Glossary of Block V, Week VII
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- 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.
- 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?
- 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?
- I, II, III
- 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
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
autoimmune hemolytic anemias
- Which hallmark thing is seen in complement mediated and opsonization cytotoxicity?
- MAC (membrane attack complex)
- describe the mechanism of antibody dependent cell mediated cytotoxicity
- DOES NOT INVOLVE COMPLIMENT
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
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)
3. Myobacterium avium
- 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)
- 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
- what are the two organ systems effected in Goodpasture's syndrome?
- 1. Renal (Glomerulus)
"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. attached to a surface
- 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
- 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
(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
- 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)
- 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
- 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?
- SYNERGISTIC EFFECTS
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
3. airway hyperresponsiveness
- NO EFFECT ON ANY OF THOSE!
(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)
- 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
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
MUST MONITOR SERUM LEVELS
- 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?
- 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
EQUAL IN EFFICACY
- 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?
- MAST CELL STABILIZER
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
- 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?
- PHOSPHOLIPASE A2 INHIBITOR
(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)
- 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?
- REDUCES INFLAMMATORY CELLS
(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
- corticosteroids with mineralcorticoid activity have what effects?
- ALDOSTERONE LIKE EFFECTS
Na+ reabsorption w/ K+ elimination
- Ca++ effects (reduced GI absorption, increased urinary excretion)
- Cardiovascular effects of glucocorticoids?
- - HTN
- 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
- 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)
- 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)
- 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?
2. helminths (nematodes)
- 1. single celled
- 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. amoebae
- what are the top two locations in a human for parasite colonization?
- 1. intestinal
- 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)
- 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)?
- 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"
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