severe Persistent)
what is the treatment of choice for intermittent (Class I) asthma?
inhaled, short acting B2 agonist
what is the treatment of choice for mild persistent (Class II) asthma?
low dose inhaled steroid
(for long-term control combine with long-acting inhaled B2 agonist)
what is the preferred long-term treatment of severe persistent asthma?
high dose inhaled steroid AND long acting B2 agonist
when does the peak serum concentration of cortisol occur?
between 6 and 8 AM
if you wanted to minimize the effects of cortisol the most, when would you administer it?
in the evening
(negative feedback will inhibit ATCH and cortisol from peaking in the morning)
if you wanted to maximize the effects of cortisol when would you dose it?
in the morning
(Mimic natural cortisol peak - produce less adrenal suppression)
how do corticosteroids get to the nucleus and alter protein synthesis
- diffuse across lipid bilayer
- binds to intracellular cytoplasmic receptors/activate the receptor
- glucocorticoid/receptor complex translocates to nucleus
- binds to DNA: either stimulates or represses genes involved in synthesis of protiens
what is the effect of glucocorticoids on neutrophils?
- Neutrophilia (lots of bands)
can alter CBC when looking for infection
- little effect on function
what cells do glucocorticoids reduce?

(also a decrease in function)
Why do glucocorticoids have such widespread activity?
inhibit phospholipase A2, a precursor for many inflammatory mediators
what effect do glucocorticoids have on blood glucose?
INCREASE blood glucose
- watch for hyperglycemia or diabetic induced state
Lipid effects of glucocorticoids
redistribution of body fat
- buffalo hump
- moon facies
- supraclavicular area
Skin effects of glucocorticoids
thinning of skin
easy bruising
corticosteroids with mineralcorticoid activity have what effects?

Na+ reabsorption w/ K+ elimination
- Ca++ effects (reduced GI absorption, increased urinary excretion)
Cardiovascular effects of glucocorticoids?
- increased vascular reactivity to vasoactive substances (increases a-adrinergic receptors = vasoconstriction)
skeletal muscle effects of glucocorticoids?
- skeletal muscle wasting and weakness (myopathy)
(mostly proximal limb muscles)
what are the advantages of using synthetic corticosteroids?
- greater antiinflammatory potency
- little or no mineralcorticoid activity
- increase or decrease absorption
- longer 1/2 lives
1. what is the most common oral corticosteroid used?
2. what is the most common IV, IM corticosteroid?
1. prednisone
2. Methylprednisolone
which corticosteroids have the highest mineralcorticoid activity?
(highest Na+ retaining potency)
which corticosteroids have the lowest antiinflammatory potency and the highest equivalent dose?
short acting corticosteroids?
intermediate acting corticosteroids
what is the difference between prednisone and prednisolone?
prednisone must be metabolized to an active metabolite for activity, prednisolone doesn't
uses of triamcinolone?
joint injections
IM injections (ie. allergy)
long acting corticosteroids?
dexamethasone (oral or IV)
betamethasone (inhaled/intranasal)
a cushingoid like adverse effect is...?
redistribution of body fat in the characteristic manner
what are some ocular adverse effects of glucocorticoids? (3)
infections (with local eye drops)
which musculoskeletal adverse effect, if we see it, we can be almost sure it was caused by corticosteroids?
aseptic necrosis of femoral or humeral head
what is the mechanism of steroid-induced osteoporosis?
- decreased absorption of Ca++ and PO4(secondary hyperparathyroidism)
- inhibition of osteoblasts
what is the time frame of steroid induced osteoporosis?
6-12 mo. - rapid bone loss
what is the prednisone dose that (above it) significant bone loss will occur?
5 mg
how can we prevent steroid induced osteoporosis
- supplemental Ca++ intake
- supplemental vitamin D
- raloxifene (SERM)
- Biphosphonates
- Calcitonin nasal spray
what happens if steroid withdrawal is not tapered?
adrenal suppression will occur
what is considered long term steroid use?
>4 wks
takes HPA axis over a year to return to normal function
signs/symptoms of a steroid withdrawal that is too rapid?
- addison's like s/s
(feel horrible, ORTHOSTATIC HYPERTENSION, neurological symptoms)
what are three things you can do to lower the adverse effects and HPA suppression?
1. Shortest term and lowest dose
2. alternate day administration
3. early morning dosing
how many cells in the following parasites?
1. protozoa
2. helminths (nematodes)
3. arthropods
1. single celled
2. multicellular
3. multicellular
ascaris is an example of?
a helminth (ascaris)
how can parasites be identified in the human host (in the lab)? (2)
blood smears
"stylized" eggs in feces
what is the name of the host type where sexual reproduction occurs?
definitive host
where do protozoa undergo sexual and asexual reproduction?
both in definitive host
where do helminths undergo sexual and asexual reproduction?
sexual - definitive host
asexual - non-definitive host
protozoa that move by..
1. ameboid
2. cilia
3. flagella
4. none
...are called
1. amoebae
2. ciliates
3. flagellates
4. sporozoans
what are the top two locations in a human for parasite colonization?
1. intestinal
2. blood
what is the name of the protozoa that causes malaria?
what is the definitive host of the plasmodium spp?
once plasmodium is injected into the human - where does it go?
the liver
after the liver - where does the plasmodium go?
to the RBCs
how is plasmodium transferred?
mosquito bites infected human, blood with protozoa enters GI tract of mosquito. plasmodium transforms and enters salivary gland - then mosquito bites an uninfected person
what are the two categories of helminths?
1. platyhelminthes (flatworms)
2. Nematodes (roundworms)
two groups of flatworms (Platyhelminthes)?
trematodes (flukes)
cestodes (tapeworms)
type of roundworm?
subtype of medical interest?
Annelids (segmented worms)
leech is only one of clinical interest.
what characteristic do all or most trematodes have in common? (3)
1. two anterior suckers, one ventral sucker
2. most are hermaphroditic
3. all must infect a mollusc (snail) host.
what is a clinically important trematode (flatworm)?
(blood fluke)
what is different about schistosoma compared to other trematodes?
they are not hermaphroditic
they mate for life
how does schistosoma infect humans?
lives in (snail in) water, then leaves snail to penetrate the skin of a human that is in that water
regarding cestodes (tapeworms):
the adults are divided into what 3 segments?
1. scolex (head)
2. strobilia (segmented body)
3. proglottids (at neck - each a self contained hermaphroditic reproductive unit)
how does schistosoma evade the immune system?
the eggs absorb human antigens onto their surfaces.
name a type of cestode (tapeworm)
Taenia saginata
(tapeworm occupies beef)
what is the role of the proglottid in a cestode?
old mature proglottids rupture and disintegrate -> releases eggs that exit with feces.
Taenia - how is it transmitted to humans?
from grass - to cattle - burrows in muscle of cattle - humans eat cattle
SOLUTION: cook meat well
which type of helminth has both an "in" and "out" hole?
Nematodes (roundworms)
where do nematodes like to colonize?
the intestine
what is an example of a nemotode that lives in human muscle but shouldn't be there?
(from uncooked pork)
what is unique about the sex of nematodes?
no hermaphrodites
all separate sexes, even have a reproductive system!
what is the most common intestinal nematode?
"giant roundworm of man"
Ascaris lumbricoides
what is a place ascaris likes to colonize?
the lungs, respiratory system and throat!
how does hookworm get into humans?
bare feet
(larva lay in soil)
what is the memory key for symptoms of SLE?
Immunoglobulins (anti-dsDNA, antiSm, antiphospholipid)
Malar rash
Discoid rash
Antinuclear antibody
Mucositis (oropharyngeal ulcers)
Neurologic disorders
Serositis (pleuritis, pericarditis)
Hematologic disorders
Renal disorders